case study 81 acne vulgaris

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Case 81 – Acne vulgaris

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Case-based learning: acne vulgaris

Causes, diagnosis and management options for a range of patients, including those with mild or moderate acne.

JL / Shutterstock.com

Acne is a common skin condition that affects 90% of people at some point during their teenage years [1] . Although predominately an adolescent condition, acne can persist into adult life. Estimates of the prevalence in those aged 40 years and over have ranged from 26% in females and 12% in males, to more than 40% in both sexes [2] , [3] . Research suggests that acne can be associated with significant psychological morbidity, impair the individual’s quality of life and can lead to suicide ideation [4] , [5] , [6] .

Pathophysiology

Acne is a disease of the pilosebaceous follicles (PSF) that are present over the surface of the skin, except for the palms of the hands and soles of the feet. There is a much higher concentration of PSF in the T-zone of the face (i.e. the forehead and nose), the chest and the back.

Although the precise cause of acne remains unclear, at least four factors are implicated in the pathophysiology:

• The release of inflammatory agents in the skin;
• Proliferation of the anaerobic organism Cutibacterium acnes (formerly known as Propionibacterium acnes ), which is present within functionally blocked follicles;
• An increased production of altered sebum;
• Abnormal keratinocyte proliferation and differentiation (ductal hypercornification or comedogenesis).

An inflammatory response is also believed to precede abnormal keratinocyte proliferation [7] . C. acnes can activate toll-like receptors (TLRs) that are present on the surface of keratinocytes and monocytes. These receptors form part of the innate immune system, and the stimulation of TLRs on monocytes and keratinocytes release the pro-inflammatory cytokines interleukin (IL)-8 and IL-12 [8] .

In addition, C. acnes has several other effects, including the production of lipase enzymes that act as chemoattractant for neutrophils [9] and the release of tumour necrosis factor alpha and various proteases and hyaluronidases that contribute towards tissue injury [10] , [11] (see Figure 1 and Figure 2). 

Figure 1: Structure of a blocked pilosebaceous follicle

The androgen-mediated increased output of altered sebum serves as a substrate for Cutibacterium acnes , which degrades sebum triglycerides, releasing irritant fatty acids that may induce comedogenesis. Epithelial keratinocytes lining the pilosebaceous follicle undergo abnormal desquamation and block the follicular opening. Increased production of altered sebum allows C. acnes to flourish in a blocked follicle

Figure 2: Actions of Cutibacterium acnes

Cutibacterium acnes within the blocked follicle activates toll-like receptors (TLRs) on monocytes and keratinocytes inducing release of pro-inflammatory cytokines. Additional agents produced by C. acnes contribute towards tissue damage as well as initiation of comedogenesis

The onset of adolescence is characterised by an increase in the production of sex hormones (mainly androgens) that cause sebaceous gland hyperplasia with a corresponding increase in the output of sebum. This gives the skin a greasy appearance and, while this is the first clinical symptom of acne, it is not a prerequisite. It is believed that alterations in the composition of sebum, rather than the quantity, is associated with acne.

Changes in sebum composition include increased levels of squalene, alterations in the ratio of fatty acids and a reduction in the levels of linoleic acid [12] . Sebum serves as a substrate for C. acnes, which produces a lipase enzyme that hydrolyses sebum triglycerides into glycerol and free fatty acids [13] . Two fatty acids — palmitic acid and oleic acid — appear to be involved in the production of pro-inflammatory cytokines, which can contribute to inflammation in acne, as well as ductal hypercornification [14] , [15] .

The final factor is abnormal desquamation (shedding) of the epithelial keratinocytes lining the PSF. The main driver for comedogenesis remains unclear but in vitro work with isolated sebaceous glands has shown that peptidoglycan, a component of the C. acnes cell wall , activates keratinocyte TLR-2, stimulating the release of interleukin-1 (IL-1), which leads to comedone formation [16] . Indeed, the addition of IL-1 to isolated PSFs leads to comedone formation [17] . 

Types of acne

The main inflammatory lesions (see Figure 3) are:

• Papules — erythematous lesions, less than 5mm in diameter;
• Pustules — white/yellow-fluid-filled lesions, less than 5mm in diameter;
• Nodules — painful, solid lesions deep within the skin, larger than 5mm in diameter, with varying degrees of erythema. Can lead to scarring;
• Cysts — similar to nodules but filled with pus. Can lead to scarring.

Figure 3: Types of acne

Source: Source: Primary Care Dermatology Society

Comedogenesis leads to the blockage of the PSF and the earliest acne lesion, a ‘microcomedone’, from which all other acne lesions subsequently develop. If this blockage occurs close to the surface of the skin, the resultant keratinocyte plug causes distension of the follicular orifice and melanin present within the desquamated cells reacts with the atmosphere and turns black. This produces open comedone (known as a ‘blackhead’; see Figure 4), whereas if the blockage occurs within the lumen of the PSF, then a closed comedone (or ‘whitehead’) is formed. Closed comedones can remain stable or progress to become inflammatory lesions.

Figure 4: Open comedones

Source: St Bartholomew’s Hospital / Science Photo Library

Causes of acne 

There is evidence for a link between genes and acne. By using genetic modelling based on acne severity scores, one study showed that 81% of the variance of acne could be attributed to genetic factors [18] . Furthermore, a case-controlled study in patients in China found that the risk of acne occurring in a relative of a patient with acne was significantly greater than in unaffected relatives [19] . A more recent study identified further genomic loci at which genetic variation is associated with acne susceptibility [20] . 

Patients often perceive that diet has an impact on acne, with one study reporting that 92% of patients felt that diet affected their condition [21] . Although the evidence base is controversial, foods with a high glycaemic index (e.g. white bread, cakes and biscuits), as well as milk and dairy products, are thought to aggravate acne [22] , [23] , [24] . It has been suggested that consuming high glycaemic index foods results in an insulin-triggered rise in free insulin-like growth factor-1 (IFG-1), which elevates androgens, sebum synthesis and, ultimately, the development of acne [25] . Indeed, it has been found that patients with acne consume more carbohydrate [26] and that lowering the glycaemic index of the diet reduces levels of IGF-1 [27] . Furthermore, when patients with Laron syndrome, who lack IGF-1, were treated with IGF-1, they developed acne [28] . 

Drug-induced acne

A wide range of drugs have been documented as causing an acne-like eruption, including oral corticosteroids, anabolic steroids, progestogens, lithium and anti-epileptics [29] . Clinically, drug-induced acne is defined by a sudden onset of a monomorphic eruption of inflammatory papules and pustules that are pruritic and follicular, with an absence of comedones [30] . 

Polycystic ovary syndrome (PCOS) is a common endocrine disorder of unknown aetiology [31] . PCOS often first presents during adolescence alongside hyperandrogenism symptoms, such as acne, and hirsutism and/or anovulation. Acne occurs in 10–34% of women with PCOS [32] .

Lifestyle factors

Several lifestyle factors thought to be associated with acne include:

• Smoking  — there is conflicting evidence about the link between smoking and acne; one study found that older women who are smokers have a greater incidence of comedonal acne [33] , whereas another study found no association [34] ;
• Cosmetics  — it is considered that cosmetics can worsen acne severity by effectively blocking the PSFs [35] . It is generally advised that patients use make-up products that are labelled ‘non-comedogenic’; 
• Stress  — evidence suggests that acne can worsen during periods of stress [36] . One study identified that sebocytes have receptors for corticotrophin-releasing hormone and other neuroendocrine factors, which may explain the link [37] .

Case studies

Case study 1: mild acne.

Jessica* is a 15-year-old girl who attends the pharmacy one day after school. She spends time looking at the shelves of facial washes. You approach her and ask if she needs any assistance. She asks for something to treat her spots and you offer to take her into the consultation room. On examination, you notice that she has several open and closed comedones on her face with a small number of inflammatory lesions. When asked, she says that she does not have acne on her chest or back.

Jessica asks you to recommend a suitable facial wash to help get rid of her spots.

How should you respond?

Assessment and diagnosis

Your examination has revealed that the patient has mild, predominantly comedonal acne.

Treatment options

Guidelines state that a topical retinoid, benzoyl peroxide (BPO) or azelaic acid show the best efficacy in mild-to-moderate comedonal acne [38] . Therefore, a BPO formulation would be an appropriate initial over-the-counter treatment and is available as a 5% gel or a 10% wash. The drug acts via oxidation and the formation of free radicals producing comedolytic, antibacterial and anti-inflammatory effects [39] .

Advice and recommendations

The patient should be warned about common side effects, such as irritation and bleaching of fabrics [40] . Recommend that they use an adapalene-BPO gel and suggest that it is applied roughly 15 minutes after washing with soap and warm water, and then removed a few hours later to minimise irritation [41] .

If the patient prefers to use a wash, the product should be applied to the skin and left in contact for a few minutes before rinsing off. The dryness or skin irritation from BPO can be managed using emollients, in particular, products labelled as ‘oil-free’ or ‘non-comedogenic’, which often contain either dimethicone or cyclomethicone [42] .

Although the patient wants to use a facial cleanser, the value of these agents in acne remains unclear, with one review concluding that it was difficult to make any firm recommendations given the lack of well-performed studies [43] . However, a recent study using a 5% BPO gel combined with a cleanser and sun protection moisturiser resulted in high levels of patient satisfaction and treatment efficacy [44] .

The patient should be advised to apply BPO to the whole of the affected area rather than individual lesions — histological evidence shows that ‘normal’ looking skin has features of microcomedones [45] .

Finally, advise the patient to continue with the treatment for at least six weeks (a large randomised trial found that most of the treatment benefits occurred within this time frame) [46] .

Potential outcome of the advice

If there is no response to the treatment after six weeks or if the acne worsens, the patient should be referred to their GP.

Case study 2: moderate acne

Jonathan* is a 30-year-old local estate agent who works near your pharmacy. He has had with acne since adolescence but has never really bothered treating his condition. However, he has recently started a new relationship and is feeling embarrassed about his acne and asks you for an effective cream.

During a private consultation, the patient removes his shirt and, in addition to many inflamed lesions on his face, you notice a large number of papules on his back and chest, as well as the presence of some scarring on his face and chest.

Owing to the difficulty in applying topical treatments over a widespread area, referral to a GP is required. In addition, the acne has already caused some scarring, which is common, for instance, one study of nearly 1,000 patients found some level of facial scarring in 87% of patients [47] .

The most appropriate treatment for this patient would be the use of an oral antibiotic – either doxycycline or lymecycline (in preference to minocycline or tetracycline) – combined with a topical retinoid [38] . Benzoyl peroxide (BPO) can be added to the regime to help reduce the likelihood of resistance developing to the oral antibiotic [48] .

Typically, doxycycline 50–100mg daily and lymecycline 300mg daily are prescribed. Oral antibiotics can have anti-inflammatory effects, including inhibition of neutrophil chemotaxis and inhibition of pro-inflammatory cytokines [49] . Topical retinoids, such as adapalene, tretinoin and isotretinoin, bind to membrane-bound retinoic acid receptors and this leads to normalisation of keratinocyte differentiation and cohesion, comedolysis and inhibition of comedone formation [50] .

Common adverse effects experienced by those taking oral antibiotics include vaginal candidiasis (in women), gastrointestinal upset and phototoxicity. Therefore, patients should be advised to take doxycycline with food to avoid UV exposure [51] .

Topical retinoids are also associated with adverse effects, including erythema, dryness, peeling and/or burning within the first two weeks of therapy [52] . In an effort to minimise these effects, advise the patient to apply a pea-sized amount of the retinoid to the entire affected area, every other day for the first 2–4 weeks of treatment. Furthermore, the retinoid can be left in contact with the skin for 30–60 minutes before washing off. Any further irritancy can be managed by applying a non-comedogenic emollient [53] .

Using the combination regime, the patient should expect to see some response after 6–8 weeks and, ideally, oral agents should not be continued for longer than 12 weeks [40] . If treatment with oral agents is ineffective, the patient should be referred for specialist assessment.

Case study 3: polycystic ovary syndrome-induced acne

Anna* is an overweight 17-year-old student who has recently been diagnosed with polycystic ovary syndrome (PCOS). She comes to the pharmacy with a new prescription for co-cyprindiol. You know from your records that Anna has previously had acne; she was prescribed doxycycline but it was ineffective. Anna mentions that she did not get much time to discuss her new diagnosis with the GP or how to take her new medicine, and asks you for advice.

There are no treatments specifically licensed for PCOS. Co-cyprindiol is given to manage the patient’s acne and is a suitable first-line treatment when someone is not planning to conceive. Co-cyprindiol serves a dual function, being an effective contraceptive (owing to ethinylestradiol), which helps to normalise menstrual irregularities, and an anti-androgenic agent, cyproterone acetate. This latter component competes with dihydrotestosterone for androgen receptors and, therefore, reduces testosterone production, which will improve acne and any hirsutism [31] . Alternatives to co-cyprindiol include combined oral contraceptives, which are also effective in treating acne [54] .

The patient should be advised to start taking their co-cyprindiol on the first day of their next period for 21 days and then to have a 7-day pill-free interval. Nausea and abdominal pain are common side effects and, therefore, advise the patient that if they experience any vomiting or diarrhoea, it can reduce the effectiveness of the contraceptive and additional protection should be used for at least seven days.

The drug needs to be continued for at least three months before any likely benefit can be seen. There is a risk of venous thromboembolism with co-cyprindiol; however, recent advice suggests that while the risk is 1.5–2.0 times greater with co-cyprindiol than contraceptives that contain levonorgestrel, the benefits of treatment outweigh the risks [55] .

Finally, it is helpful to advise the patient that lifestyle measures, such as a healthy diet, regular exercise and achieving a healthy weight, can improve symptoms of hyperandrogenism [56] .

*All cases are fictional.

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Am Fam Physician. 2019;100(8):475-484

Author disclosure: No relevant financial affiliations.

Acne vulgaris is the most prevalent chronic skin disease in the United States, affecting nearly 50 million people per year, mostly adolescents and young adults. Potential sequelae of acne, such as scarring, dyspigmentation, and low self-esteem, may result in significant morbidity. Typical acne lesions involve the pilosebaceous follicles and the interrelated processes of sebum production, Cutibacterium acnes (previously called Propionibacterium acnes ) colonization, and inflammation. Acne may be classified as mild, moderate, or severe based on the number and type of skin lesions. Multiple treatment agents and formulations are available, with each agent targeting a specific area within acne pathogenesis. Treatment selection is based on disease severity, patient preference, and tolerability. Topical retinoids are indicated for acne of any severity and for maintenance therapy. Systemic and topical antibiotics should be used only in combination with benzoyl peroxide and retinoids and for a maximum of 12 weeks. Isotretinoin is used for severe, recalcitrant acne. Because of the risk of teratogenicity, patients, pharmacists, and prescribers must register with the U.S. Food and Drug Administration–mandated risk management program, iPledge, before implementing isotretinoin therapy. There is limited evidence for physical modalities (e.g., laser therapy, light therapy, chemical peels) and complementary therapies (e.g., purified bee venom, low-glycemic-load diet, tea tree oil); therefore, further study is required.

Acne vulgaris is the most prevalent chronic skin disease in the United States, affecting nearly 50 million people. 1 Acne is most common in adolescents and young adults but may persist into the 30s and 40s at a cost of $3 billion. Sequelae of acne include scarring, dyspigmentation, depression, anxiety, and low self-esteem. Specific estimates of prevalence for psychiatric comorbidities vary, and further study is needed. 2 , 3

Pathogenesis

Acne vulgaris is a chronic disease originating within the pilosebaceous follicles. Four interrelated processes are involved: sebum overproduction, abnormal shedding of follicular epithelium, follicular colonization by Cutibacterium acnes (previously called Propionibacterium acnes ), and inflammation. 4 – 6

Sebum overproduction is the result of excessive androgen hormones or a heightened sebaceous gland sensitivity to normal levels of androgen hormones. 7 Inflammatory pathway activation is evident at all stages of acne progression. 7 There may also be a genetic component to acne. 8 Certain foods and drinks, particularly those with a high glycemic index (e.g., sugary drinks, starchy foods, highly processed foods) and skim milk, seem to affect acne severity. 9 , 10 Other factors that may be involved in the development or progression of acne include psychological stress, tobacco smoke, and damaged or unhealthy skin. 9 – 13

Classification

Acne lesions typically occur on the face, chest, or upper back. The lesions may be noninflammatory closed comedones (i.e., papules formed by the accumulation of sebum/keratin within the hair follicle; also called whiteheads); open comedones (i.e., distension of the hair follicle with keratin leads to opening of the follicle, oxidation of lipids, and deposition of melanin; also called blackheads); or inflammatory papules, nodules, pustules, and cysts. Inflammatory lesions result from follicle rupture triggering an inflammatory response. Based on the extent and types of lesions, acne severity may be classified as mild, moderate, or severe ( Figure 1,   Figure 2 , and Figure 3 ) . However, there is currently no universally accepted grading system for acne. 1 , 2 Several skin conditions should be considered in the differential diagnosis of acne ( Table 1 ) . 2

TOPICAL AGENTS

Acne treatment is based on severity and location on the skin ( Figure 4 ) . 2 Effective topical therapies are available over the counter and by prescription and come in multiple formulations (e.g., washes, creams, pads) and strengths, permitting individualized treatment. Table 2 , Table 3 , and Table 4 summarize the topical agents used in the treatment of acne. 1 , 2 , 14

Benzoyl Peroxide . Benzoyl peroxide is comedolytic, anti-inflammatory, and bactericidal against C. acnes . 15 Benzoyl peroxide is available over the counter and by prescription in multiple strengths and formulations, and can be used alone or in combination with topical antibiotics or retinoids. A reduction in acne lesion count may occur within days of initiating treatment with benzoyl peroxide. 15 Use of benzoyl peroxide itself does not induce bacterial resistance. 1 , 15 , 16 Benzoyl peroxide is safe to use during pregnancy. Adverse effects of benzoyl peroxide include burning, dryness, stinging, erythema, peeling, hypersensitivity, and bleaching of hair or clothing.

Topical Antibiotics . Topical antibiotics, including clindamycin 1% and erythromycin 2%, are commonly used for the treatment of mild to moderate acne in combination with benzoyl peroxide. Topical antibiotics possess anti-inflammatory and, depending on the formulation, bacteriostatic or bactericidal properties. 16 , 17 Clindamycin is favored over erythromycin because of the declining effectiveness of erythromycin, which is likely associated with emerging resistance of C. acnes . 16 – 19 To reduce the risk of resistance, use of topical antibiotics as monotherapy or maintenance therapy is not recommended, and the duration of therapy should be limited to 12 weeks. 16 – 19

Erythromycin and clindamycin are available in combination with benzoyl peroxide, and clindamycin is available in combination with retinoids. Use of combination agents is recommended to reduce the risk of resistance (benzoyl peroxide) and to enhance effectiveness (retinoids, benzoyl peroxide). 1 Topical antibiotics may have mild adverse effects, including burning, erythema, and pruritus, mainly when used in combination with benzoyl peroxide and retinoids. A rare serious adverse effect is Clostridium difficile colitis (clindamycin and erythromycin). 1

Retinoids . Retinoids are vitamin A derivatives recommended as a component in the primary treatment of noninflammatory acne and most inflammatory acne, regardless of severity. Retinoids are effective against microcomedo and comedo formation and have anti-inflammatory effects. 1 , 20 – 22 Retinoids are indicated as monotherapy for mild comedonal acne, in combination with other topical or oral agents for the treatment of moderate to severe acne , and as maintenance therapy once treatment goals are achieved and oral agents are discontinued . 1 , 14 , 17 , 20 – 23

Retinoids approved by the U.S. Food and Drug Administration (FDA) include adapalene (Differin), tazarotene (Tazorac), and tretinoin (Retin-A). Tazarotene is more effective than tretinoin or adapalene, although adapalene is less irritating than tazarotene. There are multiple formulations and strengths of tretinoin, and a gradual increase in strength minimizes skin irritation. 20 – 22 Although more costly, the topical combination agents clindamycin phosphate 1.2%/tretinoin 0.025% (Veltin, Ziana) and adapalene 0.1% or 0.3%/benzoyl peroxide 2.5% (Epiduo) may enhance compliance. Oxidation, a chemical reaction, occurs with tretinoin (except with the microsphere formulation) when used in combination with benzoyl peroxide. Because oxidation causes degradation of tretinoin, reducing its effectiveness, simultaneous application of benzoyl peroxide and tretinoin should be avoided.

Adverse effects of retinoids include erythema, dryness, pruritus, stinging, and photosensitivity (use of sunscreens is recommended). 1 Tretinoin and tazarotene are not indicated during pregnancy. 1 Several agents that contain retinoids are FDA approved for use in adolescents. Adapalene 0.1%/benzoyl peroxide 2.5% is approved for patients nine years and older, and tretinoin 0.05% micronized gel is approved for patients 10 years and older. All other retinoids are approved for patients 12 years and older. 1 , 14

Azelaic Acid . Azelaic acid 20% (Azelex) is FDA approved as an alternative treatment for acne, alone or in combination with other agents. It has mildly comedolytic, antibacterial, and anti-inflammatory properties. 1 Advantages of azelaic acid 20% include the potential for safe use in pregnancy and its effectiveness in the treatment of postinflammatory dyspigmentation. Although usually well tolerated, azelaic acid 20% may cause burning, stinging, and hypopigmentation in individuals with dark skin. 1 , 24

Dapsone . Dapsone 5% or 7.5% gel (Aczone) has anti-inflammatory and antibacterial properties and is effective as an adjunct therapy in the treatment of acne. A meta-analysis of multiple randomized controlled, double-blind trials showed that topical dapsone is more effective in adult women compared with men or adolescent females. 25 Dapsone may cause mild to moderate local irritation. Testing for glucose-6-phosphate dehydrogenase deficiency is unnecessary. 1 , 25

Other Topical Agents . There is insufficient evidence to support the use of over-the-counter therapies containing salicylic acid, niacinamide (nicotinamide), sulfacetamide, sulfur, zinc, or resorcinol. There are only two studies of aluminum chloride, with conflicting outcomes. 1

SYSTEMIC ANTIBIOTICS

Tetracyclines, macrolides, trimethoprim/sulfamethoxazole, trimethoprim, penicillins, and cephalosporins have been used effectively in the treatment of inflammatory acne. 1 , 23 , 26 Systemic antibiotics ( Table 5 1 , 2 , 14 ) are indicated in the management of moderate to severe inflammatory acne and should be used in combination with nonantibiotic topical agents to prevent resistance and enhance effectiveness. 1 , 23

A recent systematic review found that no antibiotic class, individual antibiotic, or dosage is superior. 23 However, the American Academy of Dermatology (AAD) recommends doxycycline and minocycline (Minocin) as first-line therapies based on studies indicating superiority over tetracycline and azithromycin (Zithromax). 1 , 26 Because of the risk of emerging bacterial resistance, guidelines recommend restricting macrolide use to when tetracyclines are contraindicated (i.e., in children younger than eight years and pregnant women). Trimethoprim/sulfamethoxazole and trimethoprim should be reserved for patients who are unresponsive to or intolerant of tetracyclines or macrolides. Penicillins and cephalosporins are not recommended because of limited data supporting their use; however, they may be indicated in special circumstances, such as for patients with allergies to multiple drug classes and for pregnant women. 1 , 27

Sarecycline (Seysara) is an oral, narrow-spectrum tetracycline-derived antibiotic FDA approved for the treatment of nonnodular moderate to severe acne vulgaris in children nine years and older (October 2019). Sarecycline significantly reduced inflammatory acne lesion counts when compared with placebo in two large, multicenter, randomized, double-blind studies. 28

Recent studies, systematic reviews, and consensus expert opinion support limiting use of oral antibiotics to the shortest duration possible (12 weeks or less), except in select recalcitrant cases. 1 , 23 On completion of systemic antibiotic therapy, topical retinoids should be used for maintenance of remission. 1 , 22

ISOTRETINOIN

Isotretinoin is a vitamin A derivative believed to act on all proposed mechanisms of acne development. Isotretinoin directly inhibits sebaceous gland function, resulting in decreased sebum production and comedolysis. Declining sebum production leads to decreasing C. acnes proliferation and, consequently, diminishes chemotactic inflammatory modulator release, which lessens cutaneous inflammation. 1 The effectiveness of isotretinoin is well established, and the therapy is FDA approved for the management of severe, recalcitrant nodular acne. 1 , 29 , 30 The AAD endorses the use of isotretinoin in treatment-resistant or relapse-prone acne or acne that is causing significant psychosocial distress or scarring. 1 Recommended starting dosages are 0.25 to 0.4 mg per kg per day for moderate acne and 0.5 mg per kg per day for severe, recalcitrant acne. After one month, the dosage for severe, recalcitrant acne should be titrated as tolerated to 1 mg per kg per day with the goal of a 120-mg to 150-mg cumulative dose to reduce the risk of relapse and need for retreatment. 1

Common dose-dependent adverse effects of isotretinoin include xerosis, cheilitis, acne flare-up, dry eyes, headache, and elevated lipid and hepatic enzyme levels. Previously suggested associations between isotretinoin and inflammatory bowel disease, mood disorders, and suicidal ideation have not been confirmed in more recent studies, and some studies have shown improvement of depressive symptoms in patients taking isotretinoin. 1 , 31 , 32 Patients receiving isotretinoin should be counseled about associated risks. 1

A systematic review and meta-analysis found no evidence to support periodic laboratory monitoring in healthy patients on typical dosages of isotretinoin after initial assessment. 33 However, consensus guidelines based on expert opinion recommend monitoring liver function and lipid panels until stability is assured. 1 , 33 Because of isotretinoin's risk of teratogenicity, patients, pharmacists, and prescribers must register with the FDA-mandated risk management program, iPledge, before initiating therapy. 1 All female patients who may become pregnant must have pretreatment and posttreatment contraceptive counseling and monthly urine pregnancy tests.

HORMONAL AGENTS

Combination oral contraceptives are antiandrogenic, effective in the management of inflammatory and comedonal acne in menarchal females, and FDA approved for treatment of acne in females older than 15 years who also desire contraception. There are currently four combined oral contraceptives approved for the treatment of acne vulgaris (ethinyl estradiol/norgestimate, ethinyl estradiol/norethindrone acetate/ferrous fumarate, ethinyl estradiol/drospirenone, ethinyl estradiol/drospirenone/levomefolate). Use should be considered for menarchal females unresponsive or intolerant to past therapies, for temporal association of acne outbreaks with menses, or for females with signs and symptoms of hyperandrogenism (acne, hirsutism, oligomenorrhea). 1 , 34 Although several agents are approved for use in acne treatment, none has demonstrated superiority over others. Combination oral contraceptives are best used with other acne treatments, because improvement may take at least three months. 1 , 34

ANTIANDROGENS

There are limited studies demonstrating the effectiveness of spironolactone (aldosterone receptor antagonist) and flutamide (androgen receptor blocker) in the treatment of acne. Based on expert opinion and current evidence, the AAD consensus panel recommends the use of spironolactone for its antiandrogenic properties in women with resistant and hormonally mediated acne. Spironolactone should be used in conjunction with contraception because of the risk of fetal antiandrogenic effects. The AAD does not recommend the use of flutamide because of the potential for serious adverse effects. 1 , 35 Breast tenderness, menstrual irregularities, and hyperkalemia may occur in patients treated with spironolactone.

CORTICOSTEROIDS

Prednisone (5 mg to 15 mg daily) has demonstrated effectiveness in the treatment of acne and may be used as an adjunct in select patients; however, the potential adverse effects limit its use. Prednisone is indicated for the treatment of acne fulminans, prevention of acne fulminans–like eruptions in patients initiating isotretinoin, treatment of severe nodulocystic acne in pregnancy (after the first trimester), and in patients with adrenal hyperandrogenism. 1 , 27 Intralesional triamcinolone injections reduce inflammation and pain in nodular acne. 1

PHYSICAL MODALITIES

Laser and light-based modalities have been studied in the treatment of noninflammatory and moderate to severe inflammatory acne; however high-quality evidence is lacking. Photodynamic therapy has been studied most extensively. 1 , 36 There is limited evidence to support chemical peels and comedo extraction for the management of comedonal acne. 1

COMPLEMENTARY THERAPIES

Dietary interventions (i.e., low-glycemic-load diets and avoidance of dairy or skim milk), acupuncture, cupping, herbal medicines, tea tree oil, and purified bee venom have been recently reviewed for the treatment of acne. Although of low quality, there is evidence that purified bee venom, tea tree oil, a low-glycemic-load diet, or avoidance of skim milk is associated with a reduction in skin lesions. 9 , 10 , 37

Reassessment and Referral

Goals of therapy in patients with acne vulgaris include reduction in comedonal and inflammatory lesions, improvement of psychosocial symptoms, and avoidance of scarring. 2 Therapeutic interventions for acne should have a minimum duration of eight weeks to assess effectiveness, unless the patient has an allergy or experiences intolerable adverse effects. If the patient shows inadequate improvement after sequential interventions, referral to a dermatologist is recommended. 2

This article updates previous articles on this topic by Titus and Hodge 2 and Feldman, et al. 38

Data Sources: We performed electronic searches of PubMed, the Cochrane database, and Essential Evidence Plus using the MeSH terms acne, vulgaris, treatment, treat, therapy, prevention, prophylaxis, grading, classification, microbiology, endocrinology, hormone, topical, retinoid, antibacterial, antibiotic, contraceptives, corticosteroid, isotretinoin, complementary, alternative, diet, etiology, pathophysiology, Propionibacterium acnes , light therapy, spironolactone. Search dates: April 2018, June 2018, and July 2019.

Zaenglein AL, Pathy AL, Schlosser BJ, et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol. 2016;74(5):945-73.e33.

Titus S, Hodge J. Diagnosis and treatment of acne. Am Fam Physician. 2012;86(8):734-740. Accessed July 11, 2019. https://www.aafp.org/afp/2012/1015/p734.html

Kim K, Ha I, Kim E, et al. A comparative study of biological and metabolic biomarkers between healthy individuals and patients with acne vulgaris: a cross-sectional study protocol. Medicine (Baltimore). 2017;96(45):e8554.

Zouboulis CC. Acne and sebaceous gland function. Clin Dermatol. 2004;22(5):360-366.

Toyoda M, Morohashi M. Pathogenesis of acne. Med Electron Microsc. 2001;34(1):29-40.

Ghosh S, Chaudhuri S, Jain VK, et al. Profiling and hormonal therapy for acne in women. Indian J Dermatol. 2014;59(2):107-115.

Tanghetti EA. The role of inflammation in the pathology of acne. J Clin Aesthet Dermatol. 2013;6(9):27-35.

Zhang M, Qureshi AA, Hunter DJ, et al. A genome-wide association study of severe teenage acne in European Americans. Hum Genet. 2014;133(3):259-264.

Mahmood SN, Bowe WP. Diet and acne update: carbohydrates emerge as the main culprit. J Drugs Dermatol. 2014;13(4):428-435.

Fiedler F, Stangl GI, Fiedler E, et al. Acne and nutrition: a systematic review. Acta Derm Venereol. 2017;97(1):7-9.

Jović A, Marinović B, Kostović K, et al. The impact of psychological stress on acne. Acta Dermatovenerol Croat. 2017;25(2):1133-1141.

Yang YS, Lim HK, Hong KK, et al. Cigarette smoke-induced interleukin-1 alpha may be involved in the pathogenesis of adult acne. Ann Dermatol. 2014;26(1):11-16.

Yamamoto A, Takenouchi K, Ito M. Impaired water barrier function in acne vulgaris. Arch Dermatol Res. 1995;287(2):214-218.

Eichenfield LF, Krakowski AC, Piggott C, et al.; American Acne and Rosacea Society. Evidence-based recommendations for the diagnosis and treatment of pediatric acne. Pediatrics. 2013;131(suppl 3):S163-S186.

Mohd Nor NH, Aziz Z. A systematic review of benzoyl peroxide for acne vulgaris. J Dermatolog Treat. 2013;24(5):377-386.

Tan HH. Topical antibacterial treatments for acne vulgaris: comparative review and guide to selection. Am J Clin Dermatol. 2004;5(2):79-84.

Gamble R, Dunn J, Dawson A, et al. Topical antimicrobial treatment of acne vulgaris. Am J Clin Dermatol. 2012;13(3):141-152.

Mills O, Thornsberry C, Cardin CW, et al. Bacterial resistance and therapeutic outcome following three months of topical acne therapy with 2% erythromycin gel versus its vehicle. Acta Derm Venereol. 2002;82(4):260-265.

Simonart T, Dramaix M. Treatment of acne with topical antibiotics: lessons from clinical studies. Br J Dermatol. 2005;153(2):395-403.

Tanghetti E, Dhawan S, Green L, et al. Randomized comparison of the safety and efficacy of tazarotene 0.1% cream and adapalene 0.3% gel in the treatment of patients with at least moderate facial acne vulgaris. J Drugs Dermatol. 2010;9(5):549-558.

Thiboutot D, Arsonnaud S, Soto P. Efficacy and tolerability of adapalene 0.3% gel compared to tazarotene 0.1% gel in the treatment of acne vulgaris. J Drugs Dermatol. 2008;7(6 suppl):s3-s10.

Thielitz A, Gollnick H. Topical retinoids in acne vulgaris: update on efficacy and safety. Am J Clin Dermatol. 2008;9(6):369-381.

Bienenfeld A, Nagler AR, Orlow SJ. Oral antibacterial therapy for acne vulgaris: an evidence-based review. Am J Clin Dermatol. 2017;18(4):469-490.

Thiboutot D. Versatility of azelaic acid 15% gel in treatment of inflammatory acne vulgaris. J Drugs Dermatol. 2008;7(1):13-16.

Stein Gold LF, Jarratt MT, Bucko AD, et al. Efficacy and safety of once-daily dapsone gel, 7.5% for treatment of adolescents and adults with acne vulgaris. J Drugs Dermatol. 2016;15(5):553-561.

Garner SE, Eady A, Bennett C, et al. Minocycline for acne vulgaris. Cochrane Database Syst Rev. 2012(8):CD002086.

Chien AL, Qi J, Rainer B, et al. Treatment of acne in pregnancy. J Am Board Fam Med. 2016;29(2):254-262.

Moore A, Green LJ, Bruce S, et al. Once-daily oral sarecycline 1.5 mg/kg/day is effective for moderate to severe acne vulgaris. J Drugs Dermatol. 2018;17(9):987-996.

Vallerand IA, Lewinson RT, Farris MS, et al. Efficacy and adverse events of oral isotretinoin for acne: a systematic review. Br J Dermatol. 2018;178(1):76-85.

Hitzeman N. Family physicians are well-suited to prescribe isotretinoin. Am Fam Physician. 2016;94(5):342-344. Accessed July 11, 2019. https://www.aafp.org/afp/2016/0901/p342.html

Alhusayen RO, Juurlink DN, Mamdani MM, et al.; Canadian Drug Safety and Effectiveness Research Network. Isotretinoin use and the risk of inflammatory bowel disease. J Invest Dermatol. 2013;133(4):907-912.

Huang YC, Cheng YC. Isotretinoin treatment for acne and risk of depression [published correction appears in J Am Acad Dermatol . 2018;78(2):431]. J Am Acad Dermatol. 2017;76(6):1068-1076.e9.

Lee YH, Scharnitz TP, Muscat J, et al. Laboratory monitoring during isotretinoin therapy for acne [published correction appears in JAMA Dermatol . 2016;152(1):114]. JAMA Dermatol. 2016;152(1):35-44.

Arowojolu AO, Gallo MF, Lopez LM, et al. Combined oral contraceptive pills for treatment of acne. Cochrane Database Syst Rev. 2012(7):CD004425.

Layton AM, Eady EA, Whitehouse H, et al. Oral spironolactone for acne vulgaris in adult females: a hybrid systematic review. Am J Clin Dermatol. 2017;18(2):169-191.

Barbaric J, Abbott R, Posadzki P, et al. Light therapies for acne. Cochrane Database Syst Rev. 2016(9):CD007917.

Cao H, Yang G, Wang Y, et al. Complementary therapies for acne vulgaris. Cochrane Database Syst Rev. 2015(1):CD009436.

Feldman S, Careccia RE, Barham KL, et al. Diagnosis and treatment of acne. Am Fam Physician. 2004;69(9):2123-2130. Accessed July 11, 2019. https://www.aafp.org/afp/2004/0501/p2123.html

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Acne Vulgaris Case Study

J.S., age 16, comes to your office for a routine physical examination. You notice that she has facial acne that she is hiding with heavy makeup. She has tried Clearasil inconsistently without relief. She works at a fast food restaurant as a cook after school and on the weekends. Her mother has made her stop eating chocolates and greasy foods, but that has not seemed to help her. She is concerned because her prom is in 6 weeks and she wants her face clear. On physical examination, there are open and closed comedones as well as papules on her face and back. No scarring is evident. J.S.confides that she has recently become sexually active.

Diagnosis:  Acne Vulgaris

Answer the following questions. Include two references, cited in APA style.

• List specific treatment goals for J.S.
• What drug therapy would you prescribe? Why?
• What are the parameters for monitoring the success of the therapy?
• Describe specific patient education based on the prescribed therapy.
• List one or two adverse reactions for the selected agent that would cause you to change therapy.
• What would be the choice for second-line therapy?
• What over-the-counter or dietary supplement would you recommend to J.S.?
• What dietary and lifestyle changes should be recommended for J.S.?
• Describe one or two drug–drug or drug–food interactions for the selected agent.

You will receive two points for each correct answer and two points for using correct grammar and spelling and providing references cited in APA style.

Case Review in Adolescent Acne: Multifactorial Considerations to Optimizing Management

Janet Selway

Dermatology Nursing. 2010;22(1) 

• Abstract and Introduction
• Pathophysiology of Acne
• Diagnostic Considerations
• Treatment Options
• Decision Point: What is an Appropriate Treatment Plan for This Particular Patient?
• Treatment Selection and Patient Instruction

S.R., a 16-year-old high school student, presented to the clinic for a requisite physical for work as a summer camp counselor. The NP noticed facial acne and asked if it was bothersome. Relieved at the question, S.R. stated that she had been bothered by facial acne for the past 3 years. She described facial breakouts that began gradually, varied in severity, worsened during menses, and never completely cleared. She was disappointed with her recent yearbook pictures and admitted the breakouts contributed to feelings of low self-esteem. She tried over-the-counter 5% benzoyl peroxide (BP) gels and washes, as well as multiple facial cleansing products, without improvement. S.R. followed her mother's advice to eliminate chocolate and fried foods from her diet, but also without improvement. She had a normal PAP test result and well-woman examination 3 months earlier. She was prescribed norgestimate/ethinyl estradiol at that time; however, she did not fill the prescription for fear that hormone therapy would worsen her acne and cause weight gain. In addition to normal physical examination results, her menstrual cycle was regular, and the endocrine system review was negative. She was not taking any medications and denied any allergies. A physical examination revealed a healthy young woman with 15 open and closed comedones, 10 papules, and 5 pustules on each half of the face and involving the forehead, cheeks, and chin (see Figure 1). No nodules or cysts were present. Additional history and physical examination findings were noncontributory.

Initial presentation of acne on forehead. Source : Reprinted with permission from Interactive Medical Media LLC. Available at: https://www.dermnet.com .

Dermatology Nursing. 2010;22(1) © 2010  Jannetti Publications, Inc.

Cite this: Case Review in Adolescent Acne: Multifactorial Considerations to Optimizing Management -  Medscape  - Jan 01, 2010.

BP = benzoyl peroxide * Lesion count is per half of face (Hayashi, Akamatsu, & Kawashima, 2008) +/– Recommended situationally, either as part of a combination of therapy (retinoids, BP/antibiotic) or in female patients only (hormonal therapy) Source : Gollnick et al., 2003.

Source: Baldwin, 2006.

Source: Magin et al., 2006.

Authors and Disclosures

Janet Selway Janet Selway, DNSc, CRNP, is an Assistant Professor, School of Nursing, University of Delaware, Newark, DE.

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Dermatology: how to manage acne vulgaris

Alexander kc leung.

1 Department of Pediatrics, The University of Calgary, and The Alberta Children’s Hospital, Calgary, Alberta, Canada

Benjamin Barankin

2 Toronto Dermatology Centre, Toronto, Ontario, Canada

Joseph M Lam

3 Department of Dermatology and Skin Sciences, University of British Columbia and BC Children’s Hospital, Vancouver, British Columbia, Canada

Kin Fon Leong

4 Pediatric Institute, Kuala Lumpur General Hospital, Kuala Lumpur, Malaysia

Kam Lun Hon

5 Department of Paediatrics and Adolescent Medicine, The Hong Kong Children’s Hospital, Hong Kong

Acne vulgaris is the most common skin disease that can lead to disfigurement and psychological distress. This article aims to provide a narrative updated review on the management of acne vulgaris.

A PubMed search was performed with Clinical Queries using the key term “acne”. The search strategy included clinical trials, meta-analyses, randomized controlled trials, observational studies and reviews. The search was restricted to articles published in English.

Treatments of acne include proper skin care, topical medications, oral medications and procedural therapies. Topical agents are the first-line treatment for mild-to-moderate acne and can be used as combination therapy for more severe acne. Systemic therapies are usually prescribed for the initial treatment of moderate-to-severe acne as well as for acne that is refractory to topical therapies.

Topical retinoids are the drugs of choice for the treatment and maintenance therapy of patients with mild-to-moderate acne vulgaris. Depending on the severity of the acne, topical retinoids may be used alone or in combination with benzoyl peroxide and topical or oral antibiotics. Oral antibiotics are an important therapy for inflammatory acne unresponsive to topical therapy. Neither topical nor oral antibiotics should be used as monotherapy. Oral contraceptives and/or spironolactone are useful for many women with acne. Oral isotretinoin is the drug of choice for severe, extensive, nodular acne vulgaris but is also often used in moderate cases where scarring is evident, acne-related psychosocial distress is significant or other treatment modalities have failed.

Introduction

Acne vulgaris is a common, chronic, inflammatory disorder of the pilosebaceous unit (comprising the hair follicle and sebaceous gland) caused primarily by increased sebum production, hyperkeratinization of the follicle, bacterial colonization and inflammation. The condition is characterized by chronic or recurrent development of comedones, erythematous papules and pustules most commonly on the face but may also involve the neck, trunk and proximal upper extremities. Although generally considered a benign, self-limited condition, acne vulgaris may cause severe psychological problems and disfiguring scars. This article provides an updated review on acne with a focus on the management of this condition.

A PubMed search was performed in July 2021 with Clinical Queries using the key term “acne”. The search strategy included clinical trials, meta-analyses, randomized controlled trials, observational studies and reviews published within the past 10 years. The search was restricted to the English language. The information retrieved was used in the compilation of this article.

Epidemiology

The global prevalence of acne vulgaris in the general population is estimated at approximately 9.4%. 1 The condition typically begins at puberty when sex hormones begin to be produced and occurs most frequently in adolescents and young adults, with progressive reduction in prevalence with increasing age thereafter. 2 Although uncommon, acne may occur in the neonatal period and develop de novo in adulthood. 3 The prevalence of acne in boys increases from 40% at age 12 years to 95% at age 16 years. 4 , 5 In girls, the prevalence increases similarly from 61% to 83%. 4 , 5 During adolescence, there is a male predominance, particularly with more severe forms of acne. 2 , 6 In contrast, during adulthood, the condition is more common in women than in men. 6 Mild acne is more common in Caucasians whereas severe acne tends to be more common in Asians and Africans. 7

There is growing evidence that diet may contribute to the development of acne. 8 – 11 A 2021 systematic review of 53 studies (11 interventional clinical trials and 42 observational studies) showed that a high glycaemic-load diet, foods with a high glycaemic index, dairy products, chocolate and fatty food have a positive effect on the development of acne. 12 On the other hand, fatty acids, vegetables and fruit tend to protect against the development of acne. 12 Studies have also shown that vitamin D deficiency, high-dose vitamin B6 and vitamin B12 supplements and whey protein supplements may be associated with acne. 13 , 14 Other predisposing factors include genetic predisposition (family history of severe acne), obesity, oily/seborrheic skin, higher skin surface pH, emotional stress, repetitive mechanical trauma, exposure to excess sunlight, pre-menstruation, mechanical occlusion (e.g. headbands, shoulder pads, surgical masks, N95 respirators), topical application of greasy products or occlusive preparations, medications (e.g. anabolic steroids, hydantoin, benzodiazepines, ramipril, adalimumab, cyclosporin, isoniazid, lithium, iodides), congenital adrenal hyperplasia, adrenal tumours, polycystic ovarian syndrome and body dysmorphic disorders. 15 – 29

Pathogenesis

Acne vulgaris is a chronic inflammatory process of the pilosebaceous unit. The condition usually occurs with the onset of puberty due to increased production of androgens by the adrenals and gonads and/or increased sensitivity of androgen receptors. 30 , 31 Obstruction of the pilosebaceous canal may result from follicular hyperkeratinization, hypertrophy of the sebaceous gland with increased production of sebum, and shedding of keratinocytes in clumps leading to the formation of a follicular plug, all of which are under the influence of androgens. 32 – 40 When the normal flow of sebum onto the skin surface is obstructed by follicular hyperkeratosis, a microcomedo is formed. As the sebum accumulates, the microcomedo enlarges into a visible comedo. 17

In the pilosebaceous gland, triglycerides are hydrolysed into free fatty acids and glycerol by lipase produced by Cutibacterium acnes , formerly known as Propionibacterium acnes . 4 , 5 , 33 , 40 C. acnes , which increases dramatically at the time of puberty, is a key promoter of inflammation in acne. 4 , 5 , 33 , 40 The free fatty acids, once released into the skin through follicular breakdown, are cytotoxic and contribute to the inflammatory reaction. 5 , 40 Pro-inflammatory cytokines, such as IL-1, IL-8, IL-12 and defensins, are then produced by the recruited inflammatory cells, leading to the formation of inflammatory papules, pustules and, in severe cases, cysts and nodules. 3 , 6 , 41 Serum calprotectin, a biomarker of inflammation, is elevated in patients with acne. 42 Recent evidence suggests that C. acnes can activate components of the innate and adaptive immune systems and biofilms of C. acnes can promote follicular hyperkeratosis. 43 , 44

Clinical manifestations

Acne vulgaris manifests most commonly in areas of the body that have abundant sebaceous glands, such as the face and, to a lesser extent, the trunk, where sebaceous follicles predominate. 5 , 39 , 40 At times, the neck and proximal upper extremities may also be affected. 5 , 40 The initial stage of the disease begins with the pathognomonic comedo, a clogged follicle, which may be either closed or open. 38 , 40 A closed comedo (colloquially known as whitehead) appears as a white or flesh-coloured, domed-shaped papule without a readily visible central pore and without any clinical signs of inflammation ( Figure 1 ). 40 It is flask-shaped with the narrowest portion connected to the skin surface. 40 As the follicular opening is enlarged and eventually opened with continued distension as a result of keratin and sebum build-up, an open comedo (colloquially known as blackhead) is formed. 6 An open comedo typically presents as a flat or slightly raised black lesion with a central, dilated, follicular orifice containing a black keratotic plug, typically measuring 1–3 mm in diameter ( Figure 2 ). 40 , 43 The black surface of the open comedo is oxidized melanin not oxidized fat or dirt. 40 , 43

Numerous closed comedones on the forehead of a 16-year-old girl.

Multiple open comedones on the face of a 17-year-old boy.

Blackheads do not generally become inflamed unless the pilosebaceous canal is disrupted by external forces, such as may occur by squeezing the lesion, thus patients should be advised to not ‘play’ with their lesions. 40 Whiteheads may either open up their pores resulting in blackheads or they may rupture. 40 With rupture of the obstructed follicle and release of free fatty acids into the surrounding tissue, an inflammatory reaction ensues, resulting in erythematous papules ( Figure 3 ), pustules, papulopustules ( Figure 4 ) and, occasionally, nodules and cysts depending on the location and amount of the tissue involved and the magnitude of the inflammatory response. 38 , 40 Nodules and cysts comprise severe nodulocystic acne ( Figure 5 ). 31

Multiple inflammatory papules on the cheek.

Closed and open comedones, inflammatory papules and pustules over the forehead of a 13-year-old boy.

Nodulocystic acne on the face.

Several clinical variants exist. Acne conglobata (also known as conglobate acne), found predominately in young males, is a severe, destructive and highly inflammatory form of acne marked by the presence of grouped and polyporous comedones, nodulocystic lesions, burrowing, interconnecting deep-seated abscesses, and draining sinus tracts with purulent, foul-smelling discharge ( Figure 6 ). 5 , 40 , 45 – 47 The condition may lead to significant scarring. 48 Acne conglobata is more commonly found on the posterior back and chest but may extend to the buttocks. 5 , 40 , 45 , 47 Less commonly, the lesion can appear on the face, proximal arms, shoulders, abdomen and scalp. 45

Acne conglobata presenting as grouped comedones, nodulocystic lesions, abscesses and draining sinus tracts on the back.

Acne fulminans (also known as acne maligna) is a rare form of acne characterized by the sudden onset of painful, haemorrhagic pustules, friable plaques and large, necrotic, ulcerating nodules mainly on the back but may involve the chest, face, neck and shoulders in association with systemic manifestations such as malaise, fever, chill, weight loss, diffuse myalgia, polyarthralgia, erythema nodosum, hepatosplenomegaly, bone lesions, increased inflammatory markers (e.g. leukocytosis, neutrophilia, elevated erythrocyte sedimentation rate or C-reactive protein) and elevated liver enzymes. 12 , 38 , 49 – 51 Characteristically, comedones are uncommon and polyporous comedones are absent. 48 The condition typically occurs in individuals aged 13–16 years with a male to female ratio of 3:1. 49 , 50 Acne fulminans may be an isolated disorder and may be triggered by isotretinoin therapy 6 or may present as part of syndromes such as pyogenic arthritis, pyoderma gangrenosum and acne (PAPA), synovitis, acne, pustulosis, hyperostosis and osteitis (SAPHO), pyogenic arthritis, pyoderma gangrenosum, acne and hidradenitis suppurativa (PAPASH) or pyoderma gangrenosum, acne and hidradenitis suppurativa (PASH). 52 , 53

Acne excoriée, or ‘picker’s acne’, results from excessive picking and scratching of the acne lesions. 6 , 54 Typically, acne excoriée presents with comedones and inflammatory papules. 6 Picking or scratching of the acne lesions exacerbates the acne lesions and may result in excoriations, erosions, ulcerations, scabs and scars. 54 Affected individuals may have obsessive-compulsive personality and body dysmorphic disorders. 6 , 54 The condition is more common in young women. 6

Neonatal acne is either present at birth or shortly thereafter, usually within 6 weeks of life. 55 , 56 The condition is more common in boys. 57 Presumably, neonatal acne results from stimulation of sebaceous glands by maternal and neonatal androgens and colonization of sebaceous glands by Malassezia species. 55 Neonatal acne is characterized by papules and pustules usually on the face (forehead, cheeks and nose) ( Figure 7 ) and tends to resolve spontaneously over weeks to months. 55 , 56

A 5-week-old boy with neonatal acne on the face. Note the presence of papules and pustules.

Infantile acne typically presents between 6 weeks and 12 months of age with a male predominance. 58 Lesions consist of closed and open comedones, inflammatory papules, pustules, nodules, and cysts ( Figure 8 ). 57 , 58 The site of predilection is the face, especially the cheeks. 58 Infantile acne may result from increased sensitivity of sebaceous glands to circulating androgens or, less commonly, from increased production of androgens. 56 , 58 Lesions usually resolve within 12 months of initial onset. 58

Multiple comedones and inflammatory papules over the cheeks of a 9-month-old boy.

Mid-childhood acne is rare and typically presents between 1 and 7 years of age. 55 , 56 Clinically, mid-childhood acne is characterized by comedones, inflammatory papules and pustules on the face. 56 Mid-childhood acne should always raise the concern for underlying causes of hyperandrogenism such as late-onset congenital hyperplasia, Cushing syndrome or a virilizing tumour. 55 , 56

Preadolescent acne, defined by the appearance of acne between 7 and 11 years of age, typically presents with comedones on the central forehead. 55 , 56 Lesions gradually evolve to inflammatory papules and pustules with time and involve the centre of the face. 56 Acne in this age group is usually normal and presumably caused by isolated premature adrenarche. 30 , 59 At times, it may be the first sign of true precocious puberty, late-onset congenital hyperplasia, polycystic ovarian syndrome or a virilizing tumour. 55 , 56

Acne tarda refers to the late onset of acne or persistence/relapse of acne in the third and fourth decade of life. 36 , 60 , 61 In adult women, late-onset acne tends to involve the chin, jaw line and neck with a predominance of inflamed papules and pustules with relatively few comedones ( Figure 9 ). 6 , 60 – 62 Acne tarda in women is most associated with premenstrual flares. 6 , 60 , 61

Acne on the chin and neck of a 35-year-old woman presenting predominately with inflamed papules and pustules.

Diagnosis and diagnostic evaluation

The diagnosis is mainly clinical based on the characteristic lesions (closed comedones, open comedones, inflammatory papules, pustules, inflamed nodules and inflamed nodulocystic lesions) in a characteristic distribution (face, neck, back, chest, shoulders or upper arms). Laboratory investigations are usually not necessary unless clinically indicated. Serum concentrations of testosterone, androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate and, in women of childbearing age, luteinizing hormone and follicle-stimulating hormone may be measured and pelvic ultrasound should be performed to look for polycystic ovarian syndrome if there is a suspicion of hyperandrogenism (e.g. hirsutism, clitoromegaly, very early development of pubic or axillary hair). 15 , 58

Differential diagnosis

Acne should be differentiated from bacterial folliculitis, pityrosporum folliculitis, acne keloidalis nuchae, milia, miliaria rubra, syringomas, perioral dermatitis, sebaceous hyperplasia, nevus comedonicus, papulopustular rosacea, keratosis pilaris, molluscum contagiosum, facial angiofibromas in tuberous sclerosis, eruptive vellus hair cysts, steatocystoma multiplex and verruca vulgaris ( Table 1 ). 63 – 69 The distinctive features of each condition allow a relatively straightforward differentiation from acne.

Differential diagnosis of acne vulgaris.

Drug-induced acne or acneiform eruption can be caused by corticosteroids, anabolic steroids, testosterone, isoniazid, lithium, halogens, lithium, isoniazid, epidermal growth factor receptor inhibitors, vascular endothelial growth factor inhibitors, TNF antagonists and capecitabine. 70 , 71 Compared to classic acne lesions, drug-induced acne is characterized by a history of drug intake, sudden onset of monomorphous, inflammatory papules or papulopustules with few, if any, comedones, unusual age of onset, lesions on the face and neck as well as unusual locations beyond the seborrheic areas, and disappearance of lesions when the offending medication is discontinued ( Table 1 ). 71

Acne should be differentiated from skin lesions of Birt–Hogg–Dube syndrome (triad of acrochordons, fibrofolliculomas and trichodiscomas), Cowden syndrome (facial trichilemmomas and acral keratosis) and Muir–Torre syndrome (facial keratoacanthomas and sebaceous neoplasms) ( Table 1 ). 34 , 72

Complications

Post-inflammatory hyperpigmentation and, less commonly, hypopigmentation may result; the risk is higher in dark-skinned individuals (skin phototypes IV–VI). 6 , 7 Scarring may result in susceptible individuals, especially with severe variants such as acne conglobata and acne fulminans. In general, the deeper the inflammatory process, the more likely acne lesions will result in permanent scarring. 5 , 40 , 73 However, even comedonal acne can result in acne scarring. 40 It has been shown that early and effective treatment of acne vulgaris may reduce the risk of scarring. 6 Acne scars are typically atrophic in nature and, based on their distinctive physical characteristics, can be divided into three basic types, namely boxcar scars (punched-out, U-shaped angular scars with sharply demarcated vertical edge) ( Figures 10 and ​ and11), 11 ), ice pick scars (small, deep punched-out pits, sharply demarcated and V-shaped) ( Figure 12 ) and rolling scars (wider and shallower than ice pick scars; rounded, sloping edges, having a wavelike or undulating appearance; combination of several of these scars in a region of the skin gives a rolling appearance) ( Figure 13 ). 39 , 74 , 75 Conversely, acne scars can also be thick such as hypertrophic scars (scars remain within the confines of the original wound borders) ( Figure 14 ) and keloid scars (lesions outgrow the boundaries of the wound scars, invading surrounding normal tissue, and may be pruritic or tender) ( Figure 15 ). 40 , 74 , 75

Boxcar scars on the right cheek.

Boxcar scars (close-up view).

Ice pick scars on the chin.

Rolling scar on the left cheek.

Hypertrophic scars over the chest of a 16-year-old boy.

Keloid scars over the left shoulder of a 14-year-old girl.

Morbihan disease, characterized by persistent erythema and solid oedema of the upper two-thirds of the face, is a rare complication of acne. 6 , 76 Rarely, dystrophic calcinosis cutis may result from inflammatory acne. 77

Both active acne and post-inflammatory hyperpigmentation/hypopigmentation and scars from previous acne, especially those on the face and in women, are apt to be embarrassing and psychologically traumatic and may result in anxiety, emotional stress, low self-esteem, feelings of unattractiveness and worthlessness, depression, suicidal ideation, and even suicide. 60 , 61 , 78 – 81 Self-consciousness related to acne can have an adverse effect on interpersonal and sexual relationships, daily and social activities, and quality of life. 82 – 89

Acne vulgaris is characterized by a chronic inflammatory and relapsing course for years. With proper treatment, the overall prognosis is good. The prevalence of acne tends to decrease with increasing age in adulthood and beyond. 69 However, some patients are left with residual scars, the treatment of which is often difficult and not optimal. 7

The goals of treatment are to provide the patient with the best appearance possible and to minimize scarring and psychological sequelae. The aims of therapy are to prevent follicular hyperkeratosis, reduce C. acnes , inhibit fatty acid production and sebum secretion and eliminate comedones. 6 , 40 In general, topical agents used for the treatment of acne vulgaris have a favourable safety profile. 90 Therefore, topical agents are the first line of treatment for mild-to-moderate acne and can be used as combination therapy for more severe acne. 17 , 90 , 91 Systemic therapies are usually prescribed for the initial treatment of moderate-to-severe acne as well as acne that is refractory to topical therapies. 92

Skin hygiene

Patients should be advised to use gentle skin cleansers rather than scrubs and soaps (especially harsh or drying soaps) as well as non-comedogenic skin care and cosmetic products. 92 Patients can also be advised to pat dry their face after washing rather than rubbing and exfoliating. They should avoid aggressive scrubbing of the skin and picking or squeezing of acne lesions as this can increase the risk of scar formation. 69 , 92 Use of soap-free face wash and oil-free moisturizers and sunscreens is advisable. 60 , 61 , 93

Topical therapy

Many topical agents are available for the treatment of acne vulgaris. The choice should be based on, amongst others, patient age, sites and severity of the acne, efficacy, safety, and cost of the medication, and patient preference. Most patients would benefit from a combination of medications. 94 Generally, patients with dry skin prefer lotions or creams whereas patients with oily skin may prefer gels. 91

Topical retinoids (e.g. tretinoin, tazarotene, adapalene, trifarotene), a diverse group of vitamin A derivatives that modulate gene expression, are the drugs of choice for the treatment and maintenance therapy of patients with mild-to-moderate acne vulgaris. 24 , 31 , 92 , 95 – 100 These agents inhibit keratinocyte proliferation, thereby reducing obstruction of the follicle and preventing the formation of microcomedones. 17 , 101 , 102 In addition, these agents have an anti-inflammatory effect. 17 They are effective for the treatment of comedones, inflammatory papules and pustules. 24 , 92 The major side effects are local skin dryness, flaking, erythema, thinning of the stratum corneum, burning sensation and irritation. 5 , 40 Some patients may have an exacerbation of acne, so called ‘retinoid flare’ during the first month of treatment. 90 , 92 Topical retinoids are usually applied once daily, preferably at night, due to the photolability and photosensitivity associated with their use. 92 With the use of topical retinoids, regular use of broad-spectrum sunscreens and of protective wide-brimmed hats when outdoors should be advised. 92 Typically, patients are started on low concentrations of topical retinoids; the dosing should be slowly titrated up to minimize irritation, which may impact compliance. Topical tazarotene, a retinoid prodrug, is classified as a pregnancy category X drug (whilst the other retinoids are classified as category C; trifarotene is not assigned a category) and should be avoided during pregnancy or lactation. 92 Depending on the severity of acne, topical retinoids may be used alone or in combination with another agent such as benzoyl peroxide and topical or oral antibiotics. 99 , 100 , 102 A 2019 systematic review of 54 clinical trials evaluating the safety, efficacy and tolerability of topical retinoids for the treatment of acne showed that topical retinoids are safe and efficacious for the treatment of acne. 103 They are slower to work, so patience is key. Topical retinoids also improve skin tone and hyperpigmentation and reduce atrophic scarring. Optimal results can be obtained when they are used in combination with an antimicrobial agent. 103 , 104 The difference in efficacy of topical retinoids appears minor. 103 Amongst topical retinoids, adapalene has the best tolerability profile and the least irritating effect. 24 , 103

Benzoyl peroxide is a potent topical antimicrobial with rapid bactericidal action. 5 , 40 The bactericidal effect on C. acnes is due to the oxidation of bacterial proteins. Benzoyl peroxide inhibits the lipolysis of sebum triglycerides and decreases the inflammation of acne lesions. 5 , 40 In addition, benzoyl peroxide has a modest keratolytic and comedolytic effect. 34 , 99 , 100 The medication is usually applied once a day. 92 Use of benzoyl peroxide does not induce bacterial resistance and the medication is safe to use during pregnancy or lactation. 98 , 105 , 106 Benzoyl peroxide can be used as monotherapy or, more commonly, in conjunction with topical retinoids or antibiotic therapy to increase the efficacy of treatment. 105 , 107 – 110 A 2021 systematic review shows that benzoyl peroxide in combination with adapalene is more effective than either treatment used alone, but may cause more side effects. 111 Side effects associated with the use of benzoyl peroxide include skin dryness, peeling of the skin, erythema, stinging, burning, contact dermatitis, and bleaching of clothing, linen and hair. 106 Skin irritation often decreases with time. 31 Just like with retinoids, it is useful to start slowly with benzoyl peroxide-based products to minimize irritation and to improve overall compliance. The Global Alliance to Improve Outcomes in Acne suggests benzoyl peroxide plus a topical retinoid as the first-line therapy for most patients with inflammatory acne. 109 The European Evidence-Based (S3) Guideline for the Treatment of Acne recommends benzoyl peroxide plus topical adapalene or benzoyl peroxide plus topical clindamycin for the treatment of mild-to-moderate acne. 112

Topical antibiotics have anti-inflammatory properties and, depending on the formulation, are either bactericidal or bacteriostatic. 106 Compared with oral antibiotics, topical antibiotics have the benefit of less systemic toxicity and systemic side effects. 113 Topical antibiotics should not be used as monotherapy because of the risk of developing bacterial resistance. 24 , 92 , 101 , 114 – 116 Combining topical antibiotics with topical retinoids or benzoyl peroxide will improve the therapeutic outcome and will reduce the emergence of antibiotic-resistant strains of C. acnes . 24 , 92 , 101 , 102 , 114 , 115 Generally, topical antibiotics should not be given to patients who are concurrently receiving oral antibiotics. 108 Topical antibiotics, such as clindamycin, erythromycin, dapsone and minocycline, have been successfully used in the treatment of acne. 34 In general, topical antibiotics alone are very well tolerated. Most topical antibiotic regimens use either clindamycin or erythromycin, which are available in a variety of vehicles such as a gel or solution. 113 , 116 , 117 The cutaneous side effects associated with the use of clindamycin or erythromycin include local dry skin, erythema, peeling, pruritus, occasional burning and Clostridium difficile colitis. 90 , 106 Dapsone is a sulfone antibiotic with anti-inflammatory and antibacterial properties. 106 The medication exerts its antibiotic effect by inhibiting bacterial DNA synthesis. 55 , 118 Dapsone is available in 5% and 7.5% gel formulations and is effective as an adjunct treatment for acne vulgaris. 55 , 92 , 94 , 106 The medication is often used in individuals with sensitive skin and in women with acne. 99 , 100 It is also a viable addition to the armamentarium for the treatment of truncal acne. 72 Side effects of topical dapsone include dryness, peeling, erythema and pruritus at the application sites. 55 , 92 , 106 Temporary orange-brown staining of the skin due to dapsone oxidation may occur when dapsone and benzoyl peroxide are used concomitantly. 92 , 106 , 118 Topical minocycline is an alternative topical antibiotic that can be used as an adjunct treatment for acne vulgaris. 92 , 97

Azelaic acid is a naturally occurring, saturated, straight-chained acid that has antibacterial, anti-inflammatory, antikeratinizing, comedolytic, tyrosinase-inhibiting and antioxidant properties. 90 , 118 Topical azelaic acid (e.g. 15% or 20% gel) has been used with success for the treatment of acne vulgaris and post-inflammatory hyperpigmentation. 7 , 52 , 90 , 118 , 119 The medication has a favourable safety profile and is safe during pregnancy or lactation. Side effects are mild and consist mainly of local erythema, dryness, burning, stinging, pruritus, dysesthesia and hypopigmentation in dark-skinned individuals. 116 , 118 No bacterial resistance to azelaic acid has been reported. 90 , 118

Superficial chemical peels, such as lactic acid, retinoic acid, alpha hydroxyl acid, pyruvic acid, salicylic acid, mandelic acid, glycolic acid, Jessner solution and 10–25% trichloroacetic acid, have keratolytic action and can be used for comedonal and mild inflammatory acne lesions. 15 , 120 – 123 The appropriate peel should be chosen based on acne activity and the skin type of the patient. 122

Clascoterone (cortexolone 17 α-propionate) is a topical androgen receptor inhibitor that competes with androgens, specifically dihydrotestosterone, for binding to the androgen receptors within the sebaceous glands and hair follicles. 92 , 124 The medication was approved by the FDA in 2020 for use in individuals aged 12 years or older. 92 Clascoterone 1% cream has good efficacy for both non-inflammatory and inflammatory acne lesions, especially when combined with a topical retinoid. 124 Irritation of the skin is a potential side effect. 92 As clascoterone is rapidly hydrolysed to cortexolone, hypothalamic–pituitary–adrenal axis suppression is possibly associated with its use. 124

A short course of topical steroids may be helpful in severe acute inflammatory lesions. 4 , 40 Fluorinated steroids should not be used as they may cause steroid acne or periorificial dermatitis in susceptible individuals.

New and emerging topical agents that have shown promise for the treatment of acne vulgaris include insulin-like growth factor 1 inhibitors, phosphodiesterase inhibitors, acetylcholine inhibitors, acetyl coenzyme A carboxylase inhibitors, 5-lipoxygenase inhibitors, ectopeptidase inhibitors, IL-1, IL-1α, IL-1β and IL-17A blockers, melanocortin receptor antagonists, peroxisome proliferator-activated receptor modulators, omiganan pentahydrochloride, antimicrobial peptides, lupeol, gold and silver nanoparticles, sodium hypochlorite and epigallocatechin-3-gallate. 3 , 44 , 97 , 109 , 125 – 131 Well-designed, large-scale, randomized, double-blind and placebo-controlled studies are necessary to confirm the efficacy and safety of these novel topical agents in order to make formal recommendations regarding their use in the management of acne vulgaris.

Topical therapy can be used, if necessary, for the treatment of post-inflammatory hyperpigmentation. In this regard, post-inflammatory hyperpigmentation can be treated by the use of sun protection (sunscreen, hat, sunglasses), topical hydroquinone, topical azelaic acid, topical retinoids, topical modified Kligman’s formula or superficial chemical peels (e.g. lactic acid, alpha hydroxyl acid, linoleic acid, salicylic acid, polyethylene glycol, Jessner solution and 10–25% trichloroacetic acid). 7 , 102 , 109

Systemic therapy

Oral antibiotics are an important therapy for acne unresponsive to topical therapy and the more inflammatory types of acne lesions, including pustules, nodular lesions and abscesses. 31 , 40 , 98 They are particularly useful for acne involving the back because of difficulties of applying topical treatments to large areas that are difficult to reach. 31 , 41 , 131 These agents administered systemically produce a significant reduction in C. acnes . 98 In addition, oral antibiotics have intrinsic anti-inflammatory properties, exerting their action through the inhibition of neutrophil chemotaxis and the alteration of macrophage and cytokine production. 99 , 100 , 132 Tetracyclines (doxycycline, minocycline, sarecycline) are preferred because of greater efficacy and better tolerability. 108 , 116 , 131 In general, tetracyclines should be taken on an empty stomach as the absorption of tetracyclines is inhibited by food. 55 The recommended dose of doxycycline and minocycline is 50 or 100 mg daily or twice daily. 108 Sarecycline given once daily can be used in individuals aged 9 years and older. 108 Due to its narrow spectrum of activity, efficacy and safety in individuals 9 years and older, some authors now consider sarecycline to be the antibiotic of choice in the treatment of acne. 133 The recommended dose of sarecycline is based on body weight (60 mg, 100 mg and 150 mg for individuals weighing 33–54 kg, 55–84 kg and 85–136 kg, respectively). 108 Side effects of tetracyclines include nausea, vomiting, diarrhoea, oesophagitis, photosensitivity, pigment deposits in the skin, mucous membrane and teeth (young children), vaginal candidiasis, dizziness, tinnitus, hepatotoxicity, C. difficile colitis, allergic reactions, drug hypersensitivity syndrome, lupus-like syndrome, pseudotumor cerebri and impairment of growth. 55 , 73 , 98 , 106 , 132 The use of tetracyclines is contraindicated for pregnant individuals, individuals with childbearing potential and individuals aged 8 years or younger. 108 Azithromycin (500 mg one to three times per week) and erythromycin (500 mg twice a day) are the macrolides most often used when tetracyclines are contraindicated (e.g. children ≤8 years of age, pregnant women or breastfeeding mothers). 101 Treatment with cephalexin (500 mg twice a day for adults) and trimethoprim-sulfamethoxazole (160/800 mg once to twice a day for adults) is discouraged because of limited data to support their efficacy, unless tetracyclines and macrolides are contraindicated. 101 , 108 To reduce the risk for the development of antibiotic resistance, oral antibiotics should not be used as monotherapy. 109 , 134 , 135 Rather, they should be used in combination with a topical retinoid or preferably benzoyl peroxide. 60 , 61 , 99 , 100 , 135 In general, oral antibiotics should be limited to the shortest possible duration. The maximum duration of continuous treatment with oral antibiotics should be limited to no more than 6 months; long-term use of oral antibiotics is not recommended. 73 , 98 , 101 , 108

Oral isotretinoin (13-cis-retinoic acid) decreases sebum production, follicular keratinization and intrafollicular concentration of C. acnes . 4 , 40 , 108 In addition, oral isotretinoin has a direct anti-inflammatory effect. 108 It is the drug of choice for severe, extensive, nodular acne vulgaris but is also often used in moderate cases where scarring is evident, acne-related psychosocial distress is significant or other treatment modalities have failed. 91 , 108 , 109 , 112 , 136 Oral isotretinoin shows superior efficacy in the management of severe acne. 112 , 137 , 138 The considerable benefits must be weighed against their potential risks. 137 , 138 The medication is typically given as monotherapy and initiated at a low dose (e.g. 0.5 mg/kg/day) for the first month of therapy to minimize the risk of isotretinoin-induced acne flare due to intense sebocyte apoptosis and the subsequent release of antigens and inflammatory response. 108 , 138 , 139 , 140 The dose can then be increased to 1 mg/kg/day if needed, reaching a total cumulative dose typically within 120–150 mg/kg often given over approximately 6 months, though higher doses or longer durations may be needed. 140 Oral isotretinoin is highly lipophilic and should be taken with food (especially high-fat meals), which will increase absorption of the medication. 137 , 140 Side effects are dose related and include cheilitis, cutaneous erythema, mucocutaneous and ophthalmic dryness, palmoplantar desquamation, cutaneous atrophy, pruritus, epistaxis and acne flare. 140 Other adverse reactions include alopecia, photosensitivity, corneal opacities, decreased night vision, headache, nausea, vomiting, myalgias, arthralgias, delayed wound healing, pseudotumour cerebri, bone marrow suppression, hepatotoxicity, periostitis, hyperostosis and, rarely, Stevens–Johnson syndrome. 41 , 139 , 140 Currently, the causal relationship between isotretinoin therapy and depression, suicidal ideation and inflammatory bowel disease has not been established. 137 – 140 Laboratory abnormalities associated with the use of isotretinoin include hypertriglyceridaemia, hypercholesterolaemia, abnormal liver function tests, elevated erythrocyte sedimentation rate, anaemia, thrombocytosis and leucopenia. 4 , 40 , 140 As isotretinoin is teratogenic, women of childbearing age should not be given oral isotretinoin until pregnancy is excluded and an effective form of contraception is being used during treatment and for 1 month after stopping the medication. 4 , 38 , 40 Isotretinoin is also contraindicated in individuals with a history of hypersensitivity to isotretinoin or its component. 140 Concomitant treatment with isotretinoin and tetracyclines should be avoided because of the risk of pseudotumour cerebri. 140 Additionally, vitamin A supplementation may increase the side effects of isotretinoin and should therefore be avoided. 140

For women in post-menarche with acne, hormonal therapy is a therapeutic option. 69 The use of oestrogens in the form of oral contraceptives in the treatment of acne is based on the ability of oestrogen to suppress the stimulatory effect of androgens on pilosebaceous units leading to decreased size and function of sebaceous glands with a resultant reduction in sebum production and keratinous material accumulation. 108 The use of oral contraceptives should be considered in women in post-menarche typically over the age of 15 years with moderate-to-severe, recalcitrant, pustulocystic or nodulocystic acne who do not respond or are intolerant to conventional therapy as well as in those who experience premenstrual flares, especially along the jawline and lower face, and in those with evidence of hyperandrogenism (e.g. hirsutism, oligomenorrhoea) such as those with polycystic ovarian syndrome. 4 , 15 , 40 , 55 , 106 For post-pubertal women who desire a contraception method and who have no contraindications to oral contraceptives, an oral contraceptive is preferred to spironolactone as hormonal therapy for acne vulgaris, though the two are often combined for enhanced efficacy. 108 Oral contraceptives containing both oestrogen and progestin (e.g. ethinyl oestradiol and norgestimate; ethinyl oestradiol and norethindrone; ethinyl oestradiol and drospirenone; and ethinyl oestradiol, drospirenone and levomefolate) rather than progestin-only contraceptives should be used, as the latter are not effective and may worsen acne vulgaris. 101 , 106 , 108 , 137 Side effects of oral contraceptives include headaches, nausea, bloating, moodiness, breast tenderness, breakthrough bleeding, amenorrhoea, hypertension, thromboembolism and, rarely, myocardial infarction and stroke. 137

Spironolactone is an antiandrogen that blocks androgen receptors (thereby inhibiting the biosynthesis of androgen), inhibits 17-β-hydroxysteroid dehydrogenase (thereby halting the conversion of androstenedione to testosterone), inhibits 5-α-reductase (thereby halting the conversion of testosterone to dihydrotestosterone) and may increase the concentration of sex hormone-binding globulin (thereby decreasing the concentration of free testosterone and dihydrotestosterone). 108 Spironolactone should be considered in women who use oral contraceptives, are refractory to topical acne therapy, have hyperandrogenism or present with late-onset (>25 years old) acne vulgaris. 141 The recommended oral dose is 25–100 mg per day, given once or twice daily. 118 Some authors prefer spironolactone to oral antibiotics due to concerns of bacterial resistance. 142 Side effects of oral spironolactone include menstrual irregularities, breast enlargement, breast tenderness, polyuria, headache, fatigue, dizziness, nausea, anorexia, vomiting, diarrhoea, orthostatic hypotension and hyperkalaemia. 108 , 137 , 138 , 142 To minimize the adverse events of menstrual irregularities and breast tenderness, spironolactone is often prescribed with an oral contraceptive. 97 , 100 Pregnancy should be avoided and adequate contraceptive measures should be instituted during spironolactone therapy due to concerns of feminization of the male fetus. 7 , 126 , 142

Oral corticosteroids may be considered as an adjunct treatment of acne fulminans, aggressive conglobate acne, severe inflammatory acne and severe acne flare-ups associated with initiation of isotretinoin treatment. 73 , 106 In addition, oral corticosteroids can be used in patients with congenital adrenal hyperplasia to suppress adrenal production. 108

The rationale for the use of probiotics in the treatment of acne vulgaris is based on their potential to correct dysbiosis and to mend the epidermal barrier. 138 , 143 Preliminary studies showed that oral administration of probiotics as an adjunct therapy played an effective role in the treatment of mild-to-moderate acne. 144 Because of the heterogeneity of the available trials, the highly dynamic microbiome that might change over time and the lack of long-term safety data, well-controlled randomized clinical trials are needed to determine the true efficacy of probiotics before they can be recommended for the treatment of acne vulgaris. 143

Procedural therapies

Manual extraction of comedones, electrocauterization of macrocomedones, intralesional infiltration with triamcinolone, and the draining of cysts and abscesses have been used in selected patients for the treatment of acne lesions. 53 , 139 , 145 Laser and light therapy, as well as photodynamic therapy, have been used in the treatment of acne with varying success. 105 , 121 , 146 A 2018 Cochrane systemic review of 71 randomized controlled trials ( n =4211) on the use of different modalities of light therapies for acne yielded mixed results. 147 Well-designed randomized controlled trials on the efficacy of the different modalities of laser and light therapy are needed.

Several physical modalities are helpful in the management of atrophic scars resulting from acne. 4 , 148 Dermabrasion can help in treating superficial scars if conducted carefully. Deeper scars can be smoothed by dermal fillers such as hyaluronic acid, l -poly-lactic acid, polymethylmethacrylate, platelet-poor plasma gel, platelet-rich plasma and autologous fibroblasts. 55 , 139 , 148 – 156 Other treatment options include chemical peels, skin microneedling, traditional non-fractional ablative laser resurfacing, ablative fractional laser resurfacing, non-ablative fractional laser resurfacing, dermaroller, radiofrequency, punch excision, punch lift/elevation and subcision. 55 , 148 – 162 A 2016 Cochrane systematic review of 24 randomized controlled trials (789 individuals aged 18 years or older) examining the efficacy of a wide range of interventions for the treatment of acne scars found insufficient evidence to recommend any particular intervention as the intervention of choice. 163 The authors attributed this to underpowered studies, poor methodology, different baseline variables and a lack of standardized outcome measures. 163 A 2017 systematic review of 36 articles on the efficacy and side effects of dermabrasion, microneedling, dermal fillers and chemical peeling for the treatment of acne scars found that those interventions have varying degrees of efficacy, each with both advantages and disadvantages. 164 Nevertheless, all of the previously discussed interventions are safe with few side effects. 164 More high-quality placebo-controlled trials with a large number of patients are needed to clarify the efficacy and safety of various interventions for the treatment of acne scars.

For hypertrophic acne scars and keloids, treatment may be required for cosmetic purposes. Intralesional corticosteroid injections are the most effective and the first-line treatment for hypertrophic scars and keloids. 159 , 165 , 166 If treatment with intralesional corticosteroid monotherapy is unsuccessful, one may consider multimodality therapy such as liquid nitrogen followed by intralesional steroids, followed by silicone gel sheeting and/or pulsed-dye laser therapy. 165 , 166 If these measures result in an insufficient response, surgical excision with preoperative, intraoperative and postoperative corticosteroid injections as well as pressure dressing, if applicable, can be considered. 165 , 166

Complementary therapies

In some cultures, complementary therapies are popular for the treatment of acne. Low-quality evidence suggests topical application of tea tree oil or bee venom may reduce the total number of acne skin lesions. 167 Several studies have shown that topical application of tea tree oil products is as effective as topical benzoyl peroxide or salicylic acid for the treatment of mild-to-moderate acne. 167 Many other plant-derived therapies, such as basil oil and seaweed derivatives, have demonstrated some positive effects against acne lesions. 168 There is generally a lack of high-quality evidence for the use of herbal medicine, acupuncture or cupping therapy for acne. 169

Acne vulgaris is a common, chronic, inflammatory disorder of the pilosebaceous unit that affects most adolescents with inflammatory lesions on the face and trunk and may progress to scars. The condition can lead to emotional stress and the impact on quality of life can be significant. The management of acne vulgaris can be a challenge in daily clinical practice. As timely and proper treatment of acne may reduce the risk of scarring, early and effective treatment is of utmost importance. This article provides an updated review on acne with a focus on the management of this condition.

Acknowledgements

Contributions: AKCL is the principal author. BB, JML, KFL and KLH are coauthors who contributed and helped with the drafting of this manuscript. All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole and have given their approval for this version to be published.

Disclosure and potential conflicts of interest: AKCL and KLH are associate editors of Drugs in Context and confirm that this article has no other conflicts of interest otherwise. This manuscript was sent out for independent peer review. All authors declare that they have no conflicts of interest relevant to this manuscript. The International Committee of Medical Journal Editors (ICMJE) Potential Conflicts of Interests form for the authors is available for download at: https://www.drugsincontext.com/wp-content/uploads/2021/09/dic.2021-8-6-COI.pdf

Funding declaration: There was no funding associated with the preparation of this article.

Correct attribution: Copyright © 2021 Leung AKC, Barankin B, Lam JM, Leong KF, Hon KL. https://doi.org/10.7573/dic.2021-8-6 . Published by Drugs in Context under Creative Commons License Deed CC BY NC ND 4.0.

Article URL: https://www.drugsincontext.com/dermatology-how-to-manage-acne-vulgaris

Provenance: Invited; externally peer reviewed.

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Global, regional, and national burdens of acne vulgaris in adolescents and young adults aged 10-24 years from 1990 to 2021: a trend analysis

Affiliations.

• 1 Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
• 2 State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
• 3 4+4 Medical Doctor Program, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
• 4 Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
• PMID: 39271178
• DOI: 10.1093/bjd/ljae352

Background: Acne vulgaris is a common skin condition affecting adolescents and young adults worldwide, yet data on its burden and trends remain limited. We aimed to investigate trends in the burden of acne vulgaris among adolescents and young adults aged 10-24 years at global, regional, and national levels.

Methods: We retrieved data from the Global Burden of Disease Study (GBD) 2021 for individuals aged 10-24 years in 204 countries and territories from 1990 to 2021. We analyzed the numbers, age-standardised rates, and average annual percentage changes (AAPCs) of the prevalence, incidence, and disability-adjusted life-years (DALYs) for acne vulgaris at the global, regional, and national levels. Additionally, we examined these global trends by age, gender, and Socio-demographic Index (SDI).

Results: Globally, the age-standardised prevalence rate of acne vulgaris among adolescents and young adults increased from 8,563.4 per 100,000 population (95% UI 7,343.5-9,920.1) in 1990 to 9,790.5 (95% UI 8,420.9-11,287.2) per 100,000 population in 2021, with an AAPC of 0.43 (95% CI 0.41-0.46). The age-standardised incidence rate and age-standardised DALY rate also showed a similar upward trend. Regionally, Western Europe had the highest age-standardised prevalence, incidence, and DALY rates, while North Africa and the Middle East had the largest increase in these rates. By SDI quintile, the high SDI region had the highest age-standardised prevalence, incidence, and DALY rates from 1990 to 2021, whereas the low-middle SDI region had the lowest burden of acne vulgaris but experienced the most significant increase in these rates. Globally, the age-standardised prevalence rate of acne vulgaris in 2021 was approximately 25% higher in females than in males (10,911.8 per 100,000 population vs. 8,727.8 per 100,000 population). Among all age groups, adolescents aged 15-19 years had the highest age-specific prevalence rate, while adolescents aged 10-14 years experienced the largest increase from 1990 to 2021 (AAPC = 0.50, 95% CI 0.48-0.52).

Conclusions: The burden of acne vulgaris among adolescents and young adults has continued to increase in nearly all countries since the 1990s. Managing this condition remains a significant challenge, necessitating more effective and targeted interventions to control the acne burden.

© The Author(s) 2024. Published by Oxford University Press on behalf of British Association of Dermatologists. All rights reserved. For commercial re-use, please contact [email protected] for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact [email protected].

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Global, regional, and national burdens of acne vulgaris in adolescents and young adults aged 10-24 years from 1990 to 2021: a trend analysis

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Zhou Zhu, Xiaoying Zhong, Zhongyu Luo, Mingjuan Liu, Hanlin Zhang, Heyi Zheng, Jun Li, Global, regional, and national burdens of acne vulgaris in adolescents and young adults aged 10-24 years from 1990 to 2021: a trend analysis, British Journal of Dermatology , 2024;, ljae352, https://doi.org/10.1093/bjd/ljae352

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Acne vulgaris is a common skin condition affecting adolescents and young adults worldwide, yet data on its burden and trends remain limited. We aimed to investigate trends in the burden of acne vulgaris among adolescents and young adults aged 10-24 years at global, regional, and national levels.

We retrieved data from the Global Burden of Disease Study (GBD) 2021 for individuals aged 10-24 years in 204 countries and territories from 1990 to 2021. We analyzed the numbers, age-standardised rates, and average annual percentage changes (AAPCs) of the prevalence, incidence, and disability-adjusted life-years (DALYs) for acne vulgaris at the global, regional, and national levels. Additionally, we examined these global trends by age, gender, and Socio-demographic Index (SDI).

Globally, the age-standardised prevalence rate of acne vulgaris among adolescents and young adults increased from 8,563.4 per 100,000 population (95% UI 7,343.5-9,920.1) in 1990 to 9,790.5 (95% UI 8,420.9-11,287.2) per 100,000 population in 2021, with an AAPC of 0.43 (95% CI 0.41-0.46). The age-standardised incidence rate and age-standardised DALY rate also showed a similar upward trend. Regionally, Western Europe had the highest age-standardised prevalence, incidence, and DALY rates, while North Africa and the Middle East had the largest increase in these rates. By SDI quintile, the high SDI region had the highest age-standardised prevalence, incidence, and DALY rates from 1990 to 2021, whereas the low-middle SDI region had the lowest burden of acne vulgaris but experienced the most significant increase in these rates. Globally, the age-standardised prevalence rate of acne vulgaris in 2021 was approximately 25% higher in females than in males (10,911.8 per 100,000 population vs. 8,727.8 per 100,000 population). Among all age groups, adolescents aged 15-19 years had the highest age-specific prevalence rate, while adolescents aged 10-14 years experienced the largest increase from 1990 to 2021 (AAPC = 0.50, 95% CI 0.48-0.52).

The burden of acne vulgaris among adolescents and young adults has continued to increase in nearly all countries since the 1990s. Managing this condition remains a significant challenge, necessitating more effective and targeted interventions to control the acne burden.

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Helicobacter pylori and acne vulgaris: is there a relationship?

• Original Paper
• Open access
• Published: 14 September 2024
• Volume 316 , article number  621 , ( 2024 )

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• Ahmed Abdelfattah Afify   ORCID: orcid.org/0000-0002-7163-5383 1 ,
• Hanan Mohamed Ahmed Saleh 1 &
• Abeer Farrag Hussein 1  

Background: Helicobacter pylori (H. pylori) is a gastric Gram-negative, spiral-shaped microaerophilic pathogen. H. pylori may play a potential pathogenic role in extra-intestinal diseases such as hepatobiliary, respiratory, and dermatological disorders. The latter included chronic urticaria, psoriasis and rosacea. The first report in literature on the relationship between H. pylori and acne vulgaris (AV), found association between severe AV and H. pylori infection. There are very limited data in AV patients addressing the impact of H. pylori infection on various severities. In this context, the aim of the present work was to determine the association of H. Pylori infection among AV patients and correlate it with the disease severity. Methods: This case-control study included 45 Patients with AV and 45 age and sex matched healthy volunteers as a control group. H. pylori antigen in stool and serum H. pylori antibody IgG using commercially available ELISA kits was tested in all included subjects. Results: The percentage of participants with a positive H. pylori antigen in stool and positive H. pylori antibody in serum in the whole study population was 35/90 (38. 9%) and 41/90 (45. 6%). On comparing between the percentages of positive H. pylori antigen in stool and positive H. pylori antibody in serum between the patients with AV and healthy controls, a highly statistically significant difference was found between the two groups ( P  < 0.001, P  = 0.006). On comparing between the percentages of positive H. pylori antigen in stool and positive H. pylori antibody in serum in the patients with different grades of acne severity and healthy controls, the rate of positive H. pylori antigen in stool and positive H. pylori Ab in serum was significantly associated with severity of acne comparing with healthy controls ( p  < 0. 001). Conclusion: The rate of H. pylori infection in patients with AV is high so it may influence the pathogenesis of this skin disease. Patients with severe AV had higher rates of H. pylori antigen in stool and H. pylori antibody in serum as compared to the patients with mild AV and healthy controls.

Avoid common mistakes on your manuscript.

Introduction

Acne vulgaris (AV), is one of the most common dermatologic complaints [ 1 ]. About 85% of adolescent population and 3% of the adults between the age of 35–44 years have this disease worldwide [ 2 ].

It is a chronic inflammatory disorder of the pilosebaceous unit. The pathogenesis of AV includes disturbed sebaceous gland activity associated with hyperseborrhoea and alterations in sebum fatty acid composition, dysregulation of the hormone microenvironment, interaction with neuropeptides, follicular hyperkeratinization, Propionibacterium acnes (P. acnes), induction of inflammation and dysfunction of the innate and adaptive immunity [ 3 ]. Acne can be manifested in both inflammatory and noninflammatory forms [ 4 ].

Helicobacter pylori (H. pylori) is a gastric Gram-negative, spiral-shaped microaerophilic pathogen closely associated with gastric and extra-gastric diseases [ 5 , 6 ]. Appropriately half of the global population is infected with H. pylori, and the prevalence of H. pylori varied among regions, which appeared to be explained by the differences in economic and social conditions [ 7 ].

The most common routes of H. pylori transmission are oral-to-oral and fecal-to-oral routes. The colonization of H. pylori itself does not cause any symptoms, and < 20% of all infected patients will develop symptoms following infection [ 8 ].

It has been shown that H. pylori may play a potential pathogenic role in extra-intestinal diseases such as hepatobiliary, respiratory, cardiovascular, and dermatological disorders. The latter included chronic urticaria, psoriasis, henoch-schonlein purpura, rosacea, behcet’s disease, alopecia areata and sweet’s syndrome [ 9 ].

The first report in the literature on the relationship between H. pylori and AV, found that there is association between severe AV and H. pylori infection [ 10 ].

Khalid et al. (2021) suggested that AV and H. pylori infection may be related. However, there is insignificant evidence to support a casual association between H. pylori infection and AV per se. More so, there are very limited data in AV patients addressing the impact of H. pylori infection on various severities [ 11 ].

In this context, the aim of the present work was to determine the association of H. Pylori infection among AV patients and correlate it with the disease severity.

Patients and methods

Participants.

This case-control study included 45 Patients with AV and 45 age and sex matched healthy volunteers as a control group. They were recruited from the Dermatology outpatient clinic, Ain Shams University Hospitals and Teba specialized hospital in Luxur government. The study was done in the period from November 2021 to October 2022. Patients < 12 years and > 40 years, patients with a history of drug intake that affects H. pylori such as proton pump inhibitors, clarithromycin, tetracyclines, amoxicillin or metronidazole within the previous 1 month and patients who received any topical or systemic treatment for AV in the past 3 months were excluded. After the approval of Ethics Committee of Faculty of Medicine, Ain Shams University (Approval number: FMASU 670 / 2021), all participants signed an informed consent after explaining for them the objective of the study.

I- Full history taking including personal history, drug history, family history and history of the present illness with special emphasis on: Onset, course and duration of the disease.

II- Clinical examination:

(a) General examination. (b) Dermatological examination: The AV patients were examined for the type of acne (Comedonal, inflammatory or mixed) and the site of AV (Forehead, cheeks, nose, chin, arms, chest and upper back).

III– Severity indices:

For evaluation of severity of the disease, patients with AV were classified into mild, moderate, severe according to the global acne grading system (GAGS). The GAGS score ranges from 0 (no acne), 1–18 (mild acne), 19–30 (moderate acne), 31–38 (severe acne), and > or = 39 (very severe acne) [ 12 ].

lV- Laboratory investigations:

H. pylori antigen in stool (catalogue no. HPY35-k01, Eagle Biosciences) and serum H. pylori antibody IgG (Catalog No: KA0219, Abnova company) using commercially available ELISA kits following the manufacturer guidelines.

Sample collection, handling and storage

Stool specimen collection, handling and storage.

Fresh stool samples were collected from each participant in the study and control group into stool sample collection containers. A minimum of 1–2 mL liquid stool sample or 1–2 g solid sample was the needed sample. The collected fecal sample was transported to the lab in a frozen condition (-20 °C). If the stool sample was collected and tested the same day, it is allowed to be stored at 2–8 °C.

Blood specimen collection, handling and storage

Blood (the volume of blood needed 1 milliliter) samples were taken from each participant in the study and control group and was directly transferred to laboratory for detection of H. pylori immunoglobulin G (Ig G) antibody in serum. Serum prepared from a whole blood specimen obtained by acceptable medical techniques. This kit is for use with serum samples without additives only. Specimens may be refrigerated at 2–8 C o for up to 7 days.

Assay procedure

All samples and standards were prepared as instructed.

H. pylori Ag in stool was measured with monoclonal antibodies-based ELISA kit by sandwich technique by the following steps

A sufficient number of H. Pylori monoclonal antibody-coated microwell strips were placed in a frame to run H. Pylori negative control (1x Assay buffer), positive control and unknown samples induplicate. 100µL of controls (use1x Assay buffer as a negative control) and diluted patient stool samples were added into the designated microwell. Mix by gently tapping the plate. The plate was covered with one plate sealer. Cover with foil or other material to protect from light. The plate was incubated at room temperature for 1 h. The plate sealer was removed and aspiration of the contents of each well was done. Each well was washed 5 times by dispensing 350µL of working wash solution into each well, then complete aspiration of the contents was done. 100 µl of Stop Solution was added to each well and mixed gently. The color change was measured spectrophotometrically at a wavelength of 450 nm.

IgG antibodies against H. pylori in human serum was assessed with ELISA by the following steps

The desired number of coated wells were secured in the holder. 1:40 dilution of test samples, negative control, positive control, and calibrator was prepared by adding 5 µl of the sample to 200 µl of sample diluent. Mix well. 100 µl of diluted sera, calibrator, and controls were dispensed into the appropriate wells. For the reagent blank, 100 µl sample diluent was dispensed in 1 A well position. They were mixed well for 10 s and incubated at room temperature for 30 min. At the end of the incubation period, liquid was removed from all wells. The microtiter wells were rinsed and flicked 4 times with diluted wash buffer (1×) and then one time with distilled water. 100 µl of enzyme conjugate was dispensed to each well and mixed gently for 10 s. Incubation at room temperature for 30 min was done. Enzyme conjugate was removed from all wells. The microtiter wells were rinsed and flicked 4 times with diluted wash buffer (1×) and then one time with distilled water. 100 µl of TMB Reagent was added to each well and mixed gently for 10 s and incubated at room temperature for 20 min. 100 µl of Stop Solution was added to each well including the 2 blanks and mixed gently for 30 s (the blue color changed to yellow color at that moment). The optical density was determined at 450 nm with a microtiter plate reader.

Interpretation of the results

The concentration value of the patients and controls samples were determined from a calibration standard curve which was constructed by plotting the optical density of each standard with respect to the corresponding units’ values, using a linear regression equation.

Statistical methodology

The data were analyzed using Statistical Package for Social Science (IBM Corp, released 2013. IBM SPSS statistics for windows, V. 22. 0. Armonk, NY. USA). Parametric quantitative data were expressed as mean ± standard deviation (SD). Non-Parametric quantitative data were expressed as median and IQR. Qualitative data were described as frequency and percentage.

The categorical variable was analyzed with frequency and percentage. Chi-squared test was used to evaluate the differences in categorical data. Kruskal-Wallis Test was used to evaluate the differences in nonparametric quantitative variables which was not normally distributed and involving more than two groups. Adjusted Mann-Whitney U Test was used to evaluate the differences between two nonparametric quantitative variables. Spearman correlation was used to evaluate the correlation between two variables. All P values were two-tailed and P-value ≤ 0.05 was considered statistically significant and ≤ 0.01 was considered statistically highly significant.

Demographic data

This case-control study included 45 Patients with AV and 45 age and sex matched healthy volunteers as a control group. Sex distribution among the whole study population were 58 females (64. 4%) and 32 males (35. 6%). Age among the whole study population were from 12 to 37 years with mean age = 18.7 ± 4.4 years.

Included AV patients were 29 females (64. 4%) and 16 males (35. 6%). Age ranged from 13 to 36 years with mean age = 18.6 ± 4.5 years (Table  1 ).

Included healthy individuals were 29 females (64.4%) and 16 males (35.6%). Age ranged from 12 to 37 years with mean age = 18.7 ± 4.3 years (Table  1 ). There was no statistically significant difference in age and sex between the two groups ( P  = 0.743, P  = 1) (Table  1 ).

Clinical data

Duration of AV range from 7 to 144 months with a median (36 months). Family history of AV was positive in 39 patients (86.6%). The type of AV was inflammatory in 12 patients (26. 7%), comedonal in 6 patients (13.3%) and mixed in 27 patients (60. 0%).

Involved acne sites were (forehead & cheeks) in 13 patients (28. 9%), (forehead, cheeks and nose) in 3 patients (6. 7%), (forehead, cheeks, nose and chin) in 12 patients (26. 7%), (forehead, cheeks, nose, chin, chest and upper back) in 7 patients (15. 6%), (forehead, cheeks, nose and chest) in 3 patients (6. 7%), (forehead, cheeks, nose and upper back) in 3 patients (6. 7%), (forehead, cheeks, chin, chest and upper back) in 1 patient (2. 2%), (forehead, cheeks, nose and upper back) in 1 patient (2. 2%), (forehead, cheeks and chin) in 1 patient (2. 2%) and (forehead, cheeks and upper back) in 1 patient (2. 2%).

According to the GAGS assessment, the severity of AV was classified as mild in 16/45 (35. 56%), moderate in 16/45 (35. 56%), and severe in 13/45 (28. 88%) of the patients.

Laboratory data

The percentage of participants with a positive H. pylori antigen in stool in the whole study population was 35/90 (38. 9%). The percentage of participants with a positive H. pylori antibody in serum in the whole study population was 41/90 (45. 6%).

On comparing between the percentages of positive H. pylori antigen in stool between the patients with AV and healthy controls, a highly statistically significant difference was found between the two groups ( P  < 0.001) (Table  2 ).

On comparing between the percentages of positive H. pylori antibody in serum between the patients with AV and healthy controls, a highly statistically significant difference was found between the two groups ( P  = 0.006) (Table  2 ).

On comparing between the percentages of positive H. pylori antigen in stool in the patients with different grades of acne severity and healthy controls, the rate of positive H. pylori antigen in stool was significantly associated with severity of acne comparing with healthy controls ( p  < 0. 001) (Table  3 ).

On comparison, the patients with severe AV had significantly higher rate of H. pylori Ag in stool (92. 3%) as compared to healthy controls (20%, p  < 0. 001) and compared to patients with mild AV (25%, p=. 001), while no statistical significance between mild AV-moderate AV ( p  = 0. 183), healthy controls-mild AV ( p  = 1. 000), healthy controls-moderate AV (p=. 017) and moderate AV-severe AV ( p  = 0. 621) (Table  3 ).

On comparing between the percentages of positive H. pylori antibody in serum in the patients with different grades of acne severity and healthy controls, the rate of positive H. pylori Ab in serum was significantly associated with severity of acne comparing with healthy controls ( P  < 0. 001) (Table  4 ).

On comparison, the patients with severe AV had significantly higher rate of H. pylori Ab in serum (92. 3%) as compared to healthy controls (31. 1%, p  = 0. 001) and compared to patients with mild AV (31. 3%, p=. 007), while no statistical significance between healthy controls-mild AV ( p  = 1. 000), healthy controls-moderate (p=. 188), mild AV-moderate AV ( p  = 0. 465) and moderate AV-severe AV ( p  = 0. 666) (Table  4 ).

Correlation between different variables of AV patients and H. pylori Ag in stool and ab in serum

The number of AV involved sites and severity of AV were significantly correlated with H. pylori Ag in stool and H. pylori Ab in serum (Table 8). While there was no statistically significant correlation between (the type of AV, onset of AV and duration of AV) and H. pylori Ag in stool and H. pylori Ab in serum (Table  5 ).

Acne vulgaris is one of the most common skin diseases worldwide that significantly affects the patients’ life quality and often associated with anxiety and depression [ 13 ].

It is a chronic inflammatory skin disorder. Multiple factors contribute to acne pathogenesis, including increased sebum production, aberrant keratinization of the pilosebaceous duct, bacteria such as P. acnes, hormonal influences, the skin microbiome and chronic inflammation [ 14 ].

There is a growing concern toward the role of H. pylori in the pathogenesis of many skin diseases [ 9 ]. It was found that H. pylori infection is involved in the development of rosacea. It is suggested that rosacea patients should be tested for H. pylori infection, the H. pylori-positive rosacea patients should be treated with eradication of H. pylori, so as to enhance the therapeutic effect on rosacea [ 15 ].

This study was conducted to determine the prevalence of H. pylori infection in patients with AV and to correlate it with the disease severity.

In this study H. pylori antigens in stool were detected in 57. 8% of patients with AV and H. pylori (IgG) antibodies in serum were detected in 60% of patients with AV and these were significantly higher from the rates in healthy controls. Also, when the patients were stratified according to the severity of acne, the group presented with severe AV had significantly higher rate of positive H. pylori antigen in stool and positive H. pylori antibody in serum as compared to the healthy controls and mild AV patients. However, the differences between healthy controls and patients with mild or moderate AV were not statistically significant. The above-mentioned findings agreed with the observations of Khodaeinai et al., (2014) the first report in the literature on the relationship between H. pylori and AV, showed in his case-control study on 100 (25 control, 75 cases) individuals. The rate of H. pylori infection was found in 56% of control group, 60% in the cases of mild AV, 72% of moderate and 88% of severe AV patients. Frequency of H. pylori infection was significantly associated with severity of acne comparing with controls. Mean serum IgG was also significantly high in the group with severe disease [ 10 ].

Also, our findings agreed with the findings in Saleh et al., (2020) which showed that the patients with severe AV had significantly higher levels of fecal H. pylori antigen as compared to the patients with mild AV, moderate AV, and healthy controls (P <. 001) [ 16 ]. Also, Khalid et al., (2021) in his cross-sectional study which included 135 patients, 48 (35.56%) females and 87 (64.44%) males with male to female ratio of 1.8:1.0. The frequency of H. pylori infection in patients of AV was seen in 107 (79.26%) patients [ 11 ].

A prospective cohort study was done by Khashaba et al., (2020) to detect the prevalence of H. pylori in AV patients of different severities and the impact of its eradication on clinical outcome. It included 66 patients along with 22 controls. There was statistically significant increase in anti-Helicobacter immunoglobulin G index in severe acne group and statistically significant decrease in total lesion count after triple therapy in all groups ( P  = 0.002, 0.04, 0.001) [ 17 ].

In our study the number of AV involved sites and severity of AV were positively correlated with the rates of H. pylori antigen in stool and H. pylori antibody in serum. The observations of our study indicate that the prevalence rate of H. pylori infection in patients of AV is high and H. pylori infection may be related to increasing the severity of AV.

A possible mechanism for the association of AV and H. pylori infection may be related to that H. pylori leads to formation of increased number of reactive oxygen species like inflammatory cytokines and superoxide. These toxic metabolites enhance the inflammation of the gastric mucosa as well as pilosebaceous units in skin leading to AV [ 16 ].

Secondly, there is a mechanism suggested that H. pylori infection might significantly be associated with seborrhea. Another possible mechanism which can lead to the development of AV is the direct involvement of H. pylori. According to researches, there may be cross-mimicry between H. pylori and extra digestive antigens present in the skin. Further H. pylori produces an enzyme, lipase. This enzyme has significant role in the pathogenesis of AV. This lipase activity of H. pylori significantly correlates the association of H. pylori with AV [ 11 ].

Additionally, the antibiotics that are known to be effective in AV such as metronidazole, tetracycline, and doxycycline, are also effective against H. pylori infection. Such observation may also suggest a possible role of H. pylori infection, in the pathogenesis of AV [ 18 ].

So, we conclude that the rate of H. pylori infection in patients with AV is high so it may influence the pathogenesis of this skin disease. Patients with severe AV had higher rates of H. pylori antigen in stool and H. pylori antibody in serum as compared to the patients with mild AV and healthy controls.

Data availability

No datasets were generated or analysed during the current study.

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Dermatology, venereology and andrology department, Faculty of medicine, Ain Shams University, Cairo, Egypt

Ahmed Abdelfattah Afify, Hanan Mohamed Ahmed Saleh & Abeer Farrag Hussein

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Afify, A.A., Saleh, H.M.A. & Hussein, A.F. Helicobacter pylori and acne vulgaris: is there a relationship?. Arch Dermatol Res 316 , 621 (2024). https://doi.org/10.1007/s00403-024-03300-w

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Received : 04 January 2024

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Published : 14 September 2024

DOI : https://doi.org/10.1007/s00403-024-03300-w

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