Acne (overview) L70.0

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 28.07.2022

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Synonym(s)

Acne; acne vulgaris; Classic acne; Vulgar Acne

Definition
This section has been translated automatically.

Common, chronic inflammatory, polyetiological disease of the sebaceous follicles, which occurs in a large part of the population in adolescence in western industrial nations. A chronic-continuous or relapsing course is typical.

Acne develops from a complex interaction of different pathogenetic factors. As a result of the plug-like occlusion of the follicular excretory duct and simultaneous seborrhoea, the sebum is backed up into the follicular gland unit = comedo (acne comedonica). Follicular pustules (acne papulopustulosa) develop as a result of purulent melting. In severe courses (acne conglobata), follicular ruptures due to comedone components lead to pronounced inflammatory processes deep into the dermis, with furunculoid, frequently confluent, painful abscesses (acne conglobata). Leading clinical symptoms are seborrhoea, comedones and papulo-pustules. Due to the chronicity of the disease, treatment is designed as a months- or years-long management.

Classification
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According to predominant efflorescences, 3 clinical types are distinguished, with transitional forms being more typical than rare:

Special forms of acne vulgaris

Occurrence/Epidemiology
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Worldwide disease.

In Germany, 70-80% of all adolescents show signs of acne vulgaris of varying severity.

In the USA, 40-50 million people are affected annually. Affected are mainly male, less frequently female adolescents, and young adults aged 12-24 years.

In a British population study of women > 25 years, acne prevalence was 54%.

In a French study of women aged 24-40 years, prevalence was 41%.

In a U.S. study, prevalence figures were 51% for women aged 30-39 years, 26% for women aged 30-39 years, and 15% for women aged 40-49 years.

Women are more commonly affected by late acne or acne tarda than men.

Etiopathogenesis
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Acne results from a complex interaction of different pathogenetic factors. As a result of the plug-like occlusion of the follicular excretory duct, with simultaneous seborrhea, sebum is backed up into the follicular gland unit = comedo(acne comedonica). Follicular pustules develop as a result of purulent melting(acne papulopustulosa). In severe courses(acne conglobata), follicular ruptures caused by comedone components lead to pronounced inflammatory processes deep into the dermis, with furunculoid, often confluent, painful abscesses(acne conglobata). Leading clinical symptoms are seborrhea, comedones and papulo-pustules. Due to the chronicity of the disease, treatment is designed as months- or years-long management.

A polyetiological mechanism is postulated for the etiopathogenesis of acne. The following factors play a role:

  • Genetic factors
    • Insulin resistance and hyperinsulinemia; elevated levels of IGF-1 (see insulin-like growth-factor under growth factors) correlate with the total number of acne lesions.
    • Identical twins have a high concordance regarding acne.
    • Relevant gene polymorphisms are found in genes coding for androgen receptors, for enzymes of androgen metabolism, for tumor necrosis factor-alpha and for insulin-like growth factor.
  • Seborrhea (sebum is the "fuel of the acne flame"!)
    • Sebum is produced holocrine from sebocytes, main components are triglycerides, fatty acid esters and squalene. Androgens regulate sebum production. The adrenal dehydroepiandrosterone sulfate (DHEA-S) is the primary physiological control hormone. It is enzymatically converted in sebocytes to more potent androgens such as testosterone and dehydrotestosterone.
    • The ratio: saturated fatty acids/unsaturated fatty acids is increased.
    • Composition of the sebum is altered
  • Cornification disorders
    • In the infundibulum of the sebaceous follicle, there is a differentiation disorder of the keratinocytes with increased proliferation as well as increased adhesiveness to each other. Here, interleukin-1 plays an initiating role. The resulting proliferation-retention hyperkeratosis leads to the formation of initially clinically invisible microcomedones; further comedone growth leads under dilatation of the follicular ostium to open comedones darkened by melanin. Free palmitic acid and oleic acid have a comedogenic effect and induce the follicular cornification disorder.
  • Bacterial colonization and biofilm formation by Propionibacterium acnes
    • Propionibacteria produce a matrix of glycocalyx polymers that are thought to increase keratinocyte adhesiveness (Degitz K et al. 2017). Free oleic acid in acne sebum promotes hyperconolization of the site germ P. acnes. Furthermore, propionibacteria produce esterases that release irritant fatty acids from triglycerides.
  • Insulin-like-growth-factor 1 (IGF-1)
    • Insulin-like-growth-factor 1 (IGF-1): IGF-1 is an important growth hormone during adolescence. The growth factor is elevated in acne patients. It induces sebocytic lipogenesis in lipocytes and acts costimulatory with androgens (Melnik BC 2015). IGF-1 as well as insulin inhibits the transcription factor FoxO1 in sebocytes with a concomitant increase in mTORC1 activity (Mirdamadi Y et al. 2015). Acne does not occur in congenital IGF1 deficiency(Laron syndrome) or in individuals with nonfunctional androgen receptors.
  • Insulin
    • Acne is combined with increased insulin resistance(dietary factors; muscle building products (kolek products, casein concentrates leading to bodybuilding acne)). IGF-1 as well as insulin inhibit the transcription factor FoxO1 in sebocytes (Mirdamadi Y et al. 2015). Known insulin resistance in acne associated syndromes such as PAPA syndrome, SAPHO syndrome.
  • Body Mass Index: A high "body mass index" is a risk factor for adolescent acne expression (Sas K et al. 2019).
  • FoxO1: The Fox O1 protein (see forkhead box genes below) is a central switch in insulin regulation as well as glucose metabolism. FoxO1 inhibits important transcription factors of lipid synthesis such as: PPARgamma, LXRalpha, SREBP1 as well as the kinase mTORC1. Furthermore, FoxO1 inhibits the androgen receptor (AR).
  • Isotretinoin compensates for the consequences of increased insulin/IGF-1 signal transduction with nuclear FoxO1 deficiency. The prodrug, which is isomerized to all-trans-retinoic acid in the cell, upregulates FoxO transcription factors through activation of the retinoic acid receptor(RAR) via numerous intermediate steps. Thus, isotretinoin initiates FoxO-mediated programmed cell death (apoptosis) of sebum-producing cells (sebocytes).
  • Inflammation with interactions between sebaceous glands and perifollicular connective tissue.
    • The importance of innate immunity for acne focuses in the activation of the inflammasome. P. acnis is thought to play an activating role through secretion and activation of proinflammatory mediators (IL-1beta, NLPRP-3 inflammasome, activation of caspase-1 pathway).
  • Sebaceous gland hyperplasia (mostly androgen stimulated)
    • In women, polycystic ovary syndrome(PCOS) should be considered!
  • Psychological factors
  • Smoking may promote acne.
  • Nutrition
    • (High glycemic index foods, dairy products). These lead to a dietary increased hyperglycemic load, induction of insulin and IGF-1. In combination with the already high serum IGF1 levels in adolescence, this constellation leads to promotion of seborrhea and follicular hyperkeratosis (Melnik BC 2015).
  • Medications:
    • Anticontraceptives with a restandrogenic component (e.g., 19-nortestosterone derivatives).
    • DHEA-S
    • Anabolic steroids
    • Lithium
    • Vitamin B supplements (esp. vitamin B12 - Kang D et al. 2015).
    • EGFR inhibitors: The use of EGFR inhibitors, depending on therapy duration, shows follicular (acneiform) papulo-pustular exanthema in the area of seborrheic zones in a period of 2 weeks. Comedones are typically absent. The severity of the exanthema is considered a measure of therapeutic response to EGFR inhibitors. EGF is thought to exert a control function on the inflammatory processes of acne vulgaris (Aydingoz IE et al. 2021).

Acne fulminans is defined as acne conglobata with a severe immunological systemic reaction (sickness, fever, bone pain, vasculitis).

Manifestation
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V.a. in adolescents and young adults; more pronounced in boys or men than in girls or women.

In Germany, 70-80% of all adolescents show signs of acne of varying severity.

In the USA, 40-50 million people are affected annually. Affected are mainly male, less frequently female adolescents, and young adults aged 12-24 years.

In a British population study of women > 25 years, acne prevalence was 54%.

In a French study of women aged 24-40 years, prevalence was 41%.

In a U.S. study, prevalence figures were 51% for women aged 30-39 years, 26% for women aged 30-39 years, and 15% for women aged 40-49 years.

Women are more likely to be affected by late acne or acne tarda than men.

Localization
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Infestation of the so-called seborrhoic zones. Here mainly face, shoulders and back, upper sternal area.

Clinical features
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Comedones, papules and pustules, nodules, abscesses, cysts, scars.

Laboratory
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In severe and unclear cases of both sexes: BSG, CRP, BB, IgG, IgM, IgA, IgM, IgA, zinc, α-1-antitrypsin, TPHA.

If necessary, exclusion of HIV infection.

Women with signs of cycle disorders or androgenisation: total testosterone, free testosterone, SHBG, prolactin, DHEAS, androstendione.

Optional: LH, FSH, blood sugar, insulin, DHT, cortisol, estradiol, TSH.

Histology
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Follicular hyperkeratosis, enlarged sebaceous glands.

Diagnosis
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  • medical history: time of onset, progression (spontaneous, insidious), family history, cosmetics, medications, previous treatment, allergies, endocrinological diseases
  • If necessary, laboratory values (see laboratory below)
  • Hair type, physique (androgenisation in women)
  • Determination of severity based on primary and secondary fluorescence and the severity of the manifestation
  • Antibiogram from smear of comedone content, pustules or papules
  • Antibiogram from a smear taken from the nasal mucosa (colonisation with Gram-negative germs, staphylococci, dermatophytes, yeasts, moulds)
  • Biopsy if necessary
  • Counting of precursor efflorescences on the cyanoacrylate preparation
  • If necessary: skin function tests (lipometry, TEWL)

General therapy
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The therapy depends on the type of acne, the severity of the acne, the age of the patient and the skin type.

  • Graduation of acne to assess the success of therapy is useful before starting therapy: e.g. counting of all acne lesions per half of the face or in a 20 x 20 cm field and classification according to open/closed, papules, papulopustules, nodules. See below Acne comedonica, Acne papulopustulosa.
  • Cleaning: Purely mechanical with a microfiber glove, Claroderm and water without further additives.
  • Regular, not too frequent washing with pH-neutral soaps is recommended, e.g. Sebopona, Cetaphil, Satina, Eubos, Stephalen Waschgel, Sebamed flüssig. Antiseptic or antibacterial cleansers are not indicated, as they neither capture Propionibacterium acnes nor act in the depth of the follicle. O/W-type creams or emulsions are suitable for skin care, e.g. Toleriane, Physiane, Hydranorm, Avène Cleanance, Lutsine Kerafnia, Eucerin Rebalance, Eucerin Creme-Gel. Tinted acne therapeutics such as Aknichthol-Lotio are good as color-regulating topicals to cover inflammatory redness.
  • Avoid comedogenic topicals, especially cosmetics. If make-up is not avoided, make-up suitable for acne should be used, e.g. Unifiance by La Roche Posay or Lutsine make-up pencil, in each case after testing the color shade.
  • In terms of food, a reduction of the glycemic load (high proportion of unsaturated fatty acids, legumes, vegetables >> fruit) should be brought about by a wise selection.

External therapy
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The available acne therapeutics are used alone or in combination for the different forms of acne according to their optimal effect.

  • Retinoids: Tretinoin and isotretinoin are the classic first- and second-generation retinoids, respectively. Tretinoin is available in concentrations of 0.025 to 0.1% in the form of creams, solutions and gels (see below gels, hydrophilic, gels, hydrophobic), isotretinoin, previously available as 0.05 to 0.1% gel or cream (e.g. Isotrex®), currently out of sale, see table below. For seborrheic skin type, gels and solutions should be preferred, for normal skin gels and creams. Application is initially 1 time/day, preferably in the evening, as slight redness occurs, possibly also burning and itching. If well tolerated, can be increased to 2 times/day. All other external acne therapeutics should be discontinued until habituation to vitamin A acid has occurred. The corners of the mouth and eyelid region should be avoided. In about 30% of patients, after 2-4 weeks of treatment, pustules appear as a result of rupture of the microcomedones. Despite this apparent blossoming of acne, treatment should be continued. After about 4 weeks, "hardening" has occurred and the irritations recede. Direct sun exposure should be avoided as tretinoin and isotretinoin lower the erythema threshold and are not light stable.
  • Since the end of 2020, there is a 4th generation retinoid: trifarotene, Selgamis®. This selectively binds to the retinoid receptor gamma and at the same time has an anti-inflammatory effect. The large-area application (max. 2 g on face and trunk) also allows the treatment of acne on the trunk.
  • Adapalene: (Differin® Gel/Cream) is a synthetic polyaromatic retinoid of the third generation. In addition to comedolytic activity, it has stronger anti-inflammatory activity than tretinoin and isotretinoin. It only needs to be used 1 time/day.
  • Adapalene/ Benzoyl Peroxide (BPO) (e.g. Epiduo® Gel 0.1%/2.5%): The combination of retinoid and BPO is an approach that combines the advantages of both therapeutic modalities and does not involve the risk of antimicrobial resistance. Apply 1 time/day, in the evening, as a thin film on the acne affected skin areas, after the skin has been previously cleansed (e.g. Dermowas) & dried.
  • Tazarotene: Application (off-label use) of tazarotene (e.g. Zorac Gel 0.1%) overnight or 2 times/day for 5-10 minutes is according to studies comparable to the effectiveness of above mentioned retinoids.
  • Notice. Topical retinoids are suitable for maintenance therapy because they have an anticomedogenic effect and thus prevent the formation of new microcomedones. The success of therapy can usually only be assessed after 3 months: reduction of the number of efflorescences (acne comedonica, acne papulopustulosa) by > 50% is considered a good response, reduction by > 75% a very good response. Treatment should be continued as long as signs of clinical activity are still present.
  • Azelaic acid: The substance has an antimicrobial effect at high concentrations, but the effect is not as pronounced as with benzoyl peroxide. Azelaic acid is used in a concentration of 20% (Skinoren). The onset of action is delayed compared to other external acne therapeutics. Temporary irritation, scaling, burning, itching may occur in the first 2-4 weeks. As a rule, azelaic acid is often better tolerated than other external acne therapeutics, especially in sensitive skin (atopics). Azelaic acid can be administered during pregnancy. In addition to the cream form, a gel preparation is available.
  • Salicylic acid: Possesses a demonstrable comedolytic effect; keratolytic activity is too weak in most concentrations used to be expected to have any effect on acne here. Salicylic acid is used externally in various concentrations and combinations with other active ingredients. For preparations see Table 1.
  • Benzoyl peroxide (BPO): Has a keratolytic and strong antimicrobial effect without the risk of developing resistance. Gram-positive germs, which are found in abundance in sebaceous glands, are rapidly destroyed. This applies in particular to Propionibacterium acnes. BPO is available in 1.5/3/5/10% concentration in creams, emulsions, hydrogels and alcoholic gels, e.g. Akneroxid® Gel 5%-10%, Akneroxid L Suspension, Benzaknen® 5%-10%, Benzaknen® W Suspension, Sanoxit® 2.5-10%, Sanoxit® MT Suspension, Akneroxid® Gel 5%-10%. Emulsions are often better tolerated than gels. As a rule, the preparation is applied thinly 1 time/day. After application of benzoyl peroxide, there is initially slight skin irritation with drying of the skin, redness and scaling in the first days to weeks. A habituation effect usually occurs within a few weeks. Special caution should be exercised when used on atopic skin. Rarely, contact sensitization to BPO may occur. Patients must be alerted to the fact that BPO will discolor or bleach hair, clothing, and bedding, towels, etc. Benzoyl peroxide can be used as a gel in 3.0, 5.0 or 10.0% concentration as a formulation (see below Benzoyl Peroxide Gel NRF 11.25.). Benzoyl peroxide /Clindamycin: Good clinical effects can be achieved by the BPO/CLN combination (DUAC®-Gel ). This combination is superior to monotherapy with azelaic acid (Schaller 2016).
  • Abrasives (peeling agents): Aluminum oxide (e.g. Brasivil) or polydimethylsilicone resin (e.g. Jaikin) have a mild peeling effect, but usually do not reach the comedones. Caution is advised in particular with simultaneous therapy with preparations such as vitamin A acid, benzoyl peroxide or azelaic acid.
  • Peeling substances: α-hydroxy acids such as lactic acid and glycolic acid for the reduction of hyperkeratoses are recommended again and again, see also below Chemical peeling.
  • Fruit acids (α-hydroxy acids): α-hydroxy acids reduce corneocyte adhesion and thus keep the follicular ostia open, which leads to a reduction in the number of comedones. The indication is mainly follicular hyperkeratosis. Application: 1 time/day, in case of good tolerance 2 times/day. Subsequent chemical peeling with 70% glycolic acid and manual physical acne therapy bring faster success. α-Hydroxy acids can also be used with sun exposure. Onset of action after 6 weeks.
  • Antibiotics: Three main groups of antibiotics are used in external acne therapy:
    • Tetracyclines
    • Erythromycin (e.g., Aknemycin® ointment/solution, Eryaknen® 2-4% gel).
    • Clindamycin (e.g., Basocin® acne solution; Basocin® acne gel; DUAC® gel [combination with BPO]).
  • Nadifloxacin (Nadixa® cream) has also recently been approved. However, the growth inhibition of Propionibacterium acnes with externally applied antibiotics is inferior to that of benzoyl peroxide. According to study results, clindamycin and erythromycin show the best success in inflammatory acne. Local side effects consist of redness, scaling, and burning of the skin. Rarely, bloody diarrhea and colitis (including pseudomembranous colitis) may also occur after topical application of clindamycin. Topical antibiotics are usually used in combination with topical retinoids (Aknemycin® plus), salicylic acid, BPO or abrasives and should be time-limited due to the risk of resistance development. Long-term use may result in selection of the bacterial spectrum in favor of gram-negative pathogens, in the sense of gram-negative folliculitis.
  • Glucocorticoids: They can be used in ointment or cream form for a few days in cases of highly inflammatory acne. Intralesional application is possible in abscessed nodules.

Radiation therapy
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UV phototherapy: The use of UVB rays or UVA u. UVB rays leads to an improvement of the symptoms. UV phototherapy is outdated due to an unfavorable risk-benefit ratio.

Although photodynamic therapy is effective, it cannot be recommended as a routine procedure because of the not insignificant side effects (Degitz K et al. 2017).

Combined light therapy using LED mask with blue and red light (wavelength 445 nm and 630 nm) shows a sifnificant reduction of inflammatory and non-inflammatory acne efflorescences in the studies (Nestor MS et al. (2016)

Internal therapy
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Systemic treatment is reserved for the severe form of acne vulgaris which is not optimally accessible to external therapy.

Antibiotics (tetracyclines and macrolide antibiotics [e.g. erythromycin, roxithromycin]) are the standard preparations. The antibiotic of first choice is minocycline (e.g. skid, acnosan, clinomycin), followed by doxycycline (e.g. doxacne).

  • Tetracycline: Minocycline is generally better tolerated than doxycycline, but much more expensive. The initial dosage of minocycline is 50 mg p.o. 2 times/day. (with meal), then reduction to a maintenance dose of 50 mg/day. Doxycycline: once/day 50 mg p.o. Tetracycline (Tefilin): 1500 mg/day, possibly higher doses, initial 3 times/day 500 mg (before meal, no milk) for 1-2 months. The phototoxic effect of this group of substances must be taken into account; it is less pronounced with doxycycline than with tetracycline hydrochloride; minocycline is considered safer in this respect.
  • Notice! Many tetracyclines have a phototoxic effect!

    Notice: Many tetracyclines are phototoxic. No combination with systemic retinoids!

  • Macrolide antibiotics: Erythromycin (e.g. Erythromycin-ratiopharm) should be given in a dosage of 500-1000 mg/day; Roxithromycin (Roxithromycin-ratiopharm) in a dosage of 150-300 mg/day.

    Notice! Dangers of long-term systemic antibiotic treatment include development of resistance, Gram-negative folliculitis and renewed blooming of papulopustules!

Hormone therapy (only for women): cooperation with gynaecologists.

  • Estrogens: Estrogens inhibit sebum production. The most common contraceptives contain 50 mg ethinylestradiol (= sufficient quantity to inhibit sebum production). Hormone therapy is reserved exclusively for women with severe acne and a minimum age of 16 years. Not a therapy of the 1st choice.
  • Anti-androgens: In acne patients an accelerated androgen metabolism in the sebaceous glands with a consecutively increased rate of mitosis in the sebocytes and stimulation of lipid synthesis can be observed. Cyproterone acetate (CPA) has an antiandrogenic and progesterone effect. It inhibits all androgen-dependent organs and thus also the sebaceous glands. The indication is only given for women. Due to the expected cycle disorders, a combination with ethinylestradiol is indicated. Combination preparations are for example Clevia, Diane 35 or Climen. Chlormadinone acetate and megestrol acetate are less effective than cyproterone acetate, a reduction in sebum reduction occurs after several cycles; e.g. Esticia, Gestamestrol N (2 mg chloromadinone acetate and 50 μg Mestranol). In severe cases, estrogen therapy can be supplemented by the administration of 5-10 mg CPA (e.g. Androcur 10 mg) over 15 days (see Table 3).
    Cave! Thromboembolic complications occur especially in smokers, overweight patients or patients with arteriosclerosis.
    Patients with livedo racemosa, Sneddon syndromeare excluded from antiandrogenic therapy. The formulation of antiandrogens belongs in the hands of the gynaecologist. The indication is set by the dermatologist, dosage, implementation and control of the therapy is left to the gynaecologist. The duration of therapy should be at least 1 year, if necessary years, also in combination with isotretinoin. An improvement of the acne can be expected at the earliest after 2-3 months of therapy. Problems arise when the hormone therapy is discontinued: rebound with eruption of papulopustules.

Isotretinoin (e.g. acne normin) is indicated according to the European Directive (EMA) in severe inflammatory forms of acne vulgaris with the risk of permanent scarring. The prescription for acne conglobata or nodular acne is undisputed.

Notice! When isotretinoin is prescribed for women of childbearing age, a pregnancy test must be carried out before the start of therapy and safe contraception must be requested one month before the start of therapy, throughout the course of therapy and one month after the end of therapy (some authors recommend up to 3 months).

Cave! Teratogenicity: Not allowed in women of childbearing age. The civil law and possibly also criminal law responsibility is therefore explicitly with the treating physician!
Recurrences: As a rule, adequate therapy with isotretinoin leads to long lasting remissions (weeks to years). After discontinuation of the isotretinoin, a relapse may occur. This is usually milder than the original acne. The recurrence rate is inversely proportional to the therapeutic dose administered. With a cumulative dose < 120 mg/kg bw, a relapse is much more likely than with a total dose > 120 mg/kg bw, which is why this dose should be reached if possible. In case of recurrence, renewed therapy may be necessary in some cases.

Combinations with hormones: In cases of severe inflammatory acne conglobata or acne fulminans, combination therapies with hormones (antiandrogens, anticontraceptives, glucocorticoids) are possible. In particular, the use of glucocorticoids for a limited period of time can, in individual cases of severe inflammatory acne, result in a significant reduction of the inflammatory reaction.

Care measures: In order to reduce the unpleasant side effects of dry lips, locally refatting lip care products, e.g. Rolip Emulsion, Rolip Mandelic, Labello or similar can be used.

Progression/forecast
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Acne usually starts around the age of 12. However, clinical symptoms may occur in some patients as early as the 7th to 9th year of life. In most cases it ends spontaneously, at the end of the growth phase, between the ages of 17 and 25. In some patients, however, the acne continues into the fourth and fifth decade (persistent acne) or does not begin until older age (acne tarda).

Naturopathy
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see also under phytotherapy

In a double-blind, placebo-controlled study (n=82), the daily intake of lactoferrin (250mg/day p.o.) in combination with vitamin E and zinc proved to be successful in mild to moderate acne vulgaris (Chan H et al. 2017).

Remediation of the microbiome (totality of all microorganisms and their genes) whereby a connection between gut - and skin microbiome, the so-called gut-skin axis, is known. A disturbance of this microbiome, a dysbiosis, has been described in acne patients. Probiotics also have an inhibiting effect on the proliferation of C. acnis.

Order therapy: Avoidance of triggering causes, see also under diet/living habits, reduction of psychological stress, avoidance of manipulation of the acne florescences.

Hydrotherapy: moist compresses with astringent, drying plants like oak bark, black tea

Peloid therapy: masks with healing clay for pustules and papules

Phytotherapy, see below

Tables
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Keratolytic/comedolytic topicals in acne therapy

Active agents

Preparation

Concentration

Example preparations

Monopreparations

Tretinoin

solution

0,05%

Airol

Cream

0,05%

Cordes VAS, Airol

Isotretinoin

Gel, Cream

0,05%

Isotrex

0,1%

Benzoyl peroxide

Gel

2,5%

PanOxyl Acne, Clinoxide, Sanoxit

5%

PanOxyl Acne, Sanoxite, Benzacne

10%

Sanoxite, Benzacnene

Emulsion

5%

PanOxyl mild

10%

PanOxyl W emulsion

Cream

2,5%

PanOxyl mild

5%

PanOxyl mild, clinical oxide

10%

Clinoxide forte

Washing emulsion

10%

PanOxyl W, benzacne

Azelaic Acid

Cream

15%

Skinoren

Adapalene

Cream, Gel

0,1%

Differin

Salicylic acid

Solution

5%

214

10%

214

Sulphur

Cream

3%

Sulphur Diasporal

Combinations of active ingredients

Combination preparations

Adapalene Benzoyl peroxide Gel 0,1-0,3%/2,5% Epiduo®

Salicylic Acid

Lactic acid

Solution

0,5/0,2%

Aknederm Tincture N

Salicylic Acid

Na-Bituminosulf.

Lotio

0,5/1%

Aknichthol N/soft

ammonium bit.

Zinc oxide

Ointment

2/10%

Aknederm Ointment New

Salicylic acid

Lactic acid

Tincture

0,5/0,2%

Akaderm Tincture N

Sulfur Diaspora

Sulphur

Camphor

Milk

0,1/0,36%

l

Locally acting antibiotics

Generic

Preparation

Concentration

Example preparation

Tetracycline

Ointment

3%

Imex ointment, Achromycin ointment

Erythromycin

Solution

2%

Acnefug El

Gel

2%

Aknederm Ery Gel

Emulsion

1%

Aknemycin

Cream

2-4%

Erythromycin cream hydrophilic 0.5/1/2

or 4% (NRF 11.77.)

Ointment

2%

Aknemycin ointment

Clindamycin

Gel

1%

Basocin, Zindaclin

Solution

1%

Basocin Acne Lsg.

Clindamycin/BPO

Gel

1%/5%

Duac Acne Gel

Nadifloxacin

Cream

1%

Nadixa

Hormone therapy for severe acne in women

Example preparation

Dosage

Application period

Diane 35

2 mg cyproterone acetate/35 μg ethinyl estradiol +

1st-21st day of cycle, 7 days off.

Androcur 10

5-10 mg cyproterone acetate

1st-15th day of cycle1/2-1 tbl/day.

Acne therapeutics according to efficacy

Active substance

Follicular hyperkeratosis

Seborrhea

Microbial colonisation

Inflammation

External

Benzoyl Peroxide

(+)

-

+++

+

Azelaic acid

+

-

++

+

Isotretinoin

++

+

+

-

Tretinoin

++

-

+

-

Adapalene

++

-

+

++

Salicylic acid

+

-

+

(+)

Resorcinol

-

(+)

+

+

Sulphur

-

(+)

-

-

Alumina

++

(+)

-

-

Tioxolone

-

+

+

+

Na-Bituminosulf.

-

+

(+)

-

Internal

Chlormadinone acetate

-

+

-

-

Cyproterone acetate

-

++

-

-

Isotretinoin

++

+++

(+)

++

Tetracyclines

-

-

++

+

- not effective; (+) weakly effective; + moderately effective; ++ strongly effective; +++ very strongly effective

Mild forms

Moderate forms

Severe forms

Acne comedonica

Acne papulopustulosa

Acne papulopustulosa (severe)

Nodular acne

Nodular acne/ A. conglobata

1st choice

Topical retinoid

Topical retinoid + top. antibact. drug

Oral antibiotic + top. Retinoid ± BPO

Oral antibiotic + top. Retinoid ± BPO

Oral isotretinoin

Alternatives

Other top. Retinoid or azelaic acid or salicylic acid

Topical retinoid + top. antibact. drug + other top. retinoid or azelaic acid or salicylic acid Retinoid or azelaic acid

Other oral antibiotic + other topical retinoid ± BPO

Oral isotretinoin or other oral antibiotic + other topical retinoid ± BPO

High dose oral antibiotic + top. Retinoid + BPO

Alternatives for women

See below 1st choice

S.u. 1st choice

Oral antiandrogen + top. Retinoid/azelaic acid ± top. antibact. drug

Oral antiandrogen + top. Retinoid ± oral antibiotic ± other antibact. drug

High dose oral antiandrogen + top. Retinoid ± other top antibacterial drug

Maintenance therapy

Topical retinoid

Topical retinoid ± BPO

Diet/life habits
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Scientifically, a triggering of acne vulgaris by food was not proven for a long time. In the meantime, there is a solid evidence on the pathophysiological connection between acne and nutrition, in particular the western dietary style. However, insulin, IGF-1 (see insulin-like growth factor), hyperglycemic diet, highly processed cereal products, polyunsaturated fats and milk play a role in the pathogenesis of acne. High dairy consumption leads to a significant increase in insulin and IgF-1, comparable to a high glycemic index diet. This leads to a stimulation of anabolic signaling pathways with increased lipid synthesis, increased proliferation activity of the follicular epithelium and thus triggering of the acne florescences (see table). Lifestyle habits, lack of sleep, stress, environmental factors like air pollution, climate and solar radiation also play an important role.

Meals should be interspersed with breaks of several hours to reduce insulin and IGF 1 (insulin-like growth factor) levels.

Recommendations for the prophylaxis and dietary treatment of acne before (modified after B. Melnik)
Acne promoting factors Prophylaxis/recommendations
Food and luxury food with acne-inducing effect Food and luxury food without acne-inducing effect
Milk, milk products, cream cheese, whey protein concentrates raw vegetables, fruits, vegetables, blue berries, soy products, tomatoes
Milk chocolate, sweets, lemonade, potato chips, corn flakes, other carbohydrates with a high glycemic index such as: fine flours: white bread, rice, potatoes, wheat pasta, fast food Wholemeal bread and cow's milk free cereals, plenty of fibre with high fibre content, no fast food.
Saturated fats e.g. in lard, pork liver, liver sausage, egg yolk High in omega-3 fatty acids, e.g. sea fish, seafood, chia, linseed, hemp seed, algae.
Smoking Abstain from smoking
Frequent snacks between meals and breaks Taking complete breaks from food intake for several hours at a time
Sweetened soft drinks (e.g. Coca Cola) Mineral water, unsweetened tea, also green tea
Lack of exercise, overweight

Sport, ideal weight

Phytotherapy external
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Phytopharmaceuticals are sufficiently effective exclusively for mild to moderate acne.

The indication acne only exists for the mahonia bark in 10 % ointment preparation.

Furthermore, externals with extracts of the Mediterranean myrtle (Myrtacin®) have proved successful. This product is contained as keracnyl (Ducray) among others. Myrtacin destroys the biofilm of the propionibacterium acnes. Myrtle-saw palmetto extracts: in clinical studies, an antimicrobial and anti-acne effect could be proven by a combination of nicotinamide, saw palmetto and myrtle extracts (active ingredient is myrtacin). This naturopathic combination inhibits the formation of a biofilm by propionibacteria (Keracnyl®). It can be used as first-line therapy for minimal to moderate inflammatory acne.

Furthermore, tanning drugs, as well as anti-inflammatory plant ingredients (as aqueous poultices) can help to alleviate the pustular form of acne. These include:

  • Hamamelis
  • moist compresses with black tea
  • Tea tree oil - cave wrongly stored tea tree oil - allergic skin reactions! increased peroxide formation with irritation!
  • Camomile
  • Sage
  • Peloids: As an alternative or complementary treatment, masks with healing earth can considerably reduce pustules and papules. Following the healing earth mask, a moisturizing cream should be applied.

Note(s)
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The capsule material of Isotretinoin contains peanut ingredients! This drug is contraindicated in peanut allergies. Alternatively, a "low dose" dosage (the peanut-free) of acitretin (0.3 mg/kg bw) can be used.

Literature
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  1. Aydingoz IE et al (2021) The investigation of the amounts and expressions of epidermal growth factor, epidermal growth factor receptor, and epidermal growth factor receptor gene polymorphisms in acne vulgaris. J Cosmet Dermatol 20:346-351.
  2. Bacharach-Buhles M et al (2011) Acne. hautnah dermatologie 27: 327.
  3. Burkhart CN et al (2003) Microbiology's principle of biofilms as a major factor in the pathogenesis of acne vulgaris. Int J Dermatol 42: 925-927
  4. Chan H et al. (2017) A randomized, double-blind, placebo-controlled trial to determine the efficacy and safety of lactoferrin with vitamin E and zinc as an oral therapy for mild to moderate acne vulgaris. Int J Dermatol 56:686-690.
  5. Cordain L et al (2002) Acne vulgaris: a disease of Western civilization. Arch Dermatol 138: 1584-1590.
  6. Degitz K et al (2017) Acne. J Dtsch Dermatol Ges 15: 709-721.
  7. Fiorini-Puybaret C et al.(2011) Pharmacological properties of Myrtacine® and its potential value in acne
  8. treatment. Planta Med 77:1582-1589.
  9. Itoh Y (2002) Photodynamic therapy for acne vulgaris with topical 5-aminolevulinic acid. Arch Dermatol 136: 1093-1095.
  10. Kang D et al. (2015) Vitamin B12 modulates the transcriptome of the skin microbiota in acne
  11. pathogenesis. Sci Transl Med 7:293ra103.
  12. Kawashima M et al (2014) Is benzoyl peroxide 3% topical gel effective and safe in the treatment of acne vulgaris in Japanese patients? A multicenter, randomized, double-blind, vehicle-controlled, parallel-group study. J Dermatol 41:795-801
  13. Leyden JJ (2003) A review of the use of combination therapies for the treatment of acne vulgaris. J Am Acad Dermatol 49: S200-210.
  14. Melnik B (2010) Acne vulgaris, dermatologist 61: 115-125.
  15. Melnik BC et al (2015) Linking diet to acne metabolomics, inflammation, and comedogenesis: an update.
  16. Clin Cosmet Investig Dermatol 8:371-388.
  17. Mirdamadi Y et al. (2015) Insulin and insulin-like growth factor-1 can modulate the
  18. phosphoinositide-3-kinase/Akt/FoxO1 pathway in SZ95 sebocytes in vitro. Mol Cell Endocrinol 415:32-44.
  19. Plewig G (2010) How acne vulgaris develops. Dermatologist 61: 99-106
  20. Sas K et al (2019) High Body Mass Index is a Risk Factor for Acne Severity in Adolescents: A
  21. Preliminary Report.Acta Dermatovenerol Croat 27:81-85.
  22. Schaller M et al.(2016) A multicentre,randomized, single-blind, parallel-group study comparing the efficacy and tolerability of benzoyl peroxide 3%/clindamycin 1% with azelaic acid 20% in the topical treatment of mild-to-moderate acne vulgaris. J Eur Acad Dermatol Venereol 30:966-973.
  23. Seaton ED et al (2003) Pulsed-dye laser treatment for inflammatory acne vulgaris: randomised controlled trial. Lancet 362: 1347-1352.
  24. Skidmore R et al (2003) Effects of subantimicrobial-dose doxycycline in the treatment of moderate acne. Arch Dermatol 139: 459-464
  25. Zouboulis CC (2014) Acne vulgaris. Dermatologist 65:733-747
  26. Gürtler A (2021) Acne and nutrition - relevance for clinical practice. Compendium Dermatology 2021: 35-41.
  27. Baldwin H et al (2020) Effects of diet on acne and its response to treatment. Am J Clin Dermatol 22:55-65.
  28. Szanto M et al (2019) Targeting the gut-skin axis-probiotics as new tools for skin disorder management? Exp Dermatol 28: 1210-1218
  29. Goodarzi A et al (2020) The potential of probiotics for treating acne vulgaris: a review of literature on axne and microbiotica. Dermatol Ther 33: 13279
  30. Aubert J et al (2018) Nonclinical and human pharmacology of the potent and selective topical retinoic acid receptor-γ agonist trifarotene. Br J Dermatol 179:442-456.
  31. Nestor MS et al (2016) Efficacy and Tolerability of a Combined 445nm and 630nm Over-the-counter Light Therapy Mask with and without Topical Salicylic Acid versus Topical Benzoyl Peroxide for the Treatment of Mild-to-moderate Acne Vulgaris. J Clin Aesthet Dermatol 9: 25-35

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Please ask your physician for a reliable diagnosis. This website is only meant as a reference.