Acne (overview) L70.0

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 15.02.2021

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Synonym(s)

Acne; acne vulgaris; Classic acne; Vulgar Acne

Definition
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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 the predominant efflorescences, 3 clinical types are distinguished, whereby transitional forms are more typical than rare:

Special forms of Acne vulgaris

Occurrence/Epidemiology
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Worldwide disease.

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

In the USA, 40-50 million people contract the disease every year. Most affected are male, less often female adolescents; and young adults aged 12-24 years.

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

In a French study among women aged 24-40, the prevalence was 41%.

In a US study, the prevalence was 51% for women aged 30-39, 26% for women aged 30-39 and 15% for women aged 40-49.

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

Etiopathogenesis
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Acne develops from a complex interaction of different pathogenetic factors. As a result of the plug-like occlusion of the follicular excretory duct, sebum is backed up into the follicular gland unit = comedo(acne comedonica) in the presence of seborrhoea. 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 months- or years-long management.

Polyetiological mechanism. Frequently caused by:

  • Genetic factors
    • Insulin resistance and hyperinsulinemia; elevated levels of IGF-1 (see insulin-like growth-factor under growth factors) correlate with 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.
  • Seborrhoea (sebum is the "fuel of the acne flame"!)
    • Sebum originates holocrinally from sebocytes, main components are triglycerides, fatty acid esters and squalene. Androgens regulate sebum production. The adrenal dehydroandrosterone sulfate (DHEA-S) is the primary physiological control hormone. It is converted in sebocytes to enzymatically more potent androgens such as testosterone ud 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 an increased adhesiveness among each other. Interleukin-1 plays an initiating role in this process. 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 comedogenic effects 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 in adolescence. The growth factor is increased in acne patients. It induces sebocytic lipogenesis in lipocytes and acts costimulatory with androgens (Melnik BC 2015). IGF-1 as well as insulin inhibit FoxO1 transcription factor in sebocytes with concomitant increase in mTORC1 activity (Mirdamadi Y et al 2015). The Fox O1 protein (see forkhead box genes below) is a central switch in insulin regulation and glucose and lipid metabolism. Acne does not occur in congenital IGF1 deficiency(Laron syndrome) or in individuals with non-functioning 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 like PAPA syndrome, SAPHO syndrome.
  • Body Mass Index: High "body mass index" is a risk factor for adolescent acne expression (Sas K et al. 2019).
    FoxO1: FoxO1 inhibits key transcription factors of lipid synthesis. Furthermore, Fox O1 inhibits the androgen receptor (AR) as well as other transcription factors of lipid biosynthesis (PPARgamma, LXRalpha, SREBP1) and the kinase mTORC1. In this regulatory chain, ultimately that of IGF-1 leads to an induction of sebocytic lipogenesis.
  • 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. Isotretinoin thus 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 the secretion and activation of proinflammatory mediators (IL-1beta, NLPRP-3 inflammasome, activation of the 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, an induction of insulin and IGF-1. In combination with the already high serum IGF1 levels in adolescence, this constellation leads to a 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).

Acne fulminans is acne conglobata with a severe immunological systemic reaction (feeling sick, fever, bone pain, vasculitis).

Manifestation
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This is particularly true for adolescents and young adults; it is more pronounced for boys or men than for girls or women.

In Germany, 70-80 of all young people show signs of acne of varying degrees of severity.

In the USA, 40-50 million people are affected annually. Affected are mainly male, less often female adolescents; and young adults between 12-24 years of age.

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

In a French study among women aged 24-40, the prevalence was 41%.

In a US study, the prevalence was 51% for women aged 30-39, 26% for women aged 30-39 and 15% for women aged 40-49.

Women are more frequently 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.

  • A graduation of the acne to evaluate the success of the therapy is useful before starting the therapy: e.g. counting of all acne lesions per half of the face or in a 20 x 20 cm field and division into open/closed, papules, papulopustules, nodules. S.u. Acne comedonica, acne papulopustulosa.
  • Cleaning: Purely mechanical with a microfibre glove, Claroderm and water without further additives.
  • We recommend regular, not too frequent washing with pH-neutral soaps, e.g. Sebopona, Cetaphil, Satina, Eubos, Stephalen wash gel, Sebamed liquid. Antiseptic or antibacterial detergents are not indicated as they neither catch the Propionibacterium acnes nor act in the depth of the follicle. Creams or emulsions of the O/W type are suitable for the care, e.g. Toleriane, Physiane, Hydranorm, Avène Cleanance, Lutsine Kerafnia, Eucerin Rebalance, Eucerin Cream-Gel. Tinted acne therapeutics such as Aknichthol-Lotio are well suited as colour-regulating external agents to cover the inflammatory redness.
  • Avoid comedogenic topicals, especially cosmetics. If make-up is not avoided, a make-up suitable for acne should be applied, e.g. Unifiance from La Roche Posay or Lutsine Make-up Pen, after testing the colour shade.
  • With food, a wise choice should be made to reduce the glycaemic load (high content of unsaturated fatty acids, legumes, vegetables, fruit).

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

  • Retinoids: Tretinoin and Isotretinoin are the classic retinoids of the first and second generation. Tretinoin is offered in concentrations of 0.025 to 0.1% in the form of creams, solutions and gels (see below gels, hydrophilic, gels, hydrophobic), isotretinoin is available as 0.05 to 0.1% gel or cream (e.g. Isotrex®), see table below. Gels and solutions should be preferred for seborrhoeic skin type, gels and solutions for normal skin gels and creams. The application should be done once a day, preferably in the evening as a slight reddening occurs, possibly also burning and itching. If well tolerated, application can be increased to 2 times/day. All other external acne therapeutics should be discontinued until the patient has become accustomed to vitamin A acid. The corner of the mouth and the eyelid region should be left out. In about 30% of the patients, after 2-4 weeks of treatment, pustules appear due to ruptures of the microcomedones. Despite this apparent blooming of the acne, further treatment should be continued. After about 4 weeks, hardening has occurred and the irritations subside. Direct exposure to the sun should be avoided as tretinoin and isotretinoin lower the erythema threshold and are not light stable.
  • Adapalen: (Differin® gel/cream) is a synthetic polyaromatic retinoid of the third generation. In addition to its comedolytic activity, it is more anti-inflammatory than tretinoin and isotretinoin. It only needs to be used once a 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 a day, in the evening, as a thin film on the acne affected areas after cleansing (e.g. Dermowas) and drying the skin.
  • Tazarotene: Application (off-label use) of Tazarotene (e.g. Zorac Gel 0.1%) overnight or 2 times/day for 5-10 minutes is comparable to the effectiveness of the above mentioned retinoids according to studies.
  • Notice! Topical retinoids are suitable for maintenance therapy as they have an anticomedogenic effect and thus prevent the new formation of microcomedones. The success of therapy can usually only be assessed after 3 months: a decrease in the number of efflorescences (acne comedonica, acne papulopustulosa) by > 50% is considered a good response, a decrease of > 75% a very good response. Treatment should be continued as long as there are signs of clinical activity.
  • Azelaic acid: The substance has an antimicrobial effect in 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 and itching may occur during the first 2-4 weeks. As a rule, azelaic acid is often better tolerated than other external acne therapeutics, especially in sensitive skin (atopic patients). Azelaic acid can be administered during pregnancy. Besides the cream form a gel preparation is available.
  • Salicylic acid: Has a verifiable comedolytic effect; the keratolytic activity is too weak in most of the used concentrations to have an effect on acne. Salicylic acid is used externally in various concentrations and combinations with other active ingredients. For preparations see table 1.
  • Benzoyl peroxide (BPO): Has keratolytic and strong antimicrobial effects without the danger of developing resistance. Gram-positive germs, which are abundant in sebaceous glands, are rapidly destroyed. This is especially true for 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 once a day. After application of benzoyl peroxide, skin irritation may occur at first, with drying of the skin, redness and scaling in the first days to weeks. A habituation effect usually sets in within a few weeks. Special care should be taken when applying on atopic skin. In rare cases contact sensitization to BPO may occur. Patients must be informed that BPO discolors or bleaches 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 with the BPO/CLN combination (DUAC® gel). This combination is superior to monotherapy with azelaic acid (Schaller 2016).
  • Abrasives (peeling agents): Aluminium oxide (e.g. Brasivil) or polydimethyl silicone resin (e.g. Jaikin) have a slight peeling effect, but usually do not reach the comedones. Caution is required especially in case of 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 hyperkeratosis are recommended again and again, see below chemical peeling.
  • Fruit acids (α-hydroxy acids): α-hydroxy acids reduce corneocyte adhesion and thus keep the follicle ostia open, this leads to a reduction of the number of comedones. The indication is mainly for follicular hyperkeratosis. Application: 1 time a day, 2 times a day if well tolerated. 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. Effect begins after 6 weeks.
  • Antibiotics: There are three main groups of antibiotics 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]).
  • In addition, nadifloxacin (Nadixa® cream) has 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 results in inflammatory acne. Local side effects include redness, scaling and burning of the skin. In rare cases, bloody diarrhoea and colitis (including pseudomembranous colitis) may occur even after topical application of clindamycin. The use of topical antibiotics is usually in combination with topical retinoids (Aknemycin® plus), salicylic acid, BPO or abrasives and should be limited in time due to the risk of developing resistance. Long-term use may result in a selection of the germ spectrum in favour of Gram-negative pathogens, in the sense of Gram-negative folliculitis.
  • Glucocorticoids: They can be used in ointments or creams for a few days in cases of severe inflammatory acne. In case of abscessed nodules, an intralesional application is possible.

Radiation therapy
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UV phototherapy: The use of UVB rays or UVA and UVB rays leads to an improvement of the symptoms. UV phototherapy is no longer up to date due to an unfavourable benefit-risk ratio.

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

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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Myrtle and saw palmetto extracts: clinical studies have shown an antimicrobial and antiacnogenic effect of a combination of nicotinamide, saw palmetto and myrtle extracts (active ingredient is myrtacin). This natural combination inhibits the formation of a biofilm by propionibacteria (Keracnyl®). It can be used as first-line therapy for minimal to moderate inflammatory acne.

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

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%

083

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

-

-

++

+

- t 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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There is no scientific evidence of food triggering acne vulgaris. However, insulin, IGF-1 (see below insulin-like growth factor), hyperglycaemic food and milk apparently play a role in the pathogenesis of acne. A high milk consumption leads to a significant increase in insulin and IgF-1, comparable to a diet with a high glycaemic index (see table below).
Recommendations for prophylaxis and dietary treatment of acne before (modified according to B. Melnik)
Acne promoting factors Prophylaxis/recommendations
Food and stimulant with acne-inducing effect Food and luxury food without acne-inducing effect
Milk, dairy products, cream cheese, whey protein concentrates Raw vegetables, fruit, vegetables, blue berries, soya products, tomatoes
Milk chocolate, sweets, potato chips, cornflactes, other carbohydrates with a high glycemic index such as: white bread, rice, potatoes, wheat noodles, fast food Wholemeal bread and cow's milk-free muesli, plenty of fibre with high fibre content, no fast food
Saturated fats e.g. in lard, pork liver, liver sausage, egg yolk Frequent consumption of sea fish
Smoking Abstention from smoking
Frequent snacks and snacks during breaks Several hours of complete pause with food intake
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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Externals with extracts of the Mediterranean myrtle (Myrtacin®) have proven effective for mild to moderate acne. Extracts of the drug Myrti folium are widely used as expectorants.

Furthermore, anti-inflammatory plant ingredients (in the form of watery compresses) can help to alleviate the pustular form of acne. These include:

  • chamomile
  • Sage
  • Hamamelis
  • and, with some caution, also tea tree oil (Bacharach-Buhles 2011).

Peloids: Alternatively or as a supplement, masks with healing clay can significantly reduce pustules and papules. A moisturizing cream should be applied after the healing earth mask.

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. Bacharach-Buhles M et al. (2011) Acne. close dermatology 27: 327
  2. 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
  3. 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.
  4. Cordain L et al (2002) Acne vulgaris: a disease of Western civilization. Arch Dermatol 138: 1584-1590
  5. Degitz K et al (2017) Acne. J Dtsch Dermatol Ges 15: 709-721
  6. Fiorini-Puybaret C et al.(2011) Pharmacological properties of Myrtacine® and its potential value in acnetreatment
    . Planta Med 77:1582-1589.
  7. Itoh Y (2002) Photodynamic therapy for acne vulgaris with topical 5-aminolevulinic acid. Arch Dermatol 136: 1093-1095
  8. Kang D et al (2015) Vitamin B12 modulates the transcriptome of the skin microbiota in acnepathogenesis
    . Sci Transl Med 7:293ra103.
  9. 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
  10. Leyden JJ (2003) A review of the use of combination therapies for the treatment of acne vulgaris. J Am Acad Dermatol 49: S200-210
  11. Melnik B (2010) Acne vulgaris, dermatologist 61: 115-125
  12. Melnik BC et al (2015) Linking diet to acne metabolomics, inflammation, and comedogenesis: an update.
    Clin Cosmet Investig Dermatol 8:371-388.
  13. Mirdamadi Y et al (2015) Insulin and insulin-like growth factor-1 can modulate thephosphoinositide-3-kinase/Akt/FoxO1
    pathway in SZ95 sebocytes in vitro. Mol cell endocrinol 415:32-44.
  14. Plewig G (2010) How is acne vulgaris formed. dermatologist 61: 99-106
  15. Sas K et al (2019) High Body Mass Index is a Risk Factor for Acne Severity in Adolescents:
    APreliminary Report.Acta Dermatovenerol Croat 27:81-85.
  16. 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.
  17. Seaton ED et al (2003) Pulsed-dye laser treatment for inflammatory acne vulgaris: randomised controlled trial. Lancet 362: 1347-1352
  18. Skidmore R et al (2003) Effects of subantimicrobial doxycycline in the treatment of moderate acne. Arch Dermatol 139: 459-464
  19. Zouboulis CC (2014) Acne vulgaris. Dermatologist 65:733-747

Disclaimer

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