Acne (overview) L70.0

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

Acne results from a complex interaction of various 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 seborrhea. 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.

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

• Acne comedonica
• Acne papulopustulosa
• Acneconglobata.

Special forms of acne vulgaris

• Acne inversa
• Acne excoriée des jeunes filles
• Acne fulminans
• Acne mechanica
• Acne medicamentosa (drug-induced acne)
• Chlorine acne
• Acne neonatorum (see Pityrosporum folliculitis of the infant)
• Acne infantum
• Acne tropicalis
• Acne venenata
• Majorca acne
• Acne tarda
• Occupational acne
• Oil acne
• Tar acne
• X-ray acne

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, the 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.

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).

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.

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

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.

Follicular hyperkeratosis, enlarged sebaceous glands.

• 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)

• Childhood:
  • Pityrosporum folliculitis of the infant.
  • Acne infantum.
• Adulthood:
  • Acne inversa
  • Hidradenitis suppurativa
  • Acne triad
  • Acne tetrad
  • Folliculitis
  • Nevus comedonicus
  • Acne medicamentosa
  • syphilitic recurrent exanthema
  • Trichostasis spinulosa
  • Elastoidosis cutanea nodularis et cystica.

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.

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.

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 due to 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).

Systemic treatment is reserved for the severe form of acne vulgaris that is not optimally amenable to external therapy.

Antibiotics (tetracyclines and macrolide antibiotics [e.g., erythromycin, roxithromycin]) are the standard preparations. The antibiotic of choice here is minocycline (e.g., Skid, Aknosan, Klinomycin), followed by doxycycline (e.g., Doxakne ).

• Tetracyclines: Minocycline is generally better tolerated than doxycycline, but much more expensive. Minocycline dosage is 50 mg p.o. 2 times/day initially (with meal), then reduction to a maintenance dose of 50 mg/day. Doxycycline: 1 time/day 50 mg p.o. Tetracycline (Tefilin): 1500 mg/day, higher dose if necessary, initially 3 times/day 500 mg (before meal, no milk) for 1-2 months. Attention should be paid to the phototoxic effect of this group of substances, 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. Do not combine with systemic retinoids!

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

  Notice. Dangers of long-term systemic antibiotic treatment include development of resistance, gram-negative folliculitis, and reflorescence of papulopustules!

Hormone therapy (only for women): Collaboration with gynecologists. Hormonal therapy in girls who are not yet sexually active should be started no earlier than two years after menarche. On the other hand, in the case of contraceptive needs and acne, the prescription of an antiandrogenic OH is the 1st choice therapy.

• Estrogens: Estrogens inhibit sebum production. A few contraceptives contain 50 µg ethinylestradiol (= sufficient amount to inhibit sebum production), but are rarely used in practice. Standard doses are 20-35 µg. Natural estrogens (estradiol valerate, estradiol, estestrol) are also used.
• Antiandrogens: In acne patients, accelerated androgen metabolism is observed in the sebaceous glands with a consequent increase in the mitotic rate in the sebocytes and stimulation of lipid synthesis. Cyproterone acetate (CPA) has a 100% antiandrogenic and progesterone effect. It inhibits all androgen-dependent organs and thus also the sebaceous glands. The indication is only in women and limited to moderate and severe acne, hirsutism and androgenetic alopecia. Because of the expected cycle disturbances, a combination with ethinylestradiol is indicated. Combination drugs include Diane 35, Juliette, Jennifer 35.
  Dienogest has 40% antiandrogenic efficacy (Valette, Maxim, Aristelle) and is approved for acne therapy in addition to contraception. Drospirenone has 30% antiandrogenic efficacy (Yasmin, Petibelle, Xellia) and additional antimineral corticosteroid activity. Chlormadinone acetate has 20% antiandrogenic efficacy.
• In severe cases, COC therapy can be supplemented by administration of 5-10 mg CPA (e.g., Androcur 10 mg) for 15 days (see Table 3).
• Caution. Thromboembolic complications occur especially in smokers, overweight patients or patients with arteriosclerosis.
  Patients with livedo racemosa and Sneddon's syndrome should be excluded from antiandrogen therapy. The prescription of antiandrogens belongs in the hand of the gynecologist. The indication is made by the dermatologist, dosage, implementation and control of the therapy are left to the gynecologist. The duration of therapy should be at least 1 year, if necessary years, also combination with isotretinoin. Improvement of acne can be expected after 2-3 months of therapy at the earliest. Problems arise when hormone therapy is discontinued: rebound with eruption of papulopustules.

Isotretinoin (e.g. acnenormin) is indicated according to the European Directive (EMA) for severe inflammatory form of acne vulgaris with the risk of permanent scarring. Indisputable is the prescription for acne conglobata or nodular acne.

Notice. When prescribing isotretinoin for women of childbearing age, it is essential to perform a pregnancy test before starting therapy and to require safe contraception one month before starting therapy, throughout the course of therapy, and one month after the end of therapy (some authors recommend up to 3 months).

Caution. Teratogenicity: Not approved in women of childbearing potential. The civil and possibly also criminal responsibility therefore lies explicitly with the treating physician!
Recurrences: As a rule, sufficient therapy with isotretinoin leads to long-lasting remissions (weeks to years). After discontinuation of isotretinoin, recurrence may occur. This is usually milder than the original acne. The recurrence rate is inversely proportional to the therapeutic dose administered. At a cumulative dose < 120 mg/kg bw, recurrence is much more likely than at a total dose > 120 mg/kg bw, so this dose should be reached if possible. In the event of relapse, repeat therapy may be required in some cases.

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

Care measures: To mitigate the unpleasant side effects of dry lips, locally re-lubricating lip care products, e.g. Rolip Emulsion, Rolip Mandelic, Labello or similar can be used.

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).

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

Keratolytic/comedolytic topicals in acne therapy

Locally acting antibiotics

Hormone therapy for severe acne in women

Acne therapeutics according to efficacy

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.

Phytopharmaceuticals are sufficiently effective exclusively for mild to moderate acne.

The only indication for acne is mahonia bark in a 10 % ointment preparation.

Furthermore, externals with extracts of Mediterranean myrtle (Myrtacin®) have proven effective. This is contained, among others, as Keracnyl (Ducray). Myrtacin destroys the biofilm of 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!
• Chamomile
• Sage
• Peloids: Alternatively or complementary, masks with healing clay can significantly reduce pustules and papules. Following the healing earth mask, apply a moisturizer.

for mild acne pustulosa external: Echinacea purpura radix

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.

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