Acne (overview) L70.0

Common, chronic inflammatory, polyetiological disease of the sebaceous follicles that occurs in adolescence in the majority of the population in western industrialized nations. A chronic-continuous or relapsing course is typical.

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 every year. It mainly affects male adolescents and young adults between the ages of 12 and 24, but less frequently female adolescents.

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

In a French study of women aged between 24 and 40, the prevalence was 41%.

In a US study, the prevalence figures were 51% for women aged 20-29, 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.

Acne arises from a complex interplay of various pathogenetic factors. As a result of the plug-like closure of the follicular excretory duct and simultaneous seborrhea, the sebum is backed up into the follicular gland unit = comedo(acne comedonica). Follicular pustules(acne papulopustulosa) develop due to purulent melting. In severe cases (acneconglobata), follicular ruptures due to comedone components lead to pronounced inflammatory processes deep into the dermis, with furunculoid, often confluent, painful abscesses(acne conglobata). The main clinical symptoms are seborrhea, comedones and papulo-pustules. Due to the chronicity of the disease, treatment is designed to last for months or years.

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

• Genetic factors
  • Insulin resistance and hyperinsulinemia; elevated levels of IGF-1 (see insulin-like growth factor) correlate with the total number of acne lesions.
  • Identical twins have a high concordance with regard to 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 holocrinally from sebocytes; the main components are triglycerides, fatty acid esters and squalene. Androgens regulate sebum production. The adrenal dehydroepiandrosterone sulphate (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 and increased adhesiveness to each other. Interleukin-1 plays an initiating role here. The resulting proliferation-retention hyperkeratosis leads to the formation of initially clinically invisible microcomedones; further comedone growth with dilatation of the follicular ostium leads to open comedones that are darkly colored by melanin. Free palmitic acid and oleic acid have a comedogenic effect and induce the follicular keratinization disorder.
• Bacterial colonization and biofilm formation by Propionibacterium acnes
  • Propionibacteria (Propionibacterium acnes, now called Cutibacterium acnes) 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 elevated in acne patients. It induces sebocytic lipogenesis in lipocytes and has a costimulatory effect with androgens (Melnik BC 2015). IGF-1 and insulin inhibit the transcription factor FoxO1 in sebocytes while simultaneously increasing mTORC1 activity (Mirdamadi Y et al. 2015). Acne does not occur in cases of congenital IGF1 deficiency(Laron syndrome) or in people with dysfunctional androgen receptors.
• Insulin
  • Acne is combined with increased insulin resistance(dietary factors; muscle-building products (colec products, casein concentrates, which lead to bodybuilding acne). IGF-1 and 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 the development of acne in adolescents (Sas K et al. 2019).
• FoxO1: The Fox O1 protein (see forkhead box genes below) is a central switch in insulin regulation and glucose metabolism. FoxO1 inhibits important transcription factors of lipid synthesis such as: PPARgamma, LXRalpha, SREBP1 and the kinase mTORC1. FoxO1 also inhibits the androgen receptor (AR).
• Inflammatory readiness with interactions between sebaceous glands and perifollicular connective tissue.
  • The significance of innate immunity for acne is focused on the activation of the inflammasome. P. acnis is ascribed 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) must be taken into account!
• Psychological factors
• Smoking can promote acne.
• Diet - foods with a high glycemic index, dairy products. These lead to a diet-related increased hyperglycaemic load and induction of insulin and IGF-1. In combination with the already high IGF1 serum levels in adolescence, this constellation leads to a promotion of seborrhoea and follicular hyperkeratosis (Melnik BC 2015).
• Medication:
  • Anticontraceptives with a restandrogenic component (e.g. 19-nortestosterone derivatives)
  • DHEA-S
  • Anabolic steroids
  • Lithium
  • Vitamin B supplements (especially vitamin B12 - Kang D et al. 2015)
  • EGFR inhibitors: The use of EGFR inhibitors shows, depending on the duration of therapy, a follicular (acneiform) papulo-pustular exanthema in the area of the seborrhoeic zones within a period of 2 weeks. Comedones are typically absent. The severity of the exanthema is considered an indicator of the therapeutic response to EGFR inhibitors. It is assumed that EGF exerts a control function for the inflammatory processes of acne vulgaris (Aydingoz IE et al. 2021).

Acne fulminans refers to acne conglobata with a severe immunological systemic reaction (feeling of illness, fever, bone pain, vasculitis).

Mainly 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 every year. It mainly affects male adolescents and young adults between the ages of 12-24, with female adolescents affected less frequently.

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

In a French study of women aged between 24 and 40, the prevalence was 41%.

In a US study, the prevalence figures were 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.

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

In severe and unclear cases of both sexes, the following laboratory values are recommended: ESR, CRP, BB, IgG, IgM, IgA, zinc, α-1-antitrypsin, TPHA.

Exclusion of HIV infection if necessary.

Women with indications of cycle disorders or androgenization: total testosterone, free testosterone, SHBG, prolactin, DHEAS, androstenedione.

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

Follicular hyperkeratosis, enlarged sebaceous glands.

• Medical history: time of onset, progression (spontaneous, gradual), familial accumulation, cosmetics, medication, previous treatment, allergies, endocrine disorders
• If necessary, laboratory values (see laboratory below)
• Hair type, physique (androgenization in women)
• Determination of severity based on primary and secondary lesions and severity of manifestation
• Antibiogram from swab of comedone contents, pustules or papules
• Antibiogram from a swab of the nasal mucosa (colonization 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.

• A grading of the acne to assess the success of the therapy is useful before starting therapy: e.g. counting 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 wash gel, Sebamed liquid. Antiseptic or antibacterial cleansers are not indicated as they do not target Propionibacterium acnes or act deep within the follicle. Creams or emulsions of the O/W type are suitable for care, e.g. Toleriane, Physiane, Hydranorm, Avène Cleanance, Lutsine Kerafnia, Eucerin Rebalance, Eucerin Cream-Gel. Tinted acne therapies such as Aknichthol-Lotio are well suited as color-regulating topicals to cover the inflammatory redness.
• Avoid comedogenic topicals, especially cosmetics. If make-up is not avoided, make-up suitable for acne should be used, e.g. Unifiance from La Roche Posay or Lutsine make-up pencil, in each case after testing the color shade.
• The glycemic load of food should be reduced by making a wise choice (high proportion of unsaturated fatty acids, pulses, vegetables >> fruit).
• Rehabilitation as part of a measure to ensure the ability to work (especially in the case of acne inversa). If necessary, dietary advice or in the case of psychological involvement: behavioral medicine-oriented rehabilitation (VOR).

• In the treatment of acne scars, ablative, non-ablative lasers and radiofrequency microneedling have proven to be useful forms of therapy (Teymour et al. 2023)

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

• Retinoids: Tretinoin and isotretinoin are the classic retinoids of the first and second generation 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 a 0.05 to 0.1% gel or cream (e.g. Isotrex®), is currently no longer marketed, see table below. Gels and solutions should be preferred for seborrhoeic skin types, gels and creams for normal skin. Initially apply once a day, preferably in the evening, as slight reddening occurs, possibly also burning and itching. If well tolerated, this can be increased to 2 times/day. All other external acne treatments should be discontinued until the patient has become accustomed to the vitamin A acid. Avoid the corners of the mouth and eyelid region. In about 30% of patients, pustules appear after 2-4 weeks of treatment as a result of ruptures of the microcomedones. Despite this apparent blossoming of the acne, treatment should be continued. After about 4 weeks, "hardening" has taken place and the irritations recede. Direct sun exposure should be avoided as tretinoin and isotretinoin lower the erythema threshold and are not light-stable.
• A 4th generation retinoid has been available since the end of 2020: trifarotene, ^Selgamis®. This binds selectively to the retinoid receptor gamma and also has an anti-inflammatory effect. The large-area application (max. 2 g on face and trunk) also enables the treatment of acne on the trunk.
• Adapalene: (^Differin® gel/cream, ^Dipalene® gel/cream) is a synthetic polyaromatic retinoid of the third generation. In addition to its comedolytic efficacy, it has a stronger anti-inflammatory effect than tretinoin and isotretinoin. It only needs to be applied once a day.
• Adapalene/benzoyl peroxide (BPO) (e.g. ^Epiduo® Gel 0.1%/2.5% or ^Epiduo® Forte 0.3%/2.5%): The combination of the polyaromatic retinoid and BPO is an approach that combines the advantages of both therapeutic modalities and does not involve the risk of antimicrobial resistance. Apply once a day, in the evening, as a thin film on the areas of skin affected by acne, 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.
• Remember! Topical retinoids are suitable for maintenance therapy as they have an anti-comedogenic effect and thus prevent the formation of new microcomedones. The success of therapy can generally only be assessed after 3 months: a reduction in the number of efflorescences (acne comedonica, acne papulopustulosa) of > 50% is considered a good response, a reduction of > 75% a very good response. Treatment should be continued as long as there are still 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 in the first 2-4 weeks. As a rule, azelaic acid is often better tolerated than other external acne therapies, especially by sensitive skin (atopics). Azelaic acid can be administered during pregnancy. In addition to the cream form, a gel preparation is also available.
• Salicylic acid: Has a demonstrable comedolytic effect; the keratolytic activity is too weak in most concentrations used to be expected to have an effect on acne. Salicylic acid is used externally in different concentrations and combinations with other active agents. 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 abundant in sebaceous glands, are quickly destroyed. This applies in particular to Propionibacterium acnes. BPO is available in 1.5/3/5/10% concentrations 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 applying benzoyl peroxide, skin irritation may initially occur with drying of the skin, redness and scaling in the first few days to weeks. A habituation effect usually sets in within a few weeks. Special care should be taken when applying to atopic skin. Contact sensitization to BPO may occur in rare cases. Patients must be made aware of the fact that BPO discolors or bleaches hair, clothing, bedding, towels, etc. Benzoyl peroxide can be used as a gel in 3.0, 5.0 or 10.0% concentration as a formulation (see benzoyl peroxide gel NRF 11.25. below). 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): Aluminum oxide (e.g. Brasivil) or polydimethyl silicone resin (e.g. Jaikin) have a slight peeling effect, but generally do not reach the comedones. Caution should be exercised 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 hyperkeratosis are repeatedly recommended, see also chemical peeling below.
• 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 given for follicular hyperkeratosis. Application: 1 time/day, 2 times/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. Effective 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 been used for some time. 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 with inflammatory acne. Local side effects include redness, scaling and burning of the skin. Rarely, bloody diarrhea and colitis (including pseudomembranous colitis) can also occur after topical application of clindamycin. Topical antibiotics are generally used in combination with topical retinoids (Aknemycin® plus), salicylic acid, BPO or abrasives and should be limited in time due to the risk of resistance developing. Long-term use can lead to a selection of the germ 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 the case of highly inflammatory acne. Intralesional application is possible for abscessing nodules.
• A topical combination therapy of tretinoin, benzyl peroxide and clindamycin is the gold standard of topical therapy and is superior to therapy with single substances and two combinations.

UV phototherapy: The use of UVB rays or UVA and UVB rays leads to an improvement in symptoms. UV phototherapy is no longer up to date 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 an LED mask with blue and red light (wavelength 445 nm and 630 nm) shows a significant reduction in inflammatory and non-inflammatory acne efflorescences in studies (Nestor MS et al., 2016).

Systemic treatment is reserved for severe forms of acne vulgaris that are not optimally responsive to topical therapy.

Antibiotics (tetracyclines and macrolide antibiotics [e.g., erythromycin, roxithromycin]) are the standard treatments. The first-line antibiotic in this context is minocycline (e.g., Skid, Aknosan, Klinomycin), followed by doxycycline (e.g., Doxakne).

• Tetracyclines: Minocycline is generally better tolerated than doxycycline, but is significantly more expensive. The initial dosage of minocycline (Skid®) is 50 mg orally twice daily (with a meal), then reduced to a maintenance dose of 50 mg per day. Doxycycline (e.g., Doxyderma): 50 mg orally once daily. Tetracycline (Tefilin): 1,500 mg daily, or higher if necessary; initially 500 mg three times daily (before meals, no milk) for 1–2 months. Be aware of the phototoxic effects of this group of substances; these are less pronounced with doxycycline than with tetracycline hydrochloride, and minocycline is considered safer in this regard.

• Note! Many tetracyclines are phototoxic!

  Note! Do not combine with systemic retinoids!

• Macrolide antibiotics: Erythromycinshould be administered at a dose of 500–1000 mg per day; roxithromycinat a dose of 150–300 mg per day.

  Note! Risks associated with long-term systemic antibiotic treatment include, among others, the development of resistance, Gram-negative folliculitis, and a recurrence of papulopustules!

Hormone therapy (for women only): Collaboration with gynecologists is essential. Hormone therapy for girls who are not yet sexually active should be started no earlier than two years after menarche. However, if contraception is needed and the patient has acne, prescribing an antiandrogenic oral contraceptive is the first-line therapy.

• Estrogens: Estrogens inhibit sebum production. A few contraceptives contain 50 µgof ethinyl estradiol (a sufficient amount to inhibit sebum production), but they are rarely used in clinical practice. Standard doses are 20–35 µg. Natural estrogens (estradiol valerate, estradiol, estestrol) are also used.
• Antiandrogens: In patients with acne, accelerated androgen metabolism is observed in the sebaceous glands, leading to an increased mitotic rate in the sebocytes and stimulation of lipid synthesis. Cyproterone acetate (CPA) has 100% antiandrogenic and progesterone effects. It inhibits all androgen-dependent organs, including the sebaceous glands. It is indicated only for women and is limited to moderate and severe acne, hirsutism, and androgenetic alopecia. Due to the expected menstrual irregularities, combination therapy with ethinyl estradiol is indicated. Combination preparations include, for example, Diane 35, Juliette, and Jennifer 35.
  Dienogesthas 40% antiandrogenic efficacy (Valette, Maxim, Aristelle) and is approved for the treatment of acne in addition to contraception. Drospirenonehas 30% antiandrogenic efficacy (Yasmin, Petibelle, Xellia) and also has an antimineralocorticoid effect.Chlormadinone acetatehas 20% antiandrogenic efficacy.
• In severe cases, COC therapy can be supplemented with 5–10 mg of CPA (e.g., Androcur 10 mg) administered over 15 days (see Table 3).
• Caution! Thromboembolic complications occur particularly in female smokers, overweight patients, or patients with atherosclerosis.
  Patients with livedo racemosa or Sneddon syndrome must be excluded from antiandrogen therapy. The prescription of antiandrogens is the responsibility of the gynecologist. The indication is established by the dermatologist, while the gynecologist is responsible for the dosage, administration, and monitoring of the therapy. The duration of therapy should be at least 1 year, or several years if necessary, and may be combined with isotretinoin. Improvement in acne can be expected after 2–3 months of therapy at the earliest. Problems may arise upon discontinuation of hormone therapy: a rebound effect with an eruption of papulopustules.

Isotretinoin (e.g., Aknenormin) is indicated, in accordance with the European Directive (EMA), for severe inflammatory forms of acne vulgaris with a risk of permanent scarring. Its prescription for acne conglobata or nodular acne is undisputed.

• Note! When prescribing isotretinoin to women of childbearing age, a pregnancy test must be performed before starting therapy, and effective contraception must be used one month before the start of therapy, throughout the entire course of treatment, and for one month after the end of therapy (some authors recommend up to 3 months).
• Caution! Teratogenicity: Not approved for women of childbearing age. Civil and, where applicable, criminal liability therefore lies expressly with the treating physician!
• Recurrences: As a rule, adequate therapy with isotretinoin leads to long-lasting remissions (ranging from weeks to years). Recurrence may occur after discontinuation of isotretinoin. This recurrence is generally milder than the original acne. The recurrence rate is inversely proportional to the therapeutic dose administered. With a cumulative dose < 120 mg/kg body weight, recurrence is significantly more likely than with a total dose > 120 mg/kg body weight; therefore, this dose should be achieved whenever possible. In the event of a recurrence, repeat therapy may be necessary in some cases.
• Skincare measures: To alleviate the unpleasant side effect of dry lips, locally moisturizing lip care products, such as Rolip Emulsion, Rolip Mandelic, Labello, or similar products, can be used. 

• Combination with Antihistamines: Additional administration of H1 antihistamines may be considered during systemic isotretinoin therapy. In particular, there is evidence for desloratadine (5 mg/day) to reduce initial acne exacerbations and pruritus, as well as, in some cases, to improve the clinical response. However, a relevant effect on isotretinoin-induced cheilitis has not been established. In addition to H1 receptor blockade, additional anti-inflammatory effects and an influence on sebocyte lipid production are discussed as possible explanations. Due to the limited evidence to date, this combination has not been established as routine standard therapy; its use is off-label.

• Combinations with Hormones: In cases of severe inflammatory acne conglobata or acne fulminans, combination therapies with hormones (antiandrogens, contraceptives, glucocorticoids) are possible. In particular, the temporary use of glucocorticoids can, in individual cases of severely inflammatory acne, result in a significant reduction in the inflammatory response.  

IL-17A Antibodies: Treatment approaches for severe acne vulgaris using a monoclonal antibody directed against interleukin IL-17A havenot proven successful (Thiboutot M et al. 2023). 

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 for mild to moderate acne vulgaris (Chan H et al. 2017).

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

Order therapy: Avoidance of triggering causes, see also under diet/lifestyle, reduction of psychological stress, avoidance of manipulation of the acne lesions

Hydrotherapy: Moist compresses with astringent, drying plants such as oak bark, black tea

Peloid therapy: masks with healing clay for pustules and papules

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.

Herbal medicines are sufficiently effective only for mild to moderate acne.

Positive monographsexist for: 

• Violae herba cum flore
• Arctii radix
• Echinacea pallida root
• Echinacea purpurea root

No monograph available:Galbanum

The indication for acne applies only to mahonia bark in a 10% ointment formulation.

Furthermore, topical preparations containing extracts of Mediterranean myrtle (^Myrtacin®) have proven effective. This is included, among other products, in^Keracnyl® (Ducray);^Myrtacin® destroys the biofilm of Propionibacterium acnes.  

Myrtle-saw palmetto extracts: Clinical studies have demonstrated an antimicrobial and anti-acne effect from a combination of nicotinamide, saw palmetto, and myrtle extracts (the active ingredient is Myrtacin). This naturopathic combination inhibits the formation of a biofilm by Propionibacterium acnes (^Keracnyl®). It can be used as a first-line treatment for mild to moderate inflammatory acne. 

Furthermore, tannin-containing herbs and anti-inflammatory plant compounds (as aqueous compresses) can help alleviate pustular acne. These include:

• witch hazel
• Moist compresses with black tea
• Tea tree oil— Melaleuca alternifolia —Caution: Improperly stored tea tree oil can cause allergic skin reactions! Increased peroxide formation may lead to irritation!
• Chamomile
• Sage
• Peloids: Alternatively or as a supplement, masks containing healing clay can significantly reduce pustules and papules. Apply a moisturizer afterward. 
• Zinc, e.g.,^Aknederm® ointment (new)

For mild pustular acne (external use): Echinacea purpura radix

see also under Arctii radix,

Zinc supplementation if necessary, see under Zinc

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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