4.1.1 Acne

ED80Z

Pimples, spots.

Highest prevalence in the 16 to 18 years old adolescents with about 85 %. It may sometimes occur in small children and adults of the 3rd and 4th life decade.

Very common, chronic, highly heritable inflammatory disease of the sebaceous follicles appearing in puberty. 30% of patients are adults. One can distinguish between physiological acne (60-70%) as an almost normal variant from clinical acne (30-40%) that needs medical care.

Genetic predisposition and hormonal stimulation (androgens) lead to:

• Seborrhoea as a result of increased proliferation and change of differentiation of sebocytes caused by androgens and insulin growth factor followed by increased  production of sebum including ceramides, squalenes, and cholesterol. Release of inflammatory mediators. 
• Proliferation of follicular keratinocytes (response to androgen and growth signals), retention hyperkeratosis, keratin- and integrin-pattern disturbance. 
• Low oxygen saturation and sebum components are ideal for proliferation of Cutibacterium acnes in the infundibulum. Specific C.acnes strains drive the inflammation. Increased expression of TLR-2 and 4 and other danger signals. IL-1 α and C. acnes mediators drive inflammation and corneocytes to hyperproliferate. 
• Innate immune system reacts strongly. CD 4 and CD 17 T cells accumulate and invade the follicular wall. Later macrophages.

Nutritional factors can play a role: increased carbohydrate load with stimulation of  IGF-1 and stimulation of androgens via nuclear factors (Fox O1) Symptoms.

Precursor lesion is a microcomedo, which is not visible for the naked eye. Primary lesions: open comedones (blackheads), closed comedones (whiteheads). Papules, pustules, nodules,  abscesses, fistulas, scars, keloids.

Often marked emotional reaction. Increased risk for suicidal intention. 

Primary lesion is a comedo: open comedones (blackheads), closed comedones (whiteheads). Papules, nodules, pustules, abscesses, fistulas, scars, keloids. Often marked emotional reaction. Increased risk for suicide.

Face, chest, upper back.

Forms: 

• Acne comedonica: primarily comedones. 
• Acne papulo-pustulosa : primarily papules and pustules mixed with comedones. 
• Acne papulo-pustulosa nodosa : stronger inflamed and additionally with small nodules.
• Acne conglobata: nodular lesion predominate, scars, abscesses, fistulas, typical localisation (mid-face, shoulders, chest, upper back).

Special forms: 

• Late onset acne (a) persisting or (b) relapsing or (c) first onset. Most prominent in females. Often mild endocronological dysfunctions. Sometimes evident with PCOS (Polycystic ovary syndrome) and androgenic signs.
• Acne fulminans: fever, leukocytosis, arthralgias, immune-mediated vasculitis, sterile abscesses of bone, elevated CRP. 
• Acne venenata: can be an occupational induced subtype. Induction, maintenance or aggravation of acne often by medications (for example corticosteroids), cosmetics, chlorinated organic compounds (Agent Orange), iodine, oil, tar.
• Acne cosmetica: overwashing and overuse of cleansers. Occlusive cosmetics, vaseline/petrolatum.
• Acne excoriée des jeunes filles: artefactual disorder with excoriations and papules around the mouth and chin, often marked emotional component. 
• Acne neonatorum (common, relative hyperplasia of the adrenals in newborns).
• Infantile acne (after 1 year of age, uncommon, LH/FSH-induced raise in testosterone). Primary manifestation of adrenogenital syndrome.

The special acneiform type Acne inversa ( Hidradenitis suppurativa) is discussed under diagnosis 2.2.2. It  is characterized by inflammation of terminal hair follicles in intertriginous regions rich in apocrine glands.

Acne tetrade = acne conglobata, acne keloidalis nuchae, pilonidal sinus and acne inversa.

In therapy-refractory acne, causes of elevated androgen levels (hormone-producing tumours, adrenogenital syndrome, polycystic ovarian syndrome) should be excluded.

Usually not necessary. In comedonal and  papulo-pustular acne sebaceous hyperplasia with infundibular widening and perifollicular lympho-mononuclear cells. Some cells invading the follicular wall. Depending on severity degree stronger perifollicular inflammation and microabcesses and scarring.

Self-limited with downsizing around end of the second life decade. Late type acne see above.

Scars (atrophic, keloids), fistulas, pigmentary changes, sometimes skin picking as an obsessive compulsory disorder and long-term psychiatric problems.

Clinical findings.

Rosacea papulo-pustulosa, folliculitis of face and trunk, beard folliculitis. Gram-negative folliculitis. Ulerythema ophryogenes. Prurigo-type of atopic dermatitis.

PRIDE syndrome: following oncologic therapy with EGF receptor agonists.

Acne aestivalis ("Mallorca acne"): is not acne, but an acneiform reaction in predisposed persons who develop follicular irritation from sun creams and UV exposure, itchy, comedones are lacking.

Basic topical therapy in comedonic acne with retinoids (comedolytic, anticomedogenic, and anti- inflammatory). Alternatively azelaic acid.

Papulo-pustular acne grades I or II: treat sequentially or with combination preparation retinoids plus benzoyl peroxide azelaic acid.Never use topical antibiotics as monotherapy (development of resistance).

Papulo-pustular acne with nodules: treat always combined topically and systemically (often oral tetracycline such as doxycycline which has strong anti-inflammatory effects. 

Acne conglobata: Isotretinoin as first choice. Systemic tetracycline plus retinoids plus benzoyl peroxide, in women  consider antiandrogens (e.g. cyproterone acetate, chlormadinon acetate or drospirenone combined with estrogens). 

Treatment of atrophic and hypertrophic scars: chemical peels (TCA peels 20-30%), dermabrasion, microneedling, CO 2 laser, fillers, surgical defect elevation for depressed scars. Maintenance treatment to prevent relapses essential, above all topical retinoids for the prevention of the development of microcomedones.