Definition
The term acne comes from a corruption of the Greek άκμή (acne in the sense of a skin eruption) in the writings of Aëtius Amidenus.
Is a chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular
Epidemiology
Age 10 to 17 years in females; 14 to 19 in males; may appear first at 25 years or older.
Sex More severe in males than in females
Race Lower incidence in Asians and blacks; rare in Chinanodules. The cause is unknown, but heredity and age are predisposing factors.
Symptoms
Sites of predilection Face, neck, upper arms, trunk, buttocks
Duration of Lesions Weeks to months to years
Season Often worse in fall and winter
Symptoms Pain in lesions (especially nodulocystic type)
Types
- Comedones open (blackheads) or closed (whiteheads)
- Papules and papulopustules with (red) or without inflammation
- Nodules, noduloulcerative lesions, or cysts 1 to 4 cm in diameter. The soft nodules are not cysts but large secondary comedones from repeated ruptures and reencapsulations with inflammation and abscess formation.
- Sinuses draining epithelial-lined tracts, usually with nodular acne
- Scars atrophic depressed (often pitted) or hypertrophic (at times, keloid) scars
- Seborrhea of the face and scalp is often present and sometimes severe.
- Shape Round; nodules may coalesce to form linear mounds or sinus tracts.
- Arrangement Isolated single lesion (e.g., nodule) or scattered discrete lesions
(papules, cysts, nodules).
Diagnosis
Free testosterone, ovarian source in females
FSH and LH; if ratio of LH/FSH is >3 : 1, highly suggestive
DHEA-S, adrenal source of androgens
Note: In the overwhelming majority of acne patients hormones are normal.
Pathogenesis
The lesions of acne (comedones) are the result of complex interaction between hormones (androgens) and bacteria (Propionibacterium acnes) in the pilosebaceous units of individuals with appropriate genetic backgrounds.
Androgens (which are qualitatively and quantitatively normal) stimulate sebaceous glands to produce larger amounts of sebum; bacteria contain lipase that converts lipid into fatty acids.
Both sebum and fatty acids cause a sterile inflammatory response in the pilosebaceous unit; this results in hyperkeratinization of the lining of the follicle with resultant plugging.
The enlarged follicular lumen contains inspissated keratin and lipid debris (the whitehead).
When the follicle has a portal of entry at the skin, the semisolid mass protrudes, forming a plug (the blackhead).
The black color is due to oxidation of tyrosine, contained in the follicular orifice, to melanin.
The distended follicle walls may break, and the contents (sebum, lipid, fatty acids, keratin, etc.)
may enter the dermis, provoking a foreign-body response (papule, pustule, nodule).
Rupture plus intense inflammation leads to scars.
Causes of acne
Acne develops as a result of blockages in follicles.
Hyperkeratinization and formation of a plug of keratin and sebum (a microcomedo) is the earliest change.
Enlargement of sebaceous glands and an increase in sebum production occur with increased androgen (DHEA-S) production at adrenarche.
The microcomedo may enlarge to form an open comedo (blackhead) or closed comedo (whitehead). Whiteheads are the direct result of skin pores becoming clogged with sebum, a naturally occurring oil, and dead skin cells.
In these conditions the naturally occurring largely commensal bacteria Propionibacterium acnes can cause inflammation, leading to inflammatory lesions (papules, infected pustules, or nodules) in the dermis around the microcomedo or comedo, which results in redness and may result in scarring or hyperpigmentation.
Primary causes
The root cause of why some people get acne and some do not is not fully known. It is known to be partly hereditary. Several factors are known to be linked to acne:
- Family/Genetic history. The tendency to develop acne runs in families. For example, school-age boys with acne often have other members in their family with acne as well. A family history of acne is associated with an earlier occurrence of acne and an increased number of retentional acne lesions.
- Hormonal activity: several hormones have been linked to acne, the androgens testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), as well as insulin-like growth factor 1 (IGF-I) . In addition, acne-prone skin has been shown to be insulin resistant.
Development of acne vulgaris in later years is uncommon. True acne vulgaris in adult women may be a feature of an underlying condition such as pregnancy and disorders such as polycystic ovary syndrome or the rare Cushing's syndrome. Menopause-associated acne occurs as production of the natural anti-acne ovarian hormone estradiol fails at menopause.
Hormonal treatment is one of the possible acne therapy in women.
- Inflammation, skin irritation or scratching of any sort will activate inflammation. Anti-inflammatories are known to improve acne
- Stress, through increased output of hormones from the adrenal (stress) glands, although modern tests have said otherwise and point to this not being a cause.
- Hyperactive sebaceous glands, secondary to the three hormone sources above.
- Accumulation of dead skin cells that block or cover pores.
- Bacteria in the pores. Propionibacterium acnes (P. acnes) is the anaerobic bacterium that causes acne. In-vitro resistance of P. acnes to commonly used antibiotics has been increasing.
- Use of anabolic steroids.
- Any medication containing lithium, barbiturates or androgens.
- Exposure to certain chemical compounds. Chloracne is particularly linked to toxic exposure to dioxins, namely Chlorinated dioxins.
- Exposure to halogens. Halogen acne is linked to exposure to halogens (e.g. iodides, chlorides, bromides, fluorides).
- Chronic use of amphetamines or other similar drugs.
Role of diet
Many patients hold the belief that their acne is influenced by dietary factors.
In the early 1900s, a few doctors discovered European and traditional diets highly reduced chronic diseases and acne than US diet. Past doctors advise eating whole, raw food for optimum health.
Most dermatologists today are awaiting confirmatory research linking diet and acne but some support the idea that acne sufferers should experiment with their diets, and refrain from consuming such fare, including chocolate, if they find such food affects the severity of their acne.
Milk
Recently, three epidemiological studies from the same group of scientists found an association between acne and consumption of partially skimmed milk, instant breakfast drink, sherbet, cottage cheese, and cream cheese.
The researchers hypothesize that the association may be caused by hormones (such as several sex hormones and bovine insulin-like growth factor 1 (IGF-1) or even iodine present in cow milk.
Carbohydrates
The long-held belief that there is no link between diets high in refined sugars and processed foods, and acne, has recently been challenged.
The previous belief was based on earlier studies (some using chocolate and Coca Cola) that were methodologically flawed.
The recent low glycemic-load hypothesis postulates that rapidly digested carbohydrate foods (such as soft drinks, sweets, white bread) produce an overload in blood glucose (hyperglycemia) that stimulates the secretion of insulin, which in turn triggers the release of IGF-1. IGF-1 has direct effects on the pilosebaceous unit (and insulin at high concentrations can also bind to the IGF-1 receptor) and has been shown to stimulate hyperkeratosis and epidermal hyperplasia.These events facilitate acne formation. Sugar consumption might also influence the activity of androgens via a decrease in sex hormone-binding globulin link concentration.
In support of this hypothesis, a randomized controlled trial of a low glycemic-load diet improved acne and reduced weight, androgen activity and levels of insulin-like growth factor binding protein-1.High IGF-1 levels and mild insulin resistance (which causes higher levels of insulin) had previously been observed in patients with acne. High levels of insulin and acne are also both features of polycystic ovarian syndrome.
According to this hypothesis, the absence of acne in some non-Westernized societies could be explained by the low glycemic index of these cultures' diets. It is possible that genetic reasons account for there being no acne in these populations, although similar populations (such as South American Indians or Pacific Islanders) do develop acne. Note also that the populations studied consumed no milk or other dairy products.
Further research is necessary to establish whether a reduced consumption of high-glycemic foods, or treatment that results in increased insulin sensitivity (like metformin) can significantly alleviate acne, though consumption of high-glycemic foods should in any case be kept to a minimum, for general health reasons. Avoidance of "junk food" with its high fat and sugar content is also recommended.
Vitamins A and E
Studies have shown that newly diagnosed acne patients tend to have lower levels of vitamin A circulating in their bloodstream than those who are acne free.In addition people with severe acne also tend to have lower blood levels of vitamin E .
Treatement
In females, acne can be improved with hormonal treatments that are one of possible solutions.
The common combined oestrogen/progestogen methods of hormonal contraception have some effect, but the antiandrogen, Cyproterone, in combination with an oestrogen (Diane 35) is particularly effective at reducing androgenic hormone levels.
Diane-35 and newer oral contraceptive containing the progestin drospirenone.
Both can be used where blood tests show abnormally high levels of androgens, but are effective even when this is not the case.
Along with this, treatment with low dose spironolactone can have anti-androgenetic properties, especially in patients with polycystic ovarian syndrome.
In some women with acne or alopecia who have normal serum levels of free testosterone, no clinical improvement can be reached by the classical treatment with antiandrogens, isotretinoids or corticosteroids.
The hypothesis is that some of these women have an excessive activity of the enzyme 5alpha-reductase.
A retrospective study evaluates a questionnaire filled out by 12 female patients, (six of whom had acne and six of whom had alopecia, but all with normal serum levels of free testosterone) treated with finasteride (5 mg/day), an inhibitor of 5 alpha reductase.
Nine of the 12 patients benefited from the treatment.
This supports the hypothesis of an excessive activity of 5alpha-reductase enzyme in peripheral tissue in these patients.
The fact that three of the patients did not realize any change in their symptom severity implies that there must also be other pathways in the genesis of acne and alopecia in women with normal levels of free testosterone.
Further evaluation is needed to elucidate more precise indications for the administration of finasteride in women with acne and alopecia.
Guide Lines 2016
Pamela Giordano
