Chapter 141 Acne Vulgaris and Acne Conglobata
Acne vulgaris is characterized as a pilosebaceous disease with comedones, papules, and pustules, whereas acne conglobata is a more severe form, with cyst formation and subsequent scarring. The lesions occur predominantly on the face and, to a lesser extent, on the back, chest, and shoulders. It is more common in males, and onset is typically at puberty (somewhat later for the conglobata form).
Acne is the most common of all skin problems. A key factor is genetics. It is inherited in an autosomal dominant pattern with incomplete penetrance. If both parents had acne, 3 of 4 children will have acne. If 1 parent had acne, then 1 of 4 of the children will have acne.1
The on sent of acne vulgaris usually reflects an increase in pilosebaceous gland size and sebum secretion due to androgenic stimulation. The severity and progression are determined by a complex interaction among hormones, keratinization, sebum, and bacteria.
The lesions begin in the upper portion of the follicular canal, with hyperkeratinization being the first microscopic change. This leads to blockage of the canal, resulting in dilation and thinning. Eventually a comedone is formed. The formation of open or closed comedones appears to be related to the degree of keratinization and the level of blockage of the duct.
Despite a large amount of purulent exudate in pustular and cystic lesions, the only bacteria commonly cultured are normal skin species. Propionibacterium acnes is believed to release lipases that hydrolyze sebum triglycerides into free fatty acid lipoperoxides, thus promoting an inflammatory cascade.
Acne-like lesions can occur in response to various compounds: corticosteroids, halogens, isonicotinic acid, diphenylhydantoin, and lithium carbonate. Exposure to various industrial pollutants also causes acne: machine oils, coal tar derivatives, and chlorinated hydrocarbons. Cosmetics, pomades, overwashing, and repetitive rubbing can produce acne.
Acne is considered to be an androgen-dependent condition, and androgen excess, either systemic or local, is associated with more severe forms of the disease. Androgens control sebaceous gland secretion and exacerbate the development of abnormal keratinizing follicular epithelium. Endocrine disorders producing excess androgens are important etiologic factors: idiopathic adrenal androgen excess, partial defect in 21-hydroxylase, and polycystic ovary syndrome. Free testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and low sex-hormone-binding globulin levels have all been implicated.2–4 The skin of acne patients shows greater activity of 5-α-reductase, the enzyme that converts testosterone to a more potent androgen, dihydrotestosterone.5,6 This increased activity is independent of systemic levels of androgens and may explain the poor correlation between systemic levels of androgens and the severity of the acne lesions. Receptors for growth hormone and insulin-like growth factor (IGF-1) are present on the sebaceous gland and these hormones stimulate sebum production. Conditions of growth hormone excess (such as acromegaly) are associated with increased sebum production and acne. Insulin at high levels can interact with IGF-1 receptors. IGF-1 promotes expression of enzymes responsible for androgen biosynthesis and conversion. Elevated cortisol due to chronic stress thickens sebum. The stress of acne compounds this problem.
Although there is some controversy regarding diet in the etiology of acne, there is clear evidence of an association. In Western societies, acne vulgaris is a nearly universal skin disease afflicting 79% to 95% of the adolescent population. Among men and women older than 25 years, 40% to 54% have some degree of facial acne, and clinical facial acne persists into middle age in 12% of women and 3% of men. In contrast, epidemiologic evidence suggests that acne incidence rates are considerably lower in non-Western societies. For example, researchers found no cases of acne among the Kitavan Islanders of Papua New Guinea and the Ache hunter-gatherers of Paraguay.7
The exact diet for acne sufferers to follow has not been evaluated, but foods high in iodine should be eliminated and milk consumption limited.8 Milk contains estrogens, progesterone, and androgens as well as glucocorticoids and IGF-1.9 Trans fatty acids and high-fat foods should also be eliminated because they can disrupt sebaceous secretions and increase inflammation. The composition of the diet should be in the range of 45% protein, 35% carbohydrate, and 20% fat, as such a composition produces substantially less 5-α-reduction of testosterone and enhanced cytochrome P450 hydroxylation of estradiol, both therapeutic goals.10 A high-carbohydrate diet (10% protein, 70% carbohydrate, and 20% fat) has the opposite effect. A diet that encourages a high insulin response chronically could promote acne by resulting in elevated levels of IGF-1.11,12
Many dermatologists have reported that insulin is effective in the treatment of acne, suggesting impaired cutaneous glucose tolerance, insulin insensitivity, or both.13,14 The insulin was either given systemically (5 to 10 units two to three times a week) or injected directly into the lesion.
One study comparing the results of oral glucose tolerance tests in acne patients showed no differences from controls. However, repetitive skin biopsies revealed that the acne patients’ skin glucose tolerance was significantly impaired.15 One researcher of the role of glucose tolerance in acne coined the term skin diabetes to describe the disorder of acne.16 Considering the known immunosuppressive effects of sugar (see Chapter 56), all concentrated carbohydrates should be strictly eliminated.
High-chromium yeast is known to improve glucose tolerance and enhance insulin sensitivity17 and has been reported in an uncontrolled study to induce rapid improvement in patients with acne.18
Many studies have demonstrated that retinols, including oral vitamin A, reduce sebum production and the hyperkeratosis of sebaceous follicles. Retinol has been shown to be effective in treating acne when used at high and potentially toxic dosages (i.e., 300,000 to 400,000 IU/day for 5 to 6 months).19
Although dosages of vitamin A below 300,000 IU/day for a few months rarely cause toxic symptoms,19 early recognition is important. Cheilitis (chapped lips) and xerosis (dry skin) generally occur in the majority of patients, particularly in dry weather.
The first significant toxic symptom is usually headache, followed by fatigue, emotional lability, and muscle and joint pain. Laboratory tests appear unreliable for monitoring toxicity, since serum vitamin A levels correlate poorly with toxicity, and serum glutamate oxaloacetate transaminase and serum glutamate pyruvate transaminase are elevated only in symptomatic patients. Of far greater concern is the teratogenicity of massive dosages of vitamin A. Women of childbearing age should use effective birth control during treatment and for at least 1 month after discontinuation.
Contraception counseling is mandatory, and two negative pregnancy test results are required prior to the initiation of vitamin A therapy in women of childbearing potential. The baseline laboratory examination should also include cholesterol and triglyceride assessment, hepatic transaminase levels, and a complete blood count. Pregnancy tests and laboratory examinations should be repeated monthly during treatment.