Keratosis pilaris (KP) is one of the most common skin imperfections that results from follicular hyperkeratosis. It is characterized by an accumulation of corneocytes forming a keratinized plug which blocks and then dilates the hair follicle, sometimes associated with perifollicular erythema 1 (Figs 1-2). Because of its bad cosmetic appearance, KP can be socially disabling.2
Prevalence for KP is almost 40% of the total population and is increased in adolescents, predominantly girls where the prevalence is up to 80%. Studies show this phenomenon occurs in more than 85% of cases during the first two decades of life, mainly on arms, legs and buttocks. This condition is quite often familial (39 to 67% of the cases according to the authors) although no single gene mutation has yet been directly associated with keratosis pilaris. If KP reduces with age in 35% of people, it remains at the same level in 43% of the cases and even worsens for the others.1,3
There are, however, more or less strong correlations between certain states of life or pathologies and keratosis pilaris occurrence. Obesity, diabetes, pregnancy, menopause and vitamin A deficiency are thus unfavorably associated with keratosis pilaris.4,5 Keratosis pilaris is also more common for people with cutaneous dryness (ichthyosis vulgaris and atopic dermatitis), with a less efficient skin barrier and less retention of epidermal water, moreover 35% of KP patients displayed common mutations in filaggrin gene.6
On the other hand, an environmental aspect might play a role, as keratosis pilaris regresses during summer and worsens during winter cold dry episodes.2,3,7 This suggests that the air humidity reduction can be considered as an aggravating factor.
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