| Keratosis pilaris atrophicans | |
|---|---|
| Specialty | Dermatology |
| Types | Keratosis pilaris atrophicans faciei,atrophoderma vermiculatum, andkeratosis follicularis spinulosa decalvans. |
Keratosis pilaris atropicans is a group of idiopathicgenodermatoses that consists of three unique clinical entities:atrophoderma vermiculatum,keratosis follicularis spinulosa decalvans, andkeratosis pilaris atrophicans faciei.[1]
Keratosis pilaris atrophicans faciei manifests as follicular, hornypapules encircled by anerythematous halo encompassing the chin, cheeks, forehead, and eyebrows. Gradualhair loss occurs on the lateral edges of the eyebrows after this.[2]
Atrophoderma vermiculatum is characterized by the formation of keratotic, inflammatorypapules on the face that atrophicate, leave behind pitted scars that resemble honeycombs or reticula.[3]
Follichyperkeratosis andscarring alopecia arekeratosis follicularis spinulosa decalvans clinical hallmarks. Early childhood or infancy is when follicularhyperkeratosis first appears on the face, affecting the nose, forehead, cheeks, and eyebrows.Alopecia areata that leaves scars on the scalp and eyebrows starts in early childhood and gets worse. Additional related features include excessive periungal cuticles, corneal dystrophy withphotophobia, andpalmoplantar keratoderma.[4]
The aberrant keratinization of the follicular infundibulum causes keratosis pilaris atrophicans, which is characterized by irritation and blockage of the growing hair shaft.Alopecia,fibrosis,atrophy, and shrinking of the hair bulb are caused by persistent inflammation. The possibility that the genes controlling follicular keratinization are located onchromosome 18p is suggested by the association with a number of congenital disorders caused by partial monosomy or deletion in chromosomal arm 18p.[5]
It has been demonstrated that a mutation in thedesmoglein 4 gene causes autosomal recessive keratosis pilaris atrophicans.[6]
Keratosis pilaris atrophicans can be diagnosed clinically. Usually, askin biopsy is not required to make the diagnosis. When carried out, it exhibits general characteristics such as modest perifollicular inflammatory infiltration and keratotic plugs in the pilosebaceous units.[5]
For keratosis pilaris atrophicans, there are no proven treatment options. With age, the condition frequently becomes better. It is advised to use ultraviolet (UV) protection because the condition is frequently made worse by light.[5]