Porokeratosis

Ultrastructural and Biochemical Studies on a Case of Elastosis perforans serpiginosa

“…The residual part of the pathological specimen, as well as the normal specimens, were cleaned of adhering fat and muscular tissues, shredded in a homogenizer, washed with copious amounts of isotonic saline solution and then stirred for several hours [12][13][14] in 2 m NaBr solution to facilitate removal of the epidermis [16].…”

“…Histologically, the lesion shows hyperkeratotic and acanthotic epidermis, communicating channels extending from the dermis to the surface, and increased dermal elastin [1][2][3][4][5][6][7][8][9]. While patho genesis remains obscure, it has been clinically associated with heritable genetic diseases of connective tissue [10] like Marfan's syndrome [11], Ehlers-Danlos syndrome [12], osteogenesis imperfecta [13] and pseudoxan thoma elasticum [14], However, a real alteration of typical components of connective tissue has not yet been shown.…”

Porokeratosis (Mibelli).

“…Bloom and Abramowitz (1943) regard the condition as an hereditary dyskeratosis and suggest that vitamin A deficiency might be of aetiological importance; they state that Vigue, Lagarde and Lambard (1938) reported deficiency in one of their cases. This hypothesis was elaborated by Jones and Smith (1947) who were, however, unable to test it clinically.…”