1988
DOI: 10.1111/j.1600-0560.1988.tb00532.x
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Adult, acquired reactive perforating collagenosis. Report of a case including ultrastructural findings

Abstract: A case of reactive perforating collagenosis in an adult male patient with chronic renal failure. Pruritic, umbilicate papules, showing extrusion of collagen fibers through the epidermis were detected histopathologically. Electron microscopy showed absence of basal membrane beneath the perforation and collagen fibers with preserved periodicity passing through widened intercellular spaces with islands of cytoplasmic material.

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Cited by 33 publications
(12 citation statements)
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“…With regard to acquired reactive perforating collagenosis, the exact pathogenesis remains unknown although many histological, immunohistochemical and ultrastructural studies have been done 37 . Several hypotheses have been proposed, including diabetes‐linked microangiopathy, 38 microtrauma due to chronic pruritus, 38 acquired abnormalities of collagen and /or elastic fibers by some factors such as proteolytic enzyme released from polymorphonuclear cells, 39,40 dysregulation of vitamin A or vitamin D metabolism, 41,42 elevated serum and tissue concentrations of fibronectin inciting epithelial proliferation and migration, culminating in perforation, 37 and abnormal tissue remodeling associated with TGF‐β overexpression 43,44 . Considering the pathogenesis of both disorders, TGF‐β could be a key pathogenetic common factor of both IgG4‐related sclerosing disease and acquired reactive perforating collagenosis.…”
Section: Discussionmentioning
confidence: 99%
“…With regard to acquired reactive perforating collagenosis, the exact pathogenesis remains unknown although many histological, immunohistochemical and ultrastructural studies have been done 37 . Several hypotheses have been proposed, including diabetes‐linked microangiopathy, 38 microtrauma due to chronic pruritus, 38 acquired abnormalities of collagen and /or elastic fibers by some factors such as proteolytic enzyme released from polymorphonuclear cells, 39,40 dysregulation of vitamin A or vitamin D metabolism, 41,42 elevated serum and tissue concentrations of fibronectin inciting epithelial proliferation and migration, culminating in perforation, 37 and abnormal tissue remodeling associated with TGF‐β overexpression 43,44 . Considering the pathogenesis of both disorders, TGF‐β could be a key pathogenetic common factor of both IgG4‐related sclerosing disease and acquired reactive perforating collagenosis.…”
Section: Discussionmentioning
confidence: 99%
“…A number of inorganic salts, including calcium chloride, have been proposed as a direct calcifier 8 . These inorganic salts apparently change connective tissue in such a manner that it will trap calcium, however, the finding of intact collagen fibers with regular periodicity indicates that no major structural alterations of collagen triggers the process of transepidermal elimination 9 …”
Section: Discussionmentioning
confidence: 99%
“…In addition, an increasing number of patients with a perforating dermatosis in association with a systemic disorder 1 have been reported in the last two decades, 4 in whom the clinical and histological picture often presents a combination of features from the four traditional perforating skin disorders as well as from prurigo nodularis of Hyde 3 . For these conditions, whose prevalence is much higher than suggested by the few reports in the literature, 4 the term acquired perforating collagenosis (APC) was coined 5 …”
mentioning
confidence: 99%