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Authors: Vanessa Ngan, Staff Writer, 2005; Updated: Dr Aswan Tai, Junior Doctor, Peter MacCallum Cancer Centre, Melbourne, Australia; Dr Sarah Smithson, Dermatologist, Skin Health Institute, Melbourne, Australia. Copy edited by Gus Mitchell. September 2021
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Reactive perforating collagenosis is the most common type of primary perforating dermatosis. It is characterised by the transepithelial elimination of collagen from the dermis through the epidermis to the skin surface.
Reactive perforating collagenosis
The pathogenesis of reactive perforating collagenosis is unclear.
The inherited form appears to be due to a genetic abnormality in collagen causing focal damage and extrusion through the epidermis. Cold weather and skin trauma typically trigger or aggravate the skin lesions.
Microvascular insufficiency and elevated fibronectin levels in plasma, as seen with diabetes and renal failure, may play a role in the acquired form. Another theory suggests microdeposition of substances and abnormal glycosylation of collagen I and III in diabetes alter collagen fibres.
Superficial trauma, such as scratching, and cold leads to necrobiosis and epidermal thinning in susceptible patients.
Reactive perforating collagenosis is a papulonodular mucocutaneous disorder with adherent keratotic plugs and crusts.
Clinical features of reactive perforating collagenosis
The dermoscopy features of reactive perforating collagenosis are characteristic and consistent:
Dermoscopy of reactive perforating collagenosis
Reactive perforating collagenosis in skin of colour is associated with hyperpigmentation:
Hyperpigmentation related to reactive perforating collagenosis in skin of colour
Reactive perforating collagenosis can usually be diagnosed on its distinct clinical features and associated conditions, and confirmed on dermoscopy.
The main aim of treatment for reactive perforating collagenosis is to reduce itch and minimise skin trauma:
Reactive perforating collagenosis remains confined to the skin.
Familial reactive perforating collagenosis is a lifelong condition with lesions becoming larger and more numerous with age.
Individual lesions in both the familial and acquired forms are self-healing but often recur.
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