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Isomorphic response of Koebner in a patient with cutaneous small vessel vasculitis

Editor A 48-year-old woman presented with recurrent occasionally itchy erythematous palpable lesions over both the lower limbs for 4 months before consultation. She did not have any systemic symptoms like fever, pain abdomen, melena or haematuria. Occasionally, she had joint pains involving small and large joints of the limbs without any associated swelling. She did not have any significant illness in the recent past nor was on any medication. Her past medical history was normal. On cutaneous examination, there were a few palpable purpuric lesions distributed over both the lower limbs below knee. In addition, she had similar purpuric lesions arranged in a striking linear distribution just above right medial malleolus (fig. 1). On investigation, her blood cell counts, liver function tests and renal function tests were normal. Microscopic examination of urine sample showed microscopic haematuria. Stool specimen for occult blood examination did not reveal any abnormality. Chest X-ray was normal, and test for antinuclear antibody was negative. Skin biopsy taken from one of the purpuric lesions on histopathological examination revealed leucocytoclastic vasculitis. Direct immunofluorescence of skin biopsy specimen revealed deposition of IgA and C3 on the vessel wall, thus consistent with Henoch Schonlein purpura. Heinrich Koebner first described the phenomenon of development of an existing dermatosis in previously normal skin following external or internal trauma and thus the name of the phenomenon. Although many dermatoses have been reported to exhibit isomorphic response, psoriasis is the prototype. Boyd and Neldner have classified isomorphic response in four categories depending on the strength of association between trauma and development of dermatoses at the site of trauma. These include (i) true isomorphic response seen in lichen planus, psoriasis, and vitiligo; (ii) pseudo-isomorphic response seen in Behcet’s disease, molluscum contagiosum, pyoderma gangrenosum, and warts; (iii) occasional traumatic localization of lesions in many dermatoses; and (iv) poor or questionable trauma induced processes. They have argued that isomorphic response should be reserved solely for those diseases in which the phenomenon is reproducible in all manner of patients, by a variety of insults, and not due to dispersement of external infective or allergic elements. The research in the pathogenesis of isomorphic response has been largely restricted to as it occurs in psoriasis. Different patho-mechanisms including immunologic, vascular, dermo-epidermal interaction, enzymatic, neural, genetic, hormonal factors and the role of inhibitory and growth factors have been implicated in the pathogenesis of isomorphic response. Isomorphic response is rare in vasculitis, and only a few cases have been reported in English literature including a case where PLEVA was considered to be a type of vasculitis. It has also been described in a patient with anaphylactoid purpura and an ANCA-positive patient with pyoderma gangrenosum. Different factors like vasoactive amine release, vascular permeability, size and nature of immune complexes and hydrodynamic forces determine the deposition of immune complexes in immune complex mediated vasculitis. As the legs and areas of stasis are the most common areas of vasculitis, alteration of vasculature due to various reasons like gravitational stasis, wounds and scars may lead to vulnerability to vasculitis. One case have been reported, where vasculitis occurred in scars and areas of altered vascular anatomy. In our case, vasculitis occurred presumably at the site of scratching. Scratching and subsequent triple response mediated venular dilatation could have led to circulatory stasis leading to immune complex deposit and thus vasculitis. Although the explanation sounds simple, why it is reported rarely is anybody’s guess.