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© 1992 British Society for Rheumatology

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CALCINOSIS AND THE ANTICENTROMERE ANTIBODY: ITS CLINICAL, RADIOLOGICAL AND IMMUNOGENETIC ASPECTS

M. NISHIKAI, K. ITOH and A. SATO

Department of Internal Medicine and Clinical Investigation, Second Tokyo National Hospital Tokyo, Japan

Correspondence to: Correspondence to M. Nishikai MD, Department of Internal Medicine, Second Tokyo National Hospital, 2-5-1. Higashigaoka, Meguro-ku, Tokyo 152, Japan

The relationship between calcinosis and the anticentromere antibody (ACA) was studied from a clinical, radiological and immunogenetic standpoint. Ten ACA-positive scleroderma patients, 34 ACA-negative scleroderma patients, 31 ACA-positive patients without sclerodermatous skin changes and 140 ACA-negative patients with various rheumatic diseases were compared with regard to the incidence of calcinosis as measured by radiographs of hand and/or foot. Calcinosis was found in 10(100%), 12(35%), 13(42%) and eight(6%) patients in each group respectively. Frequent sites for calcinosis in the ACA-positive patients were foot (24%), hand (21%) and leg(19%). The forearm was not usually involved (6%). During the follow-up term (1.0–9.5 years; mean 4.5 years) of 11 ACA-positive patients without calcinosis, four (36%) developed new calcinosis and this incidence was significantly higher (P<0.02) than that in the ACA-negative control group (2/42; 4.8%). As a whole, 23(59%) of 39 patients with ACA showed calcinosis. In the ACA-positive patients with calcinosis, sclerodactyly (P<0.005) and CREST syndrome (P<0.001) were found more frequently than in ACA-positive patients without calcinosis. HLA-A2 was found more frequently (67%) in the ACA-positive patients with calcinosis when compared to normal subjects (41%) (P<0.02). We concluded that calcinosis seems closely related to scleroderma, especi ally those with ACA, and that the development of calcinosis requires a certain genetic background.

KEY WORDS: Calcinosis, Anticentromere antibodies, Scleroderma


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