PubMed1987
Among the cutaneous manifestations of hyperparathyroidism, cases of panniculitis with calcification of the adipose tissue and necrosis of the skin have recently been reported, the mechanism incriminated being calciphylaxis, as defined by Selye on the basis of experiments. Experimental calciphylaxis consists of local or systemic calcium deposits followed by inflammatory necrosis or sclerosis. The deposits are induced by "provoking" or precipitating factors (metal salts, albumin, traumas) after a phase of sensitization (to parathyroid hormone, vitamins D2 or D3, dihydrotachysterol), provided a critical period is allowed between these two phases; the duration of that period depends on the experimental conditions. The case reported here concerns a 64-year old obese and diabetic woman who had presented with hard and tender nodosities and plaques in her abdominal and crural panniculi, ending in extensive and hyperalgesic necrosis (fig. 1 and 2). The panniculitis had occurred in a peculiar context: at the end of an episode of renal failure complicated with secondary hyperparathyroidism (serum PTH 12.9 mIU/ml; N = 1.5-4.4 mIU/ml) with moderate increase to 5,000 of the P x Ca product. Histological examination of a nodule of the thigh disclosed multiple foci of microcalcification (fig. 3, 4, 5) within the adipose lobules, in the interadipocyte spaces, in connective tissue septa and in the adventitia of small vessels (positive Von Kossa reaction). Electron microscopy showed dense calcium deposits between adipocytes, in subcutaneous septa (fig. 6, 8) and in more or less damaged vascular walls (fig. 9). Within the microfibrillar and granular fundamental substance, microcrystals looking like hydroxyapatite crystals (fig. 7) conglomerated into pincushion-like formations becoming increasingly denser and more compact.(ABSTRACT TRUNCATED AT 250 WORDS)