Skin necrosis is a well-recognized although rare complication of continuous heparin therapy. We report the case of a 66-year-old diabetic woman with end-stage renal failure who received intermittent intravenous heparin during hemodialysis. She developed severe necrotic cutaneous ulcers over both legs, with typical histological findings. Thrombocytopenia never occurred but platelet studies demonstrated enhanced aggregation when heparin was added in vitro. Platelet-aggregating immunoglobulins produced in response to heparin can lead to thrombotic events. Thrombocytopenia usually develops prior to the onset of cutaneous lesions, but as in this case, may be absent. Heparin should be discontinued when the condition is recognized. Unfortunately, a poor outcome is frequently observed.

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The role of 1,25-dihydroxyvitamin D (1,25(OH)2D) in the pathogenesis of idiopathic hypercalciuria was studied in 37 renal stone formers who, during two 10-day periods, followed first a normal and then a low calcium diet. The following samples were taken during each diet; 24 h urine; fasting blood and urine; blood and urine following a 1 g oral calcium load. Patients were divided according to serum calcium level, 24 h urinary calcium excretion on the first diet and fasting calcium excretion on the second diet. Eight patients were found to be normocalciuric (NSF), 16 had absorptive hypercalciuria (AH), five renal hypercalciuria (RH) and eight primary hyperparathyroidism. In NSF and AH, a positive correlation was found between the fasting and the 24 hour urinary calcium (r = 0.787, P less than 0.001), while negative correlations were found between the fasting urinary calcium and the serum parathyroid hormone (r = -0.703, P less than 0.001) or the fasting urinary cyclic AMP (r = -0.434, P less than 0.01). Patients with RH had higher serum PTH and urinary cAMP levels for a given degree of fasting calciuria mainly on the low calcium diet. Mean serum 1,25(OH)2D was similar in NSF (43.6 +/- 4.5 pg/ml), AH (43.6 +/- 2.3 pg/ml) and RH (40.4 +/- 4.8 pg/ml) on the first diet; increases were similar in all groups after 10 d of calcium restriction. A positive correlation was found between the serum 1,25(OH)2D concentrations and the 24 h urinary calcium excretion on the first diet in NSF (r = 0.889, P less than 0.001) but not in AH or RH. There was no evidence of such correlation with the low calcium diet. No correlation between the calciuric response to calcium loading and the serum concentrations of 1,25(OH)2D was found. The results suggest that serum concentrations of 1,25(OH)2D may be related to urinary calcium excretion in NSF more than in AH or RH. The factors responsible for the hyperabsorption of calcium in the latter patients remain to be elucidated.

Serum 25-hydroxyvitamin D [25(OH)D], 24,25-dihydroxyvitamin D [24,25 (OH)₂D] and 1,25-dihydroxyvitamin D [1,25(OH)₂D] were studied in renal stone formers while on a diet containing 1,000 or 300 mg calcium per day. The patients were divided into four groups and identified as (a) normocalciuric (NSF), (b) absorptive hypercalciuric (AH), (c) renal hypercalciuric (RH) and (d) as having primary hyperparathyroidism (PHP). The results indicate that, on the 1,000-mg Ca diet, the mean 25(OH)D, 24,25(OH)₂D and 1,25(OH)₂D concentrations were within the normal range in all groups of patients. On the low-calcium diet, 25(OH)D concentrations decreased significantly in patients with AH and RH while 24,25(OH)₂D concentrations were not affected by the low-calcium diet. 1,25(OH)₂D concentrations increased significantly during dietary calcium restriction in all groups of patients. When the relationship obtained on each diet between the circulating 25(OH)D concentrations and the 25(OH)D/1,25(OH)₂D concentration ratio was compared, it suggested that the increase in the 1,25(OH)₂D concentrations during dietary calcium restriction may have been due to an increase in the capacity of the 25(OH)D-1α-hydroxylase, or to an increase in the circulating half-life of the hormone. These results indicate that renal stone formers are able to adapt themselves to dietary calcium restriction as shown by highly significant increases in the circulating 1,25(OH)₂D concentrations while on a low-calcium diet. Moreover, the increase in the circulating 1,25(OH)₂D concentrations did not happen at the expense of the 24,25(OH)₂D production in any of the groups of patients studied.