Sarcoidosis with extensive cutaneous ulceration. Unusual clinical presentation.

A 70-year-old white woman with sarcoidosis and insulin-resistant diabetes mellitus presented with extensive cutaneous ulcerations. Both the cutaneous lesions and the systemic features of sarcoidosis showed a dramatic improvement during oral corticosteroid therapy. When extensive cutaneous ulcerations are present, it is important to consider sarcoidosis, as these may be the only presenting sign of the disease. Unlike ulcerated necrobiosis lipoidica diabeticorum, sarcoidal ulcerations may respond well to treatment with oral corticosteroids.

Nadolol, propranolol, and thyroid hormones: evidence for a membrane-stabilizing action of propranolol.

Ten normal subjects participated in a placebo-controlled, randomized, parallel study to determine the effects on thyroid hormones of chronic (4 wk) propranolol or nadolol, including observation for 2 wk after their discontinuation. Subjects took placebo for 1 wk, then propranolol or nadolol doses increased weekly to 240 mg/day by 3 wk. After 1 wk of placebo, after 2 wk of the highest dose of propranolol or nadolol, and 2, 4, 6, 9, and 13 days after their discontinuation, thyroid hormone levels were measured by radioimmunoassay and heart rate responses to exercise were assessed. Both drugs induced equal and high degrees of exercise tachycardia inhibition. Propranolol decreased 3,3'5-triiodothyronine (T3) levels, increased 3-3'-5'-triiodothyronine (rT3) levels, tended to increase thyroxine levels, but did not increase thyroid-stimulating hormone levels. After discontinuation of propranolol, rT3 levels slowly (day 6) returned to values after placebo, suggesting delayed recovery of 5'-deiodination. There was no evidence of any rebound in T3 levels after withdrawal of propranolol. Nadolol induced no significant changes in the thyroid hormones measured. The data agree with the known effects of propranolol on thyroid hormones in normal man and show that nadolol does not have these effects when given chronically at an equivalent beta-blocking dose. The likely explanation is that the membrane-stabilizing activity of propranolol alters thyroid physiology by interfering with 5'-deiodinase.

Oncogenic osteomalacia associated with a mesenchymal chondrosarcoma.

A patient with phosphaturic osteomalacia without chemical or pathological evidence of hyperparathyroidism and subnormal urinary cyclic AMP excretion was treated with vitamin D and phosphates for 9 months with partial improvement of osteomalacia, but not phosphaturia. Subsequent removal of a mesenchymal chondrosarcoma of the foot led to prompt resolution of phosphaturia and healing of the osteomalacia. Although 1,25-dihydroxyvitamin D levels were not obtained before vitamin D therapy, the levels noted during continued severe phosphaturia preoperatively were not lower than those obtained several months postoperatively during the healing phase. Studies done 1 year after tumor removal showed normalization of phosphaturia, urinary cyclic AMP, and bone histology. We suggest that the tumor elaborated products which promoted nonparathyroid mediated phosphate excretion independently from any effects on vitamin D metabolism.

Minoxidil in refractory hypertension: benefits, risks.

The blood pressure of 18 patients with refractory hypertension was controlled by treatment with Minoxidil in combination with Propranolol and diuretics. Ten of these patients were studied prospectively and were found not to have deterioration of carbohydrate tolerance while on Minoxidil therapy. Pericardial effusions occurred in 40% of the patients, including 2 with normal renal function. This untoward effect of prolonged use Minoxidil warrants further study.