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Calcium channel blockers have become popular for the treatment of hypertension (high blood pressure) and exertional angina (chest pain brought on by exercise). The more common side effects result from the action of the drug and are predictable; however, there are adverse reactions related to the central nervous system that are unpredictable and often unrecognized. Nifedipine has caused acute psychosis, and verapamil has caused acute delirium. Diltiazem, which otherwise causes few side effects, has caused restlessness and agitation (akathisia) and acute psychosis. A case is reported of a 66-year-old woman with bipolar affective disorder (manic-depression) who was taking lithium carbonate to control manic behavior, and nitroglycerin, estrogen, and levothyroxine sodium. She was put on diltiazem to control high blood pressure, and a few days later she became confused, forgetful, and depressed. A week after she began diltiazem she was admitted to psychiatric service. She was disheveled and knew her name, but not where she was, and she believed she had just gone through the San Francisco earthquake. Blood chemistry and results of other laboratory tests were normal. Diltiazem was discontinued, and she returned to normal within one week. The symptoms were not related to her manic-depressive disorder, but were those of lithium poisoning. Both diltiazem and verapamil have been reported to cause synergistic effects with lithium, and the side effects occurred even though blood lithium levels remained within the normal range. (Consumer Summary produced by Reliance Medical Information, Inc.)

The paper presents the case history of a 15-year-old boy with traumatic tetraplegia who developed hypercalcaemia within 6 weeks of injury. The condition was initially controlled by the infusion of intravenous fluids in large amounts and by the administration of calcitonin. After 3 weeks, calcitonin became ineffective. Eventually the hypercalcaemia responded to cortisone administered in low dosage. The endocrinologic implications of this observation are discussed.

Chronic renal disease is characteristically attended by derangements in calcium homeostasis and bone metabolism.1-3 Many investigators have documented an impaired intestinal absorption of calcium in patients with chronic renal failure using either classical metabolic balance or isotopic marking techniques.3-5 This defect has also been noted in patients without manifest azotemia or acidosis 3,6 and has been confirmed in chronic experimental renal insufficiency by Kessner and Epstein.7 Liu and Chu initially considered a "resistance" to vitamin D action in the uremic individual as a cause for defective intestinal calcium absorption.8 Stanbury and Lumb3 and Dent and co-workers 9 have also suggested that the "acquired vitamin D resistance" results primarily in the defective absorption of calcium from the gastrointestinal tract. The subsequent studies of Fletcher et al made during the therapeutic trials of alkali, aluminum hydroxide, vitamin D, and calcium supplements in uremic osteodystrophic patients appear confirmatory

Dr. Arthur Schneider, Junior Assistant Resident in Medicine, the Jewish Hospital of St. Louis, and Assistant in Medicine, Washington University School of Medicine: A 66-year-old white woman was admitted to Jewish Hospital with a two-day history of abdominal pain, vomiting of bilious material, and diarrhea. There was no previous history of weight gain, cold intolerance, or constipation. In the past few months she had had some drowsiness and a gradual decrease in mental acuity. On admission, the blood pressure was 130/ 80 mm Hg, pulse rate was 76 beats per minute, and temperature was 98 F (35.0 C). The voice was deeply pitched and hoarse, the skin was dry, and the scalp hair was coarse. Rales were heard at the bases of both lungs. Examination of the abdomen revealed diffuse involuntary rigidity, rebound tenderness, and high-pitched, rushing bowel sounds. Deep tendon reflexes were abnormally delayed and symmetrical in response.The

Ten patients with recurrent renal calculi were evaluated for parathyroid function. Each patient had persistently normal serum calcium values, normal or low serum phosphorus values, and increased urinary excretion of calcium, thus satisfying the criteria for "idiopathic hypercalcuria." However, each patient had reduced tubular resorption of phosphorus (TRP) in the presence of normal renal function, consistent with hyperparathyroidism. Four grossly normal parathyroids were identified in each patient at operation; three or 3½ glands were removed in each instance. Parathyroid hyperfunction was evident by electron microscopy in six of six patients examined. The clinical and biochemical response to parathyroidectomy corroborated the diagnosis of hyperparathyroidism. The incidence of stone formation was dramatically reduced. There was a prompt and sustained fall in urinary calcium, a rise in TRP, and an insignificant fall in serum calcium value. No patient had persistent hypocalcemia despite removal of 3 or 3½ parathyroid glands. In all four patients in whom serum parathyroid hormone levels were determined, the preoperative level was significantly elevated and fell promptly to normal postoperatively.