1/5. Disorders of maternal calcium metabolism implicated by abnormal calcium metabolism in the neonate.Normal fetal and neonatal calcium homeostasis is dependent upon an adequate supply of calcium from maternal sources. Both maternal hypercalcemia and hypocalcemia can cause metabolic bone disease or disorders of calcium homeostasis in neonates. Maternal hypercalcemia can suppress fetal parathyroid function and cause neonatal hypocalcemia. Conversely, maternal hypocalcemia can stimulate fetal parathyroid tissue causing bone demineralization. We report two asymptomatic women, one with previously unrecognized hypoparathyroidism and the other with unrecognized familial benign hypercalcemia, who were diagnosed when their newborn infants presented with abnormalities of calcium metabolism. J.B. was born at 34 weeks' gestation with transient hyperbilirubinemia and thrombocytopenia. At 1 month of age he had severe bone demineralization, cortical irregularities, widening and cupping of the metaphyses, and lucent bands in the scapulae. The total serum calcium and phosphorus were normal with an ionized calcium of 5.4 mg/dL (4.6-5.4). His alkaline phosphatase, parathyroid hormone, and 1,25-dihydroxyvitamin D levels were all increased. P.B., mother of J.B., had no symptoms of hypocalcemia either prior to, or during this pregnancy. She had severe hypocalcemia and hyperphosphatemia, laboratory values typical of hypoparathyroidism. J.N. presented at 6 weeks of age with new onset of seizures and tetany secondary to severe hypocalcemia. The serum phosphorus, creatinine, alkaline phosphatase, and parathyroid hormone levels were normal. At 15 weeks of age his calcium was slightly elevated with a low fractional excretion of calcium. P.N., mother of J.N., had no symptoms of hypercalcemia either prior to, or during this pregnancy. Her serum calcium was 12.7 mg/dL and urine calcium was 66.5 mg/24 hr, with a low fractional excretion of calcium ranging from 0.0064 to 0.0073. P.N. has a brother who previously had parathyroid surgery. Both J.N. and P.N. meet the diagnostic criteria for familial benign hypercalcemia. These cases illustrate the important relationships between maternal serum calcium levels and neonatal calcium homeostasis. They emphasize the need to assess maternal calcium levels when infants are born with abnormal serum calcium levels or metabolic bone disease.- - - - - - - - - - ranking = 1keywords = bone disease, bone (Clic here for more details about this article) |
2/5. Curative effects of 1alpha-hydroxycholecalciferol on calcium metabolism and bone disease in patients with chronic renal failure.Synthetic 1alpha-hydroxycholecalciferol (1alpha-OH-D3) was given intravenously in a dose of 2.5-10 mug per day to three patients with chronic renal failure. As little as 10 mug of 1alpha-OH-D3 daily for a week improved intestinal calcium absorption to a normal level, raised serum calcium, and reduced serum alkaline phosphatase. Severe rickets which had not responded to large amounts (greater than 200 mg in total) of vitamin D2 was markedly cured with 2.5 mug of 1alpha-OH-D3 given daily for 3 weeks. These clinical data hold promise that is certainly useful in the improvement of intestinal malabsorption of calcium and bone diseases in renal failure.- - - - - - - - - - ranking = 0.50303785531594keywords = bone disease, bone (Clic here for more details about this article) |
3/5. Hypercalciuric rickets: metabolic studies and pathophysiological considerations.Extensive metabolic studies were performed in a 14-year-old boy suffering from the rare clinical entity known as childhood idiopathic hypercalciuria associated with dwarfism, renal tubular abnormalities and bone lesions. The salient features were: hyperphosphaturia with hypophosphatemia, hypercalciuria with normocalcemia, elevated serum 1,25-dihydroxycholecalciferol[1,25(OH)2D3] levels, marked intestinal hyperabsorption of calcium and phosphorus, with low serum parathyroid hormone (PTH) and urinary adenosine 3':5'-cyclic monophosphate (c-AMP). Bone biopsy confirmed the clinical and radiological diagnosis of rickets. It appears that the following pathophysiological sequence is operating: primary renal phosphate leak with hypophosphatemia, increased 1,25(OH)2D3 synthesis, enhanced intestinal calcium absorption which in turn inhibits release of PTH and c-AMP. hypercalciuria is seen to be secondary to both avid intestinal calcium absorption and depressed PTH activity, and rickets the result of phosphate depletion. Treatment with oral phosphorus only resulted in an acceleration of growth rate, cure of rickets, and return of urinary calcium excretion to normal values.- - - - - - - - - - ranking = 0.0010126184386467keywords = bone (Clic here for more details about this article) |
4/5. Bone mineral analysis using single-energy computed tomography.We present a new method for evaluating in vivo changes in bone mineralization in the peripheral skeleton, using computed tomography (CT). A set of bone mineralization indices are generated from numerous CT images of the patient's distal radius. The cross-sectional anatomy displayed by the CT scan allows for separate evaluation of the cortical and trabecular bone. Correction for possible drift of the CT number scale (Hounsfield scale) is achieved by scanning standard solutions of dipotassium hydrogen phosphate simultaneously with the forearm. Preliminary data indicate that this is a precise method for evaluating in vivo changes in bone mineralization.- - - - - - - - - - ranking = 0.0040504737545868keywords = bone (Clic here for more details about this article) |
5/5. Disorders of calcium and phosphorus metabolism in adolescents.During adolescence, there are marked changes in the metabolism of calcium and phosphorus and a dramatic increase in the rate of bone mineralization under the influence of the sex hormones, growth hormone, and insulin-like growth factor-1. More than 50% of adult bone mass is accumulated during puberty; failure to achieve maximum bone mineralization at this time may lead to osteopenia and its complications in later adulthood. This article discusses the causes, evaluation, and management of adolescents with hypocalcemia, hypercalcemia, and disorders of bone mineralization.- - - - - - - - - - ranking = 0.0040504737545868keywords = bone (Clic here for more details about this article) |