Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neonatal hyperparathyroidism usually presents as a "failure to thrive" syndrome. It may be transmitted as an autosomal dominant trait and may involve more than one offspring. We report on two brothers with neonatal primary hyperparathyroidism. One underwent a total parathyroidectomy and has lived for 14 years. Hyperparathyroidism was found in their father, suggesting autosomal dominant inheritance. The disease is fatal unless recognized early and treated. The characteristic pathological change is chief cell hyperplasia of the parathyroid glands. Near-total parathyroidectomy is the minimal operation required to control the hypercalcemia. Permanent hypoparathyroidism may be the sequel of appropriate surgical management. Treatment of the totally parathyroidectomized infant, however, is possible and can result in normal growth and development.
 ...
PMID:Hereditary neonatal hyperparathyroidism. 61 57

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.
 ...
PMID:Vitamin D toxicity. Initial site and mode of action. 66 94

The authors studied the clinical characteristics of primary and post-operative hypoparathyroidism in 39 patients. Laboratory follow-up data were compared under two different treatment programs using either AT 10 or 25 Hydroxycholecalciferol (25 OHCC). Clinical analysis revealed the atypical characteristics of primary hypoparathyroidism. From a therapeutic standpoint, AT 10 and 25 OHCC were equally effective in provoking a return to normal plasma calcium levels, except in complex cases of vitamin D resistance. 25 OHCC proved much easier to manipulate than at 10 and offered a higher security with respect tothe risk of hypercalcemia. The biological activity of 25 OHCC seems to differ from that of AT 10, especially regarding phosphorus metabolism.
 ...
PMID:[Hypoparathyroidism in adults (author's transl)]. 74 36

Here we report a highly sensitive and convenient ligand binding assay for the determination of 1,25(OH)2D3 in small volumes of human plasma. This method involves: (1) extraction of vitamin D3 and its metabolites using methanol-methylene chloride with separation of phases by centrifugation; (2) gel chromatography and high pressure liquid chromatography for the quantitative isolation of 1,25-(OH)2D3; and (3) a sensitive ligand binding assay for 1,25-(OH)2D3 employing cytosol receptor from the intestinal mucosa of rachitic chicks. Using modified rachitogenic chick diets allows early (less than 4 wks) harvesting of active receptor for 1,25-(OH)2D3 in high yield. The method includes a rapid and effective procedure for stable and long-term storage of the active cytosol receptor. A convenient dextran-charcoal means is used for the separation of receptor bound from free 1,25-(OH)2D3 resulting in the achievement of a lower (less than 5%) background (i.e., nonspecific binding) than reported for other 1,25-(OH)2D3 assays. Analysis of this receptor shows it to be a saturable, single class of binding sites with a dissociation constant (Kd) of approximately 3.7 x 10-11. The final recovery of 1,25-(OH)2D3 following extraction and chromatography is 80 +/- 3% and triplicate determinations can be made on a 3 ml plasma sample. The ligand binding assay routinely detects less than or equal to 5pg of 1,25-(OH)2D3 per assay tube and the inter- and intraassay variation, based on repeated determinations of 1,25-(OH)2D3 in pooled normal human plasma, is less than 5%. Preliminary studies indicate that our methodology will permit measurement of plasma 1,25-(OH)2D3 levels in all normal subjects and in pathophysiologic states where 1,25-(OH)2D3 levels may be below or above normal values. 1,25-(OH)2D3 values (pg/ml +/- SEM) in human plasma obtained from both normals and patients with various untreated calcium homeostatic disorders were: normals = 33.5 +/- 1.8; end-stage chronic renal failure = 5.1 +/- 1.2; primary hypoparathyroidism = 18.3 +/- 2.8; primary hyperparathyroidism = 61.4 +/- 7.1; and hyperthyroidism with associated hypercalcemia = 42.1 +/- 8.4.
 ...
PMID:An improved method for the measurement of 1,25-(OH)2D3 in human plasma. 75 33

Hyperparathyroidism during pregnancy is clearly associated with an increased incidence of neonatal morbidity and mortality. Although it is impossible to define the precise incidence of this entity, we believe that its occurrence will be seen more frequently with the increasing numbers of female patients who have successfully received renal transplants and with the routine determination of serum chemistries in the nontransplanted pregnant patient. A review of case reports since 1962 of women known to be hyperparathyroid during pregnancy revealed 80 per cent of these pregnancies to be complicated by neonatal tetany, death, or abortion. This review substantiates Ludwig's earlier report [1], which noted a 50 per cent incidence of neonatal complications despite the advances of prenatal and postnatal medical care. There have been only eight reported cases in which parathyroid resection was performed during pregnancy. Successful operation dramatically reduced the incidence of neonatal complications. An adaptive normocalcemic hyperparathyroidism occurs routinely during pregnancy. However, in the hypercalcemic hyperparathyroid pregnancy, transplacental passage of calcium leads to a profound hypercalcemia in the fetus. Since the fetal parathyroid glands are functionally responsive, parathyroid suppression is thought to occur in utero due to high calcium levels. This can lead to neonatal tetany or perhaps permanent neonatal hypoparathyroidism. When a patient presents with significant hypercalcemic hyperparathyroidism during pregnancy, we suggest that an explorative parathyroid operation be performed during the second trimester of pregnancy. After delivery, the baby's course should be carefully monitored with frequent calcium determinations. Cow's milk or other formula feedings high in phosphate content should be avoided in favor of feedings with a calcium:phosphorus ratio similar to that of human milk.
 ...
PMID:Hyperparathyroidism during pregnancy. 76 83

The rate of reversal of hypercalcaemia or hypercalciuria induced by calciferol, dihydrotachysterol, 1-alpha-hydroxycholecalciferol (1-alpha-OHD3), or 1-alpha, 25-dihydroxycholecalciferol (1-alpha, 25-(OH)2D3) was measured in three normal subjects, two patients with osteoporosis, and 14 patients with disorders resistant to vitamin D. The half time for reversal after stopping 1-alpha, 25 (OH)2D3 was less than that after stopping 1-alpha-OHD3, calciferol, or dihydrotachysterol. The differences observed were independent of the dose given or length of treatment. When 1-alpha-OHD3 or 1-alpha-25-(OH)2D3 was stopped patients with vitamin D resistant states (hypoparathyroidism, renal tubular hypophosphataemia, or chronic renal failure) showed less rapid reversal of hypercalcaemia and hypercalciuria than did normal subjects. These studies show one potential advantage of 1-alpha-25-(OH)2D3 over vitamin D, and possibly over 1-alpha-OHD3, in the management of vitamin D resistant states.
 ...
PMID:Rate of reversal of hypercalcaemia and hypercalciuria induced by vitamin D and its 1alpha-hydroxylated derivatives. 83 19

Fifty eight patients with thyrotoxicosis were examined as well as 9 patients with hypothyroidism and 40 healthy subjects. A tendence towards hypercalcemia and hyperphosphatemia, hypercalciuria, hyperhydroxiprolinuria, elevated alkaline phosphatase were found in hyperthyroidism. In hypothyroidism--hypocalcemia, hypocalciuria, hypohydroxiprolinuria. The changes are associated with the direct effect of thyroid hormones upon bone system (intensified bone metabolism with predominance of destruction). Calciuria and HOP-uria in thyrotoxicosis depend on the severity of the disease. The elevated calcium excretion in thyrotoxicosis speaks for the presence of ostemalacic component. TRP, PEI, mean diametrically opposite in hyper- and hypothyroidism, support the hypothesis of the secondary hypoparathyroidism in thyrotoxicosis and hyperparathyroidism--in the hypothyroidism.
 ...
PMID:[Studies of calcium-phosphorus metabolism in thyrotoxicosis]. 91 16

The newborn infant of a mother with hypoparathyroidism following thyroidectomy showed transient hypercalcemia and hypermagnesemia. Hypophosphatemia, as found in adult hyperparathyroidism, was not noted in this case, or in three of five other reported cases of neonatal hyperparathyroidism secondary to maternal hypoparathyroidism.
 ...
PMID:Transient neonatal hyperparathyroidism associated with maternal hypoparathyroidism. 93 15

Five patients with hypoparathyroidism (three post thyroidectomy and two idiopathic) were treated with synthetic 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3) for up to 6 months. In each case daily oral administration of 1 microgram 1,25-(OH)2-D3, either alone or with additional calcium, raised ther serum calcium into the normal range. The serum phosphorus and the renal tubular reabsorption of phosphorus fell during treatment. None of these patients developed hypercalcaemia and no other complications of treatment have been recorded. 1,25-(OH)2D3 seems to represent a significant improvement over conventional methods for treating hypoparathyroidism.
 ...
PMID:Treatment of hypoparathyroidism with 1,25-dihydroxycholecalciferol. 105 76

In three women intoxication with vitamin D or dihydrotachysterol occurred. Two patients died from complications despite successful lowering of the serum calcium, the third died after a pulmonary embolus during hypercalcaemia 5 months after cessation of vitamin D. Correct observation of the narrow therapeutic range of vitamin D preparations appears most important in the treatment of hypoparathyroidism and other indications. Particular attention should be given to the prophylaxis of over dosage. Apart from regular serum calcium estimations instruction of the patient and relatives as to the dangers and symptoms of intoxication is recommended. The issuing of a therapy identity card would meet these requirements.
 ...
PMID:[Observations in vitamin D and dihydrotachysterol poisoning]. 111 68


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>