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

Results of 1alpha-hydroxyvitamin D3 therapy in twelve children with renal bone disease are described. Nine of the twelve children showed a good response to 0.05--0.08 microgram/kg/day. Hypercalcaemia was the only side effect and proved easy to manage because of the short half-life of 1alpha-OHD3.
Clin Endocrinol (Oxf) 1977 Dec
PMID:Bone disease in children with chronic renal failure: therapy with 1alpha-hydroxyvitamin D3. 30 72

About 30% of patients with clinical osteoporosis had histological signs of osteomalacia, in spite of normal serum 25-hydroxyvitamin D3 (25-OHD3). The excess osteoid disappeared during treatment with 1alpha-hydroxyvitamin D3 (1alpha-OHD3). These patients might have reduced ability to convert 25-OHD3 to 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3). The intestinal calcium absorption increased during treatment with 1alpha-OHD3, but this was accompanied by a rise in urinary calcium excretion. Photon absorptiometry of the forearm indicated increased bone mineral content during treatment with a daily dose of 2 microgram 1alpha-OHD3 and a supplement of 1 g of calcium. This therapeutic combination, however, caused frequent episodes of hypercalcaemia, so further studies are necessary to evaluate an appropriate dose of 1alpha-OHD3 with or without a calcium supplement.
Clin Endocrinol (Oxf) 1977 Dec
PMID:Treatment of senile osteoporosis with 1alpha-hydroxyvitamin D3. 34 43

A group of seven children with different malignant processes presenting with hypercalcemia was studied. Bone destruction, diffuse metabolic abnormalities, abnormal acid-base homeostasis and recurrent hypercalcemia characterized these patients. A different mechanism leading to the production of hypercalcemia and/or bone destruction by cancer cells is considered. The results of this report suggest that parathyroid hormone production (P.T.H.) by the parathyroid glands is normal and that ectopic secretion of PTH or PTH-like material is negligible in these cases.
Cancer 1979 Dec
PMID:Hypercalcemia complicating childhood malignancies: a report of seven cases with some pathophysiological considerations. 38 12

To examine the relative importance of calcium and gastrin in regulation of calcitonin secretion, we administered graded oral doses of calcium to 10 normal men, ages 23-29 yr. Each subject had previously shown an appropriate increase in calcitonin secretion in response to a pharmacologic (0.5 mug/kg) pentagastrin injection. On separate days and in random order, each man drank 250 ml of distilled water containing 0.0, 0.5, 1.5, and 3.0 g of elemental calcium as the gluconate salt. Blood samples were drawn before and at 30, 60, 90, 120, 180, and 240 min after the oral calcium dose. The samples were analyzed for calcium by atomic absorption spectroscopy, and for gastrin and calcitonin by radioimmunoassays of established sensitivity and specificity. Ingestion of water (control) caused no change in any of the three variables. Calcium ingestion resulted in dose-related increases, within the normal range, of all three variables. Immunoreactive gastrin rose promptly, peaking at 30 min, and returning to basal levels or below by 120 min. In contrast, calcium and immunoreactive calcitonin levels rose slowly and in parallel, peaking at 120-240 min. Changes in calcitonin and changes in calcium were strongly and positively correlated, r = 0.73, when all data were pooled. Furthermore, individual linear regressions for changes in calcitonin and calcium levels (calculated separately for the three oral calcium doses in each subject) had positive slopes in 28 out of 30 sets (P < 0.01). The changes in calcitonin concentrations were much more poorly correlated with the corresponding changes in serum gastrin levels; in fact, the regression coefficient was weakly negative, r = -0.20. These results show that, at least in young adult men, changes of ambient calcium concentration within the normal range may be of major importance in physiologic regulation of calcitonin secretion. The findings are consistent with the hypothesis that calcitonin functions to prevent excessive postprandial hypercalcemia.
J Clin Invest 1979 Dec
PMID:Regulation of calcitonin secretion in normal man by changes of serum calcium within the physiologic range. 50 Aug 34

A 70-year-old woman with a long history of nasal and sinus polyps developed bilateral proptosis and left total external ophthalmoplegia. She was known to have hypercalcemia, which was later discovered to be caused by a parathyroid adenoma. X-ray studies, including computerized tomography, revealed increased radiodensity in the ethmoid sinuses (due to dystrophic calcification from the hypercalcemia), partial absence of the orbital walls from earlier surgical procedures, and bilateral rounded, retrobulbar tumors. At surgery, glistening, yellow, transparent, and encapsulated-lobulated masses were removed from the left orbit; they appeared to have prolapsed through a postsurgical dehiscence in the superomedial orbital wall. Light and electron microscopy confirmed that the lesional tissue represented polyps covered by respiratory epithelium; the yellow color was the consequence of secondary lipidization of the stromal fibroblasts.
Arch Ophthalmol 1979 Dec
PMID:Sino-orbital polyposis. 51 88

Previous nuclear disease was found twice: Mc Ardle disease, dermatomyositis. Causative factors were: strenous exercise, hyperthermia, intoxication, influenza. Myalgias and/or myoedema was recorded in ten cases, associated with an hypovolemia of variable severity in eight. Oligo-anuria was observed in eight cases. The acute renal failure (ARF) was characterized by an increase in the serum creatinin more important than the rise in the blood urea and, in some cases, severe metabolic disturbances: hyperkaliema (6 cases), hypocalcemia (5 cases), hyperphosphatemia (5 cases) and hyperuricemia (5 cases). Diagnosis was made by the increase in sera of the muscles enzymes, specially the CPK and the search for myoglobinuria, positive during the first seven days. A complete recovery of renal function was observed in the nine survivors with a transient and moderate hypercalcemia in three. Three patients had persistant neuro-muscular deficiencies. Non traumatic rhabdomyolysis is not a rare cause of ARF and should be considered when the etiology of ARF is uncertain.
Presse Med 1979 Dec 10
PMID:[Acute renal failure due to non traumatic rhabdomyolysis. 11 cases (author's transl)]. 53 Sep 46

9 patients with advanced renal failure and renal osteodystrophy documented by iliac crest biopsy were treated with 1,25-dihydroxycholecalciferol (average dose 0.53 micrograms per day) for 6 months. Under 1,25-DHCC there was a statistically significant increase in serum calcium and decrease in serum alkaline phosphatase and immune parathyroid hormone. Histomorphometric evaluation of posttreatment bone biopsies showed reduction of osteoclastic resorption and endosteal fibrosis. Osteoid volume decreased in most cases. In 3 patients with predominant fibroosteoclasia, bone turnover practically normalized. Bone mineral content of the radius (photoabsorptiometry) did not change with treatment. Transient hypercalcemia occurred in 5 patients and was easily corrected by adjustment of 1,25-DHCC dosage.
Schweiz Med Wochenschr 1979 Dec 08
PMID:[Effect of 1,25-dihydroxycholecalciferol in renal osteopathy]. 53 67

The leading symptom in patients with primary hyperparathyroidism (pHPT) is renal lithiasis and not osteopathy. The most abundant circulating forms of parathyroid hormone in pHPT represent COOH-terminal fragments with molecular weights ranging from 4000 to 7000. Radioimmunnoassays making use of antibodies directed to CCOH-terminal parts of human parathyroid hormone are therefore suitable in distinguishing patients with pHPT from control subjects and patients with hypercalcemia unrelated to hyperfunctioning parathyroid glands.
Schweiz Med Wochenschr 1979 Dec 08
PMID:[Diagnosis of primary hyperparathyroidism and differential diagnosis of hypercalcemia]. 53 70

Two thyrotoxic patients with significant hypercalcaemia are described. The hypercalcaemia failed to suppress with hydrocortisone, propranolol and calcitonin but serum calcium fell rapidly to normal with carbimazole treatment. Both patients were subsequently treated surgically and at operation no evidence of parathyroid disease was found. Thyroid disease must be controlled before co-existing parathyroid disease is diagnosed in hypercalcaemic thyrotoxic patients.
Postgrad Med J 1979 Dec
PMID:Control of hypercalcaemia in thyrotoxicosis. 54 53

In order to investigate the frequency of fasting hypergastrinaemia in primary hyperparathyroidism (A) and in chronic hypercalcaemia (B), in 40 and 16 patients respectively gastrin, parathyroid hormone (PTH) and serum calcium levels were measured and compared with those of a control group (40 subjects) with similar distribution of sex and age. Moreover, possible linear relationships between these parameters were investigated. Notwithstanding significant differences in calcium and PTH levels between the three groups (A: high PTH, high Ca++; B: low PTH, high Ca++; C: normal PTH and Ca++ levels), no significant difference in gastrin levels were found. However, in the first group, a marked increase of gastrin was observed in one patient, very probably affected by a gastrin-secreting tumor (positive secretin test). While no linear relationship between PTH and gastrin values was present in all the three groups, a significant correlation between serum calcium and fasting gastrin was detectable in the group A, ruling-out the above mentioned patient. Present data suggest that PTH does not modify gastrin levels and that chronic moderate hypercalcaemia does not raise serum fasting gastrin, at least in clinical conditions. Moreover, the frequency of hypergastrinaemia in hyperparathyroidism is very low and it seems to be present only in patients with gastrin-secreting tumors.
Acta Hepatogastroenterol (Stuttg) 1979 Dec
PMID:Fasting serum gastrin in primary hyperparathyroidism and in chronic hypercalcemia. 54 29


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