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)

Three siblings with neonatal familial hyperparathyroidism diagnosed at age 4 months, 2 months, and 5 days, respectively, were treated. Hypercalciuria, nephrocalcinosis, and renal tubular acidosis were present in each child. In all three, there were higher responses of serum parathyroid hormone to serum calcium and higher elevation of serum calcium with oral calcium loading. The metabolism of vitamin D and calcitonin seemed to be intact. Hypercalcemia associated with the abnormal response of parathyroid hormone secretion disappeared when the children passed the age of approximately 2 years, although renal tubular acidosis and nephrocalcinosis remained. An autosomal recessive inheritance seems likely.
Pediatrics 1990 Sep
PMID:Self-limited neonatal familial hyperparathyroidism associated with hypercalciuria and renal tubular acidosis in three siblings. 216 60

To examine the biochemical changes in coexisting hyperthyroidism and hyperparathyroidism, we have studied two female cases in our medical center. Both patients received biochemistry study, thyroid function test, thyroid autoantibody determination, parathyroid function tests and thyroid scan. They all had increased thyroid function. The concentration of parathyroid hormone was found to elevate in both cases. After thyroid function turned normal, hypercalcemia was still present. Both patients underwent neck operation. Parathyroid adenoma was found in both cases. The pictures of thyroid pathology showed diffuse hyperplasia in one case and lymphocytic thyroiditis in the other case.
Zhonghua Yi Xue Za Zhi (Taipei) 1990 Sep
PMID:Coexisting hyperthyroidism and hyperparathyroidism: two cases report. 217 48

More than a century ago, Jonathan Hutchingson, a surgeon-dermatologist, identified the first case of sarcoidosis at King's College, London. The disease is now known as a commonplace multisystem disorder characterized by the formation of noncaseating granulomata. The diagnosis of sarcoidosis is established by recognizing clinicoradiologic findings and providing histologic evidence of non-caseating granuloma. Serum angiotensin converting enzyme levels are high in about two thirds of the patients and hypercalcemia is a feature in one of every ten victims of sarcoidosis. Immunologic abnormalities include depression of cutaneous delayed-type hypersensitivity, accumulation of T-cells at the site of activity, hyperactive B-cells, and the presence of circulating immune complexes. The course and prognosis of the disease usually correlate with the mode of onset. An acute onset with erythema nodosum indicates a good prognosis and spontaneous resolution; whereas, an insidious onset may be followed by relentless, progressive fibrosis. Mortality and morbidity are caused by pulmonary fibrosis, cardiac arrhythmias, renal failure, neurologic involvement, and blindness. Corticosteroids and chloroquine relieve symptoms and suppress inflammation and granuloma formation.
Dis Mon 1990 Sep
PMID:Sarcoidosis. 220 9

To our knowledge apnea in infants has not been associated with hypercalcemia. We describe seven hypercalcemic infants aged 2 days to 3 months who had presented with apnea; six of the seven were otherwise healthy. The apneic attacks were brief, and normal breathing was restored spontaneously or after tactile stimulation. The attacks stopped and the apnea monitoring was discontinued when the children were 1 month to 2 years of age. The only abnormal finding common to all of the patients was hypercalcemia. Idiopathic infantile hypercalcemia was diagnosed in six of the patients and familial benign hypercalcemia in one. Our findings suggest that determination of the plasma calcium level be included in the investigation of apnea in infancy.
CMAJ 1990 Sep 15
PMID:Hypercalcemia in infants presenting with apnea. 220 5

Data were retrospectively analysed on 544 consecutive patients (362 females and 182 males, mean age 53.6 [2 weeks and 86 years]) who had been operated on for primary hyperparathyroidism between 1965 and 1989. During this period the rate of renal, bone and intestinal complications decreased from 90% in the first 5 years to 29% in the last 5 years. Organ manifestations and hypercalcaemia were often combined (70% in the early period, 30% now). The proportion of those with an asymptomatic course gradually and continuously rose to 21% now. The patients' average age at diagnosis rose from 46 +/- 10 to 58 +/- 14 years. Serum calcium concentrations in the last few years averaged 3.1 mmol/l, as high during the last few years as at the beginning of the period. Age, serum calcium concentration and parathyroid weight of the asymptomatic patients did not differ from those of the group as a whole.
Dtsch Med Wochenschr 1990 Sep 21
PMID:[Primary hyperparathyroidism. A disease picture has changed]. 220 21

The isolated perfused rat kidney was used to study the effects of amino-terminal fragments of human parathyroid hormone, hPTH(1-34), bovine parathyroid hormone, bPTH(1-84) and of PTH-related proteins, PTHrP(1-34), PTHrP(1-84), PTHrP(1-108) and PTHrP(1-141) on urinary bicarbonate excretion. PTHrP(1-34) (7 nmol/l), bPTH(1-84) (5.5 nmol/l) and hPTH(1-34) (7 nmol/l) had similar effects in increasing bicarbonate excretion with respect to the control. At lower concentrations (0.7 nmol/l) all PTHrP components, but not hPTH(1-34) or bPTH(1-84) increased bicarbonate excretion significantly. Infusions of PTHrP(1-108) and PTHrP(1-141) at 0.7 nmol/l, while associated with a rise in urinary bicarbonate concentration and excretion during the early stages of perfusion, produced a sharp decline in bicarbonate concentration and excretion in the latter part of perfusion. The different peptides produced no significant differences in glomerular filtration rate, fractional excretion of sodium or urine volume. The absence of substantial differences between the effects of hPTH(1-34) and PTHrP(1-34) are as noted in previous studies. The differences between PTHrP(1-108)/PTHrP(1-141) and PTHrP(1-34) demonstrated here are consistent with (1) the clinical manifestations of acidosis in hyperparathyroidism and alkalosis in humoral hypercalcaemia of malignancy, and (2) an independent action of a component of PTHrP beyond amino acids 1-34.
J Endocrinol 1990 Sep
PMID:Comparison of the effects of parathyroid hormone (PTH) and recombinant PTH-related protein on bicarbonate excretion by the isolated perfused rat kidney. 221 31

The appropriate use of phosphate binders, calcium supplements and especially calcitriol therapy has significantly decreased the incidence of overt secondary hyperparathyroidism in dialysis patients. Nevertheless some patients may still need parathyroidectomy, especially in the event of severe clinical signs and symptoms such as persistent hypercalcemia, pruritus, calcifilaxis, or extensive extra-skeletal calcification. Since aluminum-induced bone disease may resemble hyperparathyroidism in dialysis patients, whenever parathyroidectomy is contemplated the diagnosis of secondary hyperparathyroidism must be firmly established. Thus, a bone biopsy is mandatory prior to parathyroidectomy. It is our experience that once the patient goes to surgery the most important factor in the surgical approach is the presence of a skilled surgeon who has extensive experience in parathyroid gland surgery. The data comparing subtotal parathyroidectomy with total parathyroidectomy and autotransplantation are similar. The most important shortcoming is the lack of long-term follow-up. Recently, new data by several investigators has been advanced reintroducing total parathyroidectomy. Long-term observations in patients who despite total parathyroidectomy still have normal PTH levels are of special interest. In addition, long-term follow-up of these patients has shown that normal plasma calcium and phosphorus levels may be maintained without the use of Vitamin D; this occurred in the presence of active mineralization. However, our major objection to this procedure is the risk of aluminum-induced bone disease. At the present time we feel that the relative high incidence of recurrent hyperparathyroidism following subtotal parathyroidectomy is a reasonable trade off for the risk of aluminum bone disease which may develop in absence of PTH.(ABSTRACT TRUNCATED AT 250 WORDS)
Kidney Int Suppl 1990 Sep
PMID:Parathyroidectomy in chronic renal failure: indications, surgical approach and the use of calcitriol. 221 49

MC903 is a novel analogue of 1,25(OH)2D3 which exhibits similar inhibitory effects on cell proliferation and like, 1,25(OH)2D3, stimulates synthesis of osteoblast specific proteins by osteoblast-like cells in vitro. It is less active than 1,25(OH)2D3 in causing hypercalcemia in vivo. Since 1,25(OH)2D3 is known to stimulate bone resorption and increase the number of osteoclasts in several systems (in vivo and in vitro) we examined the effects of MC903 on the formation of osteoclast-like cells in vitro. As reported previously 1,25(OH)2D3 promoted the formation of multinucleated cells with phenotypic and functional characteristics of osteoclasts from adult human bone-marrow cultures at concentrations between 10(-8)M to 10(-12)M. Higher doses consistently suppressed multinucleated cell formation to values seen in the absence of 1,25(OH)2D3. Cells cultured in the presence of MC903 or for three weeks consistently induced the formation of multinucleated cells at concentrations 10(-8)M to 10(-12)M. As seen with 1,25(OH)2D3, MC903 also inhibited multinucleated cell formation at very high concentrations (10(-6)M). In two separate experiments MC903 appeared to be more potent than 1,25(OH)2D3 at lower concentrations (10(-10)M - 10(-12)M). From this study we conclude that MC903 is at least as potent as 1,25(OH)2D3 in inducing the formation human osteoclast-like cells in vitro. The decreased ability of MC903 to induce hypercalcemia in vivo is not therefore a result of a less marked effect than 1,25(OH)2D3 on the regulation of osteoclast formation.
Biochem Biophys Res Commun 1990 Sep 28
PMID:1,25(OH)2D3 and calcipotriol (MC903) have similar effects on the induction of osteoclast-like cell formation in human bone marrow cultures. 222 27

We have previously shown that cyclosporin A (CsA) produces high bone remodeling with resorption exceeding formation and loss of bone volume in the rat. This may have important clinical implications where CsA is widely used in organ transplantation. 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) is a bone mineralizing hormone which also has immune modifying properties. Consequently, we studied the effect of combined CsA and 1,25(OH)2D3 administration over 28 days in four groups of rats. Group A received vehicle (n = 10), group B CsA (15 mg/kg) (n = 10) alone, group C 1,25(OH)2D3 plus CsA (n = 15), and group D 1,25(OH)2D3 alone (20 ng/100 g) (n = 15). Rats were bled periodically at day 0, 7, 14, and 28 and Ca, parathyroid hormone (PTH), 1,25(OH)2D, osteocalcin (bone Gla-protein, BGP), BUN, and creatinine were measured. Rats were sacrificed on day 28 and bones were examined histomorphometrically. Compared to controls, CsA resulted in significant elevation of BGP and a transient increase in 1,25(OH)2D with excess bone remodeling and loss of bone volume. 1,25(OH)2D3 administration produced hypercalcemia, a significant rise in BGP, with suppression of PTH and increased osteoid volume. Combined therapy prevented the loss of bone volume probably due to increased osteoid tissue and enhanced osteoblast activity. Renal dysfunction, a side-affect of CsA, was not a factor. In conclusion, 1,25(OH)2D3 combined with CsA restores bone volume which is accompanied by increases in serum calcium and BGP.
Calcif Tissue Int 1990 Sep
PMID:1,25 Dihydroxyvitamin D3 modifies cyclosporine-induced bone loss. 222 90

In a girl with Williams-Beuren's syndrome psychological examination revealed mental retardation with a special mental profile, angiography revealed peripheral pulmonary stenoses, echocardiography a slight stenosis in the supravalvular aortal area and anthropometry typical facial signs. Indirect signs of hypercalcaemia were clinical signs of poor progress during infancy. The authors emphasize that accurate analysis of basic clinical signs and the natural development of the disease are the key to its diagnosis.
Cas Lek Cesk 1990 Sep 28
PMID:[How can the Williams-Beuren syndrome be recognized?]. 222 97


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