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)

Secondary hyperparathyroidism is common in dialysis patients. Intravenous calcitriol has proven to be an effective therapy for the reduction of parathyroid hormone (PTH) levels. However, the effect of i.v. calcitriol on parathyroid function, defined as the sigmoidal PTH-calcium curve developed during hypocalcemia and hypercalcemia, has not been evaluated during the prolonged administration of i.v. calcitriol. Six hemodialysis patients with marked secondary hyperparathyroidism, PTH levels greater than 500 pg/mL (normal, 10 to 65 pg/mL), were treated for 42 wk with 2 micrograms of i.v. calcitriol after each hemodialysis. Parathyroid function was evaluated before and after 10 and 42 wk of calcitriol therapy. Between baseline and 42 wk, the basal PTH level decreased from 890 +/- 107 to 346 +/- 119 pg/mL (P less than 0.02) and the maximally stimulated PTH level decreased from 1293 +/- 188 to 600 +/- 140 pg/mL (P less than 0.01). In addition, calcitriol administration significantly decreased PTH levels throughout the hypocalcemic range of the PTH-calcium curve. Although the slope of the PTH-calcium curve (with maximal PTH as 100%) decreased between baseline and 42 wk (P less than 0.05), the set point of calcium did not change. Two patients with a decrease in both basal and maximally stimulated PTH levels after 10 wk of calcitriol, developed marked hyperphosphatemia between 10 and 42 wk; this resulted in an exacerbation of hyperparathyroidism despite continued calcitriol therapy. In conclusion, prolonged i.v. calcitriol administration is an effective treatment for secondary hyperparathyroidism in hemodialysis patients provided that reasonable control of the serum phosphate is achieved. In addition, the slope of the PTH-calcium curve may be a better indicator of parathyroid cell sensitivity than the set point of calcium.
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PMID:The effect of long-term intravenous calcitriol administration on parathyroid function in hemodialysis patients. 176 May 37

From 1986 to 1990, we performed total parathyroidectomy with simultaneous autotransplantation (TPX with AT) of parathyroid tissue into the forearm in 13 patients on chronic maintenance hemodialysis with severe secondary hyperparathyroidism. The indications for surgery included persistent hypercalcemia, hyperphosphatemia, roentgenological signs of renal osteopathy, soft tissue calcifications and severe pruritus. The parathyroidectomy was performed by an experienced surgeon who removed all four parathyroid glands and transplanted 10 mm3 of parathyroid tissue into the brachioradialis muscle. After an average postoperative period of 33.5 months, 10 of 13 patients developed recurrent clinical and biochemical hyperparathyroidism requiring reoperation. Seven of these patients underwent removal of the autograft. In 5 patients, however, the success was minimal. Four of these patients had a second autograft resection, but only transient improvement resulted. Our recurrence rate after TPX with AT is very high. The histological aspect of the resected autograft is similar to tumor-like growth and this may account for the results. A therapeutic alternative to TPX with AT appears to be necessary.
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PMID:Recurrent hyperparathyroidism after total parathyroidectomy and autotransplantation in patients with long-term hemodialysis. 181 88

In a review of 11 cases of ectopic calcification (5 of which in dialyzed patients and one in a paraplegic), the authors attempt to characterize this disorder in all its various forms using histological, clinical, and chemical methods. In dialyzed patients, two contributing factors were identified: hyperphosphatemia (plus hypercalcemia) and secondary hyperparathyroidism. In hyperphosphatemic patients the calcifications are multiple, paraarticular, labile, and have a fluid-viscous consistency. In secondary hyperparathyroidism, in addition to the above metastatic calcification there is dystrophic calcification typically localized in the anterior muscles of the hip and thigh. The ectopic calcification of the non-dialyzed patients is true ossification. The precise moment of the onset of the lesion is not always discernable, but its evolution points to primary or secondary local irritation as the trigger. Ossification is the predominant phenomenon in the paraplegic as well, while the triggering mechanism is still unknown.
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PMID:Clinical, histological, and chemical characterization of ectopic calcification in dialyzed and non-dialyzed patients. 181 58

Vitamin D3 administered to patients with postoperative hypoparathyroidism increases calcium absorption from the gut and calcium blood levels but leads to hypercalciuria and may produce renal lithiasis. Thiazides decrease calcium excretion with the urine. Therefore, an effect of combined therapy with hydrochlorothiazide, vitamin D3 and calcium on hypoparathyroidism was investigated. Twenty one women were selected out of 135 patients with postoperative hypoparathyroidism. These women were constantly given vitamin D3 (30,000-225,000 IU daily) and calcium. Normocalcemia, hyperphosphatemia and hypercalciuria were noted before the treatment with hydrochlorothiazide. Therapy normalized hypercalciuria but did not change mean differences in calcemia, phosphatemia, magnesemia, blood alkaline phosphatase and phosphates and magnesium clearance factors. Hypercalcemia and necessity to withdraw hydrochlorothiazide together with change of either doses or preparation of vitamin D3 were noted in three patients, including one patient in whom both hypercalcemia and hypercalciuria with the symptoms of vitamin D3 poisoning were observed. The author suggests that combined therapy with hydrochlorothiazide, vitamin D3 and calcium prevents hypercalciuria but may require changes in vitamin D3 dosage and withdrawal of hydrochlorothiazide in some patients.
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PMID:[Effect of hydrochlorothiazide on calcium metabolism in postoperative hypoparathyroidism]. 196 53

Forty Fischer-344 rats (10 weeks old, 130 g BW) were either bilaterally ovariectomized (OVX) or sham-operated (SHAM). The rats were allocated to the following groups: SHAM; OVX; OVX + 15 ng 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]/rat/d; OVX + 30 ng 1 alpha,24R,25-trihydroxyvitamin D3 [1,24,25(OH)3D3]/rat/d; OVX + 15 ng 1,25(OH)2D3/rat/d + 30 ng 1,24,25(OH)3D3/rat/d. The vitamin D metabolites were fed orally starting 4 weeks after surgery. Urine and blood samples were taken at several time points during the experiment. Twenty-one weeks after surgery all rats were sacrificed, and the proximal tibiae and the first lumbar vertebrae were processed undecalcified for static bone histomorphometry. Ovariectomy induced a 40% reduction in vertebral cancellous bone area, and a 69% reduction in tibial cancellous bone area. This bone loss in OVX rats was associated with moderately increased biochemical and histomorphometric indices of bone formation and resorption as compared to values in sham-operated animals. Through inhibition of bone resorption, treatment of OVX rats with 1,25(OH)2D3, 1,24,25(OH)3D3, and the metabolite combination prevented the ovariectomy-induced osteopenia in the lumbar vertebra, and partially prevented cancellous bone osteopenia in the tibial metaphysis. However, OVX rats receiving 1,25(OH)2D3 alone or in combination with 1,24,25(OH)3D3 exhibited hypercalcemia, hyperphosphatemia, hypercalciuria, and impaired bone mineralization. Treatment of OVX rats with 1,24,25(OH)3D3 alone, on the other hand, only slightly increased serum calcium levels and did not impair bone mineralization. Furthermore, the inclusion of 1,24,25(OH)3D3 with 1,25(OH)2D3 partially antagonized the untoward effects of 1,25(OH)2D3 on bone mineralization. These data suggest that the actions of 1,24,25(OH)3D3 on bone metabolism might differ from that of 1,25(OH)2D3, and that 1,25(OH)2D3 and, particularly, 1,24,25(OH)3D3 may be potentially effective agents for the prophylaxis of postmenopausal osteoporosis.
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PMID:Role of vitamin D metabolites in the prevention of the osteopenia induced by ovariectomy in the axial and appendicular skeleton of the rat. 208 Jun 35

The influence of vitamin D and ultraviolet irradiation (UVI), used for prevention of vitamin D deficiency, on the state of phosphoric-calcium metabolism was studied in experiments on rats. It has been shown that daily injections of 1-5 IU of vitamin D, and UVI in biodoses from 1/8 to 1/4 promote the maintainance of the normal level of phosphoric-calcium metabolism. When UVI was applied according to the widely used "basic scheme" (in biodoses from 1/4 to 2 1/2) the following anomalies were recorded: a three-fold increase of 25-ON-D3 concentration in the blood plasma, hyperphosphatemia, a tendency to hypercalcemia. The use of higher doses of UVI led to a further increase of 25-OH-D3 level, hypophosphatemia, hypercalcemia, kidney and heart calcification. The data obtained have evidenced a possibility of vitamin D intoxication during UVI.
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PMID:[Experimental research on the effect of ultraviolet irradiation on the phosphorus-calcium metabolic status]. 216 9

An unusual case of dystrophic calcinosis that occurred following trauma is presented. Calcinosis cutis is the deposition of calcium phosphate into the skin. It is classified as dystrophic if calcium and phosphorous levels are normal and tissue damage is present, idiopathic if calcium and phosphorous levels are normal and no tissue damage is present, or metastatic if there is hypercalcemia or hyperphosphatemia. The numerous causes of underlying tissue damage associated with dystrophic calcinosis are discussed.
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PMID:Self-healing dystrophic calcinosis following trauma with transepidermal elimination. 229 40

The musculoskeletal system of 167 successful renal transplant recipients was examined for locomotor complications. Apart from avascular necrosis and spontaneous fractures, two new clinical entities were identified: tendinitis and spontaneous tendon ruptures. Tendinitis was found in the supraspinatus and calcaneal tendons in 12 patients (7.2%). Pretransplant hyperphosphatemia and posttransplant hypercalcemia were seen in patients developing tendinitis. Spontaneous tendon ruptures were observed in the calcaneal tendons in four patients (2.4%). Pretransplant hyperphosphatemia was observed in this group of patients. The cumulative dose of prednisolone was not significantly different than in asymptomatic patients.
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PMID:Tendinitis and tendon ruptures in successful renal transplant recipients. 230 93

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

The effects of salmon calcitonin (0.25 MRC mU/g body wt) on the serum calcium and phosphate levels as well as on the activity of ultimobranchial body and parathyroid glands was investigated in the frog, Rana tigrina for 15 days. The hormone evokes hypocalcemia (on day 1 and day 3) which is followed by a significant hypercalcemia on day 10. Thereafter, the level of calcium decreases again on day 15. Calcitonin induces hypophosphatemia (on day 3 and day 5). Thereafter, hyperphosphatemia is recorded on day 10. By day 15 normal serum phosphate value is achieved. After treatment with calcitonin, the ultimobranchial body becomes inactive and the parathyroid glands get activated.
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PMID:Ultimobranchial body and parathyroid gland of the frog, Rana tigrina in response to calcitonin administration. 248 19


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