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)

1,25-dihydroxyvitamin D3 has been used with success in the treatment of secondary hyperparathyroidism associated with chronic renal failure. However, frequently 1,25-(OH)2D3 induces hypercalcemia, especially in those patients ingesting large doses of calcium carbonate, precluding the administration of therapeutic doses of 1,25-(OH)2D3. In addition, control of serum phosphorus is a persistent problem in patients maintained on chronic hemodialysis and 1,25-(OH)2D3 treatment can aggravate the hyperphosphatemia. Thus, ideally an analog of 1,25-(OH)2D3 that can suppress PTH with minor effects on calcium (Ca) and phosphate (PO4) metabolism would be an ideal tool to control secondary hyperparathyroidism. We have shown that 22-oxa-1,25-(OH)2D3 (OCT), an analog of 1,25-(OH)2D3 with little calcemic activity, can suppress PTH mRNA in normal rats and in cultured bovine parathyroid cells with equipotency to 1,25-(OH)2D3. To further characterize the differential effects of 1,25-(OH)2D3 and OCT on Ca and PO4 metabolism we performed several experiments in intact and parathyroidectomized (PTX) rats. In metabolic studies in four groups of normal rats 1,25-(OH)2D3 treatment (8 ng/day) significantly increased the intestinal Ca absorption from 15.2 +/- 2.68% to 30.5 +/- 2.85% (P < 0.01), while the same dose of OCT had no effect. A dose of 200 ng/day of OCT increased intestinal Ca absorption similarly to the 8 ng/day dose of 1,25-(OH)2D3, from 10.6 +/- 2.49% to 24.8 +/- 2.35% (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Differential effects of 1,25-(OH)2D3 and 22-oxacalcitriol on phosphate and calcium metabolism. 845 54

Persistent hypercalcemia attributable to parathyroid gland hyperplasia was identified in 6 dogs with primary hyperparathyroidism. Clinical signs included polydipsia (n = 4), polyuria (n = 4), and signs caused by cystic calculi (n = 3). Abnormal clinical pathologic findings included hypercalcemia (mean, 13.6 mg/dl; range, 12.6 to 14.7 mg/dl; n = 6), hypophosphatemia (mean, 2.2 mg/dl; range, 1.4 to 2.9 mg/dl; n = 6), high serum alkaline phosphatase activity (mean, 222 IU/L; range, 161 to 286 IU/L; n = 3), and isosthenuria (mean, 1.012; range, 1.006 to 1.017; n = 6). Serum parathyroid hormone concentration was within the reference range or high (mean, 23 pmol/L; range, 7 to 119 pmol/L; reference range, 1.5 to 13 pmol/L) in all dogs. At surgery, the number of large parathyroid glands was variable, being limited to 1 gland in 3 dogs, 2 glands in 2 dogs, and 4 glands in 1 dog. All visibly large parathyroid glands were surgically removed from each dog. Serum calcium concentration decreased into or below the reference range within 72 hours of surgery in all dogs, confirming the diagnosis of primary parathyroid disease. Multiple nodules of adenomatous hyperplasia were identified in each dog. All 6 dogs were treated with vitamin D and calcium carbonate following surgery. The dog from which all 4 parathyroid glands were removed has remained eucalcemic for more than 1 year with vitamin D supplementation. Vitamin D and calcium administration was discontinued within 4 to 12 weeks of surgery in the remaining 5 dogs. These dogs remained eucalcemic without vitamin D supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Primary parathyroid gland hyperplasia in dogs: six cases (1982-1991). 847 30

The milk-alkali syndrome became rare with the advent of modern ulcer therapy with nonabsorbable antacids, histamine2 blockers, and sucralfate. An increased frequency of this syndrome seems likely with the growing popularity of the use of calcium carbonate as an antacid or as calcium supplementation to prevent osteoporosis. We treated five patients who had six episodes of the milk-alkali syndrome; four of these cases were diagnosed between 1990 and 1992. All patients were ingesting massive quantities of calcium and absorbable alkali and were unaware of the toxic effects of these compounds. All patients presented with the triad of hypercalcemia, metabolic alkalosis, and renal failure. All metabolic abnormalities were corrected, and renal function improved with appropriate supportive measures and cessation of calcium and alkali ingestion. In two patients, the renal failure was so severe that dialysis was necessary. In four patients, either the serum amino-terminal parathyroid hormone or 1,25-dihydroxycholecalciferol levels were appropriately decreased in response to hypercalcemia. The serum carboxy-terminal parathyroid hormone levels were increased because of renal failure. Since both physicians and patients are often unaware of the calcium and alkali content of many nonprescription medicines, the diagnosis of the milk-alkali syndrome, a reversible cause of renal failure, can be missed if a detailed history of such intake is not elicited. Measurement of the serum amino-terminal parathyroid hormone and 1,25-dihydroxycholecalciferol levels may help differentiate milk-alkali syndrome from primary hyperparathyroidism.
 ...
PMID:The milk-alkali syndrome. A reversible form of acute renal failure. 848 Oct 62

Standard therapy with orally administered active metabolites of vitamin D3 often does not satisfactorily control the biochemical manifestations of secondary hyperparathyroidism in uremic patients. This may be due to inadequate serum concentrations of 1,25 (OH)2D3 achieved during the treatment. Eighteen patients on chronic hemodialysis (HD) with severe hyperparathyroidism were given high doses of calcitriol (1,25 (OH)2D3) or alphacalcidol (1 alpha-OH-D3) orally, in ten evenings preceding each HD session. The effect of the treatment on circulating parathyroid hormone (PTH), serum hydroxyproline, serum alkaline phosphatase and bone isoenzyme was examined in a pilot study during 5 weeks. Irrespective the preparation given the treatment caused 71.7 +/- 22.2% reduction of intact serum PTH concentration with only moderate rise of serum calcium. A decrease of serum hydroxyproline and activity of alkaline phosphatase with its bone fraction, the direct indexes of bone turnover reduction, was also observed. With ongoing calcium carbonate therapy (3-6 g/day) 5 episodes of mild, asymptomatic hypercalcemia was observed for the 108 times of the total number of examinations; in those cases the dose of alphacalcidol was reduced. Our observations indicate that intermittent administration of 1,25 (OH)2D3 as well as 1 alpha-OH-D3 in high oral doses effectively suppress PTH synthesis in uremic hyperparathyroidism already in a couple of weeks. The effect is similar to that obtained with intravenous administration of the vitamin D3 active metabolites.
 ...
PMID:[Oral pulsatile therapy with active vitamin D3 metabolites--an efficient method of parathyroid hormone synthesis suppression in uremic patients with severe hyperparathyroidism. A pilot study]. 850 2

The occurrence of aluminum-related bone disease should be completely prevented in uremic patients by restricting the use of aluminum-phosphate binders, which can be safely replaced by oral calcium carbonate. Factors other than aluminum may lead to adynamic bone disease in uremic patients. Radiolucent bone cysts are indicative of amyloid deposits, and their occurrence and progression may be influenced by the membranes used for hemodialysis. Bone disease may persist after successful renal transplantation, and the additional deleterious effect of immunosuppressive drugs should be emphasized. Primary hyperparathyroidism is the most frequent cause of hypercalcemia in the general population. Surgery should be undertaken when there is evidence of active disease, even in asymptomatic patients. The consequences of primary hyperparathyroidism on bone mass and bone fragility remain controversial, and histologic bone studies suggest that hyperparathyroidism leads to increased bone turnover without any deleterious effect on bone volume or trabecular architecture. The diagnostic value of a newly developed immunoassay for intact parathyroid hormone and parathyroid hormone-related protein is clearly demonstrated. New bisphosphonates are of major value for the management of hypercalcemia in malignancy.
 ...
PMID:Renal osteodystrophy and hypercalcemia. 851 74

The purpose of this study is to find out whether hypercalcemia and hyperparathyroidism are rare or not in manic-depressive patients taking lithium carbonate. The subjects were 13 patients receiving lithium and 19 healthy subjects not receiving it as normal controls. Serum ionized calcium (Ca++), serum parathyroid hormone (PTH), urinary calcium and cyclic AMP(cAMP) were measured. Cervical ultrasonographic examination was also performed. The mean serum Ca++ level in the lithium administered group was significantly higher than that in the control group (P < 0.02). There was no significant difference between the serum PTH levels in the two groups. The mean urinary calcium level in the lithium administered group was below the normal range, but the mean urinary of cAMP level was within the normal range. Although a parathyroid cyst was found in one lithium administered patient on ultrasonographic examination, no swelling of the parathyroid gland was observed in the other patients in the lithium administered group or in any of the control subjects. In the present study, no distinct hyperparathyroidism was found in the patients in the lithium administered group. Lithium administration affects calcium metabolism in manic-depressive patients and hypercalcemia seems to be one of the complications needing attention at the time of lithium administration.
 ...
PMID:Effect of lithium on serum calcium level and parathyroid function in manic-depressive patients. 857 94

Milk-alkali syndrome is characterized by progressive hypercalcemia, systemic alkalosis, and renal insufficiency. After calcium carbonate is ingested with diary products, hypercalcemia and alkalosis may develop in susceptible persons, particularly those with underlying renal insufficiency. We describe a young woman who neither drank milk nor had peptic ulcer disease, yet who ingested enough calcium carbonate to require admission to an intensive care unit for acute renal failure. Chronically bulimic, she was taking Rolaids (Warner-Lambert Co, Morris Plains, NJ), which contained calcium carbonate, and was eating yogurt daily to prevent osteoporosis. We discuss the characteristics and complex metabolic interactions of the milk-alkali syndrome, a critical but generally reversible electrolyte disorder. Early recognition of coincident hypercalcemia and alkalosis and prompt cessation of calcium carbonate ingestion are essential for successful recovery. Finally, we suggest that nephrologists should discourage patients with renal insufficiency and chronic vomiting from consuming calcium-containing antacids and excessive dietary calcium.
 ...
PMID:Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome. 865 5

Milk-alkali syndrome was first described 70 years ago in the context of the treatment of peptic ulcer disease with large amounts of calcium and alkali. Although with current ulcer therapy (H-2 blockers, omeprazole, and sucralfate), the frequency of milk-alkali syndrome has decreased significantly, the classic triad of hypercalcemia, alkalosis, and renal impairment remains the hallmark of the syndrome. Milk-alkali syndrome can present serious and occasionally life-threatening illness unless diagnosed and treated appropriately. This article presents a patient with hypoparathyroidism who was treated with calcium carbonate and calcitriol resulting in two admissions to the hospital for milk-alkali syndrome. The patient was successfully treated with intravenous pamidronate on his first admission and with hydrocortisone on the second. This illustrates intravenous pamidronate as a valuable therapeutic tool when milk-alkali syndrome presents as hypercalcemic emergency.
 ...
PMID:Milk-alkali syndrome induced by 1,25(OH)2D in a patient with hypoparathyroidism. 866 42

Forty-five subjects (41 women and 4 men) in long-stay and medium-stay facilities, aged 74 to 95 years (mean 86.4 years), with 25-hydroxy-vitamin D levels less than 12 ng/ml, were treated for six consecutive months with two tablets per day of a preparation containing vitamin D3 (800 IU/day) and calcium carbonate (1 g elemental calcium/day). Serum levels of 25-hydroxy-vitamin D were very low at baseline (5.6 +/- 0.4 ng/ml) and rose significantly under treatment, to normal values, 33.2 +/- 1.2 and 40.9 +/- 2.1 ng/ml after three and six months, respectively (p < 0.001 for both comparisons). Serum calcium increased significantly, by 4.5% (p < 0.001) during the first three months, and remained at a plateau thereafter. Corrected serum calcium rose by 8.9% (p < 0.001) during the trial. No patient developed hypercalcemia. Serum parathyroid hormone levels, which were elevated at baseline (71.6 +/- 5.8 pg/ml; normal, 12 to 54 pg/ml), decreased gradually and significantly throughout the treatment period, by 43.0% and 67.1% after three and six months, respectively (p < 0.001 for both comparisons). Serum alkaline phosphatase activity fell concomitantly, by 9.9% after three months (p < 0.01) and 36.5% after six months (p < 0.001). In conclusion, the preparation used in our study is effective in correcting both the vitamin D deficiency that is prevalent in elderly institutionalized patients and the resultant increase in bone turnover.
 ...
PMID:Biochemical effects of calcium and vitamin D supplementation in elderly, institutionalized, vitamin D-deficient patients. 868 85

An 88 year old lady undergoing cyclical etidronate and calcium carbonate (with citrate) therapy for vertebral osteoporosis was found to be symptomatically hypercalcaemic at the end of the first cycle of treatment. She had been previously asymptomatic and normocalcaemic, but was subsequently found to have primary hyperparathyroidism. This condition is most prevalent in postmenopausal females--the same patient group at risk of osteoporosis. Serum calcium should be measured after commencing cyclical etidronate and calcium carbonate. If hypercalcaemia is detected primary hyperparathyroidism should be excluded as an underlying, cause.
 ...
PMID:Cyclical etidronate and calcium carbonate (with citrate) supplementation for osteoporosis unmasking primary hyperparathyroidism. 869 35


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