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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapy with orally administered calcitriol often does not adequately control the biochemical manifestations of secondary hyperparathyroidism in uremic patients. This may be due to inadequate serum concentrations of 1.25(OH)2 vitamin D and/or to insufficient dietary calcium supplementation. In the present study, therefore, we examined the effect on parathyroid function of calcitriol and calcium carbonate, administered orally, in doses sufficient to normalize the serum 1.25(OH)2 vitamin D and calcium concentrations. After nine months of combined therapy, marked suppression of immunoreactive PTH occurred in the absence of hypercalcemia. Furthermore, prolonged therapy resulted in additional suppression of the PTH concentrations comparable in magnitude to that reported following intravenous calcitriol therapy and was associated with a mild degree of hypercalcemia similar to that which occurs with intravenous therapy. Euparathyroidism was achieved in 25% of the patients by 15 months of treatment. In conclusion, secondary hyperparathyroidism can be effectively controlled with combined oral therapy without significant hypercalcemia in selected patients with end-stage renal failure. This salutary effect may result from direct actions of 1.25(OH)2D on the parathyroid gland and/or gastrointestinal tract, or from an overall action of combined treatment to restore calcium homeostasis.
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PMID:Oral calcitriol and calcium: efficient therapy for uremic hyperparathyroidism. 321 May 46

We present a case of the milk-alkali syndrome occurring in pregnancy, an association not described in the medical literature. Ingestion of calcium carbonate and calcium-containing food was precipitated by the hyperemesis of pregnancy. Complications--hypercalcemia, dehydration, renal insufficiency, and pancreatitis--resolved within days. Here, the milk-alkali syndrome was the cause of the hypercalcemia of pregnancy. This case illustrates a rare cause of and complications from the milk-alkali syndrome.
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PMID:The milk-alkali syndrome in pregnancy. Case report. 321 Oct 90

The most current form of chronic pancreatitis, i.e. chronic calcifying pancreatitis, is often related to nutritional causes. This disease is characterized by formation within the pancreatic ducts and the lumina of accini of precipitates and calculi composed of calcium carbonate and of a newly discovered protein, the pancreatic stone protein (PSP). The formation of precipitates depends on two mechanisms: (1) a non etiological disorder reducing the secretion of PSP. This small phosphoglycoprotein is a calcium stabilizer which prevents the crystallization of calcium carbonate in a super saturated solution such as pancreatic juice, (2) modifications of the pancreatic juice related to the cause of the disease. In Occidental countries the main etiological factor is alcohol consumption associated with protein-and-fat-rich or fat-poor diets. Like hypercalcaemia, another cause of the disease, a chronic consumption of alcohol increases the pancreatic secretion of secretory proteins (enzymes) via its action on the cholinergic nerves. In some tropical countries, chronic pancreatitis is observed in children and associated to malnutrition. However, according to recent studies neither kwashiorkor nor manioc consumption seem to be responsible for the occurrence of this disease.
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PMID:[Etiopathogenesis of chronic nutritional pancreatitis]. 330 3

The efficacy of calcium carbonate (CaCO3) as a phosphate binder has been limited by its tendency to cause hypercalcemia. Since standard dialysate calcium concentrations (3.0-3.5 mEq/l) increase the risk of developing hypercalcemia with large doses of CaCO3 by inducing positive calcium balance during hemodialysis (HD), we compared control of hyperphosphatemia in 41 HD patients during 4 months each of aluminum hydroxide (Al(OH)3) and CaCO3 when the dialysate calcium concentration was lowered, as required, to maintain the predialysis serum calcium concentration within the normal range. Mean predialysis serum phosphorus and calcium concentrations were 5.0 +/- 0.2 mg/dl and 9.3 +/- 0.1 mg/dl, respectively, during 4 months CaCO3 (9.2 +/- 0.3 g/day) and 4.9 +/- 0.2 g/dl and 9.1 +/- 0.1 mg/dl during the previous 4 months Al(OH)3 therapy (2.9 +/- 0.2 g/day). Reducing the dialysate calcium concentration to below 3.0 mEq/l (mean 2.1 +/- 0.04) in the 11 patients who developed hypercalcemia on CaCO3 decreased serum calcium (-1.1 +/- 0.15 mg/dl) and ionized calcium (-0.3 +/- 0.04 mEq/l) during HD, enabled CaCO3 (8.8 +/- 0.4 g/day) to be continued, and maintained predialysis serum calcium and phosphorus at 10.4 +/- 0.1 mg/dl and 5.2 +/- 0.3 mg/dl, respectively. No improvement in acidosis or biochemical hyperparathyroidism was observed during CaCO3 therapy but serum aluminum was significantly decreased after CaCO3 (p less than 0.005). We conclude that CaCO3 prevents interdialytic hyperphosphatemia as effectively as Al(OH)3 without increasing the predialysis serum calcium x phosphorus product, provided serum calcium is maintained within the normal range by adjusting the dialysate calcium concentration.
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PMID:Calcium carbonate is an effective phosphate binder when dialysate calcium concentration is adjusted to control hypercalcemia. 342 32

Hypercalcemia is associated with impaired urinary concentrating ability. To explore the mechanism(s) by which hypercalcemia impairs chloride transport in the loop of Henle, we carried out in vivo microperfusion of the loop segment in Sprague-Dawley rats rendered acutely hypercalcemic (12.1 +/- 0.1 mg/dliter) by calcium gluconate infusion. Control rats were infused with sodium gluconate and had normal plasma calcium (8.0 +/- 0.2 mg/dliter). Compared to control, fractional chloride reabsorption was decreased (61 +/- 4 to 50 +/- 3%; P less than 0.05) and early distal chloride increased 74 +/- 6 to 98 +/- 3 mEq/liter (P less than 0.001) in hypercalcemia. During hypercalcemia, infusion of verapamil failed to increase fractional chloride reabsorption (49 +/- 4%; P less than 0.05) or decrease early distal chloride (95 +/- 2; P less than 0.05) toward control values. Similarly, indomethacin did not improve fractional chloride reabsorption (48 +/- 4%; P less than 0.05) or distal chloride concentration (93 +/- 7; P less than 0.05). In control rats infused with Ringers HCO3, the addition of calcium 8.0 mEq/liter to the perfusate increased early distal calcium (9.22 to 3.11 mEq/liter) but was associated with no change in fractional chloride reabsorption (-6 +/- 6%) and a slight decrease in early distal chloride (-9 +/- 3 mEq/liter; P less than 0.05). These data are consistent with the hypothesis that an elevated plasma, not luminal calcium, concentration impairs chloride reabsorption in the loop segment, primarily the ADH-stimulated component. This may have an important role in the urinary concentrating defect of hypercalcemia.
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PMID:Role of the loop segment in the urinary concentrating defect of hypercalcemia. 348 71

Heart and heart-lung transplant recipients at Stanford (Calif) University Medical Center were routinely prescribed long-term calcium carbonate antacid therapy to aid in the prevention of peptic ulcer disease and osteoporosis associated with glucocorticoid immunosuppressive therapy. Patients consumed 4 to more than 10 g/d of elemental calcium. Since calcium carbonate also provides the essential ingredients for the development of the milk-alkali syndrome, the laboratory flow sheets of 297 heart and heart-lung transplant recipients were reviewed to examine the incidence of hypercalcemia. Sixty-five patients developed significant hypercalcemia after transplantation. Thirty-one patients were alkalotic at the time of hypercalcemia; 37 had impairment in renal function. It is likely that most of these patients had the milk-alkali syndrome. While most patients became eucalcemic by discontinuing calcium carbonate therapy, intravenous hydration and forced diuresis were used to treat severe cases. It is possible that the incidence of the milk-alkali syndrome will increase with the current popularity of prescribing calcium carbonate for the prevention and treatment of osteoporosis.
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PMID:Milk-alkali syndrome in patients treated with calcium carbonate after cardiac transplantation. 353 84

Traditionally, phosphate binders containing aluminum have been used effectively to control serum phosphorus levels in patients with chronic renal failure. In these patients, however, absorption and accumulation of aluminum in plasma and tissues can lead to debilitating pathologic conditions, including aluminum-related osteodystrophy. An alternative therapeutic approach using calcium carbonate as a phosphate binder has been proven to be effective. In a recent study of 20 patients on chronic hemodialysis, the efficacy of calcium carbonate therapy was demonstrated. Serum phosphorus levels in these patients were 4.8 +/- 0.13 mg/dL with the use of aluminum-containing phosphate binders, 7.3 +/- 0.26 mg/dL when phosphate binders were discontinued, and 4.8 +/- 0.17 mg/dL with the use of calcium carbonate (Os-CaL 500) therapy. The total amount of aluminum ingested for all 20 patients combined went from 112 g/d at the beginning of the study to 22 g/d at the end of the study. The amounts of calcium carbonate administered varied because of large variations in dietary phosphorus intake between patients. In addition, the individual distribution of phosphorus intake during the day dictated the dosing schedule. There were no adverse side effects associated with calcium carbonate therapy. A few patients ingesting large amounts of calcium carbonate to control their extremely high phosphorus levels developed hypercalcemia. However, this effect was reversible after discontinuation of calcium carbonate therapy.
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PMID:Alternative phosphate binders in dialysis patients: calcium carbonate. 360 77

The control of hyperphosphatemia in dialysis patients is frequently achieved using aluminium hydroxide (A1(OH)3) and/or calcium carbonate (Ca CO3). However, this effect is counterbalanced by risk of aluminium intoxication and hypercalcemia. An alternative to the use of these phosphate binders is the prescription of magnesium hydroxide (Mg(OH)2) in association with a magnesium free dialysate. 19 patients with subtoxic plasma aluminium concentration received such a therapy. 9 months after starting the essay 4 patients had been excluded for digestive intolerance (3 cases) and neuro-psychic symptoms related to hypermagnesemia (1 case) after therapy with maximal doses of 6 to 12 g/d. Plasma inorganic phosphorus was decreased from 2.47 +/- 0.32 to 1.86 +/- 0.40 mmol/l (P less than 0.05) and plasma aluminium from 3.03 +/- 0.93 to 1.52 +/- 0.15 mumol/l (P less than 0.05). The results have been obtained without any significant increase in plasma and red cell magnesium levels. Metabolic alkalosis has been observed in association with the increase of ion exchange resin (sodium polystyrene sulfonate: Kayexalate) to treat progressive hyperkalemia. With the exception of possible metabolic effects occurring on a long term basis, Mg(OH)2 in association with magnesium-free dialysate seems of value to treat dialysis hyperphosphatemia.
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PMID:[Magnesium hydroxide treatment of hyperphosphatemia in chronic hemodialysis patients with an aluminum overload]. 361 5

Case records from 21 dogs with hypercalcemia and hyperparathyroidism were evaluated. The dogs were greater than or equal to 7 years old, and 6 were Keeshonds. The most common clinical signs were polydipsia/polyuria, listlessness, and muscle weakness. The serum calcium concentrations were 12.1 to 19.6 mg/dl. Serum phosphorus concentrations were low in 5 dogs, within the reference range in 13 dogs, and high in 3 dogs that also had high concentrations of BUN. Twenty dogs had a parathyroid adenoma, and 1 had a parathyroid carcinoma. Nineteen dogs had their parathyroid tumor surgically removed. Within 5 days of tumor removal, 11 of the 19 dogs became hypocalcemic and the remaining 8, normocalcemic. Nine of the 11 hypocalcemic dogs developed clinical signs. Iatrogenic hypercalcemia was induced in 7 of 16 dogs treated orally with calcium carbonate plus vitamin D. Only 1 of 19 dogs that had their parathyroid tumor excised died in hypocalcemic tetany. Two additional dogs died within 2 weeks of surgery, one because of pancreatitis, the other due to renal failure. Eight dogs died 9 to 37 months after surgery of unrelated problems. Eight dogs were alive for at least 7 to 28 months after surgery.
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PMID:Primary hyperparathyroidism in dogs: 21 cases (1976-1986). 365 3

A man with severe hypercalcemia (22 mg/dl) secondary to ingestion of a calcium carbonate antacid (Tums) was admitted with obtundation and hyperreflexia, which disappeared with treatment. Laboratory values, which were consistent with milk-alkali syndrome, included low-normal serum chloride (96 mEq/L), normal phosphorus of 2.7 mg/dl (phosphorus is usually normal to increased in this syndrome), increased blood urea nitrogen (39 mg/dl), and increased serum creatinine (2.4 mg/dl). A normal C-terminal parathormone level helped distinguish this patient from patients with severe hypercalcemia due to primary hyperthyroidism. The ECG revealed a widened rather than a shortened QT interval, as well as a J wave, a broadened T wave, and a U wave with this marked hypercalcemia, all of which reverted to normal with correction of the hypercalcemia.
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PMID:Milk-alkali syndrome with a serum calcium level of 22 mg/dl and J waves on the ECG. 368 51


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