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

The milk-alkali syndrome is the association of hypercalcaemia and renal failure, with or without alkalosis, in the presence of absorption of excessive quantities of calcium, alkali, or both. Two patients with the milk-alkali syndrome are described, one representing an acute, reversible disorder and the other demonstrating a chronic syndrome with only partially reversible renal disease. Differential diagnosis is not difficult and is usually aided by the initial clinical evaluation as well as rapid response to conservative therapy. Because the initial stages of renal insufficiency are often fully reversible, the early identification and treatment of the milk-alkali syndrome can prevent progression to irreversible, chronic renal failure. Although non-absorbable antacids, H2 blockers, and sucralphate are the basis of modern treatment of peptic ulcer disease, the syndrome may still occur, especially in patients who self-treat symptoms of dyspepsia.
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PMID:The 'milk-alkali' syndrome: two case reports with discussion of pathogenesis. 400 10

Four patients with milk-alkali syndrome (MAS) presented with many of the characteristics of primary hyperparathyroidism including hypercalcemia, low or normal serum phosphorus levels, normal or increased urinary calcium levels, and inappropriately high or elevated serum parathyroid hormone levels. These laboratory findings differ from those classically described in MAS, i.e., hypercalcemia without hypercalciuria and a normal or high plasma phosphate level. Because the serum calcium level failed to return to normal after two weeks of hydration and a low calcium diet, and because of the inability to distinguish this syndrome from primary hyperparathyroidism, two of the four patients underwent neck exploration. Four normal parathyroid glands were histologically proven in each, and at autopsy in a third patient, there was no evidence of parathyroid hyperplasia or adenoma. Hypercalcemia eventually resolved in all patients with a low-calcium diet for as long as six months. Of the several features of MAS, hypercalcemia, alkalosis in the presence of azotemia, a history of increased calcium and alkali intake, and a response to dietary calcium restriction are helpful in differentiating this syndrome from primary hyperparathyroidism. Laboratory tests in patients with MAS may be confusing and the return to normocalcemia in response to a calcium deficient diet may be delayed.
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PMID:Milk alkali syndrome. Does it exist and can it be differentiated from primary hyperparathyroidism? 683 Mar 49

The milk-alkali syndrome was first identified in 1923, and continues to occur in patients ingesting large amounts of calcium and absorbable alkali, particularly as calcium carbonate. Hypercalcemia, alkalosis, and renal impairment remain hallmarks of the syndrome, which may occur in acute, subacute, and chronic forms. Although the pathophysiology of the milk-alkali syndrome has not been completely studied, it appears to involve complex interactions between ingested calcium and alkali resulting in an impairment in renal calcium and bicarbonate excretion. The diagnosis of the milk-alkali syndrome is based on a history of calcium and alkali ingestion, the presence of characteristic clinical and laboratory features, and the exclusion of other causes of hypercalcemia. Conservative treatment, including discontinuing calcium and alkali ingestion and supportive measures, is usually effective.
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PMID:The milk-alkali syndrome: current concepts. 704 33

We describe a 4 year old girl with acute Aeromonas hydrophila gastro-enteritis who presented with a combination of hypercalcemia, metabolic alkalosis, and renal impairment. Serum parathyroid hormone was not elevated. Both milk-alkali syndrome and intoxication of vitamins A and D were ruled out. The hypercalcemia, metabolic alkalosis, and renal impairment were improved by fluid infusion and intravenous administration of furosemide. Gastro-enteritis also improved with oral administration of the antibiotic norfloxacin. The association of A. hydrophila gastro-enteritis with hypercalcemia has not been described previously.
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PMID:Hypercalcemia associated with Aeromonas hydrophila gastro-enteritis. 779 54

Milk-alkali syndrome can be caused by ingesting large amounts of calcium carbonate. Coincident with the promotion of calcium carbonate as treatment for both dyspepsia and osteoporosis, milk-alkali syndrome is now a common cause of hypercalcemia severe enough to require admission to the hospital. The syndrome accounted for less than 2% of such admissions before 1990, but from 1990 through 1993, it was the cause of hypercalcemia for over 12% of these patients. Only primary hyperparathyroidism and hypercalcemia of malignancy (excluding multiple myeloma) are more common. The diagnosis of milk-alkali syndrome is made almost entirely based on the patient's history; careful attention to dietary practices and over-the-counter drug use is required, as numerous over-the-counter medications contain calcium carbonate. Modern assays for PTH demonstrate the expected suppression of PTH by hypercalcemia. Nonetheless, measurement of PTH must be performed in a timely manner as treatment with intravenous saline may result in hypocalcemia and elevated PTH soon after admission. Given the pathophysiology of milk-alkali syndrome compared to other causes of hypercalcemia, hypocalcemia with rebound hyperparathyroidism is probably unique to milk-alkali syndrome.
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PMID:Milk-alkali syndrome associated with calcium carbonate consumption. Report of 7 patients with parathyroid hormone levels and an estimate of prevalence among patients hospitalized with hypercalcemia. 789 47

A case of milk-alkali syndrome is described in a 34-year-old man taking an over-the-counter antacid preparation for gastroesophageal reflux. A Tc-99m MDP bone scan performed in the initial investigation of the hypercalcemia was markedly abnormal with a "metabolic" pattern of tracer uptake similar to that seen in hyperparathyroidism and humoral hypercalcemia. Following withdrawal of the antacid and calcium, the bone scan appearance returned to normal, as did the biochemical markers of his disease.
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PMID:Increased skeletal uptake of Tc-99m methylene diphosphonate in milk-alkali syndrome. 803 69

The relation between hypercalcemia and pancreatitis, first described in patients with hyperparathyroidism, is controversial. Other causes of hypercalcemia also have been associated with pancreatitis. In this report, the authors describe a patient with pancreatitis and the milk-alkali syndrome who had the classic triad of hypercalcemia, alkalosis, and renal insufficiency. The authors also review the literature for all the reported cases of pancreatitis associated with hypercalcemia.
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PMID:Case report: milk-alkali syndrome and pancreatitis. 807 35

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.
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PMID:The milk-alkali syndrome. A reversible form of acute renal failure. 848 Oct 62

The case described here illustrates the need to consider milk-alkali syndrome in the differential diagnosis of hypercalcemia, even in this age of histamine2 blockers and mucosal protectors. Thorough history taking and gastrointestinal workup help rule out alternative causes of hypercalcemia, such as cancer, hyperparathyroidism, and other metabolic and endocrine diseases. Milk-alkali syndrome is managed by administration of saline solution and loop diuretics and avoidance of thiazide diuretics. Patient education regarding the hazards of abusing calcium-containing antacids is essential.
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PMID:Milk-alkali syndrome. A consequence of chronic antacid abuse. 848 20

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.
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PMID:Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome. 865 5


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