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

The authors report the case of a 57 year old man who had taken for several years large quantities of alkaline drugs to relieve pain due to a gastric ulcer. This man presented acute digestive symptoms, and a confusional syndrome explained by various metabolic disturbance and especially hypercalcemia at 145 mg. Stopping the alkalis permitted within a few days the disappearance of the clinical symptoms and the correction of the laboratory disturbances. In the light of this case, the authors study the main clinical cases which have been described either in their acute form or in their chronic form (Burnett's syndrome). They discuss above all the physiopathology of these manifestations and it seems to them that the hypercalcemia is more important than the alkalosis. It remains to be explained why only a small number of subjects are exposed to these metabolic complications. There seems to be an individual hypersensitivity for under normal conditions, excess calcium is not sufficient to induce hypercalcemia.
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PMID:[Complication caused by abuse of alkalies in the treatment of ulcers]. 19 82

A 60-year-old man with a history of excessive ingestion of calcium carbonate presented with azotemia, hypercalcemia and hyperphosphatemia. His acid-base status was initially normal. Following the cessation of calcium carbonate treatment, the hypercalcemia and azotemia disappeared, and the patient was found to be in metabolic acidosis with blunted acid excretion and a urine pH of 6.1. Kidney biopsy showed focal tubular calcification; the tubular damage was apparently caused by hypercalcemia and had resulted in renal tubular acidosis. During the three months of observation since that time there has been a tendecy for spontaneous remission of the renal tubular acidosis. Impaired renal hydrogen ion excretion prevented the development of metabolic alkalosis despite ingestion of alkali initially, and was later responsible for the metabolic acidosis. Renal tubular acidosis occurring as a sequel to the milk-alkali syndrome may aggravate the danger of nephrocalcinosis in this syndrome.
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PMID:Renal tubular acidosis due to the milk-alkali syndrome. 88 14

We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.
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PMID:[A case of the milk-alkali syndrome with a small amount of milk and magnesium oxide ingestion--the contribution of sustained metabolic alkalosis induced by hypertonic dehydration]. 192 Sep 38

Hypercalcaemia is a frequent situation in clinical practice. An earlier detection is facilitated by routine analysis of serum calcium. The clinical manifestations depend on severity and the rate of onset of hypercalcaemia. Paucisymptomatic and asymptomatic presentations are the most frequent. Causes of hypercalcaemia are numerous and the mechanisms are various. PTH and vit. D play a preponderant part. In first of all iatrogenic cause are eliminated (all vit D preparations, thiazide diuretics, milk-alkali syndrome). Among non neoplastic hypercalcaemia primary hyperparathyroidism is the first diagnosis. Nephrolithiasis and asymptomatic forms are the most frequent presentations actually. The biochemical profile is not always typical. Generally the association of echography and tomodensitometry lead to the topographic diagnosis. Parathyroid surgical exploration is often necessary in difficult cases. Secondary, the other rare causes of hypercalcaemia are studied: sarcoidosis and granulomatosis disease, thyrotoxicosis and dome endocrinopathies, immobilisation hypercalcaemia, familial hypocalciuric, hypercalcaemia. All of this causes of hypercalcaemia are potentially reversible.
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PMID:[Non-neoplastic hypercalcemia]. 271 64

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

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

A case of recurrent hypercalcaemia due to chronic continuous ingestion of a calcium-containing antacid is described in whom the diagnosis was delayed because of an insufficiently detailed drug history. Specific named enquiry must be made of all the various calcium-containing drugs when seeking a history of excessive calcium intake if the diagnosis of the milk-alkali syndrome is not to be missed.
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PMID:Failure to diagnose the milk-alkali syndrome. 360 93

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

Severe hypercalcemia recurred three times during an observation period of 15 years in a woman with anorexia nervosa. The patient displayed a factitious cheese-alkalosis syndrome similar to the iatrogenic milk-alkali syndrome.
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PMID:Recurrent factitious hypercalcemia. 382 6

Critical surgical illness, commonly accompanied by shock, sepsis, multiple transfusions, and renal failure, is usually associated with low total calcium and/or low or normal ionized calcium. A seminal case of hypercalcemia in a surgical intensive care unit (SICU) patient prompted the review of 100 patients with longer than average SICU days (greater than 12) to determine the incidence, associated factors, and possible etiologies of this condition. Ten patients had elevated measured, and five others had elevated calculated, ionized calcium (5.9 +/- 0.25 mg%), an incidence of 15%. Compared to the 85 patients who did not develop hypercalcemia, this population had a significantly higher frequency of the following: renal failure, dialysis, total parenteral nutrition (TPN) usage greater than 21 days, bacteremic days greater than 1, transfusions greater than 24 units, shock greater than 1 day, SICU days greater than 36, and antibiotics used greater than 7. In addition, this group had significantly more days of hypocalcemia early in their hospital course. There was no difference in sex, age, mortality, or incidence of respiratory failure. Two patients studied in depth had renal failure requiring dialysis and no malignancy, milk-alkali syndrome, hyperthyroidism, or hypoadrenalism. Parathormone (PTH) concentrations were high normal or elevated (N terminal 20 and 21 pg/ml; C terminal 130 microliters Eq/ml and 1009 pg/ml) at the time of elevated calcium (total 9.2 to 14.6 mg%; ionized 4.9 to 8.2 mg%). Immobilization does not increase PTH. In renal failure, PTH elevation is a consequence of hypocalcemia rather than hypercalcemia. Moreover, five patients did not have renal failure. Shock, sepsis, and multiple transfusions containing citrate may lower total and/or ionized calcium and thus stimulate PTH secretion. Whatever the mechanism, approximately 15% of critically ill surgical patients develop hypercalcemia, which may represent a new form of hyperparathyroidism.
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PMID:Hypercalcemia in critically ill surgical patients. 393 94


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