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

Hypercalcemia during pregnancy or after delivery is uncommon, and mostly associated with primary hyperparathyroidism (PHPT). If unrecognized, it may increase maternal and fetal morbidity. In a very few patients with PHPT, hypercalcemic crisis develops during pregnancy and particularly after delivery, since calcium transport from the mother to the fetus is abruptly disrupted. Hypercalcemia may also develop in pregnant women due to PTH-related protein (PTHrP)-producing malignant tumors (humoral hypercalcemia of malignancy). Since PTHrP is produced physiologically in fetal and maternal tissues, hypercalcemia may occasionally develop during pregnancy, puerperium, and lactation due to excessive production of PTHrP in the placenta and/or mammary glands. PTHrP may also be involved in milk-alkali syndrome that develops during pregnancy. Although non-malignant hypercalcemia is usually mild, we report a 28-years-old pregnant woman who developed hypercalcemic crisis after normal delivery of an infant. On the first postpartum day, the corrected serum calcium concentration increased to 19.4 mg/dl with a markedly increased serum level of PTHrP (28.4 pmol/L) (normal <1.1 pmol/L). After administration of saline and pamidronate, the serum levels of calcium and PTHrP rapidly normalized. Extensive examination revealed no malignant lesion, suggesting that the placenta may have been producing an excessive amount of PTHrP (humoral hypercalcemia of pregnancy). We review case reports of non-malignant hypercalcemic crisis associated with pregnancy indexed in PubMed in which serum levels of intact PTH and/or PTHrP were described, and stress that rapid control of hypercalcemia is mandatory to save the life of the mother and the infant.
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PMID:Hypercalcemia during pregnancy, puerperium, and lactation: review and a case report of hypercalcemic crisis after delivery due to excessive production of PTH-related protein (PTHrP) without malignancy (humoral hypercalcemia of pregnancy). 1861 54

This report describes the presentation and clinical course of a 40-year-old woman who had an emergency admission for eclampsia. During routine investigations, she was found to have profound hypercalcaemia, the cause of which was identified as milk-alkali syndrome, caused by self-medication with antacid tablets for dyspepsia. Treatment with aggressive rehydration, bisphosphonates and discontinuation of antacid tablets restored normocalcaemia. The patient made a full recovery with no long-term side-effects. Her male infant was safely delivered with no deleterious effects of exposure to high calcium concentrations in utero.
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PMID:Excessive calcium ingestion leading to milk-alkali syndrome. 1875 31

Milk-alkali syndrome (MAS) consists of hypercalcemia, various degrees of renal failure, and metabolic alkalosis due to ingestion of large amounts of calcium and absorbable alkali. This syndrome was first identified after medical treatment of peptic ulcer disease with milk and alkali was widely adopted at the beginning of the 20th century. With the introduction of histamine2 blockers and proton pump inhibitors, the occurrence of MAS became rare; however, a resurgence of MAS has been witnessed because of the wide availability and increasing use of calcium carbonate, mostly for osteoporosis prevention. The aim of this review was to determine the incidence, pathogenesis, histologic findings, diagnosis, and clinical course of MAS. A MEDLINE search was performed with the keyword milk-alkali syndrome using the PubMed search engine. All relevant English language articles were reviewed. The exact pathomechanism of MAS remains uncertain, but a unique interplay between hypercalcemia and alkalosis in the kidneys seems to lead to a self-reinforcing cycle, resulting in the clinical picture of MAS. Treatment is supportive and involves hydration and withdrawal of the offending agents. Physicians and the public need to be aware of the potential adverse effects of ingesting excessive amounts of calcium carbonate.
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PMID:Milk-alkali syndrome. 1948 77

We report a case of a patient presenting with a triad of hypercalcemia, metabolic alkalosis and renal failure secondary to calcium bicarbonate intake for osteoporosis prevention. It is the classical presentation of the "modern" milk alkali syndrome that presents several characteristics distinguishing it from the "old" syndrome described secondary to peptic ulcer disease treatment. Milk alkali syndrome affects middle-aged female patients taking over-the-counter calcium carbonate. Clinically, these patients present in an acute hypercalcemia crisis, responding rapidly to hydration. The phosphorus level is normal to low. Bisphosphonate should be used cautiously due to the risk of symptomatic hypocalcemia.
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PMID:Hypercalcemia, metabolic alkalosis and renal failure secondary to calcium bicarbonate intake for osteoporosis prevention--'modern' milk alkali syndrome: a case report. 1991 60

Historically, the milk-alkali syndrome developed as an adverse reaction to the Sippy regimen of milk, cream and alkaline powders as treatment for peptic ulcer disease. The classic description includes hypercalcemia, metabolic alkalosis, and renal failure. Over the past 20 years, milk-alkali syndrome has had a resurgence, as consumption of supplements containing calcium has increased. A 46-year-old man presented to the emergency department after outpatient labs to evaluate his fatigue. He was found to have acute renal failure and hypercalcemia (total serum calcium was 15.9 mg/dL). Subsequent laboratory evaluation excluded both hyperparathyroidism and malignancy as causes. A detailed history led to the diagnosis of milk-alkali syndrome. With hydration and cessation of calcium carbonate ingestion, his renal function and serum calcium levels returned to normal. Physicians should have a high index of suspicion for milk-alkali syndrome in patients with hypercalcemia. Milk-alkali syndrome is no longer a merely a historical curiosity; it is currently the third most common cause of hypercalcemia.
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PMID:Hypercalcemia and acute renal failure in milk-alkali syndrome: a case report. 2010 39

We recommend changing the name of the milk-alkali syndrome to the calcium-alkali syndrome, because the new terminology better reflects the shifting epidemiology and understanding of this disorder. The calcium-alkali syndrome is now the third most common cause of hospital admission for hypercalcemia, and those at greatest risk are postmenopausal or pregnant women. The incidence of the calcium-alkali syndrome is growing in large part as a result of the widespread use of over-the-counter calcium and vitamin D supplements. Advertising for treatment or prevention of osteoporosis has long encouraged this use. Intricate mechanisms mediating the calcium-alkali syndrome depend on interplay among intestine, kidney, and bone. New insights regarding its pathogenesis focus on the key role of calcium-sensing receptors and TRPV5 channels in the modulation of renal calcium excretion. Restoring extracellular blood volume, increasing GFR and calcium excretion, and discontinuing calcium supplementation provide best treatment.
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PMID:Got calcium? Welcome to the calcium-alkali syndrome. 2041 9

A 73-year-old man was admitted with complaints of a 2-month history of generalized weakness and numbness. Laboratory examination revealed hypercalcemia, metabolic alkalosis, and kidney injury, similar to the traditional milk-alkali syndrome. The clinical history and the response to therapy indicated that alphacalcidol and thiazide taken daily were the cause. Recently, it has been recommended the term "milk-alkali syndrome" be replaced by "calcium-alkali syndrome", which broadens the definition of the condition. This case suggests that the calcium-alkali syndrome can occur without calcium and alkali, but rather with alphacalcidol and a thiazide diuretic.
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PMID:Calcium-alkali syndrome-like symptoms manifested by daily alphacalcidol and thiazide. 2045 4

Milk-alkali syndrome is a rare cause of hypercalcemia characterized by the triad of hypercalcemia, renal insufficiency, and metabolic alkalosis that results from the overconsumption of calcium containing products. In the setting of pregnancy where there is a physiologic increase in calcium absorption, milk-alkali syndrome can be potentially life threatening. We report a case of a 26-year-old woman in her second trimester of pregnancy who presented with 2 weeks of flank pain, nausea, vomiting, anorexia, headache, and lightheadedness. The history revealed consumption of a large quantity of milk, calcium carbonate antacid, and calcium-containing prenatal vitamins. Her symptoms and hypercalcemia resolved with intravenous fluids and a loop diuretic. With the increased use of calcium carbonate for peptic ulcer disease, gastroesophageal reflux disease, and osteoporosis, milk-alkali syndrome has experienced a resurgence and must be considered in the differential diagnosis of hypercalcemia. In this clinical vignette we review the literature on milk-alkali syndrome in pregnancy and discuss important diagnostic and therapeutic considerations when managing the pregnant patient with hypercalcemia.
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PMID:Hypercalcemia in pregnancy: a case of milk-alkali syndrome. 2134 76

Milk-alkali syndrome was once considered to be of historic interest and a rare cause of hypercalcemia. Currently, it should be an important consideration in the differential diagnosis of hypercalcemia, after malignancies and primary hyperparathyroidism. The resurgence is in part due to the easy availability of over the counter (OTC) calcium preparations. We describe a 50-year-old man who presented with severe hypercalcemia on two occasions associated with renal failure and metabolic alkalosis. Extensive investigations during the first admission failed to unravel a specific cause of hypercalcemia but a thorough history during his subsequent admission helped to confirm the diagnosis of milk-alkali syndrome.
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PMID:A hidden history of heartburn: The milk-alkali syndrome. 2145 29

Most cases of hypercalcaemia are secondary to malignancy or primary hyperparathyroidism. We report a patient presenting with a triad of hypercalcemia, metabolic alkalosis, and renal failure secondary to treatment of iatrogenic hypoparathyroidism and osteoporosis. Persistent ingestion of calcium carbonate and vitamin D caused milk-alkali syndrome. The patient was managed with intravenous fluids and withdrawal of calcium carbonate and vitamin D. She responded well to the treatment and the calcium concentration, renal function and metabolic alkalosis were normalized. Milk-alkali syndrome may be important as a reemerging cause of hypercalcemia.
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PMID:Hypercalcemia associated with acute kidney injury and metabolic alkalosis. 2146 3


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