Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

93 publications concerning drug-induced pancreatitis are reviewed. A confirmed causal relationship between drug and acute pancreatitis so far exists only for 8 compounds: azathioprine, chlorothiazide, furosemide, sulfonamides, tetracycline, estrogens, valproic acid and L-asparaginase. There is less convincing, but still suggestive, evidence for a causal relationship with 5 other drugs, namely: corticosteroids, chlorthalidone, ethacrynic acid, phenformin and iatrogenic hypercalcemia. Due to inadequate or contradictory evidence, the link between a number of additional drugs and acute pancreatitis is considered possible, conditional or doubtful. Finally, the scant literature concerning the pathogenesis and histological lesions of drug-induced pancreatitis is briefly reviewed.
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PMID:[Acute drug-induced pancreatitis]. 392 79

No single pathophysiologic factor has been identified as the cause of recurrent acute pancreatitis. A systematic search should be undertaken in every patient to identify one of a myriad of factors that have been shown to play a part in causing this distressing illness. The abuse of alcohol remains the likeliest cause, and further research may reveal an inborn error of metabolism that jeopardizes some people. Biliary tract disease, gallstones, choledochal cyst, papillary stenosis, and duodenal diverticula show a clear relationship. Metabolic disorders such as hypercalcemia, hyperlipidemia, and hyperparathyroidism remain suspect. Systemic illnesses such as systemic lupus erythematosus and cystic fibrosis must be considered. Development anomalies such as pancreas divisum may precipitate acute pancreatitis through aberrant anatomic structures. Cancer must always be disproved. Not yet firmly established but worthy of thorough investigation are uncommon causes, such as the ingestion of certain drugs or combinations of drugs and trauma, either recent or past. Pancreatitis remains frightening for those with the disease and puzzling and frustrating for the medical people who treat it. A careful history and investigation in accordance with a systematic diagnostic plan that includes many disparate factors will lead to identification of the cause in the majority of patients.
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PMID:Pathophysiologic factors in recurrent acute pancreatitis. 393 40

The long-held tenet that a cause and effect relation exists between primary hyperparathyroidism and pancreatitis has recently been questioned. To clarify this association, records of 1475 patients seen with pancreatitis during a 10-year period were reviewed. Five patients (0.4%) were identified with primary hyperparathyroidism. The four men and one woman ranged in age from 31 to 57 years. Four had recurrent pancreatitis over a 2-10 yr period before hyperparathyroidism was diagnosed. One patient had hypercalcemia noted 1 year prior to developing pancreatitis. Four patients had associated potential causes of pancreatitis including alcohol abuse, gallstones, and hypotension. Pancreatitis was severe in each patient. Two patients had more than four admissions for acute pancreatitis, one patient underwent pseudocyst drainage and distal pancreatectomy for chronic pancreatitis, one patient underwent pancreaticojejunostomy for chronic pancreatitis, and one patient died from hemorrhagic pancreatitis. Four patients have undergone successful parathyroidectomy and have had no further attacks of pancreatitis on follow-up ranging from 1 to 4 years. Hyperparathyroidism is rarely associated with pancreatitis, but when this combination occurs, the pancreatitis is likely to be severe. Despite its rarity, a cause and effect relationship is still suggested by the fact that parathyroidectomy seems to prevent recurrence of pancreatitis.
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PMID:The association of primary hyperparathyroidism and pancreatitis. 399 75

Six patients receiving total parenteral nutrition (TPN) developed hypercalcemia and acute pancreatitis. Four were long-term home TPN patients, and two were short-term hospital TPN patients. Causes of pancreatitis other than hypercalcemia were not found. The etiology of the hypercalcemia remained unclear and in particular was not due to calcium infusion or hyperparathyroidism. In 4 patients in whom it was measured, the plasma parathyroid hormone was normal (in 2) or nondetectable (in 2). Hypercalcemia and pancreatitis subsided with discontinuation of TPN. Thus, some patients receiving TPN develop hypercalcemia, and in some of these pancreatitis ensues.
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PMID:Pancreatitis in association with hypercalcemia in patients receiving total parenteral nutrition. 677 4

Four families with familial hypocalciuric hypercalcaemia were studied. The probands presented with abdominal pain, which in three was due to acute pancreatitis; in two the condition was life threatening. Serum concentrations of calcium, magnesium, phosphate, and immunoassayable parathyroid hormone, urinary calcium excretion, and the rate of renal tubular reabsorption of phosphate were measured; the findings were compared with results in 10 patients with primary hyperparathyroidism matched for serum calcium concentration to establish differences between the diseases. Familial hypocalciuric hypercalcaemia should be suspected in patients with hypercalcaemia in whom daily urinary calcium excretion is below 5 mmol (200 mg) provided renal insufficiency, vitamin D deficiency, and ingestion of drugs that reduce calcium excretion have been excluded. Most cases appear to run a benign course, but some may suffer considerable morbidity. Surgical treatment should be reserved for patients with severe complications, when all parathyroid tissue should be removed.
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PMID:Familial hypocalciuric hypercalcaemia and acute pancreatitis. 678 29

Plasma levels of calcitonin (CT) are highest in patients with medullary thyroid carcinoma (MTC). Plasma CT is also raised in some patients with carcinoma such as that of the breast, the lung or the pancreas, and in pheochromocytoma. It must be kept in mind, however, that plasma CT can be similarly raised in patients with renal failure, non-tumoral pulmonary disease or acute pancreatitis. In hypercalcemia patients with primary hyperparathyroidism the plasma CT is normal or only marginally elevated. It is speculated that the raised levels in pregnant and lactating women and in new-born infants prevent excessive bone destruction at times of greater physiological need for calcium. Larger molecular weight forms than monomeric CT (1--32) are circulating at least in plasma of patients with calcitonin-producing tumors and in renal insufficiency. The biological function of these larger molecular weight forms is not yet known. The discrepancies among the results of different laboratories can in part be explained by the immunoheterogeneity of the hormone and the different antigenic recognition sites of the antisera used. The measurement of plasma CT levels is nevertheless important for the diagnosis of MTC and may prove useful in some patients with malignant tumors unrelated to the C-cells of the thyroid gland. CT-radioimmunoassay may be improved by using antibodies specific to the different forms of circulating calcitonin.
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PMID:[The differential diagnosis of hypercalcitoninism]. 733 Jun 42

A case of hypercalcaemia in a pregnant patient on substitution therapy for hypoparathyroidism is reported. The clinical picture included transient cerebral disturbances, acute pancreatitis and persistent partial blindness. Calcium metabolism in pregnancy is discussed, and a possible mechanism for the sequence of events is postulated. The relevant literature is reviewed.
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PMID:Hypercalcaemia in pregnancy: a case report. 740 2

To determine the frequency of gastrointestinal symptoms in primary hyperparathyroidism, we retrospectively analyzed 100 consecutive patients seen at Emory University Hospital from Jan 1, 1977 through March 1, 1979. At the time of diagnosis, 28 patients complained of nausea, 19 of vomiting, 29 of abdominal pain, and 33 of constipation. One patient presented with acute pancreatitis and 14 had ulcer disease (two gastric and 12 duodenal ulcers). Hypercalcemia increases gastric acid secretion and may account for associated ulcer disease and the ulcer-like pain in primary hyperparathyroidism. The mechanisms causing the other gastrointestinal symptoms in hypercalcemia remain to be elucidated. These symptoms abate on correction of hyperparathyroidism.
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PMID:Primary hyperparathyroidism and the gastrointestinal tract. 746 39

The pathogenesis of acute pancreatitis is poorly understood, despite well-recognised precipitating factors. Current evidence suggests that the earliest abnormalities of acute pancreatitis arise within acinar cells, but the key intracellular trigger has yet to be identified. Within the pancreas, physiological concentrations of secretagogues bind to G-protein-linked cell-surface receptors on acinar cells, evoking short, oscillatory spikes of acinar cytosolic-free ionised calcium ([Ca2+]i), an ubiquitous intracellular messenger. Specific effects within acinar cells include initiation of enzyme release through the phosphorylation cascades of stimulus-secretion coupling. Low resting levels of [Ca2+]i are restored by Ca(2+)-ATPase, which pumps calcium into the endoplasmic reticulum and out of the cell. If high concentrations of [Ca2+]i persist, toxicity results, intracellular signalling is disrupted, and cell damage occurs. Sustained elevations in acinar [Ca2+]i result from exposure to high concentrations of secretagogues, high doses of which also induce acute pancreatitis. Similarly, sustained elevations of [Ca2+]i may result from ductal hypertension, alcohol, hypoxia, hypercalcaemia, hyperlipidaemia, viral infection, and various drugs--all factors known to precipitate acute pancreatitis. We suggest that these factors precipitate acute pancreatitis by causing either excessive release of acinar [Ca2+]i, or damage to the integrity of mechanisms that restore low resting levels of [Ca2+]i, and that the consequent calcium toxicity is the key trigger in the pathogenesis of acute pancreatitis.
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PMID:Is an elevated concentration of acinar cytosolic free ionised calcium the trigger for acute pancreatitis? 747 53

Acute pancreatitis as a manifestation of hyperparathyroidism (HPT) has been reported in the literature but the concept of causal relationship has been disputed. We report a case of acute pancreatitis where the presence of hypercalcemia led to the diagnosis of primary HPT. No other current risk factors for pancreatitis were identified and no symptoms of HPT were present prior to this episode. We review the literature regarding the role of HPT in the pathogenesis of acute pancreatitis.
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PMID:Acute pancreatitis as the first manifestation of hyperparathyroidism in an otherwise asymptomatic patient. 749 84


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