Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Drug histories were taken from 100 patients in their first attack of acute pancreatitis, and each was matched with a control subject of the same sex who was admitted to hospital as an emergency with acute abdominal pain, whose serum-amylase was within the normal range, and whose age was within three years of the pancreatitis patient's. The major differences between the patient groups was in the use of cardiovascular agents, and this was primarily due to a statistically significant excess of diuretic takers among the pancreatitis patients. There was an associated excess of intake of digoxin and antihypertensive and anti-anginal agents, but neither difference was statistically significant. Other categories of drugs showed no substantial differences. The difference between the pancreatitic patients and controls is almost entirely accounted for by takers of cyclopenthiazide with potassium chloride and of frusemide, especially the former. Further clinical and experimental evidence is required before the role of diuretics and/or potassium chloride in causing acute pancreatitis can be determined.
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PMID:Drug-associated primary acute pancreatitis. 7 39

Surgical procedures can be accomplished successfully in patients with uremia provided certain principles of perioperative management are observed. Preoperative dialysis minimizes the biochemical derangements and improves fluid balance, hypertension and hemostasis. Drug schedules are adjusted in consideration of abnormal metabolism in renal disease. Anesthetic management is modified in recognition of potentially adverse or altered activity of anesthetic agents and neuromuscular relaxants. The lightest plane of anesthesia consistent with expeditious operative technique is maintained, since adequate tissue oxygenation is dependent upon increased cardiac output in these invariably anemic patients. Intraoperative hyperventilation sustains the usual compensatory mechanism for uremic metabolic acidosis in the conscious patient, thereby averting increments in serum potassium levels associated with increasing acidosis. Postoperative morbidity may include shunt thrombosis, infection, impaired wound healing, bleeding, pericarditis, pleuritis and pancreatitis. Hypervolemia and hyperkalemia are best managed by early postoperative dialysis. A period of nutritional support using intravenous essential L-amino acids and hypertonic glucose appears promising, especially when gastrointestinal dysfunction exists.
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PMID:Renal failure and the surgeon. 40 28

Sweat electrolytes were carried out in 84 adult patients with calcific pancreatitis, 51 with noncalcific pancreatitis, and the results compared to 37 adult controls. Of the patients with calcific pancreatitis, 33.5% had sweat sodium levels greater than 90 mEq/liter and 14.4% a level greater that 120 mEq/liter. Patients with noncalcific pancreatitis also had a high incidence of elevated sweat sodium levels. Sweat potassium levels were less discriminating, and there appeared to be high sweat calcium levels in a few patients so tested. The reasons for the elevated sweat sodium levels in pancreatitis is not readily apparent, and the possible relationship to heterozygous forms of cystic fibrosis is discussed.
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PMID:Sweat electrolytes in chronic pancreatitis. 62 82

Two elderly diabetic patients with abdominal pain were demonstrated to have complications of phenformin hydrochloride therapy. The first developed severe lactic acidosis treated with sodium bicarbonate given intravenously and followed by rebound alkalosis. The second showed severe acidosis (specimens for lactate determination were unfortunately unsatisfactory for analysis) and similar alkalotic rebound after therapy. She then developed severe pancreatitis, proved at operation, no cause for which other than phenformin was apparent. Poor renal and hepatic function predispose to these conditions by increasing serum phenformin levels and by decreasing urinary excretion of its metabolites. The acidosis should be treated judiciously with sodium bicarbonate administered intravenously. A rebound alkalosis, ensuring as the accumulated lactate is metabolized, is best treated by potassium chloride and ammonium chloride given intravenously. The mechanism by which phenformin causes pancreatitis is unknown, but termination of therapy causes cessation of the pancreatitis.
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PMID:Pancreatitis and severe metabolic abnormalities due to phenformin therapy. 94 43

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

It has been reported that continuous intravenous infusion of nafamostat mesilate (FUT) produces hyperkalemia due to reduced urinary excretion of potassium. The present study was performed to see whether renin-aldosterone effect is involved in this inhibition of potassium excretion. Ten patients were studied who had been given this drug (4 mg.hr-1) to prevent postsurgical pancreatitis or DIC. Urine potassium output decreased significantly from 44 +/- 5 microEq.min-1 prior to administration of FUT to 18 +/- 4 microEq.min-1 in 3 hours, sodium/potassium ratio increased significantly from 1.7 +/- 0.7 prior to administration of FUT to 5.4 +/- 3.3 in 5 hours; and plasma aldosterone decreased significantly from 92 +/- 24 pg.ml-1 prior to administration of FUT to 63 +/- 22 pg.ml-1 in 6 hours. The results suggest that hyposecretion of aldosterone may be one of the main causes of hypokalemia. Reduced secretion of aldosterone may be due to other factors than the suppression of renin-angiotensin system.
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PMID:[Effect of nafamostat mesilate on the renin-aldosterone system]. 156 May 70

The effect of local and systemic calcium administration was tested on the pancreas of cat and guinea pig. After 3 h of local calcium infusion (0.6 mmol/kg x h) via the splenic artery of the cat hemorrhagic pancreatitis could be shown. Control animals treated with potassium (1.1 mmol/kg x h) or 0.9% NaCl alone showed no morphological change in the pancreas. Intravenous administration of calcium (0.6 mmol/kg x h) led to a 1.8-fold increase in serum ionized calcium levels in the cat and a 1.6-fold increase in levels in the guinea pig. The cat showed necrosis of acinar and ductal cells throughout the gland at 12 h. In the guinea pig, acinar cell vacuolisation and cell necrosis started at 3 h, and at 9 h degeneration of entire acini, hydropic swelling and degeneration of ductal cells, and perivascular leukocytic infiltration was present. In both species, a significant increase in the number of intraductal precipitates and a significant increase in urinary amylase output was present in calcium treated animals. The findings suggest that hypercalcemia has a deleterious effect on the pancreas that causes acinar and ductal cell necrosis and eventually pancreatitis.
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PMID:Acute hypercalcemia induces acinar cell necrosis and intraductal protein precipitates in the pancreas of cats and guinea pigs. 198 43

Fourteen cases of acute severe pancreatitis complicated by non-traumatic rhabdomyolysis are described and compared to case controls. Pancreatitis of various aetiologies was confirmed by surgical diagnosis, laparotomy, abdominal paracentesis, CAT scan and post mortem. Pancreatitis was severe with a high Ranson prognostic score (7.4 +/- 0.5 vs controls 1.9 +/- 0.4, p less than 0.001), longer ICU admission and a mortality of 79%. Rhabdomyolysis occurred two to 19 days after the onset of pancreatitis (with a median CPK peak at 6.5 days) and was accompanied by multiple organ failure in 93% of cases. Severe rhabdomyolysis and myoglobinuric renal failure occurred in three patients out of 12 with acute renal failure. Hypocalcaemia was common (93%), severe (with a mean minimum value of 1.79 +/- 0.07 vs 2.34 +/- 0.04mmol/L, p less than 0.01) and prolonged (remaining abnormal for 5.2 +/- 0.8 vs 0.07 +/- 0.07 days, p less than 0.001). Intravenous calcium supplements were required in 50% of patients. Plasma phosphate, potassium, urate and anion gap were elevated (all p less than 0.05) and accompanying clinical features included fever, ascites, leucocytosis, hypoalbuminaemia and abnormal liver function tests. Rhabdomyolysis is associated with acute several pancreatitis, appearing as a late phenomenon in the context of severe prolonged hypocalcaemia, multiple organ failure and a poor outcome.
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PMID:Acute pancreatitis and rhabdomyolysis: a new association. 195 30

This paper describes the clinical course of a young diabetic primigravida who presented to her physician with vomiting and abdominal pain. Despite the conventional doses of intravenous fluid and insulin that were used to treat her suspected diabetic ketoacidosis, she remained severely acidotic and developed increasing abdominal pain. Two hundred twenty units of regular insulin over a 5-hour period were required to reverse the lipolysis, acidemia, and abdominal pain, which characterized her severe episode of diabetic ketoacidosis. This discussion emphasizes the importance of insulin in the reversal of the hyperglycemia and acidosis that accompany a diabetic crisis. The roles of bicarbonate, phosphorous, magnesium, insulin, potassium, and fluids are discussed along with conditions such as pregnancy, infection, pancreatitis, and abdominal pain, which can complicate the management of diabetic ketoacidosis.
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PMID:Diabetic ketoacidosis and pregnancy. 216 29

Severe potassium permanganate poisoning (more than 10 g of potassium permanganate) is invariably associated with massive systemic upset and death. Multiple organ damage has been recognized as an inevitable consequence of such an overdose, although pancreatitis has not been previously reported. Death due to cardiovascular collapse and profound hypotension is a common end point in those who reach hospital, but the pathogenesis is uncertain. We report a case of haemorrhagic pancreatitis following an overdose of potassium permanganate and suggest that this complication may be an unrecognized factor contributing to the extremely high mortality rate associated with this condition.
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PMID:Haemorrhagic pancreatitis--a cause of death in severe potassium permanganate poisoning. 221 35


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