Acute pancreatitis secondary to furosemide with associated hyperlipidemia

Call, Thomas; Malarkey, William B.; Thomas, Fred B.

doi:10.1007/bf01694517

Cited by 31 publications

(5 citation statements)

References 13 publications

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“…Six clinical papers were found associating furosemide (frusemide) with acute pancreatitis, [209][210][211][212][213][214] describing 9 patients: 6 had anecdotal evidence, and 3 had positive rechalienge. 1209 ,211,212] One patient with positive recurrence had type V hyperlipidaemia and was receiving concurrent oestrogen medication, another had type II hyperlipidaemia and the third was taking thiazide medication,…”

Section: Furosemide (Frusemide)mentioning

confidence: 98%

Drug-Induced Pancreatitis

1996

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Few data exist about the incidence of drug-induced pancreatitis in the general population. 20 cases of drug-related pancreatitis were reported in Switzerland over a period of 12 years. The proportion of cases of pancreatitis caused by drugs is estimated to be around 2% in the general population, with much higher proportions in specific subpopulations, such as children and patients who are HIV positive. The literature about drug-induced pancreatitis consists mainly of anecdotal case reports. Clear evidence of a definite association with pancreatitis, by means of rechallenge tests, or consistent case reports, supported by animal experiments or data on the incidence of acute pancreatitis in drug trials exists for didanosine, valproic acid (sodium valproate), aminosalicylates, estrogen, calcium, anticholinesterases and sodium stibogluconate. An association with drug-induced pancreatitis is likely but not definitely proven for thiazide diuretics, pentamidine, ACE inhibitors, asparaginase, vinca alkaloids, some nonsteroidal anti-inflammatory drugs and clozapine. Pancreatitis is possibly caused by azathioprine, furosemide (frusemide), tetracycline, metronidazole, isoniazid, rifampicin (rifampin), sulphonamides, cyclosporin and some antineoplastic drugs. Many drugs have been reported to be associated with acute pancreatitis. However, lack of rechallenge evidence, consistent statistical data, or evidence from experimental studies on a possible mechanism prohibit definitive conclusions about most of them. The high incidence of concurrent illnesses known to induce acute pancreatitis, makes a trigger role or co-factor role for the drug seem most likely.

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Section: Furosemide (Frusemide)mentioning

confidence: 98%

Drug-Induced Pancreatitis

1996

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“…Although the patient received intravenous furosemide, it is not likely the cause of pancreatitis since the symptoms of pancreatitis occurred before the beginning of furosemide therapy. Furosemide induced pancreatitis has been reported in patients on chronic oral therapy and the onset of the symptoms was 3–5 weeks after initiation of the therapy 8 , 10 ) . Alcohol intake, gallstones, trauma, peptic ulcer disease and hypertriglyceridemia have been ruled out as a cause of the pancreatitis by the history and appropriate tests.…”

Section: Discussionmentioning

confidence: 99%

Acute Pancreatitis in a Case of Multiple Myeloma with Hypercalcemia

Lee

Kim

1989

Korean J Intern Med

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A patient with hypercalcemia and newly diagnosed multiple myeloma developed acute pancreatitis. Other etiologic factors for pancreatitis were excluded. Hypercalcemia secondary to hyperparathyroidism is associated with acute pancreatitis. In English literature, only one other case has been published where the hypercalcemia of multiple myeloma may have caused pancreatitis. Pancreatitis should be considered in patients with hypercalcemia and multiple myeloma who develop nausea/vomiting, and abdominal pain.

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“…All post-OLTx patients are on multiple medications, several of which are well known to be associated with pancreatitis. All post-OLTx patients receive large doses of corticosteroids and most also receive intermittent treatment with furosemide, two drugs known to cause pancreatitis (15)(16)(17)(18)(19)(20)(21). The use of azathi-oprine has been associated with pancreatitis as well (22)(23)(24)(25).…”

Section: Discussionmentioning

confidence: 99%

Pancreatitis Following Liver Transplantation

et al. 1988

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Since 1981, when the liver transplantation program was initiated at the University of Pittsburgh, we have been impressed with the prevalence of pancreatitis occurring following liver transplantation in patients transplanted for hepatitis B-related liver disease. To either confirm this clinical impression or refute it, the records of the 27 HbsAg+ patients and those of an additional 24 HbsAg- but HbcAb and/or HbsAb+ patients who underwent orthotopic liver transplantation were reviewed to determine the prevalence of clinical pancreatitis and hyperamylasemia (biochemical pancreatitis) following liver transplantation (OLTx). Post-OLTx hyperamylasemia occurred significantly more frequently in HbsAg+ patients (6/27) than it did in the HbsAg- patients (0/24) (P less than 0.05). More importantly, clinical pancreatitis occurred in 14% (4/27) of the HbsAg+ patients and 0% (0/24) of the HbsAg- patients. Interestingly, in each case, the pancreatitis was associated with the occurrence of acute hepatitis B infection of the allograft. Based upon these data, we conclude that pancreatitis occurring after liver transplantation is more common in patients transplanted for active viral liver disease caused by hepatitis B than in those with inactive viral liver disease. These observations suggest that pancreatitis occurring in, at least some cases following liver transplantation for viral liver disease, may result from hepatitis B virus infection of the pancreas.

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Acute pancreatitis secondary to furosemide with associated hyperlipidemia

Cited by 31 publications

References 13 publications

Drug-Induced Pancreatitis

Drug-Induced Pancreatitis

Acute Pancreatitis in a Case of Multiple Myeloma with Hypercalcemia

Pancreatitis Following Liver Transplantation

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