Ranitidine‐associated recurrent acute pancreatitis

Herrmann, R; Shaw, Rachel; Fone, D. J.

doi:10.1111/j.1445-5994.1990.tb01028.x

Cited by 30 publications

(10 citation statements)

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“…One report concerns an old woman who developed three bouts of acute pancreatitis after (re) starting ranitidine [10]. In addition, there exist five case reports in the Swedish Adverse Drug Reactions Register, and one of these cases developed a new attack of acute pancreatitis after re-exposure to ranitidine.…”

Section: Discussionmentioning

confidence: 97%

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A Swedish case-control network for studies of drug-induced morbidity – acute pancreatitis

Blomgren

Sundström

Steineck

et al. 2002

Eur J Clin Pharmacol

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Section: Discussionmentioning

confidence: 97%

“…Case reports concerning H 2 antagonists and acute pancreatitis exist [10,11,12]. One report concerns an old woman who developed three bouts of acute pancreatitis after (re) starting ranitidine [10].…”

Section: Discussionmentioning

confidence: 99%

A Swedish case-control network for studies of drug-induced morbidity – acute pancreatitis

Blomgren

Sundström

Steineck

et al. 2002

Eur J Clin Pharmacol

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“…The difference in recent risk between ulcer and nonulcer subjects makes it unlikely that acid inhibition is a general cause of pancreatitis. There have been case reports of pancreatitis in takers of acid inhibitory drugs, in which re-challenge has been followed by recurrence, 12,13 and an observational study has suggested, although without clear conclusions, that treatment precipitates the disease. 14 On the other hand, in a 15 however, the numbers of current users were small (six, five and three, respectively) and the confidence intervals around the point estimates were large.…”

Section: Discussionmentioning

confidence: 99%

Discrepancies between population‐based data and adverse reaction reports in assessing drugs as causes of acute pancreatitis

Lancashire¹,

Cheng²,

Langman

2003

Aliment Pharmacol Ther

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SUMMARYBackground: Many drugs are believed, clinically, to cause acute pancreatitis. We used information held on the UK General Practitioner Research Database to compare risks for drugs for which reports of pancreatitis were common or uncommon. Methods: Drug prescriptions were examined in 3673 patients with acute pancreatitis and in matched controls. Odds ratios were calculated for recent (1-90 days before the episode), past (91-360 days before the episode) or continuing (prescription in both periods) use. Results: Odds ratios were markedly increased for recent antisecretory use in non-ulcer patients only [all H 2 -antagonists, 12.4 (9.5-16.4); all proton pump antagonists, 9.3 (6.6-13.0)], with smaller increases for past [3.1 (2.5-3.7) and 3.5 (2.6-4.6), respectively] and continuing [2.6 (2.2-3.1) and 3.7 (2.9-4.7), respectively] use in patients without ulcer. Recent users of mesalazine showed a markedly increased risk [9.0 (1.8-44.6)], with smaller increases in past and continuing users [4.5 (1.3-16.0) and 2.5 (1.2-5.0), respectively]. Odds ratios for other drugs, suspect or not, were modestly increased, irrespective of whether the use was recent, past or continuing. The presence of gall-stones was not associated with a modified risk. Conclusions: Mesalazine, azathioprine and antisecretory drugs in non-ulcer subjects may increase the risk of pancreatitis, but warnings of drug-induced pancreatitis are generally not accompanied by increased population risks.

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“…Cimet idine treatment of experimental ulcer in the rat led to acute pancreatitis in one study [ 166], but not in another [ 167], The difference is explainable, because in the first study ulcers were induced by carbachol which itself can induce pancreatitis in the rat [ 168]. Two anec dotal cases of ranitidine-induced pancreatitis were also reported [169]. In summary, data are not consistent enough to support the asso ciation of H2-blocking agents and acute pan creatitis.…”

Section: H2-blocking Agentsmentioning

confidence: 78%

Drug-Induced Acute Pancreatitis: Further Criticism

Frick¹,

Speiser²,

Bimmler³

et al. 1993

Dig Dis

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A comprehensive literature search was performed to collect all available data on drug-induced pancreatitis. Strong evidence for an association with acute pancreatitis has been described for anticholinesterases, calcium 2’,3’-dideoxyinosine, estrogen, L-asparaginase, salicylates, thiazide-diuretics, valproic acid, and vinca alkaloids. Weak evidence has been found for antituberculous agents, azathioprine, biguanides, cisplatinum, cyclosporine A, H2-blocking agents, loop diuretics, 6-mercaptopurine, metronidazole, pentamidine, steroids, sulfonamides, sulindac and tetracycline. Many cases were associated with underlying conditions known to induce acute pancreatitis themselves. It is concluded that for none of the drugs studied the available data are consistent enough to support a definite association with acute pancreatitis. Nevertheless, the data suggest that drugs may be a trigger or a cofactor in inducing pancreatitis.

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Ranitidine‐associated recurrent acute pancreatitis

Cited by 30 publications

References 0 publications

A Swedish case-control network for studies of drug-induced morbidity – acute pancreatitis

A Swedish case-control network for studies of drug-induced morbidity – acute pancreatitis

Discrepancies between population‐based data and adverse reaction reports in assessing drugs as causes of acute pancreatitis

Drug-Induced Acute Pancreatitis: Further Criticism

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