vasculitis
Ranitidine (Zantac) Adverse Reactions
Similar to other H2 antagonists, adverse reactions during ranitidine therapy are infrequent. Adverse reactions during ranitidine therapy occur rarely and are usually mild and transient. In 1997, one safety review from the manufacturer noted that data available from more than 26,000 patients in controlled clinical trials in over a decade of use indicated that ranitidine was associated with adverse events in roughly 20% of patients treated, but the incidence was not significantly different from the number reported with placebo (i.e., 27%).
GI adverse reactions have been reported in patients receiving ranitidine. These reactions include diarrhea or constipation, nausea/vomiting and abdominal pain. Although rare, hepatitis, jaundice, and elevated hepatic enzymes have been reported with ranitidine. Pancreatitis, a rare but serious reaction, has also been reported.
Although data exist associating ranitidine with various types of blood dyscrasias, the overall incidence of these reactions is low. Neutropenia and thrombocytopenia are the most commonly encountered blood count changes. Other factors including underlying diseases or additional drugs may have contributed to these hematologic alterations. If the dyscrasia is ranitidine-mediated, recovery is usually rapid after ranitidine discontinuation. Rare cases of agranulocytosis, leukopenia, pancytopenia or aplastic anemia have all been reported. Exceedingly rare cases of immune hemolytic anemia have also been reported.
The relationship of ranitidine to reported CNS adverse reactions is unclear in many cases. Headache, which is sometimes severe, is the only CNS reaction that seems to be causally associated with ranitidine administration. Reversible mental status changes, including agitation, confusion, delirium, hallucinations, hostility, paranoia, depression, and disorientation, have been reported following ranitidine therapy. Most of these reactions have been reported in critically-ill elderly patients. Other CNS adverse reactions include blurred vision, dizziness, insomnia, malaise, and vertigo. A review of central nervous system reactions to H2-blockers revealed that the incidence rate varies widely depending on the specific report, and that no single H2-antagonist is more likely to induce CNS reactions than another. The CNS reactions appear to be primarily idiosyncratic and not dose-related. The incidence of CNS-related events for all H2-blockers is estimated at 0.2% for outpatients and up to 1.9% of hospitalized inpatients.
Gynecomastia and sexual dysfunction, including libido decrease and impotence (erectile dysfunction), have been seen during ranitidine therapy in male patients, but the incidence is rare and similar to the incidence of these events in the normal male population. It should be noted that cimetidine, another H2-blocker, more commonly produces these effects due to cimetidine’s antiandrogenic activity, and the use of ranitidine, when substituted for cimetidine in such patients, often results in resolution of cimetidine-induced endocrine dysfunction.
Dermatologic and hypesensitivity-mediated reactions are rarely reported and include maculopapular rash, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, alopecia, and vasculitis. Hypersensitivity, including anaphylactoid reactions, angioedema, bronchospasm, fever, or eosinophilia have been reported, but are rare. Rare musculoskeletal events include arthralgia and myalgia, but causality has not been established.
As with other H2-blockers, rare and idiosyncratic reports of sinus tachycardia, sinus bradycardia, atrioventricular (AV block), and premature ventricular contractions (PVCs) have occurred during ranitidine therapy.
Small increases in serum creatinine may occur during ranitidine therapy, but the increase does not reflect a decrease in renal function. Ranitidine can compete with creatinine for proximal tubular secretion. This uncommon drug-induced alteration in plasma creatinine concentration may be of clinical significance only when GFR is estimated or calculated by using serum creatinine.
[ Last revised: 4/13/2004 10:46:00 PM ]
References
. Cantu TG, Korek JS. Central nervous system reactions to histamine-2 receptor blockers. Ann Intern Med 1991;114:1027 - 34.
. Aymard JP, Aymard B, Netter P, et al. Haematological adverse effects of histamine H2 - receptor antagonists. Med Toxicol 1988;3:430 - 48.
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