Acid Reducer (CIMETIDINE) (cimetidine)

Dosage of cimetidine hydrochloride is expressed in terms of cimetidine.

Accumulation of cimetidine may occur in patients with severe renal failure; therefore, the lowest effective dosage of the drug should be used. In patients with creatinine clearances of less than 30 mL/minute, the manufacturer recommends oral or IV cimetidine dosage of 300 mg every 12 hours. Dosage may be adjusted on the basis of gastric acid secretory response. Dosage intervals may be cautiously decreased from every 12 hours to every 8 hours or less, if necessary. In patients with severe renal impairment, accumulation of the drug may occur and the longest dosage interval compatible with an adequate response should be used. For the prevention of upper GI bleeding in critically ill patients, the manufacturer states that patients with renal impairment (creatinine clearance less than 30 mL/minute) can receive one half of the usual cimetidine dosage. When hepatic impairment is also present, further reduction in dosage may be necessary. Because hemodialysis greatly reduces blood cimetidine concentrations, cimetidine should be administered at the end of dialysis and every 12 hours during the interdialysis period.

Cimetidine and cimetidine hydrochloride are administered orally. Cimetidine hydrochloride may also be given by IM or slow IV injection or by intermittent or continuous slow IV infusion, in hospitalized patients with pathologic hypersecretory conditions or intractable ulcer, or when oral therapy is not feasible. Antacids may be given as necessary for relief of pain in patients with ulcers but should not be administered simultaneously with oral cimetidine. Commercially available prefilled syringes of cimetidine hydrochloride are intended for IM injection or for preparation of IV admixtures; because the drug must be diluted prior to IV administration, the prefilled syringemust not be used for direct IV injection.

Parenteral solutions of cimetidine hydrochloride should be inspected visually for particulate matter and discoloration prior to administration whenever solution and container permit.

No dosing information is available for this tab.

No dosing information is available for this tab.

Cimetidine, apparently through inhibition of hepatic microsomal enzyme systems, reduces the hepatic metabolism of some drugs including coumarin anticoagulants (e.g., warfarin), phenytoin, propranolol, some benzodiazepines, lidocaine, metronidazole, triamterene, some tricyclic antidepressants, terfenadine (no longer commercially available in the US), and theophylline, thereby decreasing elimination and increasing blood concentrations of these drugs. Cimetidine may also decrease hepatic blood flow and thereby increase the bioavailability of drugs with high hepatic extraction ratios. Clinically important effects have occurred when cimetidine and coumarin anticoagulants were administered concomitantly; if the drugs must be administered concurrently, prothrombin time should be carefully monitored and dosage adjustment of the anticoagulant may be necessary. Adverse clinical effects have also been reported when cimetidine was administered concomitantly with phenytoin, lidocaine, or theophylline. In one study in patients receiving 300 mg of an extended-release theophylline preparation twice daily concomitantly with cimetidine 800 mg at bedtime or 300 mg 4 times daily, steady-state peak serum theophylline concentrations and area under the serum concentration-time curve were increased less substantially with the bedtime regimen than the 4-times-daily regimen. Dosage of drugs metabolized by microsomal enzyme systems or those with high hepatic extraction ratios may require adjustment when concomitant cimetidine therapy is initiated or discontinued, especially drugs with low therapeutic ratios or in patients with renal and/or hepatic impairment.

Cimetidine has reduced hepatic and renal clearances of triamterene, probably via inhibition of cytochrome P-450 microsomal hydroxylation and competition for renal tubular secretion, respectively. Minimal alteration in the natriuretic and potassium-sparing effects of triamterene occurred, but the possibility of a clinically important interaction during concomitant use should be considered.

Cimetidine may potentiate the myelosuppressive effects (e.g., neutropenia, agranulocytosis) of myelosuppressive drugs (e.g., alkylating agents, antimetabolites) or therapies (e.g., radiation). Concomitant cimetidine therapy has been reported to potentiate the neutropenic and thrombocytopenic effect of carmustine alone or combined with radiation therapy.

Some antacids may reduce the absorption of cimetidine. In one study, various aluminum and magnesium hydroxides antacids were shown to reduce the bioavailability of cimetidine when the drugs were administered concomitantly under fasting and nonfasting conditions, but not when the antacid was given 1 hour before or after cimetidine in the fasting state, or 1 hour after cimetidine was taken with food. Some interference with absorption of cimetidine by antacids has also been reported in other studies, but in some studies antacids were not shown to reduce absorption of cimetidine. To prevent any potential interaction, antacids should probably be taken 1 hour before or after cimetidine in the fasting state, or 1 hour after cimetidine is taken with food.

Alteration of gastric pH may affect the absorption of certain drugs (e.g., ketoconazole). If concomitant therapy with such drugs is needed, they should be administered at least 2 hours prior to cimetidine administration.

Currently available data suggest that consumption of moderate amounts of alcohol (e.g., 0.3 g/kg of body weight) by individuals receiving H2-receptor antagonists, including cimetidine, is unlikely to result in clinically important alterations in blood alcohol concentrations and/or alcohol metabolism, although the possibility of such alterations in predisposed individuals cannot be definitely excluded. Increases in blood alcohol concentrations have been noted in some studies in healthy individuals receiving cimetidine or some other H2 antagonists concomitantly with alcohol; however, conflicting data exist, which may be related to the effects of various patient-specific factors (e.g., gender, ethnic group, hepatic function, chronic alcoholism) on alcohol metabolism and/or to differences in study design (e.g., alcohol dose and time of administration, fasting vs fed state). Although controversy exists regarding the potential for psychomotor impairment with increases in alcohol absorption and/or blood alcohol concentration induced by H2-receptor antagonists, patients receiving these drugs should observe the usual precautions regarding alcohol intake and performance of hazardous tasks requiring mental alertness or physical coordination (e.g., driving, operating machinery).

There are no contraindication interactions for this drug.

There are no severe interactions for this drug.

There are no moderate interactions for this drug.

There is no enhanced messaging for this drug.

There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

There is no enhanced messaging for this drug.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

No enhanced messaging available.

No enhanced messaging available.

Reproduction studies in rats, rabbits, and mice at doses up to 40 times the normal human dose of cimetidine have revealed no evidence of impaired fertility or harm to the fetus. However, there are no adequate and controlled studies to date using cimetidine in pregnant women, and the drug should be used during pregnancy only when clearly needed.

Since cimetidine is distributed into milk, nursing should generally not be undertaken during therapy with the drug. Women who are pregnant or nursing should seek the advice of a health professional before using cimetidine for self-medication.

No enhanced messaging available.