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Duodenal Ulcer

Acute Therapy

Cimetidine and cimetidine hydrochloride are used for the short-term treatment of endoscopically or radiographically confirmed active duodenal ulcer. Antacids may be used concomitantly as needed for relief of pain; however, simultaneous administration of cimetidine and antacids is not recommended since some antacids have been reported to interfere with absorption of cimetidine. (See Drug Interactions.)

In controlled studies in patients with endoscopically confirmed duodenal ulcer receiving supplemental antacids, reported rates of ulcer healing for cimetidine were consistently higher than those for placebo. Ulcer healing rates from controlled studies employing various dosage regimens have averaged 68, 73, and 80% at 4 weeks and 80, 80, and 89% at 6 weeks for cimetidine 300 mg 4 times daily, 400 mg twice daily, and 800 mg at bedtime daily, respectively. At 8 weeks, healing rates have averaged 92 and 94% for 400 mg twice daily and 800 mg at bedtime daily, respectively. In a controlled study comparing various bedtime cimetidine dosages and placebo in patients with endoscopically proven duodenal ulcer who received supplemental antacids (up to 72 mEq neutralizing capacity daily) during the first week of therapy, 800 mg at bedtime daily was more effective than 400 mg at bedtime daily, with corresponding 4-week healing rates of 75 and 66%; 1600 mg at bedtime daily was not significantly more effective (81% healing rate) than the 800-mg regimen. Nocturnal pain relief occurred in more than 80% of patients after 1 day of the 800-mg regimen and daytime pain relief occurred in approximately 70% of patients after 2 days of therapy with this regimen; the 800-mg regimen was more effective than the 400-mg regimen in providing daytime and nocturnal pain relief at 4 weeks but was similar to the 1600-mg regimen. In this study, ulcer healing was less likely in patients who were smokers and in those with larger ulcers than in other patients. In one well-controlled study comparing 4 weeks of oral therapy with 1.2 g of cimetidine daily to that with 1- and 3-hour postprandial and bedtime administration of magnesium and aluminum hydroxides antacid tablets, 64% of cimetidine-treated and 52% of antacid-treated duodenal ulcer craters and erosions were healed. In another well-controlled 4-week trial comparing placebo to 1- and 3-hour postprandial and bedtime administration of an antacid suspension containing magnesium and aluminum hydroxides with simethicone, 78% of antacid-treated and 45% of placebo-treated duodenal ulcer craters disappeared. The rate of ulcer healing reported with antacid in this study is similar to that reported for cimetidine in other studies, but diarrhea occurred in 30-60% of antacid-treated patients.

Ulcer healing may occur within the first 2 weeks of cimetidine therapy and occurs in most patients within 4 weeks of therapy, but short-term therapy (i.e., up to 8 weeks) for the treatment of active duodenal ulcer will not prevent ulcer recurrence following acute healing and discontinuance of the drug. Current epidemiologic and clinical evidence supports a strong association between gastric infection with Helicobacter pylori and the pathogenesis of duodenal and gastric ulcers; long-term H. pylori infection also has been implicated as a risk factor for gastric cancer. For additional information on the association of this infection with these and other GI conditions, .

Conventional antiulcer therapy with H2-receptor antagonists, proton-pump inhibitors, sucralfate, and/or antacids heals ulcers but generally is ineffective in eradicating H. pylori, and such therapy is associated with a high rate of ulcer recurrence (e.g., 60-100% per year). Follow-up of cimetidine-treated patients has revealed no differences in frequency or time to onset of ulcer recurrence between treated patients and controls. A limited number of uncontrolled studies have shown recurrence of ulcer 1 month after cimetidine withdrawal in 41% of patients and as early as 1 week in some patients. In some studies, rate of recurrence was slightly higher after acute cimetidine therapy than after some other forms of acute therapy, but cimetidine-treated patients generally had more serious disease initially.

The American College of Gastroenterology (ACG), the National Institutes of Health (NIH), and most clinicians currently recommend that all patients with initial or recurrent duodenal or gastric ulcer and documented H. pylori infection receive anti-infective therapy for treatment of the infection. Although 3-drug regimens consisting of a bismuth salt (e.g., bismuth subsalicylate) and 2 anti-infective agents (e.g., tetracycline or amoxicillin plus metronidazole) administered for 10-14 days have been effective in eradicating the infection, resolving associated gastritis, healing peptic ulcer, and preventing ulcer recurrence in many patients with H. pylori-associated peptic ulcer disease, current evidence principally from studies in Europe suggests that 1 week of such therapy provides comparable H. pylori eradication rates. Other regimens that combine one or more anti-infective agents (e.g., clarithromycin, amoxicillin) with a bismuth salt and/or an antisecretory agent (e.g., omeprazole, lansoprazole, H2-receptor antagonist) also have been used successfully for H. pylori eradication, and the choice of a particular regimen should be based on the rapidly evolving data on optimal therapy, including consideration of the patient's prior exposure to anti-infective agents, the local prevalence of resistance, patient compliance, and costs of therapy.

Current evidence suggests that inclusion of a proton-pump inhibitor (e.g., omeprazole, lansoprazole) in anti-H. pylori regimens containing 2 anti-infectives enhances effectiveness, and limited data suggest that such regimens retain good efficacy despite imidazole (e.g., metronidazole) resistance. Therefore, the ACG and many clinicians currently recommend 1 week of therapy with a proton-pump inhibitor and 2 anti-infective agents (usually clarithromycin and amoxicillin or metronidazole), or a 3-drug, bismuth-based regimen (e.g., bismuth-metronidazole-tetracycline) concomitantly with a proton-pump inhibitor, for treatment of H. pylori infection. For a more complete discussion of H. pylori infection, including details about the efficacy of various regimens and rationale for drug selection, .

Maintenance Therapy

Cimetidine is used in reduced dosage as maintenance therapy following healing of active duodenal ulcer to reduce ulcer recurrence. In placebo-controlled studies, duodenal ulcer recurrence rates after 1 year were 10-45% in patients receiving 400 mg of cimetidine daily at bedtime vs 44-70% in those receiving placebo. Other antiulcer therapies, with the exception of H. pylori eradication regimens (see Uses: Duodenal Ulcer), have been associated with ulcer recurrence rates similar to those with cimetidine. Interindividual variation in these rates may depend in part on smoking, duration and severity of peptic ulcer disease, gender, and genetic factors. Because the efficacy of cimetidine in preventing duodenal ulcer recurrence appears to be substantially reduced in patients who are cigarette smokers compared with nonsmokers, patients who are cigarette smokers should be advised of the importance of discontinuing smoking in the prevention of ulcer recurrence. Maintenance therapy with cimetidine has been continued for up to 5 years in some patients.

Pathologic GI Hypersecretory Conditions

Cimetidine and cimetidine hydrochloride are used for the treatment of pathologic GI hypersecretory conditions (e.g., Zollinger-Ellison syndrome, systemic mastocytosis, and multiple endocrine adenomas). The drug reduces diarrhea, anorexia and pain, and promotes healing of intractable ulcers in patients with these conditions. Although total gastrectomy has been considered the treatment of choice for Zollinger-Ellison syndrome, treatment with an H2-receptor antagonist is now generally preferred in most patients because of lesser risks.

Gastric Ulcer

Cimetidine is used in the short-term treatment of active, benign, gastric ulcer.

In studies in patients with gastric ulcers receiving supplemental antacids, cimetidine promoted healing of ulcers in up to 70% of patients after 4 weeks and in 66-100% of patients after 6 weeks; in controlled studies, healing rates were consistently higher with cimetidine than placebo, with ulcers healing in up to 55% of patients receiving placebo and supplemental antacids. The usefulness of cimetidine therapy for longer than 8 weeks in the treatment of active benign gastric ulcer remains to be clearly determined. When cimetidine is used in the treatment of gastric ulcer, it should be kept in mind that symptomatic response does not preclude the presence of a gastric malignancy; there have been rare cases of transient healing of gastric ulcers despite subsequently documented malignancy.

Current epidemiologic and clinical evidence supports a strong association between gastric infection with H. pylori and the pathogenesis of gastric ulcers, and the ACG, NIH, and most clinicians currently recommend that all patients with initial or recurrent gastric ulcer and documented H. pylori infection receive anti-infective therapy for treatment of the infection. The choice of a particular regimen should be based on the rapidly evolving data on optimal therapy, including consideration of the patient's prior exposure to anti-infective agents, the local prevalence of resistance, patient compliance, and costs of therapy. (See Duodenal Ulcer: Acute Therapy, in Uses.) For a more complete discussion of H. pylori infection, including details about the efficacy of various regimens and rationale for drug selection, .

Gastroesophageal Reflux

Cimetidine is used for the short-term (12 weeks) treatment and symptomatic relief of endoscopically diagnosed erosive esophagitis in patients with gastroesophageal reflux disease (GERD). By increasing gastric pH, H2-antagonists have relieved heartburn and other symptoms of reflux and have been associated with somewhat higher healing rates of endoscopically proven esophagitis when compared with placebo and have reduced antacid consumption.

Suppression of gastric acid secretion is considered by the ACG to be the mainstay of treatment for GERD, and a proton-pump inhibitor or histamine H2-receptor antagonist is used to achieve acid suppression, control symptoms, and prevent complications of the disease. The ACG states that a histamine H2-receptor antagonist administered daily in divided doses is effective in many patients with less severe GERD, and over-the-counter (OTC) antacids and histamine H2-receptor antagonists are appropriate for self-medication as initial therapy in such individuals. A histamine H2-receptor antagonist is particularly useful when taken before certain activities (e.g., heavy meal, exercise) that may result in acid reflux symptoms in some patients. The ACG states that H2-receptor antagonists generally may be used interchangeably, although the drugs may differ in potency and in their onset and duration of action. However, proton-pump inhibitors are more effective (i.e., provide more frequent and more rapid symptomatic relief and healing of esophagitis) than histamine H2-receptor antagonists in the treatment of GERD. Although higher doses and more frequent administration of histamine H2-receptor antagonists appear to increase their efficacy, such dosages are less effective and more expensive than proton-pump inhibitor therapy. Once-daily administration of a histamine H2-receptor antagonist at full dosage is not considered to be appropriate therapy for GERD.

In controlled studies in patients with GERD and endoscopically confirmed esophageal erosions and/or ulcers, cimetidine was substantially more effective than placebo in healing lesions. In one controlled study, healing rates were 45, 52, or 26% after 6 weeks and 60, 66, or 42% after 12 weeks of therapy with cimetidine 800 mg twice daily, 400 mg four times daily, or placebo, respectively. In a second controlled study, healing rates were 50 or 20% after 6 weeks and 67 or 36% after 12 weeks of therapy with cimetidine 800 mg twice daily or placebo, respectively. The manufacturer states that by most measures, cimetidine provided greater improvement of daytime and nocturnal heartburn symptoms than placebo in these studies.

Cimetidine (300 mg 4 times daily) also has been used in combination with metoclopramide (10 mg 4 times daily) in a limited number of patients who failed to respond adequately to cimetidine alone. In one study, combined therapy was more effective than cimetidine alone in providing symptomatic relief and endoscopic improvement of esophagitis. However, the ACG states that frequent adverse CNS effects of metoclopramide have appropriately decreased regular use of the drug for GERD. Although some clinicians have suggested that a histamine H2-receptor antagonist also may be used in combination with bethanechol in patients who fail to respond to a histamine H2-receptor antagonist alone, the ACG states that bethanechol has limited efficacy in the treatment of GERD.

Short-term therapy (i.e., up to 12 weeks) with H2-receptor antagonists for the treatment of GERD will not prevent recurrence following ulcer healing and discontinuance of such therapy. Esophagitis has recurred within 6 months in up to 80% of patients following discontinuance of H2-receptor antagonist therapy. Because GERD is considered a chronic disease, many patients with GERD require long-term, even lifelong, treatment. The ACG states that proton-pump inhibitors are effective and appropriate as maintenance therapy in many patients with the disease. Maintenance therapy with an H2-receptor antagonist also has been used to reduce recurrence of GERD. However, many patients initially responding to proton-pump inhibitors experience symptomatic relapse and failure of esophageal healing with subsequent use of a histamine H2-receptor antagonist.

For further information on the treatment of GERD, .

Upper GI Bleeding

Cimetidine is used for the prevention of upper GI bleeding in critically ill patients that results principally from stress-related mucosal damage (erosive gastritis, stress ulcers). While current evidence suggests that prophylactic therapy with cimetidine, particularly via continuous IV infusion, is more effective than placebo and in appropriate regimens probably at least as effective as antacids in reducing the incidence of occult and/or overt GI bleeding in critically ill patients (e.g., those with major traumatic injury, hypotension/ shock, sepsis, extensive burns, respiratory, renal, and/or hepatic insufficiency, coagulopathy), the cost-benefit of such therapy, particularly when employed extensively in the intensive care setting, remains controversial. Most studies on the efficacy of preventive therapy mainly have measured occult (a questionable end point) and/or overt GI bleeding as therapeutic end points while few have attempted to document erosions and/or clinically important ulceration per se. In addition, few studies have measured and/or distinguished effects of preventive therapy on clinically important end points (e.g., serious upper GI bleeding, transfusion requirements, hemoglobin/hematocrit, hypovolemia, death, need for surgical and or other intervention to arrest GI bleeding) or determined objective benefit (e.g., short-term survival, morbidity, duration of hospital stay).

Some evidence indicates that the development of clinically important bleeding and progression to ulceration from stress-related GI erosions occur only rarely under current standards of care (e.g., those aimed at preventing hypovolemia, sepsis, hypoalbuminemia, anemia, and malnutrition and those resulting in reduced use of vasopressors and corticosteroids and in improved ventilatory support) in intensive care settings, even in the absence of preventive therapy. Generally absent from current evidence of efficacy is a clear indication of substantial morbidity and/or mortality reduction associated with prophylactic therapy for upper GI bleeding. These and other factors currently complicate interpretation of available data. Thus, while some clinicians recommend routine prophylactic therapy for upper GI bleeding in a large proportion of critically ill hospitalized patients, other clinicians state that such therapy should be employed more selectively in those clearly at appreciable risk of clinically important bleeding. Unfortunately, establishment of clear patient selection criteria based on appropriate cost-benefit analyses requires further study and elucidation. Factored into such consideration, however, is recognition that currently available therapies appear to be more effective in preventing than in treating upper GI bleeding once it becomes clinically important. It is for this reason and because of the often unpredictable clinical outcome of patients requiring intensive care that some clinicians recommend routine prophylaxis, at least initially; however, consensus currently does not exist on the precise role of prophylactic therapy for upper GI bleeding.

Analysis of pooled data from several studies (most of them controlled and randomized) indicates that prophylactic therapy with H2-receptor antagonists, including cimetidine, in critically ill patients appears to be more effective than no therapy or placebo in preventing occult and overt upper GI bleeding. While at least one such analysis suggests that the drugs also appear to be more effective than no therapy or placebo in reducing clinically important upper GI bleeding (e.g., overt bleeding accompanied by reduced blood pressure and/or a decreased hemoglobin or requiring red blood cell transfusion), some clinicians have questioned this conclusion. In addition, a clear benefit of prophylactic therapy on survival has not been established to date. While some studies indicate that cimetidine may be less effective than antacids in preventing upper GI bleeding in critically ill patients, other data indicate that H2-antagonists, including cimetidine, when administered in appropriate regimens (e.g., IV infusions that adequately increase and maintain gastric pH) probably are at least as effective as antacids when prevention of only overt rather than occult (microscopic) and/or overt bleeding is considered the minimum therapeutic end point.

Some studies indicate that cimetidine may be effective for the treatment of upper GI bleeding (e.g., secondary to hepatic failure, esophagitis, or gastric or duodenal ulcers) when hemorrhage is not caused by the erosion of major blood vessels. However, the effect of the drug on upper GI bleeding appears to be a moderate one, and additional study to further evaluate the effect of cimetidine therapy on morbidity and mortality in such bleeding is necessary.

Other Uses

Cimetidine may be used for self-medication for relief of symptoms of occasional heartburn (pyrosis), acid indigestion (hyperchlorhydria), or sour stomach.

Some studies indicate that cimetidine also may be effective for the treatment of stress ulcers and peptic esophagitis.

Cimetidine has been used concomitantly with an antihistamine (H1-receptor antagonist) for the prevention and management of various allergic conditions and of various urticarias including dermatographism, thermal (heat- and cold-induced) urticarias, and chronic idiopathic urticaria. Use of an H2-receptor antagonist such as cimetidine concomitantly with an antihistamine for the management of urticarias has generally been reserved for patients who did not experience adequate relief with an antihistamine alone; the addition of an H2-receptor antagonist occasionally may provide some additional benefit.

Dosage and Administration


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. (See Drug Interactions.) 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 syringe must 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.

IM Injection

For IM administration, cimetidine hydrochloride injection may be given undiluted. Transient pain may occur at the site of IM injection.

Intermittent Direct IV Injection

Cimetidine hydrochloride injection must be diluted prior to IV administration. For IV injection, 300 mg of cimetidine is diluted to a total of 20 mL with 0.9% sodium chloride injection or another compatible IV solution and injected over a period of not less than 5 minutes. Rapid IV injection of the drug has been associated with cardiac arrhythmias and hypotension. (See Cautions: Cardiac Effects.)

Intermittent IV Infusion

For intermittent IV infusion, 300 mg of cimetidine is added to at least 50 mL of 5% dextrose injection or another compatible IV fluid and infused over 15-20 minutes. Alternatively, ADD-Vantage vials labeled as containing 300 mg of cimetidine can be used, reconstituted according to the manufacturer's directions.

Alternatively, cimetidine hydrochloride that is commercially available as a diluted solution (6 mg of cimetidine per mL) in 0.9% sodium chloride may be used for intermittent IV infusion, infused over 15-20 minutes. The commercially available diluted solution should only be administered by IV infusion. The container should be checked for minute leaks by firmly squeezing the bag. The injection should be discarded if the seal is not intact or leaks are found or if the solution is cloudy or contains a precipitate. Additives should not be introduced into the injection container. The injection should not be used in series connections with other plastic containers, since such use could result in air embolism from residual air being drawn from the primary container before administration of fluid from the secondary container is complete.

Continuous IV Infusion

For continuous IV infusion, 900 mg of cimetidine is added to 100-1000 mL of a compatible IV solution (See Chemistry and Stability: Stability) and infused over 24 hours; use of a controlled-infusion device (e.g., pump) is recommended when the volume to be infused over 24 hours is smaller than 250 mL. The infusion rate should be adjusted to individual patient requirements.


Dosage of cimetidine hydrochloride is expressed in terms of cimetidine.

Parenteral Dosage

The usual adult IM or IV dosage of cimetidine is 300 mg every 6-8 hours. If necessary, parenteral dosage may be increased by increasing the frequency of administration, but the manufacturer recommends that IM or intermittent IV dosage not exceed 2.4 g daily. When feasible, IV dosage should be adjusted to maintain an intragastric pH of 5 or greater.

When cimetidine is administered by continuous IV infusion in adults, the drug usually is infused at a rate of 37.5 mg/hour, but the rate should be individualized according to patient requirements. For patients requiring more rapid increases in GI pH, an initial 150-mg IV loading dose may be required. In one study in patients with pathologic hypersecretory conditions, the average dosage by continuous IV infusion required to maintain gastric acid secretion at 10 or less mEq/hour was 160 mg/hour, but individual requirements varied considerably, ranging from 40-600 mg/hour.

Oral Dosage

Duodenal Ulcer

For the treatment of active duodenal ulcer, the usual adult oral dosage of cimetidine is 800 mg daily at bedtime. Because clinical studies have shown that reduction of nocturnal gastric acid secretion is the most important factor in healing duodenal ulcers, there does not appear to be a rationale, except for familiarity of use, for dosing regimens other than once-daily administration of cimetidine at bedtime. Increasing dosage to 1.6 g daily at bedtime does not substantially increase healing rate in most patients, although earlier healing may occur in some patients. Currently, the 800-mg bedtime regimen is considered the dosage of choice for most patients with active duodenal ulcer since it provides a high healing rate, maximal pain relief, decreased potential for drug interactions, and maximal patient compliance. In patients with an ulcer larger than 1 cm in diameter and who are heavy smokers (i.e., 1 pack or more daily), more rapid healing may be achieved with 1.6 g daily at bedtime and this regimen can be used as an alternative to the 800-mg regimen when it is considered important to increase the likelihood of healing within 4 weeks in these patients. Although healing may occur within the first 2 weeks of therapy in some patients and within 4 weeks in most patients, cimetidine therapy should usually be continued for 4-6 weeks, unless healing is confirmed earlier. Patients whose ulcer is not healed or those with continued symptoms after 4 weeks of therapy may benefit from an additional 2-4 weeks of full therapeutic dosage. Use of cimetidine at full therapeutic dosage for periods longer than 6-8 weeks is rarely needed for healing duodenal ulcers. Other regimens for the treatment of active duodenal ulcer in adults have included 300 mg 4 times daily with meals and at bedtime, 200 mg 3 times daily and an additional 400-mg dose at bedtime, or 400 mg twice daily given in the morning and at bedtime.

For maintenance therapy following healing of acute duodenal ulcer to reduce ulcer recurrence, the usual oral dosage of cimetidine is 400 mg daily at bedtime in adults. Maintenance therapy with higher dosages or more frequent administration does not increase efficacy.

Pathologic GI Hypersecretory Conditions

For the treatment of pathologic hypersecretory conditions (e.g., Zollinger-Ellison syndrome), the usual adult oral dosage of cimetidine is 300 mg 4 times daily with meals and at bedtime. Larger than usual dosage may be necessary, but total dosage usually should not exceed 2.4 g daily; dosage increases should be made by increasing the frequency of administration. Therapy should continue for as long as clinically necessary.

Gastric Ulcer

For the treatment of active benign gastric ulcer, the usual adult oral dosage of cimetidine is 800 mg at bedtime or 300 mg 4 times daily with meals and at bedtime. Currently, the 800-mg bedtime regimen is preferred for most patients with active benign gastric ulcer because of the decreased potential for drug interactions and maximal patient compliance. Therapy in controlled clinical trials was limited to 6 weeks, and efficacy for more than 8 weeks remains to be clearly determined. Patients with gastric ulcers should be monitored to ensure rapid progress to complete healing.

Gastroesophageal Reflux

For the short-term treatment and symptomatic relief of endoscopically diagnosed erosive esophagitis in patients with gastroesophageal reflux disease (GERD), the usual adult oral dosage of cimetidine is 1.6 g daily given in divided doses as 800 mg twice daily or 400 mg 4 times daily (e.g., before meals and at bedtime). Lower oral dosages (e.g., 300 mg 4 times daily) also have been used effectively for the symptomatic relief of GERD in adults.


For self-medication in relieving symptoms of occasional heartburn, acid indigestion, or sour stomach in patients 12 years of age or older, a cimetidine dosage of 200 mg once or twice daily or as directed by a clinician is recommended. For self-medication, the manufacturer recommends that the dosage of cimetidine not exceed 400 mg in 24 hours and that therapy at the maximum dosage not exceed 2 weeks of continuous use unless otherwise directed by a clinician.

Parenteral and Oral Dosage for Other Uses

For the prevention of upper GI bleeding in critically ill patients, cimetidine usually is administered to adults by continuous IV infusion at a rate of 50 mg/hour for up to 7 days; the manufacturer states that the safety and efficacy of continuously infused cimetidine for more prolonged periods have not been established. The manufacturer also indicates that an initial loading dose is not required when the drug is administered prophylactically in such patients. However, some clinicians recommend initiating cimetidine therapy in critically ill patients with a 300-mg IV loading dose administered over 5-20 minutes, followed by a continuous IV infusion initiated at a rate of 37.5-50 mg/hour and titrated according to gastric pH (e.g., maintenance of a pH of at least 3.5-4) by additional 25-mg/hour increments, generally up to a maximum rate of 100 mg/hour. Intermittent IV doses of the drug appear to be less effective in preventing upper GI bleeding than continuous IV infusions.

In the treatment of upper GI bleeding, peptic esophagitis, and stress ulcers, IV or oral dosage of 1-2 g daily, administered in 4 divided doses, has been used.

Pediatric Dosage

When the potential benefits are thought to outweigh the possible risks (see Cautions: Pediatric Precautions), a pediatric cimetidine dosage of 20-40 mg/kg daily in divided doses has been used in a limited number of children.

Dosage in Renal and Hepatic Impairment

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.


Nervous System Effects

Headache has been reported in 2.1 and 3.5% of patients receiving 800 and 1600 mg, respectively, of cimetidine daily; headache was reported in 2.3% of those receiving placebo. Headache may be mild to severe and resolves following discontinuance of the drug. Dizziness and somnolence (usually mild) have been reported in about 1% of patients receiving the drug.

Reversible confusional states (e.g., mental confusion, agitation, psychosis, paranoia, depression, anxiety, hallucinations, hostility, delirium, disorientation) have occurred occasionally following administration of cimetidine, especially in geriatric and/or severely ill patients, such as those with renal and/or hepatic insufficiency or organic brain syndrome; however, overdosage of the drug may have been involved in some cases. In addition, a clear risk for such patients and a dose relationship have not been established, and such reactions may be idiosyncratic in nature. Controlled studies are needed to more fully elucidate any relationship between the incidence of these nervous system effects and certain risk factors. Confusional states have usually occurred within 2-3 days after initiating cimetidine and resolved within 3-7 days following discontinuance of the drug. In some patients, these confusional states have been mild and have not required discontinuance of the drug. Delusions in the absence of a confusional state also have been reported. Agitation, lightheadedness, restlessness, and profuse sweating and flushing were noted in a few patients receiving 1-2 g of the drug daily. One geriatric patient with erosive gastritis and renal failure experienced twitching of the right side of the body which disappeared when IV cimetidine dosage was reduced from 1.2 g daily to 600 mg daily. An acute dystonic reaction that was temporally related to cimetidine therapy also has been reported.

Fever occurred within several days to 2 weeks after initiating cimetidine therapy and generally resolved within 24 hours after discontinuance of the drug; fever has recurred within 24 hours following rechallenge in several patients. It has been suggested that cimetidine-induced fever may result from inhibition of H2 receptors in the thermoregulatory area of the hypothalamus, although other mechanisms may be involved.

GI Effects

Mild, transient diarrhea has been reported occasionally in patients receiving cimetidine. Adynamic ileus with dilated colon has been reported in several burn patients receiving cimetidine for the treatment of stress ulcer, but this may have been related to their extensive burns. Perforation of chronic peptic ulcers also has been reported in several patients receiving cimetidine. Pancreatitis, which subsided following discontinuance of the drug, also has occurred.

Dermatologic and Sensitivity Reactions

Transient maculopapular or acneiform rashes and urticaria have been reported occasionally in patients receiving cimetidine. Mild rash and, very rarely, severe generalized dermatologic reactions such as Stevens-Johnson syndrome, epidermal necrolysis, erythema multiforme, exfoliative dermatitis, and generalized exfoliative erythroderma have been reported in patients receiving histamine H2-receptor antagonists. Hypersensitivity reactions, including anaphylaxis and vasculitis, have occurred rarely in patients receiving cimetidine but resolved following discontinuance of the drug. Fever also has been reported, but nonallergic mechanisms may be involved, at least in some cases. (See Cautions: Nervous System Effects.)

Cardiovascular Effects

Following rapid IV administration of cimetidine hydrochloride, cardiac arrhythmias and hypotension have been reported rarely. Sinus bradycardia, although principally reported following IV administration of the drug, has also been reported following oral administration; bradycardia usually resolves within 24 hours after discontinuance of the drug but cardiac arrest and, rarely, death have occurred in a few patients who received the drug IV or in overdosage. AV block also has been reported rarely. Other arrhythmias reported rarely during IV therapy with the drug include atrial premature contractions, palpitation, and unifocal ventricular premature contractions and atrial fibrillation, multifocal ventricular premature contractions, ventricular tachycardia, and ventricular fibrillation associated with impaired left ventricular function.

Hematologic Effects

Use of cimetidine has been associated with neutropenia in a few patients (about 0.001% of patients receiving the drug) and agranulocytosis has occurred rarely; recurrence with rechallenge has been reported. Most patients had serious concomitant illnesses and were receiving drugs and/or treatment known to produce neutropenia. Reversible agranulocytosis occurred in one patient 4 months after 5 weeks of cimetidine treatment for duodenal ulcer. Thrombocytopenia and a few cases of aplastic anemia have been reported.

Renal Effects

Small increases in plasma creatinine, presumably secondary to competitive renal tubular secretion, frequently have occurred early in cimetidine therapy, but these increases have not been progressive and disappeared at the end of therapy or when the drug was withdrawn. Interstitial nephritis, which subsided following discontinuance of the drug, also has occurred.

Hepatic Effects

Increases in serum AST (SGOT), ALT (SGPT), and alkaline phosphatase concentrations have been reported in patients receiving cimetidine but were not usually clinically important; in a few of these patients, concurrent mild centrilobular necrosis was noted. Although rare, adverse hepatic effects have usually been reversible and cholestatic or mixed cholestatic-hepatocellular in nature. However, although severe parenchymal injury is considered highly unlikely, as with other H2-receptor antagonists, fatalities have been reported very rarely. Periportal hepatic fibrosis has been reported in at least one patient receiving cimetidine. Rarely, hepatitis, which subsided following discontinuance of the drug, has occurred.

Respiratory Effects

Nosocomial Pneumonia

While the risk associated with prophylactic H2-antagonist or antacid therapy in critically ill patients generally has been considered low, an association between the development of nosocomial pneumonia in such patients, particularly those receiving prolonged prophylaxis, those hospitalized for long periods, and/or those who are intubated, and elevated gastric pH secondary to therapy with these drugs has been reported. However, many clinicians have questioned these findings, and in at least 2 studies, including one that analyzed pooled data from several studies, the incidence of nosocomial pneumonia actually appeared to be increased in critically ill patients receiving placebo compared with that in patients receiving H2-receptor antagonists and/or antacids, despite a lower average gastric pH in the placebo group. In another study in mechanically ventilated neurosurgical patients receiving H2-antagonist therapy, although gastric colonization with gram-negative bacteria was positively correlated with increasing gastric pH, gastric contents did not appear to be an important source of pathogens for nosocomial infections, even in those with high gastric pH. Further study is needed to determine the risk, if any, of prolonged increased gastric pH in critically ill patients.

Hyperinfection with Strongyloides stercoralis has been reported rarely in immunocompromised patients receiving cimetidine.

Community-acquired Pneumonia

Administration of gastric antisecretory agents (e.g., H2-receptor antagonists, proton-pump inhibitors) has been associated with an increased risk for developing certain infections (e.g., community-acquired pneumonia). A possible association between chronic administration of gastric acid-suppressive drugs and occurrence of community-acquired pneumonia has been evaluated using a large Dutch database (Integrated Primary Care Information [IPCI]) containing information on approximately 500,000 patients, 364,683 of whom (average follow-up: 2.7 years) were selected for evaluating any such association. During the 8-year population-based, case-control study, gastric acid suppressants were first prescribed in 19,459 individuals (10,177 received H2-receptor antagonists [mean duration of use: 2.8 months] and 12,337 received proton-pump inhibitors [mean duration of use: 5 months]; some individuals received both drugs). Most patients did not undergo endoscopy and were treated empirically for upper GI symptoms. In this study, first occurrence of pneumonia (confirmed by radiography or microbiologic testing in 18% of patients) was reported in 5551 individuals; development of pneumonia occurred in 185 individuals while receiving gastric acid suppressants and in 292 individuals who had discontinued such use.

The adjusted relative risk for development of pneumonia (or the incidence rate) was 0.6, 2.3 and 2.5 per 100 person-years for individuals not receiving acid-suppressive drugs, for those receiving H2-receptor antagonists, and for those receiving proton-pump inhibitors, respectively. Patients using gastric acid suppressants developed community-acquired pneumonia 4.5 (95% confidence interval of 3.8-5.1) times more often than those who never used such drugs. When evaluating use of all gastric acid suppressants, current use of the drugs was associated with a small (27%) overall increase in the risk of pneumonia (adjusted odds ratio 1.27 and 95% confidence interval of 1.06-1.54). Higher risks were observed for current users of H2-receptor antagonists and proton-pump inhibitors; the adjusted relative risk for developing community-acquired pneumonia was 1.63 (95% confidence interval of 1.07-2.48) or 1.89 (95% confidence interval of 1.36-2.62), respectively, for these classes of drugs compared with those who discontinued using these agents. Estimates for developing pneumonia were higher (1.7 [95% confidence interval of 0.8-2.9] for H2-receptor antagonists and 2.2 [95% confidence interval of 1.4-3.5] for proton-pump inhibitors) when only laboratory-confirmed cases of pneumonia were considered for analysis.

Although there was variation among individual H2-receptor antagonists and individual proton-pump inhibitors, the numbers were small and the heterogeneity was not considered significant. For patients currrently receiving proton-pump inhibitors, a dose-response relationship for developing pneumonia was observed; individuals using more than one defined daily dose of these drugs had a 2.3-fold increased risk for developing pneumonia compared with those who discontinued gastric acid suppressants. Such a dose-response relationship for developing pneumonia was not observed in patients receiving H2-receptor antagonists; however, dose variation of these drugs was limited. Among current users of H2-receptor antagonists or proton-pump inhibitors, the risk for developing pneumonia was most pronounced among those who initiated such therapies within the past 30 days.

Although the exact mechanism for development of community-acquired pneumonia in patients receiving gastric acid suppressants has not been fully elucidated, it has been suggested that reduction of gastric acid secretion by acid suppressive therapy and consequent increases of gastric pH may result in a favorable environment for the development of infection. Intragastric acidity constitutes a major nonspecific defense mechanism of the stomach to ingested pathogens; when gastric pH is less than 4, most pathogens are killed, while at higher gastric pH, pathogens may survive. Since for the effective management of upper GI symptoms, intragastric pH should be maintained above 4 for several hours, acid suppressive therapy may lead to insufficient elimination or, even, increased colonization of ingested pathogens.

It should be considered that certain patients (e.g., those with pleuritic chest pain, hypothermia, systolic hypotension, tachypnea, diabetes mellitus, neoplastic disease, neurologic disease, bacteremia, leukopenia, multilobar pulmonary infiltrate) are at increased risk for developing infections and in these individuals community-acquired pneumonia may be associated with increased mortality. Some clinicians state that gastric acid-suppressive drugs should be used in patients in whom community-acquired pneumonia may be severe (e.g., those with asthma or chronic obstructive lung disease, immunocompromised patients, pediatric or geriatric individuals) only when clearly needed and the lowest effective dose should be employed.

Other Adverse Effects

Mild bilateral gynecomastia and breast soreness have occurred in about 4% of patients with pathologic hypersecretory conditions and in 0.3-1% of other patients receiving cimetidine for 1 month or longer. Gynecomastia disappeared or remained unchanged throughout cimetidine therapy, and no evidence of endocrine dysfunction was found; however, gynecomastia may be related to cimetidine's weak antiandrogenic effect. Reversible alopecia has been reported rarely in patients receiving the drug.

Reversible arthralgia and myalgia have been reported rarely. In addition, in patients with preexisting arthritis, exacerbation of joint symptoms has been noted during cimetidine therapy; however, dosage reduction of cimetidine usually alleviated these symptoms. A few cases of polymyositis have been reported, but a causal relationship to the drug has not been established.

Transient pain may occur at the site of IM injection.

Precautions and Contraindications

The possibility that cardiac arrhythmias and hypotension may result from rapid IV injection of cimetidine should be considered and rapid administration avoided. (See Administration: Intermittent Direct IV Injection, in Dosage and Administration.) The possibility that reversible confusional states may occur in patients receiving cimetidine therapy also should be considered. While clear risks for such nervous system effects have not been established, the possibility that patients 50 years or older and severely ill patients as well as those with preexisting hepatic and/or renal disease may be at increased risk should be considered. (See Cautions: Nervous System Effects.)

Symptomatic response to cimetidine should not be interpreted as precluding the presence of gastric malignancy. There have been rare reports of transient healing of gastric ulcers despite subsequently documented malignancy.

The possibility that gastric acid-suppressive therapy may increase the risk of community-acquired pneumonia should be considered. (See Respiratory Effects: Community-acquired Pneumonia, in Cautions.)

In immunocompromised patients, decreased gastric acidity, including that produced by acid-suppressing agents such as cimetidine, may increase the possibility of a hyperinfection caused by Strongyloides stercoralis.

Patients should be advised to consult their clinician before using cimetidine for self-medication if they are taking theophylline, warfarin, or phenytoin. For self-medication, the manufacturer recommends that the dosage of cimetidine not exceed 400 mg in 24 hours and that therapy at the maximum dosage not exceed 2 weeks of continuous use unless otherwise directed by a clinician. Persistent abdominal pain or difficulty swallowing should be reported promptly to a clinician, since these symptoms may be indicative of a serious condition requiring alternative treatment.

Cimetidine is contraindicated in patients with known hypersensitivity to the drug.

Pediatric Precautions

The manufacturers state that since clinical experience in children is limited, cimetidine cannot be recommended for use in those younger than 16 years of age unless, in the judgment of the clinician, anticipated benefits of such therapy outweigh the potential risks. In limited clinical experience, cimetidine dosages of 20-40 mg/kg daily have been used in children. Cimetidine also should not be used for self-medication in children younger than 12 years of age unless directed by a clinician.

Mutagenicity and Carcinogenicity

In a 2-year study in rats receiving cimetidine dosages of 150, 378, and 950 mg/kg daily (approximately 8-48 times the recommended human dosage), a small increase in the incidence of benign Leydig cell tumors in each dosage group compared with the control group was observed. In a subsequent 2-year study, the incidence of these benign Leydig cell tumors was increased compared with controls in rats receiving 378 or 950 mg/kg of cimetidine but not in those receiving 150 mg/kg. These tumors were common in control as well as treated groups, and the differences became apparent only in aged rats.

Pregnancy, Fertility, and Lactation


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.


Reversible impotence has been reported in patients with pathologic hypersecretory conditions receiving cimetidine. Impotence has occurred more frequently when high dosages of cimetidine were used for at least 12 months; however, the manufacturer states that the frequency of impotence in patients receiving usual dosages of cimetidine does not exceed that reported in the general population. In controlled long-term studies in patients receiving single daily bedtime doses of cimetidine, the occurrence of impotence was similar in cimetidine-treated patients and placebo-treated patients. Although there was no impairment of mating performance or fertility, the weak antiandrogenic effect of cimetidine has reduced prostate and seminal vesicle weights in animals. Cimetidine has been reported to decrease the sperm count in males receiving usual dosage of the drug; sperm counts returned to pretreatment levels after discontinuance of cimetidine. However, in a controlled, double-blind study in healthy males receiving usual dosage of cimetidine for 6 months, no effect on spermatogenesis, sperm count, sperm motility, sperm morphology, or fertilizing capacity in vitro was observed; blood concentrations of androgen and gonadotropin were unchanged.


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.

Drug Interactions

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).



Cimetidine is rapidly and well absorbed following oral administration. A small portion of orally administered cimetidine is metabolized during first pass through the liver, resulting in an average bioavailability of 60-70% when compared to IV injection. The oral bioavailability of a single dose as 800-mg cimetidine tablets is comparable to that of a single dose as two 400-mg tablets. Food delays and may slightly decrease absorption of the drug; however, by administering cimetidine with meals, maximum blood concentrations and antisecretory effects of the drug are achieved when the stomach is no longer protected by the buffering capacity of food. Concurrent administration of some antacids may decrease cimetidine absorption. (See Drug Interactions.)

Cimetidine reduces basal gastric acid secretion by about 80% and meal-stimulated acid secretion by about 50% at blood concentrations of 0.5 mcg/mL; at blood concentrations of 1 mcg/mL, basal gastric acid secretion is reduced 90-100% and meal-stimulated acid secretion is reduced by 80%. In one study in fasting duodenal ulcer patients, peak blood cimetidine concentrations of about 1.2 mcg/mL and 1.8 mcg/mL occurred within 1 hour following oral administration of 300 mg and 400 mg of the drug, respectively; blood concentrations remained above 0.5 mcg/mL for 5 hours with both doses. Peak blood concentrations of about 5.25 mcg/mL were reached immediately and blood concentrations remained above 0.5 mcg/mL for 4 hours following IV injection of 300 mg of cimetidine in another study.

Steady-state plasma cimetidine concentrations achieved following IV infusion of the drug depend on the clearance of the drug but are proportional to the rate of infusion. In one study in patients with peptic ulcer and normal renal function, IV infusion of the drug at 37.5 mg/hour resulted in steady-state plasma cimetidine concentrations of 0.9 mcg/mL.


Cimetidine is widely distributed throughout the body and is 15-20% bound to plasma proteins. Animal studies indicate that the drug crosses the placenta. Cimetidine is distributed into milk.


Cimetidine is metabolized in the liver to sulfoxide and 5-hydroxymethyl derivatives, and possibly guanylurea, although this latter compound may result from in vitro degradation. The drug has a blood half-life of about 2 hours in patients with normal renal function, 2.9 hours in patients with creatinine clearances of 20-50 mL/minute, 3.7 hours in patients with creatinine clearances of less than 20 mL/minute, and 5 hours in anephric patients. Following IV administration of the drug in critically ill children 4.1-15 years of age, plasma cimetidine concentrations appeared to decline in a biphasic manner with a mean distribution half-life (t½α) of about 10 minutes and a mean elimination half-life (t½β) of about 1.4 hours; plasma cimetidine sulfoxide concentration also appeared to decline in a biphasic manner with t½α of 22 minutes and a t½β of 2.6 hours.

Studies show that following IV administration of radiolabeled cimetidine, 80-90% of the drug is excreted in urine within 24 hours; 50-73% is excreted unchanged and the remainder as the two metabolites. About 10% of the drug is excreted in feces. In one study, cimetidine was completely removed from the circulation after 5 hours of hemodialysis.

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