Ranitidine (Zantac)
Zantac®, Zantac® IV | Zantac 150™ | Zantac 75® | Zantac® EFFERdose® | Zantac® EFFERdose® Granules
Classification:
Antihistamines
Antihistamines
Gastrointestinal Agents
Description: Ranitidine is an antagonist at histamine H2-receptors similar to cimetidine and famotidine. The actions and indications for ranitidine differ little from other H2-blockers, except that ranitidine is 5 - 12 times as potent as cimetidine as a histamine receptor antagonist while having less affinity than cimetidine for the cytochrome P450 hepatic enzyme system. As a result, ranitidine is much less likely than cimetidine to interact with other drugs, although drug interactions with ranitidine do exist. Similar to other H2-receptor antagonists, the main use of ranitidine is in the treatment of various gastrointestinal disorders. However, for the symptomatic acute and chronic treatment of gastroesophageal reflux disease (GERD), proton pump inhibitors (PPIs) like omeprazole are considered to be more effective than H2- blockers. PPIs are also preferred over ranitidine and other H2-blockers in currently recommended treatment regimens for Helicobacter pylori-related peptic ulcer disease. Ranitidine (Zantac®) was originally approved by the FDA in June 1983. A non-prescription (OTC) form of ranitidine (e.g., 75 mg tablets) was approved in December 1995. Glaxo Wellcome also produces a formulation of ranitidine in combination with bismuth citrate (Tritec®), which was FDA approved August 8, 1996, for use in combination drug regimens to treat H. pylori. The Zantac® EFFERdose® granules for oral solution were discontinued by the manufacturer in January 2003; EFFERdose® tablets are still available. A 25-mg strength of EFFERdose® was approved by the FDA on April 12, 2004 for the treatment of GERD in children and infants >= 1 month of age.
Mechanism of Action: Ranitidine competitively inhibits the binding of histamine to receptors on gastric parietal cells (designated as the H2 receptor), thus reducing basal and nocturnal gastric acid secretion. The drug also decreases the amount of gastric acid released in response to stimuli such as food, caffeine, insulin, betazole, or pentagastrin. Ranitidine reduces the total volume of gastric juice, thereby indirectly decreasing pepsin secretion. Ranitidine has little to no effect on serum gastrin and does not impair intrinsic factor secretion. The drug does not appear to alter gastric motility, gastric emptying, esophageal pressures, biliary secretions, or pancreatic secretions. Ranitidine is not an antimuscarinic anticholinergic. Ranitidine may aid in gastromucosal healing, and it may protect the mucosa from the irritant effects caused by aspirin and nonsteroidal antiinflammatory agents. Other actions of ranitidine include an increase in gastric bacterial flora (e.g., nitrate-reducing organisms). The clinical significance of this effect is not known. H2-blockers, as single agents, do not erradicate H. pylori infection.
After bolus ranitidine doses of 100 mg IV or greater, small and transient increases in prolactin serum concentrations have been noted. Ranitidine does not affect serum concentrations or release of gonadotropin, TSH, or GH. Ranitidine may impair the release of vasopressin. Ranitidine has no effect on serum cortisol, aldosterone, androgen, or estrogen levels.
Pharmacokinetics: Ranitidine is administered either orally or parenterally. Intramuscular (IM) administration results in a bioavailability of 90 - 100% versus intravenous (IV) administration. Due to first-pass elimination, the oral bioavailability of ranitidine is about 50 - 60%. The presence of food in the GI tract does not appear to affect the extent or rate of absorption. The drug distributes throughout the body fluids and tissues, and can be found in breast milk and CSF. Using inhibition of pentagastrin-induced acid secretion as an indicator, ranitidine’s effects persist for 8 - 12 hours.
Ranitidine Tablets(Tab 300 mg) 
Ranitidine undergoes partial metabolism (30%) in the liver, and both the unchanged drug and its metabolites are excreted in the urine and feces. Following IV injection, roughly 70% of ranitidine is recovered in the urine unchanged. Following oral administration, roughly 30% of an administered dose is excreted unchanged in the urine. The half-life of the drug is 2 - 3 hours but increases to roughly 5 hours in patients with renal impairment (CrCl < 35 ml/min). Elderly patients have decreased renal function and the elimination half-life in this group is about 3 - 4 hours. Tubular secretion as well as glomerular filtration account for ranitidine renal elimination. The manufacturer states that in patients with compensated cirrhosis, there are minor but clinically insignificant alterations in ranitidine distribution, half-life, and clearance.
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References
. Howden CW, Hunt RH. Guidelines for the management of Helicobacter pylori infection. Am J Gastroenterol 1998;93:2330 - 8.
. Festen H, Schenk E, Tan G, et al. Omeprazole versus high-dose ranitidine in mild gastroesophageal reflux disease: short and long term treatment. Am J Gastroenterol 1999;94:931 - 6.
[ Revised 3/23/2006 12:40:00 PM ]
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