Ranitidine, and Cimetidine (Tagamet)

Ranitidine, and Cimetidine (Tagamet) in the Treatment of Gastric Ulcers in Horses

by Robert N. Oglesby DVM

Introduction

Introduction » Mechanism of Action/Uses » Contraindications » Overdosage Toxicity » Drug Interactions » Drug/Laboratory Interactions » Dosages » More Info & Discussions

Cimetidine (Tagamet) and ranitidine are used in horses primarily to treat gastric ulcers. An unapproved use is for the treatment of benign melanomas in horses. This article is about the uses, contraindications, toxic effects, dosages, and association drug rules that apply to this medication. Their use is compared to that of the newer treatment omeprazole (Gastroguard).

See also:

Mechanism of Action/Uses

Introduction » Mechanism of Action/Uses » Contraindications » Overdosage Toxicity » Drug Interactions » Drug/Laboratory Interactions » Dosages » More Info & Discussions

Cimetidine and ranitidine block the H2 receptors of the parietal cells, reducing gastric acid secretion, pancreatic or biliary secretion, and lower esophageal pressures are not altered by cimetidine. By decreasing the amount of gastric juice produced, they also decrease the amount of pepsin secreted. Due to frequency of administration and the occasional recurrence of symptoms following cessation, better treatments have been sought. Omeprazole has been shown to be more effective with just once daily treatment. However, it is considerably more expensive.

Cimetidine/ranitidine has an apparent immunomodulating effect as it has been demonstrated to reverse suppressor T cell-mediated immune suppression. It also possesses weak anti-androgenic activity.

They have been used for the treatment and/or prophylaxis of stomach and duodenal ulcers including:
  • uremic gastritis
  • stress-related or drug-induced erosive gastritis
  • esophagitis
  • duodenal gastric reflux
  • esophageal reflux
It has also been employed to treat hypersecretory conditions associated with gastrinomas and systemic mastocytosis. Ranitidine is a more effective treatment due to more potent and longer duration of action. Omeprazole has recently been approved for gastric ulcers and appears to be more effective than either of these treatments.

Cimetidine has also been used investigationally as a treatment for melanomas and it is felt ranitidine is not as effective for melanomas.

More Information on Cimetidine and Melanomas

Cimetidine inhibits epidermal growth factor-induced cell signaling.

Fujikawa T, Shiraha H, Nakanishi Y, Takaoka N, Ueda N, Suzuki M, Shiratori Y.

Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan. tfmty@yahoo.co.jp

BACKGROUND: Cimetidine, a histamine-2 (H2) receptor antagonist, has been demonstrated to have anticancer effects on colorectal cancer, melanoma and renal cell carcinoma. In the current study, we clarified that cimetidine inhibits both epidermal growth factor (EGF)-induced cell proliferation and migration in hepatocellular carcinoma (HCC) cell lines. METHOD: HCC cell lines (Hep3B, HLF, SK-Hep-1, JHH-2, PLC/PRF/5 and HLE) were used and cell proliferation was assessed by [3H]-thymidine incorporation assay. Cell migration was measured by in vitro cell migration assay. Biological effects of cimetidine were assessed with human EGF receptor (EGFR)-expressing mouse fibroblast cells (NR6-WT). The autophosphorylation of EGFR and the activation of other downstream effectors were analyzed by immunoprecipitation and immunoblotting. The concentration of intracellular cyclic AMP (cAMP) was measured by competitive enzyme immunoassay. RESULTS: Cimetidine inhibited both EGF-induced cell proliferation and migration in Hep3B, HLF, SK-Hep-1 and JHH-2, while cimetidine did not affect EGF-induced cell proliferation and migration in PLC/PRF/5 and HLE. Cimetidine was revealed to disrupt the EGF-induced autophosphorylation of EGFR and its downstream effectors, mitogen activated protein kinases and phospholipase C-gamma. To define the molecular basis of this negative regulation, we identified that cimetidine significantly decreased intracellular cAMP levels and that decrement of cAMP inhibited autophosphorylation of EGFR. The cell permeable cAMP analog, CPT-cAMPS reversed the cimetidine-induced inhibition of EGF-induced cell proliferation and cell migration by restoring autophosphorylation of EGFR. CONCLUSION: Cimetidine inhibited EGF-induced cell proliferation and migration in HCC cell lines by decreasing the concentration of intracellular cAMP levels. Cimetidine may be a candidate chemopreventive agent for HCC.

Contraindications

Introduction » Mechanism of Action/Uses » Contraindications » Overdosage Toxicity » Drug Interactions » Drug/Laboratory Interactions » Dosages » More Info & Discussions

                       
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