Famotidine is a highly selective histamine H2-receptor antagonist. In healthy volunteers and patients with acid hypersecretory disease it is approximately 20 to 50 times more potent at inhibiting gastric acid secretion than cimetidine and 8 times more potent than ranitidine on a weight basis. As shown in placebo-controlled trials, famotidine is effective in healing both duodenal and gastric ulcers. Famotidine 20mg twice daily or 40mg at bedtime achieves healing rates and symptom relief similar or superior to those achieved by cimetidine 800mg daily or ranitidine 300mg daily in patients with peptic ulcer disease. Results of 1 placebo-controlled study suggest that famotidine prevents recurrence of duodenal ulcer, but comparative trials are needed to establish its relative efficacy in maintenance therapy. The few non-comparative trials conducted to date also suggest that famotidine 10 to 20mg twice daily may be effective in the treatment of gastritis and reflux gastro-oesophagitis. In comparative trials, famotidine was similar in efficacy to cimetidine in the treatment of upper gastrointestinal bleeding and to ranitidine in the prevention of pulmonary aspiration of acid. In patients with Zollinger-Ellison syndrome, the potency and long duration of action of famotidine may confer an advantage over other H2-receptor antagonists--in individualised doses (mean 0.33 g/day) famotidine successfully controlled acid secretion for up to 72 months in 1 study of such patients. Accumulated clinical evidence confirms that famotidine is very well tolerated and is free of the antiandrogenic effects infrequently reported with cimetidine. Moreover, famotidine is not associated with altered hepatic metabolism of drugs. Thus, famotidine is an effective, well-tolerated alternative to cimetidine and ranitidine. Famotidine is also promising as maintenance therapy for preventing recurrence of duodenal ulcer and as initial or maintenance treatment of gastric hypersecretory disorders, but further clinical experience, particularly in the long term, is needed to define the relative efficacy and tolerability of famotidine in these indications.

Famotidine. An updated review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in peptic ulcer disease and other allied diseases.

Synopsis
Ranitidine, a histamine H2-receptor antagonist, is now well established as a potent inhibitor of gastric acid secretion effective in the treatment and prophylaxis of gastrointestinal lesions aggravated by gastric acid secretion.

Therapeutic trials involving several thousands of patients with peptic ulcer disease confirm that ranitidine 300mg daily administered orally in single or divided doses is at least as effective as cimetidine 800 to 1000mg daily in increasing the rate of healing of duodenal and gastric ulcers. Similar dosages of ranitidine have been shown to relieve the symptoms of reflux oesophagitis and heal or prevent gastrointestinal damage caused by ulcerogenic drugs. Ranitidine 150mg orally at night maintains ulcer healing in the long term. Ranitidine has also demonstrated good results in the treatment of Zollinger-Ellison syndrome and in the prevention of aspiration pneumonitis when given prior to surgery and to pregnant women at full term. It may also have a place in the management of acute upper gastrointestinal bleeding and in the prevention of stress ulcers in the intensive care setting, although these areas require further investigation. Ranitidine has been used safely in obstetric patients during labour, in children, the elderly, and in patients with renal impairment when given in appropriate dosages. The drug is very well tolerated and is only infrequently associated with serious adverse reactions or clinically significant drug interactions. Even at high dosages, ranitidine appears devoid of antiandrogenic effects.

Ranitidine is clearly comparable or superior to most other antiulcer agents in the treatment and prevention of a variety of gastrointestinal disorders associated with gastric acid secretion. With its favourable efficacy and tolerability profiles, ranitidine must be considered a first-line agent when suppression of gastric acid secretion is indicated.

Ranitidine

SUMMARY Standard techniques for selecting the bandwidth of a kernel estimator from the data in a nonparametric regression model perform badly when the errors are correlated. In this paper we propose a modified version of an existing plug-in bandwidth selector. The method is generalized to stationary error variables by estimating a functional of the residual covariance function. The proposed bandwidth selector shows good properties in asymptotic theory and in simulations without assuming a parametric model for the error process.

Choice of bandwidth for kernel regression when residuals are correlated

Simultaneous ambulatory records of gastric antral and body pH were made over 24 hours in nine healthy volunteers by means of endoscopically positioned and anchored glass electrodes. Intragastric pH was temporarily raised after the endoscopy with the median pH value 30 minutes after the procedure being 3.9 (range 1.5-7.0) for the antrum and 4.1 (range 1.5-7.0) for the body. Daytime pH (median pH value between 12 00 h and 23 00 h) was lower in the antrum (median = 1.9, range 1.6-2.6) than in the body (median = 2.7, range 1.8-4.5) (p less than 0.05) and this was because of the rise in pH on eating being less marked in the antrum than in the body. The median peak pH recorded during the evening meal was only 4.1 (range 2.4-6.2) in the antrum compared with 6.3 (range 4.4-6.7) in the body (p less than 0.01). Preprandial pH (median value over the hour prior to the evening meal) was similar in the antrum (median = 1.9, range 1.2-2.5) and body (median = 1.9, range 1.3-2.8). Night-time pH (median pH value between 23 00 h and 05 00 h) in six subjects remained low and was similar in the antrum (median = 1.4, range 1.2-1.7) and body (median = 1.3, range 1.1-1.7). In two subjects, however, there were episodes of raised night-time pH which were more marked in the antrum than in the body. Antral biopsies showed gastritis in four of the nine normal volunteers, which in three was associated with the presence of campylobacter-like organisms. This study shows the significant regional variations in day and night-time intragastric pH.

https://gut.bmj.com/content/gutjnl/30/5/573.full.pdf

Comparison of gastric body and antral pH: a 24 hour ambulatory study in healthy volunteers.

Gastric acid is of central importance in the pathogenesis of duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Pharmacological reduction of acid secretion is, therefore, the mainstay of current treatment, but the optimal degree of acid suppression remains incompletely understood. This paper considers the ideal ways of assessing and reporting the pharmacological effectiveness of acid-inhibiting drugs and relating such data to clinical efficacy. Twenty-four-hour intragastric pH measurements are widely used for this purpose, although this technique cannot measure secretion quantitatively. Data on suppression of 24-hr intragastric acidity for groups of subjects have been successfully correlated with healing rates for duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Three primary determinants of healing have been derived from antisecretory data. These are the degree of suppression of acidity, the duration of suppression of acidity, and the duration of treatment. The order of importance of these determinants varies depending on the disease. Data on 24-hr intragastric acidity should be accompanied whenever possible by data on 24-hr plasma gastrin levels, as the relationship between suppression of acidity and a rise in gastrin varies widely between individuals. It is not possible to predict the plasma gastrin level from the intragastric pH or any other measurement of intragastric acidity. Comparative data sets in groups of subjects may provide useful information. Proton pump inhibitors produce a greater and longer-lasting degree of suppression of acidity than conventional doses of H2-receptor antagonists. For this reason, they are more effective in healing duodenal ulcer and gastric ulcer. However, in view of the importance of duration of treatment, healing rates with the H2-receptor antagonists approach those obtained with proton pump inhibitors if treatment is continued for a longer time. In gastroesophageal reflux disease in particular, although the optimal degree of acid suppression is not yet defined, the consistently superior performance of proton pump inhibitors demonstrates that increased suppression of acidity is clinically beneficial.

Optimizing Acid Suppression for Treatment of Acid-Related Diseases

The interaction between smoking and the effect of histamine H2-antagonists on intragastric acidity was examined in a double blind double dummy placebo controlled study. Healthy volunteers, 11 smokers and 10 non-smokers, were given, on four separate days at least one week apart, either placebo or cimetidine 800 mg nocte or ranitidine 2 X 150 mg per day or ranitidine 300 mg nocte. Tablets were taken at 2115 and 0900 h. Smokers smoked a cigarette hourly from 0700 to 2300 h. Breakfast, lunch, and dinner were standardised. Intragastric acidity was measured with a combined intragastric glass electrode and a solid state recorder. The subjects were fully ambulatory. The three histamine H2-receptor antagonist regimens were less effective (p = 0.04) in smokers than in non-smokers, but the difference between acidity of smokers and non-smokers was small. Means of medians of pH during a 24-h period with placebo, cimetidine 800 mg, ranitidine 2 X 150 mg and ranitidine 300 mg were 1.6, 2.3, 3.1, and 2.7 in smokers and 1.5, 2.7, 3.2, and 3.1 in non-smokers, respectively. In a second part of the study seven chronic smokers were reexamined after acutely stopping smoking: inhibition of gastric acidity by histamine H2-receptor antagonists was similar before and after withdrawal. Smoking does not affect intragastric acidity in untreated volunteers and only slightly decreases the effectiveness of histamine H2-receptor antagonists on intragastric acidity. This effect best in part explains the unfavourable effect of smoking on healing of peptic ulcer in patients treated with these drugs.

https://gut.bmj.com/content/gutjnl/28/5/549.full.pdf

Does smoking interfere with the effect of histamine H2-receptor antagonists on intragastric acidity in man?

The antisecretory effect of a once daily dose of ranitidine and famotidine was examined after administration of the drugs either immediately after dinner or 3 h after dinner. A placebo-controlled mult

Reduction of gastric acidity with ranitidine or famotidine: early evening dosage is more effective than late evening dosage.

Ambulatory intragastric pH-metry is a suitable method of assessing gastric acidity under conditions of normal daily life. A detailed profile of intragastric acidity is given which is a reproducible individual characteristic. There is a circadian rhythm of gastric acidity in which pH rises during the night and after meals. pH-metry was used to determine the effects of H2-antagonists and antacids, and the results are the basis for the clinical use of intragastric pH-metry.

[Continuous intragastric pH-metry].

H 2 antagonists are more effective after early evening intake than after late intake

Doessmoking interfere withtheeffect ofhistamine H2-receptor antagonists onintragastric acidity inman?

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