Peter I. Reed

RANITIDINE AND CIMETIDINE IN PREVENTION OF DUODENAL ULCER RELAPSE: A Double-blind, Randomised, Multicentre, Comparative Trial

In a comparative trial of preventive medication for duodenal ulceration with 51 participating centres, 484 patients were recruited for a years maintenance treatment with the recommended bedtime dose of ranitidine (150 mg; n = 243) or cimetidine (400 mg; n = 241). These outpatients had recently healed duodenal ulcers, confirmed by endoscopy before and after healing, and ulcer relapse was monitored by endoscopy every 4 months. The distribution of factors likely to influence ulcer recurrence was similar in the two treatment groups. A life-table method of analysis showed that the ulcer relapse rate was consistently and significantly lower on ranitidine that on cimetidine (8% v 21%, p = 0.0018 at 4 months; 14% v 34%, p less than 0.0001 at 8 months; and 23% v 37%, p = 0.004 at 12 months). Crude relapse rate calculations, which underestimate the probability of ulcer recurrence, also confirmed the significant superiority of ranitidine 150 mg over cimetidine 400 mg nightly in preventing ulcer recurrence throughout the year.

Susceptibilities of drugs to nitrosation under simulated gastric conditions

Drugs of differing structures and pharmacological actions have been incubated at 37 degrees C and pH 2.0 under conditions simulating those within the normal fasting stomach. The nitrite concentration (25 microM) was kept as constant as possible for 3 hr in an attempt to mimic its in vivo replenishment from the saliva. The extents of N-nitrosation varied widely, but were less than those observed by Gillatt et al. (Fd Chem. Toxic. 1984, 22, 269) using the WHO Nitrosation Assay Procedure, in which the initial nitrite concentration is 40 mM, 1600 times greater, and the pH (3.0) is close to the optimum for the N-nitrosation of secondary amines. The highest yield of N-nitroso compound was obtained with the benzathine salt of penicillin G whereas some drugs, including hydrochlorothiazide and chlorthalidone, produced no detectable N-nitroso derivative. The degree of N-nitrosation was consistently reduced when the initial nitrite concentration of 25 microM was not replenished during the incubations, underlining the importance of simulating the continuous supply of nitrite from the saliva. In all instances, the reactions of the drugs with nitrous acid were inhibited and, in most cases, completely prevented by the presence of ascorbic acid (125 mg).

N-nitroso compounds in the gastric juice of normal controls, patients with partial gastrectomies, and gastric cancer patients

It has been suggested that the variation of biochemical and microbiological parameters in the gastric juice may play a role in the development of gastric cancer. In the present study we concurrently assessed the presence of N‐Nitroso compounds (NOC) and their precursors, bacteria and carcinoembryonic antigen (CEA) in the gastric juice of normal controls, patients with gastric resection, and advanced gastric cancer.

Method for group determination of total N-nitroso compounds and nitrite in fresh gastric juice by chemical denitrosation and thermal energy analysis.

A method for the determination of total N-nitroso compounds (NOC) and nitrite in fresh human gastric juice is described, which is based on earlier methods. A freshly obtained gastric juice sample is injected directly into refluxing ethyl acetate containing glacial acetic acid, HCl and HBr to determine the total concentration (A) of nitrite, total NOC and thermo- and acid-labile thermal energy analyser (TEA)-responsive compounds (TAC). Another fresh sample of the same juice (with or without the addition of sulfamic acid) is injected directly into refluxing ethyl acetate containing glacial acetic acid and HCl for determining the TAC level (B) and the total level (C) of nitrite and TAC. The NO released from nitrite, TAC and NOC is detected by TEA acting as a chemiluminescence detector. The differences between A and C and between C and B represent the concentrations of total NOC and nitrite, respectively. The method is rapid, reproducible (relative standard deviation 1-6%) and sensitive (detection limit 1.0 pmol). The behaviour of nitrite and NOC in the analytical system was studied and relevant techniques for the direct analysis of fresh gastric juice samples and for stabilization of fresh samples have been developed.

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Diet and Gastric Cancer

Although the causation of gastric cancer (GC) is complex and multifactorial the role of diet as a modulator of GC incidence has received wide recognition in recent years in the light of the progressive reduction of this cancer during the past four decades. Numerically it is still the second most common cancer world-wide and in many developing countries the most common Thus the magnitude of the problem varies with the degree of development — overall in developing countries GC ranks second after cervical cancer, while in developed countries it ranks fourth after lung, colorectal and breast cancer. There are large differences in incidence among populations, with a 2–3 fold excess in males and it increases with age in both sexes. An inverse socioeconomic as well as a North-South geographical gradient have been observed in most populations in the Northern hemisphere (Muir et al., 1987). An increased risk has been linked to certain occupations including coal mining, fishing and agriculture, and since occupations are clearly linked to socioeconomic status some of the observed excess risk might be attributable to dietary habits. The gradual decline in GC in many populations may be a reflection of the improving economic conditions (Hirayama, 1980). Epidemiological studies in migrants in the USA have also greatly helped in our understanding of the dynamics of GC and its precursor lesions. Migrants from high risk areas