Effect of different foods on the acidity of the gastric contents in patients with duodenal ulcer: Part I A comparison between two `therapeutic' diets and freely-chosen meals

Lennard-Jones, J E; Babouris, N.

doi:10.1136/gut.6.2.113

Cited by 59 publications

(11 citation statements)

References 11 publications

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“…The pH of the stomach can frequently rise above pH 4 while that in duodenal lumen is usually above this value. 26 27 Under these circumstances, in patients with peptic ulcer, in contrast with those without, more persistent erosion of the mucus barrier might be expected, even though the corrosive effect of the high acid will be absent. Duodenal mucus like gastric mucus has been shown to be digested by pepsin.…”

Section: Resultsmentioning

confidence: 99%

Mucus degradation by pepsin: comparison of mucolytic activity of human pepsin 1 and pepsin 3: implications in peptic ulceration.

Pearson¹,

Ward²,

Allen³

et al. 1986

Gut

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SUMMARY The ability to digest mucus, mucolytic activity of isolated pepsins and samples of human gastric juice has been assayed by measuring the fall in viscosity when incubated with purified pig gastric mucus glycoprotein. Pure human pepsin 1, the peptic ulcer associated pepsin, digested gastric mucus glycoprotein at a faster rate than did pure human pepsin 3 (the principal human pepsin), or the equivalent pig pepsin (pepsin A). At pH 2-0 pepsin 1 had twice the mucolytic activity of pepsin 3. Above pH 3X8 this difference became more marked and whereas pepsin 1 caused substantial mucolysis up to and including pH 5-1, pepsin 3 had minimal activity. At pH 4X0 pepsin 1 had six times the mucolytic activity of pepsin 3. Gastric juices from patients with duodenal ulcer each exhibited substantial mucolytic activity between pH 2 to 5, similar to that of pepsin 1. In contrast, gastric juice from non-symptomatic volunteers exhibited little mucolytic activity above pH 4. Analysis of the mucus glycoprotein by gel filtration showed that an increase in lower molecular weight, pepsin degraded, glycoprotein was associated with the fall in mucus viscosity for all enzyme preparations. These results showed that pepsin 1 can digest the mucus more effectively than pepsin 3 and at higher pH values. The raised concentrations of pepsin 1 in the juice of peptic ulcer patients may thus promote the ulcerative process by increased erosion of the mucus barrier under conditions likely to pertain in the duodenal bulb as well as the stomach.The mucus:bicarbonate barrier is considered to be an important component of the gastroduodenal mucosal defence mechanisms against autodigestion by the gastric juices.1-3 To function as an effective barrier the adherent mucus must be present as a continuous layer, a state maintained by a balance between its secretion from the epithelial cells and its erosion by removal from the surface into the lumen.4 Factors which swing this balance in favour of degradation of the adherent mucus might therefore be expected to decrease gastroduodenal mucosal resistance and result in mucosal damage. Agents identified in such adherent mucus erosion in vivo are proteolytic degradation and mechanical sloughing. Extensive in vitro studies show that luminal pepsins are mucolytic and dissolve adherent mucus gel by breaking down the polymeric structure

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Section: Resultsmentioning

confidence: 99%

Mucus degradation by pepsin: comparison of mucolytic activity of human pepsin 1 and pepsin 3: implications in peptic ulceration.

Pearson¹,

Ward²,

Allen³

et al. 1986

Gut

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“…Serial measurements of intragastric pH are suitable for recording the effects of diet or drugs on gastric acidity (Nichol, 1939;James and Pickering, 1949;Rowlands et al, 1952;Atkinson, 1954;Kasich and Agyros, 1958;Bingle and Lennard-Jones, 1960;Vakil et al, 1963;Lennard-Jones and Babouris, 1965;Babouris et al, 1965). The major advantage of this technique is that data can be collected during a reasonably long period in subjects whose diet and activity are similar to normal life.…”

Section: Discussionmentioning

confidence: 99%

Effect of cimetidine on 24-hour intragastric acidity in normal subjects.

Pounder¹,

Williams²,

Milton-Thompson³

et al. 1976

Gut

111

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SUMMARY The effect of H2-receptor blockade on intragastric acidity was studied in nine normal males. The pH of their gastric contents was measured at hourly daytime and two hourly nighttime intervals for 48 hours. The subjects ate identical meals, drank identical volumes of fluid, and smoked the same number of cigarettes during the two study days. Their physical activity was unrestricted in a ward environment. Blood cimetidine and plasma gastrin were measured in serial blood samples. The nine subjects were treated in random sequence with cimetidine 0 8-1 *0 g on one day and placebo capsules on the other. The drug was given in four divided doses: four subjects received it before, and five after, the three main meals. All took the fourth dose at bedtime. Replicate studies in an additional subject given placebo on both study days showed good reproducibility (r = 0O80, p < 0 01). Cimetidine therapy decreased intragastric acidity in all nine subjects. The decrease was similar in the two groups taking the drug before or after meals, mean 24 h intragastric hydrogen ion activity being lowered by 70 and 72 % respectively. Nocturnal anacidity was recorded in only two of 45 samples. Administration of cimetidine before meals produced earlier and higher drug blood levels than post-prandial medication, but when it was taken after food the blood levels were highest at the time when the buffer capacity of the food was waning. Blood concentrations of cimetidine exceeded the secretory IC50 level for most of the time between doses. The results show that cimetidine 0 8-1 .0 g/day in four divided doses produces a striking and consistent decrease of intragastric acidity. Although variation in the timing of the dose in relation to meals did not affect the decrease of acidity, the absorption data suggest that patients should take the drug after meals.Cimetidine is a new histamine H2-receptor antagonist, which in man has a potency similar to metiamide for the inhibition of acid secretion stimulated by pentagastrin or food (Black et al., 1972;Black et al., 1973;Mainardi et al., 1974;Brimblecombe et al., 1975;Burland et al., 1975;Pounder et al., 1975a;Henn et al., 1975;.The thiourea residue in metiamide, which is thought to have been responsible for the reversible marrow depression that occurred in seven patients receiving the drug, has been replaced by a cyanoguanidine moiety in cimetidine.In order to determine the optimal time of medication before starting clinical trials of the new com-

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“…Cimetidine is thought to be absorbed in the small intestine and it is likely that the rapid absorption was produced by prompt gastricemptying of the 50 ml of fluid instilled 32 min before the meal. The rapid absorption and high blood levels of the drug when given before the meal were reflected in a more profound inhibition of early acid output (Table 1) but at this stage post-prandial acid secretion is buffered by the meal itself (Lennard-Jones and Babouris, 1965;Pounder et al, 1976). When cimetidine is taken with a meal, bioavailability of the drug may be prolonged because of slower absorption from the gut.…”

Section: Discussionmentioning

confidence: 99%