Gastric emptying of two radiolabelled antacids with simultaneous monitoring of gastric pH.

The aim of this study was to assess the gastric emptying rate of two antacids using an scintigraphic technique and simultaneous monitoring of gastric pH in 16 healthy male volunteers. Ten ml of Talcid (hydrotalcite 1 g) and Maalox (Mg-Al-hydroxide), with a similar neutralization capacity, were labelled with technetium-99m using a pyrophosphate bridge. Labelled antacids were given on separate days (within 2 weeks), 1 h after a standard meal. Intragastric pH was measured for at least 4 h, using ambulatory pH-metry with a dual-crystant antimony catheter. Continuous monitoring was started 1 h prior to the meal (baseline) and lasted 3 h (post-prandial, post-antacid and final periods). The antacid capacity of labelled and unlabelled antacids was similar. The mean percentages of antacids retained in the stomach fitted a linear model. The mean half-emptying time of Talcid was 63.9 +/- 27.9 min, while that of Maalox was 57.3 +/- 23.9 min (P = NS). The recordings of gastric pH (mean values of pH for each period) showed a similar profile for both antacids. The mean pH (Maalox vs Talcid) was 1.69 vs 2.07 in the baseline period, 1.95 vs 1.93 in the post-prandial period, 1.79 vs 1.15 in the post-antacid period (P = NS) and 0.4 vs 0.52 in the final period (P < 0.05 vs prior periods). In conclusion, the gastric emptying of Talcid and Maalox was similar and pH profiles were parallel and remained unchanged for the two antacids within the first hour of intake. A significant decrease in pH was observed 1 h after intake of the antacids, suggesting a possible rebound effect.

Role of eicosanoids, nitric oxide, and afferent neurons in antacid induced protection in the rat stomach.

The mechanism underlying the mucosal protective effect of antacids is still unclear. This study shows that in rats the aluminum containing antacid, hydrotalcit, induces dose dependent protection against gastric mucosal damage caused by ethanol or indomethacin which is considerably enhanced by acidification. Hydrotalcit did not increase gastric mucosal formation or the intraluminal release of prostaglandins, and did not prevent the increase in mucosal leukotriene C4 formation in response to ethanol. Pretreatment with indomethacin did not attenuate the protective effect of unmodified or acidified hydrotalcit. Furthermore, hydrotalcit significantly reduced the gastric damage caused by indomethacin even when it was administered up to 2 hours after the ulcerogen. In indomethacin treated rats, simultaneous administration of hydrotalcit did not affect the concentrations of indomethacin in serum or inflammatory exudates nor did it attenuate the inhibition of prostaglandin release into the exudates. In hydrotalcit treated rats there was no attenuation of the increase in sulphidopeptide leukotriene release or decrease in leukocyte influx into inflammatory exudates elicited by indomethacin administration. Functional ablation of afferent neurons and inhibition of endogenous nitric oxide partially antagonised the protective effect of unmodified, but not of acidified, hydrotalcit. It is concluded that (i) the protective effect of unmodified and acidified hydrotalcit is independent of the eicosanoid system; (ii) protection against indomethacin induced gastric lesions does not require treatment before dosing of the ulcerogen and does not interfere with absorption and anti-inflammatory actions of indomethacin; (iii) endogenous nitric oxide and afferent neurons contribute partly to the effect of unmodified, but not of acidified, hydrotalcit suggesting that different mechanisms mediate their mucosal protective activity.

[Therapy of stomach ulcer--a comparison between the low dosage antacid hydrotalcite and ranitidine--results of a randomized multicenter double-blind study. Talcivent Study Group]. / Therapie des Ulcus ventriculi--Ein Vergleich zwischen dem niedrig dosierten Antazidum Hydrotalcit und Ranitidin--Ergebnisse einer randomisierten multizentrischen Doppelblindstudie. Talcivent Studiengruppe.

In a 8 week double-blind randomized multicenter trial in 159 patients with benign gastric ulcer the efficacy of hydrotalcite vs. ranitidine in expediting ulcer healing and in achieving pain relief was determined. 79 patients received hydrotalcite 1000 mg q.i.d. as tablets equalling a total neutralizing capacity of 111.2 mval and 80 patients received ranitidine (300 mg at night). Endoscopically controlled healing rates after 4 weeks of therapy amounted to 41.8% with hydrotalcite and 53.8% with ranitidine. After 8 weeks both regimen showed significant equivalent healing rates (hydrotalcite: 81.0%, ranitidine: 78.8%, p < 0.003). Ulcer pain decreased parallel in both groups. By the end of therapy 92.4% of the patients treated with hydrotalcite and 86.3% of those receiving ranitidine were free of pain. Incidence of helicobacter pylori in antral mucosal biopsies was not influenced by both treatments. We conclude that an 8-week treatment with low dose hydrotalcite therapy is as effective as ranitidine in healing benign gastric ulcers and achieving pain relief.