In this study, we examined the potential influence of duodenal pH in regulating the occurrence of the interdigestive migrating myoelectric complex (IMMC). Fasting gastroduodenal motility, duodenal pH, and plasma motilin were studied in 15 healthy subjects. During phase I, duodenal pH remained stable at 7 +/- 0.2. Phase II was accompanied by a lowering of duodenal pH, which fluctuated between 2.0 and 7.5. During late phase II, the duodenal pH increased to 6.9 +/- 0.3 and remained in the alkaline range during phase III. In six of 46 episodes of the IMMC, the occurrence of gastric phase III was delayed. This was associated with a persistently low duodenal pH (< 4) during late phase II. Despite a normal cyclic increase of plasma motilin, no gastric phase III activity was observed until the duodenal pH exceeded 7.0. Further studies showed that lowering of duodenal pH by intraduodenal perfusion of HCl prevented the occurrence of gastric phase III. We concluded that regularity of IMMC is governed by duodenal pH. An alkaline pH is essential for the initiation of gastric phase III; lowering of duodenal pH prevents its occurrence despite normal cyclic increase of plasma motilin.
Parasite-specific immunoglobulin classes were determined by the ELISA in sera of 19 patients with cystic or alveolar echinococcosis before and after 2 years (+/- 4 months) of continuous treatment with mebendazole at daily doses of 35-50 mg/kg body weight. In the majority of cases IgG decreased and IgA and IgE decreased or disappeared. In contrast, four patients with progressive disease showed reverse tendencies with increasing IgG, IgA and IgE concentrations during the same period.
The biliary excretion of mebendazole has been investigated in two patients to whom it was given for the treatment of echinococcosis, although it was found to be only partly effective. Oral mebendazole was extensively metabolized and the conjugated parent substance and its metabolites were excreted in the bile. One patient without cholestasis and with normal liver function had an apparent total biliary clearance (776 ml/min) which approached the hepatic plasma flow. The other patient with cholestasis and impairment of the hepatic drug metabolizing capacity showed a drastically reduced apparent total biliary clearance of 3.8 ml/min. The average plasma level of mebendazole was significantly lower in the former and higher in the latter patient (0.06 and 0.91 nmol/ml, respectively). The data suggest that impaired metabolism and/or biliary elimination can account for the higher plasma mebendazole level in patients with liver damage.
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