Biomedical subjects
Publications and source records attributed to K J Breen.
Diet therapy is mandatory in only a very small number of GIT disorders. While the available evidence does not support its use in other conditions, many physicians will wish to make an individual decision regarding diet therapy according to the patient's symptoms, to the patient's attitudes and expectations and very importantly, to the financial and social implications of the diet in question.
An existing intensive drug monitoring system was used to study the occurrence of pseudomembranous colitis and diarrhoea in 100 patients treated with lincomycin and clindamycin. In order to give perspective to the results an equal number of matched patients treated with ampicillin were also studied. The incidences of diarrhoea in both groups were similar (11% in the lincomycin-clindamycin group and 8% in the ampicillin group). One patient developed pseudomembranous colitis associated with two prolonged courses of lincomycin therapy. The results suggest that the risks associated with the use of lincomycin are acceptable if the drug is given for the approved specific indications.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Five cases of lincomycin-clindamycin-associated acute pseudomembranous colitis, demonstrating a spectrum of clinical, histological and radiological severity, were encountered over a five-months period. All patients presented with watery diarrhoea without the passage of macroscopic blood or pus. Two patients were seriously ill with fulminant colitis, but responded rapidly to corticosteroids given parenterally and supportive therapy. The diagnosis of acute colitis should be considered in all patients developing diarrhoea during or up to three weeks after beginning therapy with lincomycin or clindamycin and can be confirmed by sigmoidoscopic examination. Withdrawal of the antibiotic and symptomatic treatment is appropriate for mild cases of colitis, but our experience suggests that corticosteroid therapy is safe and effective in severe cases. Indiscriminate use of these antibiotics should be avoided.
Explore the source record for details and available documents.
Dose-response relationships, biochemical mechanisms, and sex differences in the experimental fatty liver induced by tetracycline were studied in the intact rat and with the isolated perfused rat liver in vitro. In the intact male and female rat, no direct relationship was observed between dose of tetracycline and hepatic accumulation of triglyceride. With provision of adequate oleic acid as a substrate for the isolated perfused liver, a direct relationship was observed between dose of tetracycline and both accumulation of triglyceride in the liver and depression of output of triglyceride by livers from male and female rats. Marked differences were observed between female and male rats with regard to base line (control) hepatic concentration of triglyceride and output of triglyceride. Accumulation of hepatic triglyceride, as a per cent of control values, in response to graded doses of tetracycline, did not differ significantly between male, female and pregnant rat livers. However, livers from female, and especially pregnant female rats, were strikingly resistant to the effects of tetracycline on depression of output of triglyceride under these experimental conditions. These differences between the sexes could not be related to altered disposition of tetracycline or altered uptake of oleic acid. Depressed hepatic secretion of triglyceride accounted only for 30 to 50% of accumulated hepatic triglyceride, indicating that additional mechanisms must be involved in the production of the triglyceride-rich fatty liver in response to tetracycline.
We have previously investigated the normal characteristics of thiamine intestinal transport in rats and found that a very low concentrations (0.06 to 2.0 muM) thiamine transport is a saturable, carrier-mediated, active process while at high concentrations (greater than 2.0 muM) transport proceeds by simple diffusion. The present studies were undertaken to characterize the effect of ethanol on thiamine transport. Intact isolated loops were used to measure rates of 35S-thiamine hydrochloride absorption into the circulation in vivo, and everted jejunal segments to measure net transmural flux, unidirectional uptake, and cellular exit of 14C-thiamine hydrochloride in vitro. Intragastric administration of ethanol (50 to 750 mg. per 100 grams of weight) reduced absorption of low thiamine concentration in vivo to 65.44 per cent of control value. A similar inhibition was noted after intravenous ethanol. Once attained, the inhibition of thiamine absorption was not related to the ethanol dose or to ethanol concentration in the blood or in the intestinal lumen; this inhibition was reversible. In contrast, ethanol did not affect absorption of high concentrations of thiamine. These findings were confirmed by the in vitro results. In transmural flux studies, the movement of low, but not high, thiamine concentration against a concentration gradient was inhibited by ethanol, so that the normal serosal/mucosal ratio of 1.5 was reduced to 1.0. Ethanol did not affect unidirectional uptake into the mucosa of either low or high thiamine concentrations, but blocked cellular exit of low thiamine concentrations from the cells into the serosal compartment. Exit of high thiamine concentrations was not affected. Ouabain, like ethanol, markedly reduced cellular exit but did not influence uptake of low thiamine concentrations. The present studies suggest that ethanol adversely affects the active, but not the passive, component of thiamine transport. Moreover, ethanol appears to block thiamine exit from the cells but does not affect cellular uptake of thiamine. The similarity to ouabain action suggests that ethanol may impair active thiamine transport by inhibiting Na-K ATPase activity.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.