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Biomedical subjects

M Y Morgan

Publications and source records attributed to M Y Morgan.

At least 55 records · Page 3Linked to original sources
PubMed1987

The measurement of 1,2-propanediol, D, L-2,3-butanediol and meso-2,3-butanediol in controls and alcoholic cirrhotics.

Plasma 1,2-propanediol, D,L,-2,3-butanediol and 2,3-meso-butanediol were measured in 29 patients with biopsy proven alcoholic cirrhosis and 10 control subjects, none of whom had measurable blood alcohol levels. None of these compounds were present in control subjects at level above 5 nmol/ml. Seventeen (59%) of 29 serum samples drawn from patients with alcoholic cirrhosis contained 1,2-propanediol in concentrations above 5 nmol/ml (range less than 5.0 nmol/ml-35.4 nmol/ml, median 5.6), 8 (28%) of 29 samples contained D,L-2,3-butanediol in concentrations above 5.0 nmol/ml (range less than 5.0 nmol/ml-211 nmol/ml) and 7 (25%) of 29 samples contained meso-2,3-butanediol in concentrations above 5.0 nmol/ml (range less than 5.0-63.4 nmol/ml). In alcohol abstinent patients with alcoholic cirrhosis elevated serum 2,3-butanediol is due neither to ingestion of diols from undistilled alcoholic beverages nor is it likely to arise directly from the metabolic products of ethanol. In future studies on the origin of 2,3-butanediol in alcoholic patients biopsy evidence of the degree of associated liver damage should be obtained.

Alcoholism↗
PubMed1987

Reductions in breath ethanol readings in normal male volunteers following mouth rinsing with water at differing temperatures.

Blood ethanol concentrations were measured sequentially, over a period of hours, using a Lion AE-D2 alcolmeter, in 12 healthy male subjects given oral ethanol 0.5 g/kg body wt. Readings were taken before and after rinsing the mouth with water at varying temperatures. Mouth rinsing resulted in a reduction in the alcolmeter readings at all water temperatures tested. The magnitude of the reduction was greater after rinsing with water at lower temperatures. This effect occurs because rinsing cools the mouth and dilutes retained saliva. This finding should be taken into account whenever breath analysis is used to estimate blood ethanol concentrations in experimental situations.

Adult↗
PubMed1986

Famotidine pharmacokinetics following oral and intravenous administration in patients with liver disease: results of a preliminary study.

The pharmacokinetics of famotidine were studied following single oral and intravenous 20-mg dose administration and after multiple oral 40-mg doses in 11 patients with alcohol-related cirrhosis of varying severity and in five healthy control subjects. No significant differences were observed, following single intravenous administration, in mean plasma famotidine half-lives or in mean plasma famotidine clearance values between the cirrhotic and control groups. Equally, values for mean maximum plasma famotidine concentrations and for mean times to peak plasma concentrations, estimated following single oral administration, were comparable between the groups. The mean (+/- s.d.) systemic availability of the drug, estimated from the areas under the curves, was 36 +/- 24% in the control subjects and 46 +/- 24% in the patients with cirrhosis. No significant increases were observed in trough plasma famotidine concentrations following multiple oral doses in the patients with cirrhosis and there was no evidence of drug accumulation. No significant changes were observed in psychometric performance in any of the patients or control subjects during the multiple-oral-dose study. Thus no significant changes occur in famotidine disposition in patients with cirrhosis even when their disease is decompensated. No reduction in drug dosage should therefore be necessary in these patients. Famotidine may produce less neurological side effects in patients with liver disease than the histamine H2-receptor antagonists used currently.

Administration, Oral↗
PubMed1985

Plasma 3-methylbutanal in man and its relationship to hepatic encephalopathy.

3-Methylbutanal is a volatile aldehyde which in the rat is derived, at least in part, from colonic bacterial breakdown of leucine. It has been proposed as a toxin of importance in the pathogenesis of hepatic encephalopathy in man. A rapid, reliable and highly reproducible method for estimating 3-methylbutanal in plasma is described using a gas-chromatograph with a head space-sampler. The mean plasma 3-methylbutanal concentration in non-fasting patients with hepatic encephalopathy, 0.244 mumol/litre (range 0-1.30) was not significantly different from the mean value in controls, 0.116 mumol/litre (0-0.349). Oral leucine feeding resulted in significant increases in plasma 3-methylbutanal concentrations in both control subjects and patients with cirrhosis. Peak leucine and 3-methylbutanal values occurred at approximately the same time and usually within 120 min of leucine ingestion. Pre-treatment with neomycin had no effect on the results of leucine feeding. No changes occurred in the clinical condition or psychometric performance of patients with cirrhosis fed leucine despite increases in plasma 3-methylbutanal of up to 700% over basal values. In man plasma 3-methylbutanal, at least in part, derives from ingested leucine independently of the action of colonic bacteria. The role of this compound in the pathogenesis of hepatic encephalopathy in man needs further exploration.

Administration, Oral↗
PubMed1985

Cholestatic jaundice in the haemolytic-uraemic syndrome: a case report.

The haemolytic-uraemic syndrome is the term used to describe the symptom complex of acute oliguric renal failure, haemolysis, and thrombocytopaenia. The pathogenesis of the syndrome is unknown though several factors have been postulated as important. Gastrointestinal disease is now recognised as a regular feature of the syndrome but hepatic involvement is uncommon and limited to occasional jaundice, hepatosplenomegaly and rises in serum transaminase values. A patient is described in whom cholestatic jaundice occurred during the prodromal illness. Its presence is unexplained but might indicate infection with an unrecognised hepatotropic agent or else lack of enteral nutrition during the prodromal phase.

Adolescent↗
PubMed1985

Lactitol in the treatment of chronic hepatic encephalopathy: an open comparison with lactulose.

Lactulose is currently the drug of choice for the treatment of hepatic encephalopathy. It is, however, only available as a syrup which is contaminated with other sugars. Consequently patients may express aversion to its excessively sweet taste and many experience nausea because of its hyperosmolarity. Lactitol is a disaccharide analogue of lactulose which can be produced as a pure crystalline powder with a low relative sweetness. Theoretically it should have the same therapeutic effects as lactulose but fewer side effects. Five patients with chronic hepatic encephalopathy on maintenance lactulose were monitored clinically, psychometrically, and by measurement of venous blood ammonia, electroencephalogram mean cycle frequency, and cerebral blood flow during three months treatment with lactulose and a similar period on lactitol. Lactitol was at least as efficacious as lactulose but was more acceptable because its cathartic effect was more predictable, its formulation was more convenient and its less sweet taste preferred. Lactitol is the ideal successor to lactulose for treatment of this condition.

Adult↗
PubMed1985

Use of CAT scanning in the diagnosis and management of hepatic artery aneurysm.

Hepatic artery aneurysms occur infrequently and are often difficult to diagnose. Non-invasive procedures such as ultrasound or computer assisted tomography have not been considered suitable for definitive diagnosis and angiography is usually required. A patient is described in whom a mycotic hepatic artery aneurysm developed during the course of subacute bacterial endocarditis. The definitive diagnosis was made using computer assisted tomography with intravenous contrast enhancement and angiography was undertaken only as a prelude to transcatheter embolisation. The same technique was used to monitor progress after embolisation precluding the need for follow up angiography. As 80% of patients with hepatic artery aneurysm present for the first time after aneurysm rupture, the mortality associated with this condition is high. More widespread use of intravenous contrast enhanced tomography for abdominal examination in patients with unexplained abdominal pain might result in earlier diagnosis of this condition.

Adolescent↗
PubMed1985

Double-blind controlled trial of bromocriptine, chlordiazepoxide and chlormethiazole for alcohol withdrawal symptoms.

Seventy-one patients undergoing withdrawal from alcohol were randomly assigned to treatment with oral bromocriptine, chlormethiazole or chlordiazepoxide. Forty-one percent had alcoholic hepatitis and/or cirrhosis. Patients were stratified into two groups: major and minor withdrawal symptoms. The latter group included a placebo tratment. Bromocriptine was ineffective in treating withdrawal symptoms, whilst chlormethiazole and chlordiazepoxide were equally effective. These findings do not support the evidence from animal and clinical studies suggesting that the disturbances in the dopaminergic system found in alcohol dependence and withdrawal can be reversed by dopamine agonists.

Adult↗
PubMed1984

Bromocriptine-associated ototoxicity.

Three patients treated with bromocriptine for chronic hepatic encephalopathy showed audiometric evidence of bilateral sensori-neural hearing-loss. Audiometrically, the hearing improved in all three patients when the bromocriptine dosage was reduced, thus suggesting that this drug may produce a reversible ototoxicity.

Adult↗
PubMed1984

Impaired oxidation of debrisoquine in patients with perhexiline liver injury.

Perhexiline maleate is an antianginal agent which depends on hepatic oxidation for its elimination. Its use may be complicated by the development of peripheral neuropathy and liver damage. The majority of patients with perhexiline neuropathy have an impaired ability to effect metabolic drug oxidation which is genetically determined. Information has not been available on drug oxidation capacity in patients with perhexiline liver injury. Drug oxidation was measured using an oxidation phenotyping procedure in four patients with perhexiline liver injury and in 70 patients with chronic liver disease serving as a control group. All four patients with perhexiline liver damage showed a substantial metabolic defect; three of the four patients (75%) showed a genetically determined impairment of oxidation capacity. The incidence of severely impaired oxidation capacity in the perhexiline group was significantly greater than in the patients with chronic liver disease (6/70; 8.6%) and in the healthy population (9%) (F = 0.0048). A clear association exists between perhexiline liver injury and diminished drug metabolic activity, suggesting that the propensity to develop perhexiline liver injury is, at least in part, genetically determined.

Adolescent↗
PubMed1982

Hepatic iron stores and markers of iron overload in alcoholics and patients with idiopathic hemochromatosis.

Liver iron concentrations were determined in 60 alcoholics with liver disease of varying severity, 15 patients with untreated idiopathic hemochromatosis, and 16 control subjects with biliary tract disease. Mean liver iron concentrations (microgram/100 mg dry weight) were significantly greater in the alcoholics (156.4 +/- 7.8 (SEM); P less than 0.05) and in patients with idiopathic hemochromatosis (2094.5 +/- 230.7; P less than 0.01) than in control subjects (53.0 +/- 7.0). Liver iron concentrations of greater than 140 micrograms/100 were found in 17 alcoholics (29%) and in all 15 patients with idiopathic hemochromatosis. Liver iron concentrations greater than 1000 micrograms/100 mg were found in all patients with idiopathic hemochromatosis but in none of the alcoholics. In the alcoholics no relationship existed between liver iron concentrations and the amount of alcohol consumed daily, the length of the drinking history, the amount of beverage iron consumed daily, or the severity of the liver disease. Serum ferritin concentrations reflected iron stores in patients with hemochromatosis and in alcoholics with minimal liver disease. However, in alcoholics with significant liver disease serum ferritin concentrations did not reflect iron stores accurately, although with normal values iron overload is unlikely. Serum iron concentration and percentage saturation of total iron-binding capacity were of little value in assessing iron status in either alcoholics or patients with hemochromatosis. Measurement of the liver iron concentration clearly differentiates between alcoholics with significant siderosis and patients with idiopathic hemochromatosis.

Alcoholism↗