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Biomedical subjects

G K Shaw

Publications and source records attributed to G K Shaw.

At least 55 records · Page 3Linked to original sources
PubMed1982

Computerized tomography of the brain in chronic alcoholism: a Survey and follow-up study.

One hundred male alcoholics from an inpatient treatment unit were examined by computerized axial tomography. All were without clinically overt signs of brain damage. Fifty age-matched normal volunteers were used for comparison. Radiological indices differed markedly between the two groups, reflecting a high incidence of cortical shrinkage and ventricular dilatation among the alcoholics. Clinicoradiological correlations are discussed and the results of follow-up with rescanning are reported. Abstinence appeared to be strongly related to slow partial resolution of the CT scan changes.

Adult↗
PubMed1982

Blood vitamin status (B1, B2, B6, folic acid and B12) in patients with alcoholic liver disease.

Blood vitamin status (B1, B2, B6, folic acid and B12) was assessed in 41 patients (M = 39; F = 2) with alcoholic liver disease. Biochemical evidence of thiamine deficiency was observed in all groups of patients. Deficiency of riboflavin was detected in patients with histologically normal liver but not in other groups. All the groups were found to be deficient in pyridoxal-5-phosphate--the active form of vitamin B6 (pyridoxine). Serum folate was decreased in all groups except in those with alcoholic hepatitis: red cell folate was, of course within normal limits in all the groups. Vitamin B12 levels were within normal limits in all groups except the cirrhotic one where it was raised. Clinico-biochemical implications of the findings are discussed. Biochemical changes in blood vitamin status may precede clinical manifestations of a disease process and may have prognostic value.

Adult↗
PubMed1981

Thyroid status in chronic alcoholics.

Serum thyroxine (T4), triiodothyronine (T3) and thyrotrophin (TSH) were measured by radioimmunoassay in 39 chronic alcoholics on admission. Two patients had a reduced circulating serum T4 and eight showed a low serum T3 level but basal TSH was not raised in any of the 39 patients. Interestingly, low T4 and T3 levels returned to normal after abstinence and high protein and vitamin supplemented diet for one week. It is clear from our observations that a normo- or hypo- rather than a hypermetabolic or hyperthyroid state is more common in drinking chronic alcoholics. Ethanol-induced "low T3 syndrome" has also been described and a mechanism of its pathogenesis is suggested.

Adult↗
PubMed1981

Vitamin utilization status in chronic alcoholics.

Chronic alcoholics are very often found to be deficient in vitamins. The object of the study was to assess the vitamin utilization of twelve drinking chronic alcoholics after intravenous therapy with polyvitamins. The following enzyme activation tests in red blood cells were used: a) Erythrocyte transketolase (ETK) activity for B1; b) Glutathione reductase (EGR) activity for B2; c) Pyridoxal-5-phosphate (PALP)--the active metabolite of vitamin B6 (pyridoxine) was directly estimated in red blood cells. Seven out of 12 patients were deficient in B1 before treatment; 6/12 in B2 and 11/12 in PALP. But all returned to normal after treatment; mean plus or minus SD of ETK activation co-efficient improved from the pre-treatment level of 1.174 plus or minus 0.135 to 1.001 plus or minus 0.009 (adequate less than or equal to 1.15); mean plus or minus SD of EGR activation coefficient from 1.265 plus or minus 0.333 to 1.015 plus or minus 0.072 (adequate less than or equal to 1.19) and PALP rose from 6.78 plus or minus 6.47 to 60.68 plus or minus 85.85 after treatment (adequate = vv10-20 ng/ml). These observations indicate the need for relevant vitamin supplementation in chronic alcoholics and also support the inclusion of intravenous polyvitamins in conventional detoxification regime for chronic alcoholics.

Adult↗
PubMed1981

Vitamin C utilization status in chronic alcoholic patients after short-term intravenous therapy.

Blood (leukocytic) ascorbic acid (vitamin C) levels were estimated in 25 chronic alcoholics (M = 21; F = 4; Age: mean +/- S.D. = 46.28 +/- 8.78; range 28-61 years) on admission before starting any treatment and on the sixth day following intravenous therapy with vitamin C -- 500 mg daily for 5 days. Twenty-four out of 25 patients (96%) were found to be deficient in blood vitamin C (mean +/- S.D. = 68.44 +/- 28.13; range = 28-148; normal range for control population = 120-300 nmol/10(8) W.B.C.). The status of blood vitamin C was significantly improved after the replenishment therapy with I/V vitamin C 500 mg daily for 5 days (mean +/- S.D. = 108.32 +/- 34.98 nmol/10(8) W.B.C.: range = 54-282.5; t = 3.76; P = less than 0.001). Still the levels did not return to within the normal range in 16 patients out of 25 (64%). In view of the biochemical deficiency of vitamin C in chronic alcoholics, it is suggested that conventional detoxification therapy for ethanol withdrawal syndrome should include polyvitamins including ascorbic acid. It is further suggested that more prolonged replenishment therapy with vitamin C, preferably by intravenous route, may be needed to normalize its blood levels in some chronic alcoholic patients.

Adult↗
PubMed1980

The effect of naftidrofuryl ('Praxilene') on hepatic microsomal enzymes.

A double-blind, placebo-controlled trial was carried out in 32 male patients to assess the effect of naftidrofuryl (40 mg i.m. 3-times for 6 days) on their serum gamma-glutamyl transpeptidase (GGT) levels. This enzyme is one of the hepatic microsomal enzymes and is now considered to be a reliable biochemical marker of enzyme induction. Measurements of serum GGT before and after treatment showed that there was no significant difference in levels between the two groups of patients. The results showed that naftidrofuryl did not increase serum GGT levels, in fact the mean post-treatment levels (36.06 +/- 10.63 I.U./l) were found to be lower than those before treatment (60.59 +/- 28.37 I.U./l). It is concluded, therefore, that naftidrofuryl may not induce hepatic microsomal enzymes and that interference with rates of metabolism, via enzyme induction, of other drugs used concurrently need not be anticipated.

Adult↗