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Biomedical subjects

A D Thomson

Publications and source records attributed to A D Thomson.

At least 73 records · Page 4Linked to original sources
PubMed1981

Leukaemic liver infiltration in AKR mice prematurely induced by immunization with human or allogeneic liver protein.

An attempt was made to produce a model of autoimmune hepatitis in AKR mice by immunization with allogeneic liver extract or a purified (human) liver-specific lipoprotein (LSP). Although a mononuclear infiltrate was found in the liver in recipients of purified liver antigen and to a lesser degree in recipients of allogeneic extract, this was associated with the development of an acute thymus-derived leukaemia. This mouse strain is normally susceptible to leukaemia after a latent period of approximately 6 to 9 months but the immunization schedule markedly reduced the age of onset of this disease.

Animals↗
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↗
PubMed1978

Alcohol and nutrition.

Alcoholic patients frequently have evidence of nutritional deficiency the consequences of which may be seen in all systems of the body. Alcoholism is theoretically a completely preventable disorder which requires more attention by the general public, practising physicians and research workers. Rehabilitation of the established alcoholic will sometimes be limited by failure to modify behaviour or because of nutritionally induced brain damage but we are beginning to understand some of the mechanisms by which malnutrition evolves (Figure 2). Better methods must be developed to limit alcohol-induced tissue injury in patients whose drinking cannot be controlled. The final mechanisms of liver injury remain to be established. Cirrhosis may be induced in animals ingesting a good diet but this does not ensure adequate delivery and utilization of nutrients at the subcellular level. Cirrhosis takes a long time to evolve and the natural history, including longitudinal nutritional profiles in man, has not been established. Therefore, although normal liver morphology is sometimes seen in alcoholics with gross stigmata of malnutrition suggesting that factors other than malnutrition are important, it may be that critical nutrients have not been deficient for long enough in these individuals or severe depletion has been intermittent. Whether or not malnutrition is of decisive importance in the toxicity of alcoholic liver injury in man, adequate replacement is essential for protection and repair of liver cells. Established daily minimal requirements are not adequate for patients with active liver disease. Hepatocyte injury reduces the capacity of this major storage site and causes release of vitamins (co-enzymes) into the circulation in the form of holoenzymes. Liver damage reduces the conversion of nutrients into their metabolically useful forms required for catabolic processes and to meet increased needs for DNA/RNA synthesis necessary for repair of damaged cells and to replace necrotic cells. The choice and route of therapy must take account of the patient's metabolic needs and their absorptive defects. The effects of alcohol and maternal undernutrition on the fetus/neonate may cause intra-uterine death or varying degrees of brain damage, thus limiting the potential of the next generation.

Alcoholism↗
PubMed1977

Polyarteritis nodosa of the liver: a report of two cases.

Two patients with liver disease due to polyarteritis nodosa are described. They presented in a similar manner, with a swinging fever, a polymorphonuclear leucocytosis and high alkaline phosphatase levels, but the natural history of the illness was different, with revocery in one and death in the other.

Aged↗
PubMed1977

Lymphocyte cytotoxicity for isolated hepatocytes in alcoholic liver disease.

To determine whether an autoimmune reaction to liver-specific proteins occurs in alcoholic liver disease, the cytotoxic effect of lymphocytes on isolated hepatocytes was determined in 27 alcoholic patients. Cytotoxicity was demonstrated in 15 of 17 patients with a histological diagnosis of alcoholic hepatitis, but in none of 10 with other forms of alcoholic liver disease. The ability of a liver-specific membrane lipoprotein to block the reaction suggests that sensitization to this antigen is responsible for the cytotoxicity. The demonstration of cytotoxicity using T cell-depleted, but not B and K cell-depleted, lymphocytes suggests an antibody-dependent cell-mediated reaction. There was a close correlation between cytotoxicity and the presence of alcoholic hyalin, liver cell necrosis, and piecemeal necrosis, but not with other histological features, immunoglobulines, autoantibodies, or standard liver function tests. The persistence of this autoimmune response, induced in some way by alcohol or one of its metabolites, may be important in the progression of acute alcoholic hepatitis to chronic liver disease.

Acute Disease↗
PubMed1976

Autoimmune reaction to a liver specific membrane antigen during acute viral hepatitis.

Lymphocyte cytotoxicity for isolated hepatocytes has been demonstrated in 93% of cases of acute viral hepatitis tested within two weeks of the onset of symptoms. The frequency of cytotoxicity during this time was similar for HBsAg positive and negative cases. However, after this time it was significantly higher in HBsAg positive than negative cases, 90% and 25% respectively (P less than 0-01). Cytotoxicity was found in B-cell, but not T-cell, enriched fractions of lymphocytes, compatible with an antibody-dependent K-cell mediated reaction. In two cases the assay remained positive on retesting six months later, and follow-up liver biopsies showed the features of chronic aggressive hepatitis. These findings suggest that, in addition to the known immunological reactions against viral antigens that occur during the acute phase of viral hepatitis, an autoimmune reaction directed against a liver specific protein is also initiated; and if this reaction persists then chronic hepatitis may develop.

Acute Disease↗
PubMed1976

The cytotoxicity of plasma from patients with acute hepatic failure to isolated rabbit hepatocytes.

The cytotoxicity of plasma from patients with various types of liver disease to rabbit hepatocytes maintained in vitro has been investigated using a microcytotoxicity assay system. Plasma from patients with fulminant hepatic failure and uncomplicated viral hepatitis showed significant cytotoxicity compared to controls. The cytotoxic effect of plasma from patients with fulminant hepatic failure was reduced by charcoal haemoperfusion, or heating and dialysis. The bile acids chenodeoxycholic acid and lithocholic acid were cytotoxic when added to control human plasma. Such toxic factors may be responsible for the delay in liver regeneration often seen in patients with fulminant hepatic failure.

Animals↗
PubMed1975

Vitamin profile of 174 mothers and newborns at parturition.

Thiamin, biotin, B12, folate, pantothenate, riboflavin, nicotinate, B6, vitamins A, E, C, and beta-cartene was estimated in the blood of 174 mothers and in the cord blood of their neonates at parturition. A vitamin profile of normal preganancy was established for mother and neonate. This was based on values obtained from 95 percent confidence limits in 74 mothers not taking oral vitamins and 133 mothers ingesting various vitamin supllements. Circulating vitamin levels in 38 neonates born to mothers with no laboratory evidence of hypovitaminemia was persented. The higher incidence of hypobitaminemia in gravidas not taking vitamins was folate, thiamin, vitamins A, C, B12, BL and nicotinate in descending order. Ingestion of vitamins supplements reduced the incidence of hypovitaminemia. A similar relationship held for neonates from these mothers. However, despite vitamin ingestion thiamin, folate, vitamins C, A, B6, B12 and nicotinate hypovitaminemia was evident. There was an approximate 1:2-5 ratio between mother and neonate blood vitamins; vitamins A, B6, E, and beta-carotene were exceptions. Vitamin B6 ran parallel, while vitamins A, B6, E, and beta-carotene ratios reversed in favor of the mother at an approximate ratio of 2:1, 4:1 and 7:1, respectively. It is concluded that vitamin profile for mother and neonate, taking into account values established from a lorge gravid population, should now permit an evaluation of the effects of hypoviteminemia on the outcome of pregnancy and infant health.

Adult↗