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Biomedical subjects

A J Arranto

Publications and source records attributed to A J Arranto.

24 records · Page 2Linked to original sources
PubMed1982

Pericellular collagen in alcoholics with liver cirrhosis.

Therapy with enzyme inducing drugs may improve the clinical state of alcoholics with liver cirrhosis. The histological changes associated with the therapy were investigated by comparing liver biopsies before and after phenobarbital and medroxyprogesterone acetate treatment, known inducers of hepatic microsomal enzyme system, in eight alcoholics with cirrhosis and two control groups, subjects with normal liver and endstage alcoholic cirrhosis. Pericellular collagen, determined morphometrically, reduced from a point value of 87.6 +/- 28.3 to 63.4 +/- 16.7 (p less than 0.01), while the fibrous septa as well as the non-fatty and fatty parenchyma did not alter significantly. Antipyrine metabolism, an index of hepatic cell function, improved from 17.4 +/- 6.4 to 45.6 +/- 22.2 ml/min (p less than 0.01). Although direct correlation between the decrease of pericellular collagen fibres and antipyrine metabolism was not significant (r = 0.410) the findings suggest that accumulation of pericellular collagen prevents mechanically and availability of the compound to the cell, thus delaying its metabolism.

Adult↗
PubMed1981

Morphologic alterations in patients with alpha-methyldopa-induced liver damage after short- and long-term exposure.

Alpha-methyldopa-induced histologic alterations were investigated in 21 patients with hepatic injury after short- and long-term exposure. Seven patients developed liver injury within 6 months and 24 after several years (mean, 5 years) of exposure. Histologic findings and clinical and biochemical data differed significantly in the two groups. Morphologic analysis of the short-term-treated group revealed marked parenchymatous degeneration, focal, confluent and massive necrosis, and inflammation. Fatty accumulation and increased fibrous trabeculae were characteristic for the patients treated for long term. All patients in the short-term-exposed group had acute and severe hepatitis. Four of them had icterus. Two patients died of hepatic coma. Patients in the long-term-treated group had for several months initially mild but increasing discomfort, dyspepsia, nausea, and colics. Liver function tests in these groups revealed differences in serum albumin, bilirubin, and transferase levels. No changes were observed in alkaline phosphatase and Thrombotest. Fat accumulation and fibrous trabeculae suggest that the alterations precede the clinical symptoms and biochemical signs of hepatitis. The findings show that alpha-methyldopa may induce hepatocellular injury after short- and long-term exposure.

Adult↗
PubMed1981

Histologic follow-up of alpha-methyldopa-induced liver injury.

Alpha-methyldopa-induced liver injury was studied in six patients by clinical, biochemical, histologic, and morphometric methods. The patients, all women, developed hepatic injury after long-term therapy lasting 2 to 8 years. Withdrawal of the drug resulted in improvement of the symptoms. Hepatitis with fibrosis and moderate to severe fatty accumulation was seen in most of the liver biopsies at onset of symptoms. Follow-up ranged from 7 to 24.5 months, at the end of which the liver function test results were in the normal range. A second liver biopsy showed significant decrease in fatty infiltration. Three patients showed a decrease in lipid content from moderate to mild or normal and two other patients from severe to moderate. A 73-year-old patient had chronic aggressive hepatitis with massive necrosis of the parenchyma after 8 years of therapy, and follow-up biopsy 12 months later showed cirrhosis. In this study alpha-methyldopa withdrawal resulted in a reduction of lipid and fibrous trabeculae content, possibly caused by alpha-methyldopa-induced derangement of liver function.

Aged↗
PubMed1981

Liver histological changes and plasma high density lipoproteins in man.

The relationship between liver histology and plasma high density lipoproteins (HDL) was investigated in 40 patients with diagnostic liver biopsy. The subjects with slight or marked changes in liver histology had low HDL cholesterol and apoprotein (A-I and A-II) levels, low HDL cholesterol/total cholesterol ratios and high triglyceride concentrations as compared with subjects with a normal liver. Plasma HDL cholesterol, HDL cholesterol/total cholesterol ratio and apoprotein A-I were directly proportional and triglycerides inversely proportional to the amount of non-fatty parenchyma in the livers. Conventional liver tests were not related to liver histology. The findings indicate that plasma HDL levels reflect alterations in hepatic parenchyma. Quantitative assessments of liver changes may hence be of significance when evaluating plasma HDL levels.

Adult↗
PubMedDate not supplied

Blood lactate, hepatic histology and microsomal enzyme activity in non-insulin-dependent diabetics.

The relationship between blood lactate levels, liver histology and microsomal enzyme activity (cytochrome P-450 content) was assessed in 32 non-insulin-dependent diabetics (NIDD) undergoing diagnostic liver biopsy. Fasting blood lactate was related to liver histology and the mean was in the low normal range in the diabetics with an intact liver, whereas higher values were noted in the diabetics with a fatty liver, inflammatory changes and an increase in fibrous trabeculae. Similarly, in the diabetics with an abnormal liver, there was a tendency for pyruvate to be elevated, and body weights and serum insulin concentrations were higher than in the NIDD with an intact liver. P-450 was inversely related to liver histology and its content was reduced in association with increases in fat and fibrous tissues. P-450 was significantly correlated with lactate (rs -0.79), pyruvate (rs -0.65) and serum insulin (rs -0.53). The results revealed close associations between blood lactate, hepatic structure and microsomal enzyme activity, and emphasize that liver function is an important consideration when lactate metabolism is evaluated in NIDD.

Aged↗