Type Of Non-alcoholic Liver Disease Research Articles

Hyperammonaemia in patients with chronic obstructive pulmonary disease and obesity: association mechanisms, detection rate and correction

To identify the frequency of hyperammonemia in patients with COPD and obesity, to analyze the degree of its influence on the COPD course and the quality of patients life, to assess the possibility of hyperammonemia correction with L-ornithine L-aspartate (LOLA). The study included 50 patients with non-acute COPD (GOLD 2), Group D, phenotype with frequent exacerbations, central-type obesity. At the 1st stage of the investigation, COPD course was evaluated, specific evaluation tests (mMRC, CCQ, CAT, SGRQ, SF-36) were used, the biochemical blood test was performed, hyperammoniemia was detected on a Pocket Chem BA PA-4140, and Number Connecting Test was performed. In the 2ndstage of the investigation, all patients were prescribed a course of treatment with LOLA and after 4 weeks the estimated parameters were compared in dynamics. After 4 weeks, comparative analysis showed reliable positive dynamics of subjective assessment of weakness, 2 scales of SGRQ questionnaire, all scales of SF-36 questionnaire, as well as reliable reduction of ammonia level by 18.26 mol/l, normal value of Number Connecting Test. Detection of hyperammoniemia in patients with COPD and obesity and its correction with LOLA seems rational in order to reduce toxic effects of ammonia on organs and systems in this category of patients.

Changes in laminin content in livers of patients with alcoholic liver disease

An increase in serum laminin levels has been reported in patients with liver disease; however, the mechanisms for this increase have not yet been clarified. In the present study, the laminin content of liver biopsy specimens obtained from patients with alcoholic liver disease and non-alcoholic liver disease was determined with a one-step sandwich enzyme-immunoassay system, using monoclonal antibodies for human placental laminin. Hepatic laminin content was significantly higher in patients with liver disease than in normal controls. In alcoholic liver disease, the content in patients with mild fibrosis was lower than in patients with advanced types of alcoholic liver disease. In non-alcoholic liver disease, the hepatic laminin content tended to increase in parallel with the progression of fibrosis. The laminin content in alcoholic liver disease was significantly higher than in the corresponding type of non-alcoholic liver disease. The ratio of laminin to total collagen content was highest in alcoholic liver disease showing mild fibrosis and decreased in parallel with the progression of fibrosis. In contrast, the ratio was low in all types of nonalcoholic liver disease. The ratio in patients with alcoholic liver disease was significantly higher than these with the corresponding non-alcoholic liver disease. Hepatic laminin content increased in parallel with the increase in hepatic type IV collagen in alcoholic liver disease, and the correlation was statistically significant. However, similar correlation was not found in non-alcoholic liver disease. These results indicate that the response to laminin synthesis to alcoholic liver disease is strong in mild fibrosis and reached a plateau at a relatively early stage of fibrosis. The stimulation for laminin synthesis in non-alcoholic liver disease is different from that in alcoholic liver disease.

Changes in type IV collagen content in livers of patients with alcoholic liver disease

An increase of serum type IV collagen levels in patients with liver disease has been reported; however, the mechanisms of this increase are not yet well known. We recently developed an assay system for type IV collagen content in liver biopsy specimens. In this study, type IV collagen content in the livers and sera of patients with alcoholic liver disease and nonalcoholic liver disease was determined. Serum and hepatic type IV collagen contents were measured with a one-step sandwich enzyme immunoassay system using monoclonal antibodies for human type IV collagen. Hepatic type IV collagen content increased significantly in liver disease. In alcoholic liver disease, type IV collagen content in patients with mild fibrosis was lower than that in advanced types of alcoholic liver disease. In nonalcoholic liver disease, hepatic type IV collagen content tended to increase with the progression of fibrosis. Type IV collagen content in alcoholic liver disease was significantly higher than that in the corresponding type of nonalcoholic liver disease. Hepatic total collagen content increased significantly in parallel with the progression of fibrosis in both alcoholic liver disease and nonalcoholic liver disease. The total collagen content in each type of alcoholic liver disease was significantly lower than that in the corresponding type of nonalcoholic liver disease. The ratio of type IV collagen to total collagen content was the highest in livers showing mild fibrosis, both in alcoholic liver disease and nonalcoholic liver disease, and decreased in parallel with the progression of fibrosis. The ratio in patients with alcoholic liver disease was significantly higher than that in those with the corresponding nonalcoholic liver disease. Hepatic type IV collagen content correlated with the intensity of the staining reactions for type IV collagen only around the sinusoidal walls in alcoholic liver disease, but not in nonalcoholic liver disease. A significant correlation was found between serum and liver type IV collagen content, although the coefficient value was not very high. These results indicate that the response of type IV collagen synthesis to liver injury is strong in mild fibrosis and reaches a plateau at a relatively early stage of fibrosis; then the content of the other types of collagen increases gradually with the progression of fibrosis. The stimulation for type IV collagen synthesis is more prominent in alcoholic liver disease than in nonalcoholic liver disease, especially at intralobular areas.

Changes in type IV collagen content in livers of patients with alcoholic liver disease

An increase of serum type IV collagen levels in patients with liver disease has been reported; however, the mechanisms of this increase are not yet well known. We recently developed an assay system for type IV collagen content in liver biopsy specimens. In this study, type IV collagen content in the livers and sera of patients with alcoholic liver disease and nonalcoholic liver disease was determined. Serum and hepatic type IV collagen contents were measured with a one-step sandwich enzyme immunoassay system using monoclonal antibodies for human type IV collagen. Hepatic type IV collagen content increased significantly in liver disease. In alcoholic liver disease, type IV collagen content in patients with mild fibrosis was lower than that in advanced types of alcoholic liver disease. In nonalcoholic liver disease, hepatic type IV collagen content tended to increase with the progression of fibrosis. Type IV collagen content in alcoholic liver disease was significantly higher than that in the corresponding type of nonalcoholic liver disease. Hepatic total collagen content increased significantly in parallel with the progression of fibrosis in both alcoholic liver disease and nonalcoholic liver disease. The total collagen content in each type of alcoholic liver disease was significantly lower than that in the corresponding type of nonalcoholic liver disease. The ratio of type IV collagen to total collagen content was the highest in livers showing mild fibrosis, both in alcoholic liver disease and nonalcoholic liver disease, and decreased in parallel with the progression of fibrosis. The ratio in patients with alcoholic liver disease was significantly higher than that in those with the corresponding nonalcoholic liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)