The efficacy of tiopronin (2-mercaptopropionyl glycine) 600 mg daily in the treatment of chronic active or chronic persistent hepatitis has been assessed in a double-blind controlled clinical trial of 12 weeks involving 165 Japanese patients with histologically proven disease. Treatment with the drug was associated with a significant improvement in abnormalities of serum transaminase and gamma glutamyl transpeptidase, with reversion towards baseline values on stopping the drug. Improvement was independent of the histological classification of the disease, or HBsAg status. The drug was well tolerated with few side-effects. The results of this short-term study indicate that tiopronin may be of value in the treatment of chronic hepatitis.
To evaluate the usefulness of antithrombin III (AT III) and alpha 2-plasmin inhibitor (alpha 2PI) in early differential diagnosis of fulminant hepatitis from the severe form of acute hepatitis, the activities of AT III and alpha 2PI were measured in plasma of 15 patients with fulminant hepatitis and 6 patients with severe form of acute hepatitis. The activities of prothrombin time (PT), hepaplastintest (HPT) and thrombotest (TT) were also evaluated. The mean values and the standard errors (SE) for PT, HPT and TT were 21.1 +/- 2.6%, 14.0 +/- 1.6% and 10.3 +/- 1.7%, respectively, in the early stage of fulminant hepatitis and 25.3 +/- 2.4%, 21.6 +/- 4.6% and 15.8 +/- 3.6%, respectively, in the severe form of acute hepatitis. No significant difference in the tests between these two diseases was noted. On the other hand, the mean values +/- SE for AT III and alpha 2PI were 13.7 +/- 4.6% and 25.6 +/- 8.6% in fulminant hepatitis and 70.2 +/- 28.5% and 98.7 +/- 9.7% in the severe form of acute hepatitis. A significant difference between the two diseases was observed. From the above, it is concluded that measuring AT III and alpha 2PI along with PT, HPT and TT is useful for early diagnosis of fulminant hepatitis.
A 63-year-old female case of cancer of the colon who developed posttransfusion hepatitis A was presented. She became ill 49 days after receiving a single unit of concentrated red cells from a donor who also developed hepatitis A 10 days after donation.
The important function of Sialic acids in glycoproteins is to prolong the half life of the glycoproteins in the circulation. In this study, the sialic acid content of plasma low density lipoprotein (LDL)-apoproteins (predominantly B-100 apoprotein, a sialoglycoprotein) was analyzed together with relative electrophoretic mobility of LDL in 46 hypercholesterolemic and normocholesterolemic diabetics and non-diabetics. There was a significant positive correlation between the LDL-sialic acid content and LDL mobility either in the non-diabetics (r=0.534, p<0.01) or in the diabetics (r=0.482, p<0.02). Thus, the effect of the LDL-sialic acids upon the LDL electric charge was apparent. However, the LDL-sialic acids in the hypercholesterolemic diabetics were significantly (p<0.01) decreased to 9.64±0.63,ag/mg LDL protein (mean±s.E.) as compared with that in the normocholesterolemic diabetics (12.85±0.62,ug/mg LDL protein). Since the relatively sialic acid-poor LDL particles are rather accumulated in plasma of diabetic patients, the grade of sialylation of glycoprotein seems to have no role in the interaction with peripheral cells and therefore, the glycoprotein turnover, as far as the LDL apoproteins are concerned. ------low density lipoprotein; apoprotein B; sialic acids; diabetes mellitus Low density lipoprotein (LDL) is the final product of very low density lipoprotein (VLDL) in plasma, carrying cholesterol to the peripheral tissues together with apoprotein B, a sialoglycoprotein (Schaefer et al. 1978). LDL is produced in the circulation through the chain delipidation cascade regulated by lipoprotein lipase and during this process triglyceride portion of VLDL is removed to form cholesterol-rich LDL (Schaefer et al. 1978). In the peripheral cholesterol utilization, the LDL particles are first bound, via apoprotein B, to the specific receptor of the cell surface, followed by internalization (Goldstein and Brown 1977).It is generally believed that patients with non-insulin dependent diabetes mellitus (NIDDM) are often associated with hypercholesterolemic, the elevation of plasma LDL. However, since lipoprotein lipase activity is known to be decreased in a diabetic state including NIDDM (Taskinen et al. 1982), it is unlikely that
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