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Biomedical subjects

T J Chen

Publications and source records attributed to T J Chen.

At least 145 records · Page 8Linked to original sources

Acute exacerbation in hepatitis B e antigen positive chronic type B hepatitis. A clinicopathological study.

During a 6-year (mean 24.5 months) follow-up study of 237 HBeAg-positive patients with biopsy-verified chronic type B hepatitis, 199 episodes of acute exacerbation (SGPT greater than 300 IU/l) were observed in 148 patients. The clinical and laboratory findings of these acute exacerbations were less severe than classic acute viral hepatitis (P less than 0.001) but with remarkable overlapping. The main histological changes of acute exacerbations were those of lobular hepatitis, even with bridging hepatic necrosis which predicted subsequent HBeAg clearance. Anti-HBc IgM was positive in 14.4% of the exacerbations. All of these findings made acute exacerbation of chronic type B hepatitis indistinguishable from acute viral hepatitis aside from chronic clinical history. Hepatitis A virus, delta agent and possibly non-A, non-B virus(es) were responsible for some of the episodes of clinical exacerbations.

Acute Disease↗

Correlation of age with the status of hepatitis B virus replication and histological changes in chronic type B hepatitis.

The interrelationships of age, hepatitis B virus (HBV)-DNA, hepatitis B e antigen (HBeAg)/antibody (anti-HBe) and hepatic histological changes were examined in a large series of patients with chronic type B hepatitis. A significant inverse relationship between serum levels of HBV-DNA and the age of patients was demonstrated:a high level of HBV-DNA (greater than 500 pg/ml) was found in 100%, 50%, 34%, 10% and 0% of patients in the second, third, fourth, fifth and sixth decade, respectively (P less than 0.001), whereas serum HBV-DNA was negative in 0%, 6%, 8%, 40%, and 50% of cases in the respective decades (P less than 0.001). The correlation of HBV-DNA with age was more pronounced in the HBeAg-negative cases, of whom 81.3% (13/16) of patients below age 40 were positive for HBV-DNA, in contrast to 33.3% (3/9) of those over 40 years (P less than 0.05). In addition, the mean age increased from 25.3 years for HBeAg-positive patients with chronic persistent hepatitis (CPH) and nonspecific reactive histological changes (NSRH), to 32.7 years for HBeAg-positive and 34.9 years for anti-HBe positive patients with chronic active hepatitis and chronic lobular hepatitis (P less than 0.001), and 40.9 years for anti-HBe positive CPH and NSRH (P less than 0.001). These data suggested that age correlated closely with the status of HBV replication and hepatic changes in chronic type B hepatitis.

Adolescent↗

Chronic hepatitis with nonspecific histological changes. Is it a distinct variant of chronic hepatitis?

A longitudinal follow-up study has been undertaken in 62 patients with clinicopathologically verified chronic hepatitis with non-specific reactive histological changes (NSRH) in comparison with 28 patients with chronic persistent hepatitis (CPH), the clinical features of which are quite similar to NSRH. In contrast to the stationary and non-progressive course of CPH, 45.2% of patients with NSRH, either HBsAg positive or negative, ran a fluctuating course with moderate to marked elevation of SGPT (greater than 200 IU/l) In HBsAg-positive patients, only those positive for HBeAg and a few negative for both HBeAg and anti-HBe had fluctuating courses. In addition, patients with apparent clinical and biochemical changes could show histological features of chronic lobular hepatitis (CLH). A few developed chronic active hepatitis and/or cirrhosis on follow-up biopsy. It is concluded that NSRH is a form of chronic hepatitis different from CPH, but similar to or representing a phase of CLH. It is suggested that NSRH should be categorized as CLH in the classification of chronic hepatitis.

Adolescent↗

Giant intracranial Masson's hemangioma. Report of a fatal case.

A giant intracranial Masson's hemangioma (intravascular papillary endothelial hyperplasia) arising from the meninges occurred in an infant. The outcome was fatal. The associated thrombocytopenia linked Masson's hemangioma to the Kasabach-Merritt syndrome.

Angiography↗

The etiology of acute viral hepatitis in an endemic area of hepatitis A and B.

To understand the etiology of acute viral hepatitis in an endemic area of hepatitis A and B, serological markers of hepatitis were studied by radioimmunoassay in a consecutive series of 145 adult patients with biopsy-verified acute viral hepatitis. Seven (4.8%) were classified as hepatitis A, 92 (63.5%) as hepatitis B, and 46 (31.7%) as hepatitis non-A, non-B. Most persons with severe acute viral hepatitis were hepatitis B antigen (HBsAg)-positive, and hepatitis A appears to play a minor role if any. The evidence also implies that non-B hepatitis may have occurred intercurrently in chronic HBsAg carriers in this area.

Adolescent↗

Uterine progesterone receptor: stabilization and physicochemical alterations produced by sodium molybdate.

Incubation of hamster uterine cytosol with millimolar concentrations of sodium molybdate prior to addition of labeled steroid increased recovery of progesterone receptor 2-fold. This stabilizing effect of molybdate was also manifest on gel electrophoresis of the receptor. In the absence of molybdate, no specific [3H]progesterone binding was detectable on polyacrylamide gel electrophoresis. But, in the presence of 5 mM sodium molybdate, a [3H]progesterone-binding species was clearly evident on the gels. The radioactivity associated with this binding was displaceable by unlabeled progesterone but not by cortisol and depended on the concentration of [3H]progesterone employed, suggesting that this binding species is a progesterone receptor. Molybdate treatment produced a small increase in receptor size on low-salt sucrose gradients (from 6-7 to S to 7.5 S). There was no effect of molybdate of receptor sedimentation in the presence of high salt (0.3 M KCl). Further analysis of this phenomenon by gel filtration suggested that this molybdate-mediated increase in receptor size was due to receptor aggregation. In low-salt buffers, molybdate treatment markedly increased the proportion of receptors contained in large aggregates (Stokes radius greater than 8.0 nm). Again, this effect was abolished in the presence of high salt. In conjunction with receptor stabilization, molybdate prevented binding of uterine progesterone receptor to DNA--cellulose. These findings suggest that sodium molybdate stabilizes the unliganded, unactivated form of the receptor. Moreover, these effects seem to be mediated through a direct interaction of molybdate with the receptor, one which results in receptor aggregation.

Animals↗