MISCELLANEOUS
Conclusion: Accelerated, multiple, double doses of HB vaccine progressively increased the sero-protection level and prevents HBV infection. Corresponding author: Manzoor Ahmad Wani. E-mail:
[email protected] http://dx.doi.org/10.1016/j.jceh.2015.07.159
hepatocytes in the activation of hepatic stellate cell and increased collagen synthesis. Conclusions: In mice, long-term treatment of AT drugs contributes HSC activation leading to development of hepatic fibrosis. These findings will help in understanding of the pathobiology of AT druginduced liver fibrosis. Corresponding author: . E-mail:
[email protected]
ANTI-TB DRUGS, ISONIAZID AND RIFAMPICIN PRODUCE HEPATIC FIBROSIS THROUGH A OXIDATIVE STRESSDEPENDENT MECHANISM
http://dx.doi.org/10.1016/j.jceh.2015.07.160
Suman Santra Ayan Biswas 1,2, Debasree Bishu 1,2, Gopal Krishna Dhali 1,2, Abhijit Chowdhury 1,2, Amal Santra 1,2,
CLINICO-SEROLOGICAL AND EPIDEMIOLOGICAL PROFILE OF INFECTIVE CAUSES OF HEPATITIS IN CHILDREN
1 Centre for Liver Research, School of Digestive & Liver Diseases, Institute of Post Graduate Medical Education & Research, Kolkata, India, 2Liver Foundation, West Bengal, Kolkata, India
Nidhi Soni, Shrish Bhatnagar, Kabeer A. Khan, Savitri Thakur
Miscellaneous
Background and Aims: Chronic hepatitis has emerged as a distinct clinical outcome in large DILI registries. AT drugs being the commonest DILI agents in India, we investigated the pathways that mediate the development of hepatic fibrosis in long-term treatment of AT drugs in mice. Methods: In a combined in vivo and in vitro experiment-based study, the extent of liver injury and development of hepatic fibrosis were evaluated in wild type BALB/c mice at different time points of AT drugs (cotreatment of INH 50 mg/kg and RMP 100 mg/kg body weight) treatment for 24 weeks. Markers of oxidative stress, hepatic inflammation, apoptosis and fibrosis were evaluated. In vitro studies with mediators released from INH treated E47 cells on LX2 cells were carried out to establish the pathways in greater detail. Results: Development of hepatic oxidative stress associated with increased expression of NADPH oxidase was observed in mice during long-term treatment of AT drugs in mice. Immunohistochemistry and quantitative polymerase chain reaction demonstrated a gradual increase of HSC activation during AT drugs treatment. Histological evidence of liver fibrosis was first observed at 3 months of these drugs treatment. In addition, increasing apoptosis of hepatocytes associated with duration of AT drugs treatment accelerated hepatic fibrosis, suggesting a causative contribution of apoptosis in this process. In vitro study on stable human cell lines also confirmed the involvement of mediators (products of oxidative stress) released from INH-treated
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Department of Pediatrics, Era’s Lucknow Medical College, Lucknow, India
Aims and Objectives: A prospective study. 1. To find out the prevalence of different infections in jaundiced patients of pediatric age group. 2. To correlate the clinical and epidemiological factors with hepatitis. Material and Methods: The study was done in Department of Pediatrics and Microbiology, Era’s Lucknow Medical College, Lucknow, UP. All patients aged between 1 and 18 years in the last 10 months with at least threefold rise in transaminases demonstrated in two samples, taken 24 hours apart, were included in the study. 80 Cases were examined as a part of ongoing study. Serology (Hepatitis A, B, C and E, leptospirosis, dengue, malaria, typhoid) and blood cultures (septicaemia) were performed on samples. Results: Maximum number of patients was aged <5 years (40%). Male to Female ratio was 1.3:1. Majority of patients were underweight (56.3%), there were 34 (42.5%) patients who had normal weight and 1 (1.3%) within normal weight category. A total of 58 (72.5%) patients were icteric and remaining 22 (27.5%) were anicteric. In the present study, we observed equal number of patients (27.2%) having both HAV and typhoid in anicteric group. The infective causes with their incidences were HAV (23/80) 28.75%, HBV (15/ 80) 18.75%, HCV (0/80) nil, HEV (9/80) 11.25%, Malaria + Dengue (12/80) 15%, Typhoid (12/80) 15%, Leptospira (2/80) 2.5% and others (7/80) 8.75%. Incidence of fulminant hepatic failure was maximum (15/80) among Hepatitis E cases followed by Hepatitis B (26.7%) and then Hepatitis A (13%). © 2015, INASL
JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
Corresponding author: Nidhi Soni. E-mail:
[email protected] http://dx.doi.org/10.1016/j.jceh.2015.07.161
Miscellaneous
The mortality rate observed in present study was (7/ 80) 8.8%. Conclusions: Acute infective hepatitis has varied aetiology. In our study, Hepatitis A is the most common casual agent of it. However fulminant hepatic failure was most commonly associated with Hepatitis E.
Journal of Clinical and Experimental Hepatology | June/July 2015 | Vol. 5 | No. S2 | S69–S81
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