Hepatitis: Anand AC

Anand AC. · No affiliation provided · Natl Med J India. · Pubmed #12540063 No free full text.

This publication has no abstract.

Anand AC, Puri P. · Army Hospital R & R, New Delhi, India. · Trop Gastroenterol. · Pubmed #18972765 No free full text.

Abstract: Rapid evolution and development in the treatment strategy of chronic hepatitis B (CHB) has taken place in the last decade. Six agents have been so far approved by the FDA for the management of HBV infection including two parenteral drugs (interferon alpha2b and pegylated interferon alpha-2a) and four oral nucleotide/nucleosides (lamivudine, adefovir dipivoxil, entecavir, and telbivudine). The two parenteral drugs have significant side effects and limited rates of HBeAg seroconversion. Lamivudine and Adefovir have been plagued by significant levels of drug resistance.The newer drugs entecavir and telbivudine have been in focus recently with claims of increased potency, with low side effects and lesser drug resistance. While these new drugs are definitely a welcome addition to the family of antiviral drugs against HBV, they are not necessarily a cure for all the evils of their predecessors.

Anand AC, Puri P. · Department of Medicine, Armed Forces Medical College, Pune, India. · J Gastroenterol Hepatol. · Pubmed #16105116 No free full text.

Abstract: Jaundice is not an unusual accompaniment of malaria. It can occur due to intravascular hemolysis, disseminated intravascular coagulation, and, rarely, 'malarial hepatitis'. Although the primary schizogony of the malarial parasite always leads to the rupture of the infected hepatocyte, alteration of the hepatic functions is uncommonly recorded due to this event. Histologically, the hepatitis or the actual inflammation in the liver has never been demonstrated. Nonetheless, the term 'malarial hepatitis' (MH) has been used in the literature to describe the occurrence of hepatocellular jaundice in patients with Plasmodium falciparum infection. The authors' own data and review of the literature indicate that it is not an uncommon entity. In endemic areas, jaundice is seen in approximately 2.5% of patients with falciparum malaria. It also appears to be a heterogeneous syndrome and one can recognize two clinical subsets. In one group there was an acute, virulent presentation with coma, renal failure and in some cases even hemorrhagic manifestations. It is only in this setting that jaundice signified a 'severe' disease as noted by the World Health Organization action program. This presentation is often confused with acute viral hepatitis and acute hepatic failure in non-endemic areas, but can be clinically differentiated.

Seth AK, Anand AC, Gedela SR, Varma PP, Baliga KV. · Department of Gastroenterology, Army Hospital (Research & Referral), New Delhi - 110 010, India. · Indian J Gastroenterol. · Pubmed #16877833 No free full text.

Abstract: Early mortality due to hepatitis C virus (HCV)-related liver failure in renal allograft recipients in the absence of fibrosing cholestatic hepatitis is reported infrequently. We report six renal allograft recipients with HCV infection who died of rapid progression to liver failure. Of these, 2 were detected anti-HCV positive at screening prior to kidney transplantation and 4 were diagnosed after transplantation following derangement of liver function (HCV RNA positive in all 4, anti-HCV positive in 2). Median interval between kidney transplantation and derangement of liver function was 11.8 months (range 2 to 25) and median interval between transplant and death was 27 months (range 11 to 53). Liver biopsy performed during the terminal illness in 3 patients and post-mortem liver histology in 2 patients showed chronic hepatitis with mean grade of 10.2 (range 9 to 12) and stage 2.4 (range 2 to 3). None had features of fibrosing cholestatic hepatitis.

Narula AS, Hooda A, Anand AC, Patrikar S. · Department of Medicine, Armed Forces Medical College, Pune 411 040, India. · Indian J Gastroenterol. · Pubmed #16204901 No free full text.

Abstract: OBJECTIVES: The impact of hepatitis C virus (HCV) infection on the success of renal transplant is controversial. We assessed the effect of HCV infection on graft and patient survival in renal allograft recipients. METHODS : We retrospectively analyzed medical records of renal allograft recipients who were transplanted between June 1990 and March 2004. Patients were divided into those positive and negative for anti-HCV antibody. Graft and patient survival were compared between the groups. RESULTS : Of 126 patients studied (median age 34.5 years, range, 16-60; 111 men), 35 were positive for anti-HCV antibody. In seven patients, the antibodies were detected for the first time after renal transplant. Mean patient and graft survival duration in the anti-HCV negative group was longer (55 [SD 2] months [95% CI, 51-58]) than in the anti-HCV positive group (50 [SD 4] months [95% CI, 43-58]) (p< 0.05). Twenty-two patients died - 8 (22.8%) in the anti-HCV positive group and 14 (15.3%) in the negative group. In the anti-HCV positive group, infections were the cause of death in 5 patients and 3 patients died of liver cell failure. In the anti-HCV negative group, corresponding figures were 13 and one. CONCLUSION: HCV infection is a bad prognostic indicator for patient and graft survival duration in renal transplant recipients. Infections are the commonest cause of death in renal transplant recipients.

Anand AC, Nagpal AK, Seth AK, Dhot PS. · Army Hospital R and R and Armed Forces Transfusion Unit, New Delhi-l 10 010. · J Assoc Physicians India. · Pubmed #15909855 No free full text.

Abstract: BACKGROUND: Hepatitis A virus (HAV) vaccination is recommended worldwide for patients with chronic liver disease to prevent decompensation due to superinfection with HAV. India being endemic for HAV, the prevalence of pre-existing antibodies against HAV due to subclinical exposure to the virus in childhood among patients with chronic liver disease may be high and, therefore, vaccination may not be needed. However, little data are available on the prevalence of HAV antibody among patients with chronic liver disease in India. METHODS: All patients with chronic liver disease seen at Gastroenterology Center, Army Hospital R and R, New Delhi during the year 2002 and diagnosed to have either chronic liver disease were tested for the presence of IgG anti-HAV antibody in their sera (using a commercial ELISA kit). All patients with acute exacerbation or rapid deterioration of a preexisting chronic liver disease were separately studied for presence of IgM anti-HAV. In addition, a matched number of patients who attended the center due to diseases other than liver disease were also studied as controls. RESULTS: One hundred and eighty seven patients of chronic liver disease and 89 controls were studied. Mean age of these two groups was 38.6 and 42.1 years and 153 (81.8%) and 78 (87.6%) of them were males respectively. Etiology of chronic liver disease was HBV infection in 91(48.7%), HCV infection in 62 (33.2%), autoimmune chronic hepatitis in 3 (1.6%), PBC in seven (3.7%) and cryptogenic 24 (12.8%). Of these 179 (95.7%) patients tested positive for IgG anti-HAV. A total of 37 hospitalisations in 29 patients were noted during the study period due to acute exacerbation of pre-existing chronic liver disease. None of these were positive for IgM anti-HAV, while 28 were positive for IgG anti-HAV. Among the controls, 87 controls (94.6%) were positive IgG anti-HAV. The prevalence of anti-HAV positivity was similar among patients with various etiologies. CONCLUSION: Vaccination against HAV is not routinely required among patients with chronic liver disease in India as there is a very high prevalence of pre-existing antibodies in these patients. HAV superinfection as a cause of acute exacerbation of chronic liver disease was not seen in this.

Anand AC, Seth AK, Nagpal A, Varma PP, Gadela SR, Baliga KV, Dutta V, Chopra GS. · No affiliation provided · Indian J Gastroenterol. · Pubmed #15627669 No free full text.

This publication has no abstract.

Anand AC. · No affiliation provided · Indian J Gastroenterol. · Pubmed #11059198 No free full text.

This publication has no abstract.