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Biomedical subjects

S K Sarin

Publications and source records attributed to S K Sarin.

At least 55 records · Page 3Linked to original sources
PubMed2000

Beneficial influence of an indigenous low-iron diet on serum indicators of iron status in patients with chronic liver disease.

The main Fe storage organ in the body is the liver. In patients with chronic liver disease, secondary Fe overload is common. Phlebotomy, often used in the West to reduce Fe overload to improve the efficacy of interferon therapy, is not socially acceptable in India. We assessed the efficacy of a low-Fe diet in reducing serum Fe levels. Nineteen patients with hepatitis B- and C-related chronic liver disease, ten with normal (< 25 mumol/l) baseline serum Fe levels (group A) and nine with high (> 25 mumol/l) serum Fe levels (group B) were included. All the subjects were advised to eat a low-Fe diet. The daily Fe intake was reduced approximately 50% by consumption of the rice-based diet. Haemoglobin, serum Fe, transferrin saturation index (TSI), ferritin and alanine transaminase (EC 2.6.1.2) levels were studied at 1 and 4 months. Dietary Fe intake and body weight were closely monitored. All patients complied with the dietary regimen and at 4 months significant (P < 0.001) reductions from baseline were seen in serum Fe (20 (SD 3) v. 12 (SD 4) mumol/l group A; 30 (SD 3) v. 19 (SD 7) mumol/l group B) and TSI (38 (SD 8) v. 23 (SD 9)% group A; 53 (SD 15) v. 34 (SD 13)%, group B) in both the groups, albeit earlier in group B subjects. Serum ferritin levels, however, reduced only in group A (112 (SD 62) v. 43 (SD 25) ng/ml, P < 0.05) and not in group B. Non-significant reductions in haemoglobin levels were seen in both groups. Alanine transaminase levels reduced significantly (P < 0.05) in both the groups (95 (SD 49) v. 44 (SD 25) IU/l, group A; 82 (SD 16) v. 51 (SD 14) IU/l group B). Thus, a low-Fe diet results in significant reductions in serum Fe and TSI levels, irrespective of baseline Fe levels. This diet should be evaluated to improve the efficacy of interferon therapy in patients with hepatitis B- and C-related chronic liver disease.

Adult↗
PubMed2000

The natural history of portal hypertensive gastropathy: influence of variceal eradication.

OBJECTIVE: The natural history and likelihood of bleeding from portal hypertensive gastropathy (PHG) present in patients with portal hypertension before endoscopic variceal obliteration may differ from that in patients who develop PHG during or after variceal eradication. METHODS: A total of 967 variceal bleeders who had achieved variceal eradication by endoscopic sclerotherapy in the recent past were prospectively studied. In all, 88 (9.1%) patients (cirrhosis in 54, noncirrhotic portal fibrosis in 18, and extrahepatic portal vein obstruction in 16) had distinct mucosal lesions. PHG alone was present in 78, PHG with gastric antral vascular ectasia (GAVE) in eight, and GAVE alone in two patients. PHG was graded as mild or severe and according to whether present before (group A) or after endoscopic intervention (group B). Patients underwent regular endoscopy at follow-up to see if the PHG was transitory (disappearing within 3 months), persistent (no change), or progressive. Bleeding from PHG lesions was defined as acute or chronic. RESULTS: Twenty-two (26%) patients had PHG before (group A) and 64 (74%) developed PHG after variceal eradication (group B). During a mean follow-up of 25.1 +/- 14.2 months, PHG lesions disappeared in group A in only two patients (9%), but in group B in 28 (44%) patients (p < 0.05). PHG lesions more often progressed in the former as compared to the latter (18% vs 9.4%, p = NS). The incidence of bleeding was higher in group A than group B (32% vs 4.7%, p < 0.02). Bleeding from PHG occurred in 10 patients (11.6%); seven of them were from group A, and all had either progressive (n = 3) or persistent (n = 4) lesions. CONCLUSIONS: PHG developing after variceal eradication is often transitory and less severe. If PHG is pre-existing, endoscopic therapy for varices could worsen the PHG, with a likelihood of bleeding. Such patients may be benefited by concomitant beta-blocker therapy.

Adolescent↗
PubMed2000

What is safe blood?

Explore the source record for details and available documents.

Bacterial Infections↗
PubMed2000

Prevalence of hepatitis GB virus C/hepatitis G virus infection in blood donors in India.

BACKGROUND: Hepatitis GBV-C/HGV is a newly described RNA virus with a parenteral route of transmission. It has been implicated in fulminant hepatitis and chronic viral hepatitis. We undertook to study the prevalence of GBV-C/HGV infection in blood donors of a tertiary care hospital in India. METHOD: Serum of 221 consecutive blood donors was tested for HBsAg, anti-HCV by EIA and HGV RNA by RT-PCR. Two sets of primers; one from the 5'non-coding region and other from NS5a region of the HGV genome, were used for amplification. RESULTS: Prevalence of HGV RNA was found to be very low in healthy blood donors. Only two of the 221 (0.9%) donors were found to be HGV RNA positive. HBsAg and AntiHCV were found to be present in 5.43% (12/221) and 1.31% (3/221) respectively. Dual infection was seen in two of the 221 (0.9%) patients; one patient had HBsAg and HGV RNA positivity, while the other, had HBsAg and AntiHCV positivity. CONCLUSION: GBV-C/HGV is an uncommon infection in healthy blood donors in India, especially when compared to the prevalence of HBV and HCV infection. It is therefore unlikely to be an important cause of transfusion associated hepatitis in India.

Adult↗
PubMed1999

Identification of a novel surface mutant of hepatitis B virus in a seronegative chronic liver disease patient.

Hepatitis B virus (HBV) with mutations in the envelope proteins can emerge during natural infections, vaccinations or interferon therapy and appears occasionally to escape virus elimination or detection. The implications of such mutations at the molecular level are often obscure. We report the identification of a new surface mutant of HBV. This mutant was identified, and isolated from a chronic liver disease patient, negative for HBsAg as well as other serological markers but positive for HBV DNA. Several mutations were observed in the surface antigen gene out of which a Thr118-Ala118 change was predicted to have a destabilizing effect on the structural integrity of the 'a' determinant and also alter the antigenicity profile of the mutant HBsAg. Besides a RNA hairpin loop was predicted for the transcript generated by the small surface protein of this mutant, which could have an inhibitory effect at the translational level. These observations thus indicate that mutations in the surface gene could lead to a considerable decrease or complete absence of properly folded surface antigen which in turn could explain the absence of reactive HBsAg in the serum of the patient.

Amino Acid Substitution↗
PubMed1999

Comparison of endoscopic ligation and propranolol for the primary prevention of variceal bleeding.

BACKGROUND AND METHODS: We compared propranolol therapy and endoscopic ligation for the primary prevention of bleeding from esophageal varices. This prospective, controlled trial included consecutive eligible patients who had large varices (>5 mm in diameter) that were at high risk for bleeding. The patients were assigned to either propranolol therapy, at a dose sufficient to decrease the base-line heart rate by 25 percent, or variceal ligation, to be performed weekly until the varices were obliterated or so reduced in size that it was not possible to continue treatment. RESULTS: Of the 89 patients, 82 of whom had cirrhosis of the liver, 44 received propranolol and 45 underwent variceal ligation. The mean (+/-SD) duration of follow-up in each group was 14+/-9 and 13+/-10 months, respectively. The mean time required to achieve an adequate reduction in the heart rate was 2.5+/-1.7 days; the mean number of sessions needed to complete variceal ligation was 3.2+/-1.1. After 18 months, the actuarial probability of bleeding was 43 percent in the propranolol group and 15 percent in the ligation group (P=0.04). Twelve patients in the propranolol group and four in the ligation group had bleeding. Three of the four in the ligation group had bleeding before their varices had been obliterated. Nine patients in the ligation group had recurrent varices, a mean of 3.7 months after the initial treatment. Five patients in each group died; bleeding from the varices was the cause of death of four patients in the propranolol group and of three in the ligation group. There were no serious complications of variceal ligation; in the propranolol group, treatment was stopped in two patients because of side effects. CONCLUSIONS: In patients with high-risk esophageal varices, endoscopic ligation of the varices is safe and more effective than propranolol for the primary prevention of variceal bleeding.

Adrenergic beta-Antagonists↗
PubMed1999

Granulocyte-macrophage colony-stimulating factor enhances the efficacy of hepatitis B virus vaccine in previously unvaccinated haemodialysis patients.

The response to vaccination with recombinant hepatitis B virus (HBV) vaccine is poor in haemodialysis patients. A defect in the antigen-presenting cells may be responsible for this hyporesponsiveness. To overcome this and to improve the response to HBV vaccine in dialysis patients, we used granulocyte-macrophage colony-stimulating factor (GM-CSF) as a vaccine adjuvant. Fifteen consecutive patients with chronic renal failure (CRF), commenced on dialysis, were stratified to receive either 40microg HBV vaccine (Engerix-B) at 0, 1, 2 and 6 months (group A, n=9) or 3microg kg-1 GM-CSF (Leucomax) on day 1 followed by the vaccination schedule described above (group B, n=6). All patients were negative for hepatitis B surface antigen (HBsAg), antibodies to hepatitis C virus (anti-HCV) and human immunodeficiency virus (HIV) serology. Titres of antibody to HBsAg (HBsAb) were quantitatively assayed, using enzyme-linked immunosorbent assay (ELISA), at 1, 2, 6 and 7 months from the first dose of vaccination. Only 44% of the patients in group A developed protective antibody levels (mean HBsAb: 22 IU l-1) Fifty per cent of responders developed protective antibody levels (HBsAb >10 IU l-1) only after the fourth dose of vaccination. In contrast, all six patients (100%) in group B developed protective levels of HBsAb (mean HBsAb: 70 IU l-1) (P<0.02). Sixty-seven per cent of the responders were protected after only the second dose of vaccination (P=0.046). No serious adverse effects of GM-CSF were observed in group B. Hence, haemodialysis patients respond poorly to HBV vaccine. GM-CSF is a safe vaccine adjuvant capable of stimulating an earlier and a stronger antibody response to HBV vaccine in haemodialysis patients.

Adjuvants, Immunologic↗
PubMed1999

Alpha-interferon therapy in chronic hepatitis due to active dual infection with hepatitis B and C viruses.

BACKGROUND: Nearly 14% of non-alcoholic chronic liver disease in India is related to hepatitis B virus (HBV) and hepatitis C virus (HCV) dual infection. There are no clear data available from the literature on the therapeutic management of these patients who often suffer an unfavourable course. METHODS: Fourteen consecutive cases of biopsy-proven chronic liver disease fulfilling the following criteria were included: Child's A or B liver disease, hepatitis B surface antigen positive, HBV-DNA positive, antibody to HCV positive and HCV-RNA positive. Seven patients had chronic liver disease (group I), while the remaining seven patients (group II) had additional disorders (non-Hodgkin's lymphoma (two), acute leukaemia (two), thalassaemia (two), chronic renal failure (one). Interferon alpha-2b (IFN) was given in a dose of 6 MIU thrice weekly for 6 months. Complete response was defined as loss of HBV-DNA and HCV-RNA at 6 months and sustained response (SR) as the sustained loss of HBV-DNA and HCV-RNA for more than 6 months during the follow-up period. RESULTS: At the end of 6 months, alanine aminotransferase (ALT) levels remained unchanged (120 +/- 40 vs 136 +/- 64 IU/L), but six of the seven (86%) patients in group I lost HBV-DNA. All three hepatitis Be antigen (HBeAg)-positive patients lost HBeAg with an early flare of ALT (at 45 +/- 12 therapy days). Two of these patients (29%) lost HCV-RNA. Thus, SR was seen in 29%, while HBV-DNA loss was found in 100% during the follow-up period. In group II patients, there was a significant decrease in ALT (308 +/- 14 vs 65 +/- 25 IU/L, P < 0.001), but only three (43%) patients lost HBV-DNA and two (29%) lost HCV-RNA. One patient with acute leukaemia and another with renal failure had a complete response to IFN, but none of the lymphoma patients showed any antiviral response. CONCLUSIONS: In chronic hepatitis due to dual infection with HBV and HCV, interferon therapy is: (i) safe; (ii) effective (more so in clearing HBV); (iii) often associated with early ALT flare; and (iv) may be less effective if non-Hodgkin's lymphoma is present.

Adult↗
PubMed1999

Acute pancreatitis associated with viral hepatitis: a report of six cases with review of literature.

Association of hepatitis viruses with acute pancreatitis in the setting of nonfulminant viral hepatitis is rare. We report six cases of nonfulminant viral hepatitis complicated by acute pancreatitis, including the first documented case of hepatitis E virus (HEV) associated acute pancreatitis. The other five patients had acute viral hepatitis caused by hepatitis A infection. Besides features of viral hepatitis, the presence of typical abdominal pain, high serum amylase, and ultrasound or CT scan features suggested the diagnosis of acute pancreatitis. This complication generally developed in the initial phase of the hepatitic illness. All of the patients had mild to moderate pancreatitis that recovered uneventfully with conservative treatment.

Acute Disease↗
PubMed1999

Transfusion-associated hepatitis in a tertiary referral hospital in India. A prospective study.

BACKGROUND AND OBJECTIVES: In Indian blood banks, screening for hepatitis B virus (HBV) is currently done by the EIA method, but no routine screening is done for hepatitis C virus (HCV). MATERIALS AND METHODS: To determine the incidence of transfusion-associated HCV hepatitis, and of any residual transfusion-associated hepatitis (TAH) after HBsAg screening, we prospectively studied 182 patients who underwent surgery and received blood transfusion. These recipients had normal alanine aminotransferase (ALT) and were negative for HBsAg (monoclonal EIA), and anti-HCV (third-generation EIA) before receiving transfusion. RESULTS: Of the 818 blood units transfused after routine screening (average 4.49+/-3.3 U/patient, range 1-14), 14 (1.7% of units) were found to be infected. Of the 182 recipients, 14 (7.69%) developed TAH during a follow-up of 6 months, 3 (21.4%) from HBV, 10 (71.5%) from HCV, and 1 (1.7%) from a coinfection of HBV and HCV. All patients with TAH due to HCV were asymptomatic. One patient with TAH due to HBV (33%) and 5 with TAH due to HCV (50%) developed chronic infection with persistently elevated ALT at 6 months. CONCLUSIONS: With the current screening practices, the incidence of TAH remains high in India and is mainly due to HCV infection. Furthermore, the screening methods for HBV also need to be improved.

Hepacivirus↗
PubMed1999

Hepatic fibrogenesis using chronic arsenic ingestion: studies in a murine model.

Chronic oral arsenic (As) ingestion has been alleged to cause hepatic fibrosis, non-cirrhotic portal fibrosis and cirrhosis of the liver. The present study was aimed to investigate if hepatic fibrogenesis and non-cirrhotic portal fibrosis (NCPF) is caused by arsenic. A significant increase in the hepatic protein and collagen was seen compared with controls; hepatic 4-hydroxyproline levels, indicative of fibrogenesis, were increased 4-14 folds with different dosages of arsenic compared to the controls. Hepatocellular necrosis and inflammation were negligible to mild in all the groups. None of the animals developed significant splenomegaly or features of non-cirrhotic portal hypertension. The results suggest that (i) prolonged oral arsenic ingestion in mice leads to significant hepatic fibrogenesis and collagen synthesis with minimal hepato-cellular injury; (ii) arsenic ingestion alone is unlikely to cause non-cirrhotic portal fibrosis or cirrhosis of liver. This murine model of arsenic feeding could be used for the evaluation of new antifibrotic agents for the liver.

Animals↗
PubMed1998

Bile duct obstruction due to portal biliopathy in extrahepatic portal hypertension: surgical management.

BACKGROUND: Varices can develop in and around the bile duct in the presence of portal hypertension, especially when it is caused by extrahepatic portal vein thrombosis. The term 'portal biliopathy' is used to describe changes in the bile duct due to these varices, which may cause bile duct obstruction. This paper reviews experience of the surgical management of patients with symptomatic portal biliopathy. METHODS: Nine patients with extrahepatic portal vein obstruction with symptomatic portal biliopathy. were reviewed retrospectively. RESULTS: Eight patients presented with jaundice, two had abdominal pain and one had recurrent cholangitis. Endoscopic retrograde cholangiography revealed abnormality of the bile duct wall, with stricture in eight patients and bile duct calculi in two. Portasystemic shunting relieved jaundice in five of seven patients, and in two a second-stage hepaticojejunostomy was required. CONCLUSION: Symptomatic biliary obstruction in patients with extrahepatic portal hypertension may be relieved by a portasystemic shunt. Rarely biliary bypass may be required and is rendered safer by previous portasystemic shunting to decompress the pericholedochal varices. A direct approach to the biliary tract without a preliminary shunt may be hazardous and is frequently unnecessary.

Adolescent↗
PubMed1998

Low-dose recombinant interferon therapy in anti-HBe-positive chronic hepatitis B in Asian Indians.

Approximately 15% of Indian patients with hepatitis B virus (HBV)-related chronic liver disease (CLD) have infection with precore mutant forms. These patients are likely to have an aggressive course. There are equivocal reports of success with interferon therapy of mutant infection in the West. This therapy has not been evaluated in precore mutant-related CLD in Asian Indians. Eighteen patients (mean age 38.2 +/- 12 years, M:F: 17:1) with biopsy proven CLD and precore mutant HBV infection (hepatitis B surface antige (HBsAg) positive, hepatitis B e antigen (HBeAg) negative, anti-HBe positive, HBV-DNA positive) were included. Interferon alpha 2b was given at 3 mIU on alternate days for 4 months. Serology, determination of HBV-DNA (both by dot-blot hybridization and polymerase chain reaction) and liver biopsy were repeated after completion of the therapy. Response to interferon therapy was defined as loss of HBV-DNA by dot-blot hybridization. Thirteen (72.2%) patients responded to the treatment (responders). Mean alanine aminotransferase levels (83 +/- 12 vs 55 +/- 29 IU/L, P < 0.01) and the histological activity index (15 +/- 1.4 vs 12 +/- 1.3, P < 0.01) significantly decreased in the responders compared with initial values. Serum albumin levels also improved at the end of the therapy (3.5 +/- 0.4 g/dL vs 3.8 +/- 0.4 g/dL, P = 0.07). During follow up, seven of the 13 (54%) responders relapsed; cirrhotics relapsed more often than chronic hepatitis patients (P < 0.05). All 18 patients, however, continued to be HBV-DNA positive at the end of follow up. This study concluded that: 1. Interferon therapy is beneficial, albeit to a limited extent, in HBV precore mutant-related chronic liver disease in Asian Indians. 2. It is ineffective in eliminating the mutant HBV infection, which explains the high relapse rate. 3. Prolonged low-dose interferon therapy alone or in combination with newer nucleoside analogues should be evaluated in these patients.

Adult↗
PubMed1998

Prevention of first variceal bleed: an appraisal of current therapies.

Primary prophylaxis of esophageal variceal hemorrhage (EVH) is an important issue in the management of patients with portal hypertension. Given the high rates of initial variceal hemorrhage and mortality in patients who have not experienced bleeding from varices, there is an urgent need for some form of primary prophylaxis in all patients with large esophageal varices. The aim of this article is to review the various therapies that have been clinically assessed in randomized controlled trials for their efficacy in prevention of initial EVH. Beta-blockers have been found to be useful in primary prophylaxis of EVH, and the consensus at present is that they should be offered to all patients with portal hypertension who are at high risk for EVH. Nitrates and other newer agents are under evaluation. Surgery is not recommended for primary prophylaxis of EVH. Endoscopic sclerotherapy has not been shown unequivocally to be efficacious, and may even be deleterious, possibly related to an unacceptably high complication rate in this clinical setting. However, it may merit further clinical evaluation in light of recent reports of benefit in certain subgroups of patients with portal hypertension. On the other hand, endoscopic variceal ligation, which has an inherently low complication rate and brings about rapid obliteration of varices, may be a better option for primary prophylaxis of EVH. In the future, preprimary prophylaxis, an attractive concept, may be considered. This would involve intervention with pharmacologic agents even before the development of portal hypertension or esophageal varices.

Endoscopy↗
PubMed1997

Long-term follow-up of gastric variceal sclerotherapy: an eleven-year experience.

BACKGROUND: Bleeding from gastric varices is often a serious medical emergency. The role of endoscopy in the management of gastric variceal bleeding is still controversial. The types of gastric varices and their respective management strategies have not been identified. METHODS: Gastric varices were observed in 209 patients with portal hypertension. Seventy-one patients (with cirrhosis 33, noncirrhotic 38) underwent gastric variceal sclerotherapy, 53 of these (75%) for gastric variceal bleeding. By use of a previously described classification, gastric varices were divided into gastroesophageal varices, type 1 (GOV1) and type 2 (GOV2), and isolated gastric varices, type 1 (IGV 1). Gastric variceal sclerotherapy was done every week using a combination technique of paravariceal and intravariceal injections with absolute alcohol. RESULTS: Emergency gastric variceal sclerotherapy arrested acute bleeding in 12 (66.7%) of 18 patients. Variceal obliteration was achieved in 43 of the 60 (71.6%) patients who underwent repeated elective sclerotherapy. Variceal obliteration was higher in patients with GOV1 (94.4%) than in those with GOV2 (70.4%) and IGV1 (41%). Rebleeding after elective gastric variceal sclerotherapy was seen in 5.5%, 19%, and 53%, respectively, in the three types of gastric varices. Gastric variceal recurrence was not seen during a mean follow-up of 24.2 +/- 22.9 months. Seventeen (24%) patients died, nearly equally from rebleeding and liver failure. CONCLUSIONS: (1) Sclerotherapy can effectively arrest acute gastric variceal bleeding and achieve gastric variceal obliteration, (2) it is more effective in patients with gastroesophageal varices, and (3) alternative therapies need to be evaluated for patients with IGV1.

Acute Disease↗