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Biomedical subjects

S K Sarin

Publications and source records attributed to S K Sarin.

At least 19 recordsLinked to original sources
PubMed2007

A randomized controlled trial of lamivudine to treat acute hepatitis B.

UNLABELLED: The role of antivirals in patients with acute viral hepatitis B (AVH-B) has not been evaluated in controlled trials. The aim of this study was to evaluate the efficacy of lamivudine in patients with AVH-B. AVH-B patients with serum bilirubin of more than 5 mg/dL were randomized to receive either 100 mg of lamivudine daily for 3 months (group 1, n = 31) or placebo (group 2, n = 40). Patients were considered to have severe AVH-B if they fulfilled 2 of 3 criteria: (1) hepatic encephalopathy; (2) serum bilirubin > or = 10.0 mg/dL; and (3) international normalized ratio (INR) > or = 1.6. At week 4, HBV DNA levels were significantly lower (P = 0.037) in group 1 (median: 3.6721 log copies/mL) than group 2 (median: 4.2721 log copies/mL). Thereafter, HBV DNA levels were comparable in the 2 groups. The improvement in serum bilirubin, ALT, and INR values was similar in the 2 groups. Twenty-two patients (71%) in group 1 and 25 patients (62.5%) in group 2 had severe AVH-B. Results were similar when patients with severe AVH-B were analyzed separately. After 12 and 18 months, 93.5% and 92.5%, respectively, of patients in the lamivudine group and 96.7% and 97.5%, respectively, of patients in the placebo group lost HBsAg. There were no deaths in either group. After 1 year, 21 patients (67.7%) in group 1 and 34 patients (85%) in group 2 developed protective anti-HBs titers (P = 0.096). All HBeAg-positive patients in both groups lost e antigen and anti-HBe developed in 71% and 87.5% of patients in groups 1 and 2, respectively (P = 0.132). CONCLUSION: Though lamivudine causes a greater decrease in levels of HBV DNA, it does not cause significantly greater biochemical and clinical improvement as compared to placebo in patients with acute hepatitis B.

Acute Disease↗
PubMed2006

Hepatic venous pressure gradient in cirrhosis: correlation with the size of varices, bleeding, ascites, and child's status.

The hepatic venous pressure gradient (HVPG) clearly reflects portal pressure in cirrhotic portal hypertension. Its relation with variceal bleeding has been well studied. We undertook to study the relation of HVPG to variceal size, Child's status, and etiology of cirrhosis. Patients with cirrhotic portal hypertension with esophageal varices underwent HVPG measurement as part of a prospective evaluation. One hundred seventy-six cirrhotics with varices (M:F, 140:36; mean age, 42.6 +/- 13.4 years), 104 with CLD related to viral etiology, 40 with alcoholic liver disease, 26 cryptogenic with cirrhosis, and 6 with miscellaneous causes of CLD underwent HVPG measurement. The mean HVPG was lower in patients with small varices (n = 77; 14.6 +/- 5.9 mm Hg) than in patients with large varices (n = 99; 19.2 +/- 6.6 mm Hg; P < 0.01). In patients with large varices, the mean HVPG in bleeders (n = 37) was higher than in nonbleeders (n = 62) (21.7 +/- 7.2 vs 17.9 +/- 6.2 mm Hg; P < 0.01). The mean HVPG was significantly higher in Child's B (n = 97; 17.4 +/- 6.9 mm Hg) and C (n = 56; 19.0 +/- 5.7 mm Hg) compared to Child's A cirrhotics (n = 23; 12.2 +/- 5.9 mm Hg; P < 0.01), and Child's C compared to Child's B cirrhotics (P = 0.05). HVPG was higher in alcoholic compared to nonalcoholic cirrhotics (20.8 +/- 7.3 vs 16.4 +/- 6.3 mm Hg; P < 0.05), but this was not significant in multivariate analysis. The HVPG was comparable between hepatitis B- and hepatitis C virus-related cirrhotics (P = 0.8). Cirrhotics with ascites had a higher HVPG than those without ascites (18.5 +/- 5.6 vs 16.6 +/- 7.6 mm Hg; P = 0.02). In multivariate analysis, only Child's status, size of varices, and variceal bleed predicted higher HVPG. HVPG is higher in cirrhotics with large varices and a history of bleed. There is a good correlation between HVPG and large varices, bleeder status, and ascites. A higher HVPG reflects more severe liver disease. The etiology of liver disease did not influence the portal pressure.

Adult↗
PubMed2006

Studies on TAQ1 polymorphism in the 3'untranslated region of IL-12P40 gene in HCV patients infected predominantly with genotype 3.

Host immunity plays an important role in viral persistence and progression of liver disease in HCV infected patients. IL-12 induces production of IFN-gamma, a potent antiviral agent. IL-12 comprises two subunits; IL-p35 and IL-12p40, which are encoded by two different genes located on chromosome 3 and 5, respectively. Single nucleotide polymorphism at A1188C in the 3'UTR of IL-12p40 gene is associated with immune mediated diseases. Association of IL-12p40 A1188C polymorphism with the outcome of HCV infection was investigated in this study. Two hundred and fifty three histologically proven chronic hepatitis C patients (43 +/- 13 years, male:female: 185:68) and 380 matched controls were included. Genotyping was performed by RFLP and confirmed by direct sequencing. To assess correlation of immune gene polymorphism with severity of HCV-related liver disease, patients were divided into those with fibrosis score of < or = 2 (mild) or > 2 (severe), and histological activity index (HAI) of = 5 (mild) or > 5 (severe). The distribution of A/A, A/C or C/C alleles in the controls was comparable to the patients. The distribution of C/C allele was significantly more common in patients with mild as compared to severe fibrosis (23.7% vs. 6.25%, P = 0.004). No significant difference was observed for any of the genetic markers with HAI or with normal or raised alanine aminotransferase (ALT). These results show that the C/C allele of IL-12p40 gene could render genetic protection against development of severe liver disease in patients infected with HCV.

3' Untranslated Regions↗
PubMed2006

Endoscopic management of liver abscesses and cysts that communicate with intrahepatic bile ducts.

BACKGROUND AND STUDY AIMS: The formation of a communication between liver abscesses or cysts and intrahepatic bile ducts is an uncommon cause of significant bile leak. Surgical management of biliary fistulas is associated with high morbidity and mortality. We performed a prospective study of endoscopic management of this type of biliary fistula. PATIENTS AND METHODS: We studied 26 patients who had either liver abscesses or hepatic cysts that had ruptured into the intrahepatic bile ducts. The presence of a biliary fistula was suspected by jaundice and/or by the appearance of bile in percutaneous drainage effluent from a liver abscess and was confirmed by endoscopic retrograde cholangiopancreatography. Once the route of the fistula between the liver abscess or cyst and the intrahepatic bile duct had been defined by cholangiography, patients underwent treatment by sphincterotomy, and either biliary stenting or nasobiliary drainage. Nasobiliary drains or biliary stents (both 7 Fr) were placed according to standard techniques. Nasobiliary drains were removed when bile leakage stopped and closure of the fistula was confirmed by cholangiography; stents were removed after an interval of 4-6 weeks. RESULTS: Of a total of 525 patients with hepatic abscesses or cysts who were seen over a 5-year period, there were 26 patients who developed a demonstrable communication between liver abscesses (n = 20; 16 amebic, four pyogenic) or hydatid cysts (n = 6) and intrahepatic bile ducts (right intrahepatic bile ducts in 22 patients, left intrahepatic bile ducts in four patients). We performed either sphincterotomy with insertion of a nasobiliary drain (n = 20) or sphincterotomy with biliary stenting (n = 6). The fistulas healed in all patients after a mean time of 4 days (range 2-20 days) after endoscopic treatment. We were able to remove the nasobiliary drainage catheters and stents 6-34 days after their placement. CONCLUSIONS: In this case series, endoscopic therapy appears to be an effective mode of treatment for biliary fistulas complicating liver abscesses and cysts.

Adult↗
PubMed2006

Profile of chronic hepatitis B virus in children in India: experience with 116 children.

BACKGROUND: Hepatitis B virus (HBV) infection in children is mostly asymptomatic and therefore the disease burden is likely to be under appreciated. There is limited information on the profile of chronic HBV infection in children from the Indian subcontinent. METHOD: In 116 (male:female 89:27) children, aged <15 years, with persistent HBsAg positivity for more than 6 months, a clinical, biochemical, virological and histological assessment was carried out. RESULTS: At presentation, 21.6% of children were symptomatic, with icterus in 12%. Features of decompensation such as ascites (7%) and gastrointestinal (GI) bleed (5%) were noted uncommonly. Five (4.3%) children had hepatocellular carcinoma (HCC) at presentation. Elevated alanine aminotransferase (ALT) was observed in 76% of subjects (median 61; range 14-815). A significantly higher proportion of children with hepatitis B early antigen (HbeAg) positive status had higher histological activity index (HAI) (84% vs 16%, P < 0.001) and fibrosis score (80% vs 20%, P = 0.007). A strong positive correlation was noted between aspartate aminotransferase (AST), ALT, HBV-DNA and histological severity of the disease (HAI > or =4, fibrosis > or =2). Median HBV-DNA levels were significantly higher in the HBeAg positive compared to the HBeAg negative group (25.6 vs 0.7 pg/mL, P = 0.004). Seventy-four percent of the mothers had evidence of past or present HBV infection. CONCLUSIONS: Majority of the children with chronic HBV infection are asymptomatic at presentation. HBeAg positive status reflects histologically more severe disease, and a higher level of HBV-DNA. Almost two-thirds of the children may have acquired their HBV infection perinataly.

Adolescent↗
PubMed2005

Endoscopic biliary drainage by nasobiliary drain or by stent placement in patients with acute cholangitis.

BACKGROUND AND STUDY AIMS: Endoscopic biliary drainage is an established mode of treatment for acute cholangitis. We compared the safety and efficacy of nasobiliary drain (NBD) placement and stent placement for biliary drainage in patients with acute cholangitis. PATIENTS AND METHODS: We recruited a total of 150 patients with severe cholangitis who required endoscopic biliary drainage. Patients were randomized to have either a 7-Fr NBD or a 7-Fr straight flap stent placed during endoscopy. Outcome measures included complications related to endoscopic retrograde cholangiopancreatography (ERCP) and the clinical outcome. RESULTS: Of the 150 patients, 75 were randomized to the NBD group and 75 to the stent group. The most common causes of biliary obstruction were common bile duct stones (n = 102) and biliopancreatic malignancies (n = 37). The site of the biliary obstruction was predominantly found to be the lower part of common bile duct in both the NBD group (n = 58) and the stent group (n = 59). Indications for biliary drainage were: a fever of > 100.4 degrees F (n = 140), hypotension (n = 23), peritonism (n = 40), impaired consciousness (n = 29), and failure to improve with conservative management (n = 45). Biliary drainage was achieved in 147 patients. Abdominal pain, fever, jaundice, hypotension, peritonism and altered sensorium improved after a median period of 2 days in both groups. Leukocyte counts became normal after a median time of 7 days in the NBD group and 6 days in the stent group. There were no ERCP-related complications. There were no instances of displacement or kinking of an NBD, occlusion of an NBD or stent, or of stent migration. Four patients died (two in the NBD group and two in the stent group) as a result of uncontrolled cholangitis after 1, 2, 4, and 6 days of biliary drainage. The success rates of biliary drainage in cholangitis were not affected by the type of endoprosthesis used (72/74 for NBD patients vs. 71/73 for stent patients), the etiology of the biliary obstruction (110/112 for benign obstruction vs. 33/35 for malignant obstruction), or the site of the biliary obstruction (28/30 for upper common bile duct obstruction vs. 115/117 for obstruction at the lower end of common bile duct). CONCLUSIONS: Biliary drainage by nasobiliary drain and drainage by stent are equally safe and effective treatments for patients with severe cholangitis.

Acute Disease↗
PubMed2004

Beneficial effects of 'lamivudine pulse' therapy in HBeAg-positive patients with normal ALT*.

Currently no therapy is given to patients with chronic hepatitis B virus (HBV) infection who are HBeAg positive with normal alanine aminotransferase (ALT) levels. Steroid priming has been shown to enhance T-helper-1 (Th-1) cell response. Lamivudine may restore immunologic competence against HBV by causing a sudden decline in the level of the virus. We examined the efficacy of lamivudine pulse therapy on the seroconversion from HBeAg to anti-HBe. This was a prospective single-blinded trial including 27 patients with chronic hepatitis B, HBeAg positive with ALT < or =1.5 times upper limit of normal (ULN). Lamivudine was administered initially for 4 weeks, then stopped for 2 weeks and later restarted and continued till 3 months after seroconversion or completion of 2 years of therapy. Twenty-six patients completed the study. Lamivudine withdrawal led to a rise in ALT levels above the ULN in 11 (42.3%) patients at 6 weeks; seven of them (63.6%) lost HBeAg compared with only two of the 15 patients (13.3%), in whom ALT levels did not rise (P = 0.011). As one patient showed a relapse, a total of eight (31%) patients responded to lamivudine pulse therapy over a mean period of 17.3 +/- 4.5 months. Responders had a higher serum albumin (P < 0.05), a lower fibrosis score (P < 0.05), and a relatively high baseline serum ALT levels (P = 0.024) than the nonresponders. YMDD mutations developed in three patients and none responded. No patient developed hepatic decompensation. Hence lamivudine pulse therapy has potential in converting HBeAg-positive, 'not-treat-worthy' (ALT < 1.5 ULN) patients to treat-worthy (ALT > 1.5 ULN) in 42%, with sustained HBeAg and HBV DNA loss in 31% patients. The effects are possibly because of a combination of antiviral and immunomodulating activities of lamivudine.

Adolescent↗
PubMed2004

Absence of hemochromatosis associated Cys282Tyr HFE gene mutation and low frequency of hemochromatosis phenotype in nonalcoholic chronic liver disease patients in India.

BACKGROUND AND AIM: Hereditary hemochromatosis (HHC) is an autosomal recessive disorder causing primary iron overload syndrome and chronic liver disease (CLD). This genetic disease is commonly associated with C282Y mutation of the HFE gene, commonly seen in the Northern European population. Minor reports on HHC are available from Asia, however, so far no genetic study is available from India. We prospectively studied the prevalence of C282Y mutation in CLD patients and healthy subjects in a tertiary care referral center in India. METHODS: A total of 249 consecutive biopsy proven CLD (HBV = 112, HCV = 72, cryptogenic = 65) patients and 134 age matched healthy controls were included. Cases of secondary iron overload, pregnancy, chronic alcoholism, age < 30 years and hepatocellular carcinoma (HCC) were excluded. A transferrin saturation index (TSI) of >60% was suggestive of a phenotypic presentation of HHC. C282Y mutation was studied by restriction fragment length polymorphism (RFLP) using genomic DNA. The 387 bp fragment obtained after polymerase chain reaction was digested with 10 units of endonuclease Rsa1. The mutation was detected by creation of an additional restriction site, giving rise to fragments of 247 111 and 29 bp. RESULTS: While the mean TSI was comparable, serum ferritin was significantly higher in CLD patients compared to controls (38 +/- 16%vs 28 +/- 13%; p = not significant (NS), and 125 +/- 18 vs 42 +/- 25 ng/mL; p < 0.001). A TSI of >60% was detected in 24 (9.64%) patients. Only one restriction site was found for endonuclease Rsa1, giving rise to two fragments of 247 and 140 bp, suggesting absence of C282Y mutation in the HFE gene in all patients. CONCLUSIONS: Almost 10% of nonalcoholic CLD patients in India have iron overload, but this is independent of C282Y mutation of the HFE gene. Large population based studies are recommended to investigate the prevalence of this rare disorder in India.

Adult↗
PubMed2003

Hepatic dysfunction in patients with extrahepatic portal venous obstruction.

BACKGROUND: Extrahepatic portal venous obstruction (EHPVO) developing due to thrombotic occlusion of the portal vein in children is generally considered a benign disease. Whether hepatic dysfunction develops in these patients in the absence of a gastrointestinal bleed has not been well studied. MATERIALS AND METHODS: Forty-three patients with EHPVO who had not bled in the last 3 months were studied. Patients were divided into those with (group I) or without ascites (group II). Matched cirrhotic patients with ascites (group III) served as controls. Clinical, biochemical, ultrasonographic, and histopathological evaluation was carried out. Portal biliopathy was assessed in five patients in group I and in 12 patients in group II by cholangiography. RESULTS: Of 43 EHPVO patients, ascites was seen in nine (21%) patients (group I). Thirty-four patients had no ascites (group II). Serum ALT (54 +/- 24 vs. 34 +/- 10 IU/l, P < 0.01), albumin (3.2 +/- 0.3 vs. 3.7 +/- 0.4 g/dl, P < 0.01), and prothrombin time difference (9.0 +/- 4.5 vs. 2.4 +/- 1.9 s, P < 0.05) were deranged in patients in group I compared with group II. Patients in group I were 4 years older, and the duration of portal hypertension was longer than in group II (11.5 vs. 5.6 year, P < 0.05). Portal biliopathy changes were significantly more severe in group I than in group II patients. Ascites was high gradient in all the patients in group I and the serum-ascitic albumin gradient was comparable between groups I and III. None of the EHPVO patients, but four cirrhotic patients, developed spontaneous bacterial peritonitis during a follow-up of 11 +/- 4 months. CONCLUSIONS: Hepatic dysfunction in the form of ascites and deranged liver functions is not uncommon in patients with EHPVO, more so in patients with prolonged portal hypertension. Based on our data it would be worthwhile to study whether prolonged portal vein thrombosis in EHPVO patients could lead to progressive liver disease.

Adolescent↗
PubMed2003

Isolated gastric varices: prevalence, clinical relevance and natural history.

BACKGROUND: Isolated ectopic gastric varices (IGV2) are present either in the body or antrum of the stomach or upper duodenum. The prevalence, natural history and clinical significance of these varices has not been adequately described. MATERIALS AND METHODS: Consecutive patients with portal hypertension, prospectively studied and diagnosed to have IGV2, were assessed for their time of appearance - primary (at first presentation) or secondary (after obliteration of oesophageal varices), association with other varices, portal hypertensive gastropathy and any overt bleeding. RESULTS: Fifty-three of the 1128 (4.7%) patients had IGV2. The IGV2 were commonly seen in the antrum (53%), duodenum (32%), or at both sites (11%) and rarely in body and fundus (4%). IGV2 were predominantly (84.9%) secondary in origin, developing after oesophageal variceal obliteration. The median time for emergence of secondary IGV2 was 8.2 months for patients with cirrhosis, 12.8 months for non-cirrhotic portal fibrosis and 10.8 months for extra-hepatic portal vein obstruction. Eight (15%) patients had primary IGV2, 6 of them had underlying portal vein obstruction. Portal gastropathy (p < 0.05) and UGI bleeding were more common in the secondary than in primary IGV2. Bleeding due to IGV2 was seen only in 3 (5.7%) patients during a mean follow-up of 36.3 +/- 12.1 months, and could be successfully managed with endoscopic ligation or obliteration. CONCLUSIONS: Isolated ectopic gastric varices are not uncommon and generally develop following obliteration of main variceal columns. They rarely bleed and often can be managed with endoscopic interventions.

Adult↗
PubMed2002

Non-cirrhotic portal fibrosis.

Non-cirrhotic portal hypertension (NCPH) comprises of diseases having an increase in portal pressure (PP) due to intraheptic or prehepatic lesions, in the absence of cirrhosis. The lesions are generally vascular, either in the portal vein, its branches or in the perisinusoidal area. Because the wedged hepatic venous pressure (WHVP) is near normal, measurement of intravariceal or intrasplenic pressure is needed to assess portal pressure. The majority of the diseases included in the category of NCPH are well characterized disease entities where portal hypertension (PHT) is a late manifestation and hence, these are not discussed. Two diseases which present only with features of PHT and are common in developing countries are NCPF and extra-hepatic portal vein obstruction (EHPVO). Non-cirrhotic portal fibrosis is a syndrome of obscure etiology, characterized by 'Obliterative portovenopathy' leading to PHT, massive splenomegaly, repeated well tolerated episodes of variceal bleeding and anemia in young adults from low socio-economic strata of life. The hepatic parenchymal functions are nearly normal. Jaundice, ascites and hepatic encephalopathy are rare. Management of variceal bleeding remains the main concern as nearly 85% of patients with NCPF present with variceal bleeding. Endoscopic variceal ligation or sclerotherapy are equally effective in about 90-95% of the patients. Gastric varices are seen in about 25% patients and a bleed from them can be managed with cyanoacrylate glue injection or surgery. Other indications for surgery include failure of endoscopic therapy to control acute bleed and symptomatic hypersplenism. The prognosis of patients with NCPF is good and 5-years survival rates in patients in whom variceal bleeding can be controlled is about > 95%.

Humans↗
PubMed2002

Non-cirrhotic portal fibrosis: current concepts and management.

Non-cirrhotic portal hypertension (NCPH) comprises diseases having an increase in portal pressure (PP) due to intraheptic or prehepatic lesions, in the absence of cirrhosis. The lesions are generally vascular, either in the portal vein, its branches or in the perisinusoidal area. Because the wedged hepatic venous pressure is near normal, measurement of intravariceal or intrasplenic pressure is needed to assess PP. The majority of diseases included in the category of NCPH are well-characterized disease entities where portal hypertension (PHT) is a late manifestation and, hence, these are not discussed. Two diseases that present only with features of PHT and are common in developing countries are non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal vein obstruction (EHPVO). Non-cirrhotic portal fibrosis is a syndrome of obscure etiology, characterized by 'obliterative portovenopathy' leading to PHT, massive splenomegaly and well-tolerated episodes of variceal bleeding in young adults from low socioeconomic backgrounds, having near normal hepatic functions. In some parts of the world, NCPF is called idiopathic portal hypertension (IPH) or 'hepatoportal sclerosis'. Because 85-95% of patients with NCPF and EHPVO present with variceal bleeding, treatment involves management with endoscopic sclerotherapy (EST) or variceal ligation (EVL). These therapies are effective in approximately 90-95% of patients. Gastric varices are another common cause of upper gastrointestinal bleeding in these patients and these can be managed with cyanoacrylate glue injection or surgery. Other indications for surgery include failure of EST/EVL, and symptomatic hypersplenism. The prognosis of patients with NCPF is good and 5 years survival in patients in whom variceal bleeding can be controlled has been reported to be approximately 95-100%.

Diagnosis, Differential↗