Heterogeneous distribution of factor V Leiden in patients from north India with venous thromboembolism.
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Biomedical subjects
Publications and source records attributed to Y Chawla.
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Hepatitis C virus (HCV), which is the major pathogen responsible for human chronic liver disease, has special tropism for hepatocytes. Although, low-density lipoprotein receptor, CD81 and negatively charged glycosaminoglycans have been proposed as candidate receptors for HCV, no confirmed receptor(s) on the hepatocytes have been identified to date. It is also suggested that additional, yet unidentified, cellular proteins may be involved in the host-viral interaction. Therefore, this study was conducted with the main aim to identify hepatocyte protein(s) that may have affinity for the HCV structural protein, envelope-2/non-structural-1 (E2/NS1) protein. For the binding studies, hepatocytes were isolated from fresh normal human liver tissues. The hepatocyte proteins on the nitrocellulose paper were reacted with recombinant E2/NS1 protein and anti-E2 (rabbit). In another approach, to rule out the possibility of binding of rec-E2/NS1 with the hepatocyte cytoplasmic proteins, hepatocyte plasma membrane proteins were passed through CNBr-activated and recombinant E2/NS1 bound sepharose-4B column. The recombinant E2/NS1 binding hepatocyte plasma membrane protein(s) were eluted and were then analyzed. Altogether, our data suggest that E2/NS1 protein of HCV binds to two hepatocyte proteins of molecular weights 25-28 kDa and 59-60 kDa. These results indicate the possible role of the above proteins (25-28 kDa and 59-60 kDa) in the viral binding to the hepatocytes.
OBJECTIVE: To study the outcome of pregnancy in women with non-cirrhotic portal hypertension (NCPH). METHOD: A retrospective analysis of 50 pregnancies in 27 women with NCPH was carried out. Pregnancy outcome was compared in extra hepatic portal vein obstruction (EHPVO) and non-cirrhotic portal fibrosis (NCPF). RESULTS: The mean maternal age was 24.60+/-2.857 years, and the disease was diagnosed during pregnancy in 15 (55.6%) patients. Variceal bleeding occurred in 17/50 (34%) pregnancies and the majority (88.2%) of them responded to endoscopic sclerotherapy. Incidence of variceal bleeding during pregnancy was lower in pregnancies where the disease was diagnosed prior to pregnancy (8.6%), and it was 43.5% in EHPVO and 25.9% in NCPF. The mean birth weight of the neonates was 2668.4+/-427.42 g, and the incidence of abortion, prematurity, small for gestational age babies and perinatal death was 20, 17.5, 12.5 and 20%, respectively. Variceal bleeding during pregnancy was associated with a higher incidence of abortion (29.4%) and perinatal death (33.3%). CONCLUSION: Variceal bleeding is the most common complication in pregnancies with NCPH. Pregnancies can be allowed and managed successfully in patients with NCPH.
Portal hypertension usually occurs in patients with fulminant hepatic failure (FHF). There is, however, no information on portal venous hemodynamics in patients with FHF. Therefore, we studied the portal venous hemodynamics in patients with FHF using duplex Doppler ultrasonography. We measured the portal vein diameter, flow velocity, and volume flow with duplex Doppler ultrasonography in 29 patients with FHF and 15 patients with uncomplicated acute viral hepatitis. No significant difference was observed in the portal vein parameters in the two groups. Nineteen patients with FHF survived. No difference in portal flow velocity and flow rate was observed between survivors and nonsurvivors. A significantly lower portal flow velocity was observed in nine patients of FHF with ascites compared with those without ascites (12.29+/-2.81 vs 16.26+/-4.87 cm/sec; P < 0.01). Portal hemodynamics do not significantly change in fulminant hepatic failure; therefore, it has no prognostic significance.
BACKGROUND: Pleural effusion in cirrhotic patients (hepatic hydrothorax) may result from migration of ascitic fluid across defects in the diaphragm. Biochemical analysis of ascitic and pleural fluid provides only indirect information about the nature and origin of the effusion. The present study was performed in order to demonstrate the presence/absence of peritoneo-pleural communication by radioisotope imaging. METHODS: Ten patients with cirrhotic ascites and pleural effusion were studied with 99mTc sulfur colloid scintigraphy to look for movement of the radiotracer from the peritoneal to the pleural cavity. Serum-ascitic albumin gradient (SAAG) and serum-pleural fluid albumin gradient (SPAG) values were determined in eight patients to examine the nature of the ascitic and pleural fluids. RESULTS: Transdiaphragmatic movement of ascitic fluid into the pleural space was demonstrated (generally within 2 h of intraperitoneal injection of the radiotracer) in eight of 10 patients; six on the right side, one on the left and one bilaterally. Two patients in whom pleural fluid was transudative on SPAG values were negative for peritoneo-pleural communications. CONCLUSIONS: Radionuclide scintigraphy is a simple, safe and relatively non-invasive method to confirm passage of ascitic fluid across the diaphragm.
BACKGROUND AND AIM: Biliary cholesterol supersaturation, gallbladder stasis and delayed intestinal transit are the key events in cholesterol gallstone formation. We studied the effect of cisapride, a prokinetic drug, on gallbladder emptying and bile composition in patients with gallstone disease undergoing cholecystectomy. METHODS: Gallbladder emptying, cholesterol saturation index (CSI) and nucleation time were studied in 21 patients with gallstone disease. Eleven patients (cisapride group, age 41.9 +/- 2.9 years) received tablet cisapride 10 mg t.i.d. for 2 weeks, while 10 patients (placebo group, age 42.1 +/- 1.9 years) received placebo for the same duration. Gallbladder emptying was repeated in all patients after a 2-week treatment with cisapride or placebo. Gallbladder bile was obtained at the time of surgery for the measurement of CSI and nucleation time. RESULTS: Residual volume of the gallbladder decreased (mean +/- SE, 18.6 +/- 2.5 mL vs 10.0 +/- 1.1 mL, P = 0.007), and the ejection fraction increased (43.5 +/- 5.3% vs 60.0 +/- 3.2%, P = 0.007) in patients in the cisapride group, while no change was observed in placebo group patients. Nucleation time was higher in the cisapride group than in the placebo group (14.9 +/- 1.3 days vs 8.0 +/- 0.9 days, P = 0.003). Patients in the cisapride group had a significantly lower cholesterol concentration (molar percentage, 5.1 +/- 0.3% vs 6.8 +/- 0.8%, P = 0.049) and CSI (1.0 +/- 0.1 vs 1.36 +/- 0.11, P = 0.034) than patients in the placebo group. CONCLUSION: Cisapride improves gallbladder emptying and bile lithogenicity in patients with gallstone disease.
BACKGROUND AND AIMS: Hyposplenism has been described in patients with alcoholic cirrhosis (AC). However, no data are available regarding hyposplenism in patients with non-alcoholic cirrhosis (NAC) and other forms of portal hypertension such as extrahepatic portal venous obstruction (EHPVO). The aim is to study the splenic functions in patients with AC, NAC, and EHPVO. METHODS: Splenic functions were assessed consecutively in 22 patients with AC, 21 with NAC, and 23 with EHPVO. The tests included pitted red blood cells (RBC; %) and Howell-Jolly bodies in the peripheral smear. Pitted RBCs > 2% with or without the presence of Howell-Jolly bodies were taken as indicators of hyposplenism. The splenic function in each group was compared with age-matched controls. RESULTS: Hyposplenism was found in 10 (45.45%) patients with AC, six (28.57%) with NAC and one (4.34%) with EHPVO. The mean pitted RBCs were significantly increased in patients with AC (mean 4.93 +/- 1.36% vs control 1.22 +/- 0.17%, P < 0.05), but not so with NAC (2.01 +/- 0.69%) and EHPVO (mean 0.99 +/- 0.1% vs control 0.66 +/- 0.1%, P > 0.05). Howell-Jolly bodies were seen in only four patients. The mean pitted RBCs were significantly higher among patients who were actively consuming alcohol (9.14 +/- 3.35%) compared to those who abstained at least for more than 24 weeks (2.0 +/- 1.3%, P < 0.05). CONCLUSION: Hyposplenism is more common in AC patients, particularly those who are actively consuming alcohol compared with those who abstain. Patients with NAC have a lower incidence of hyposplenism, while in EHPVO patients, it is uncommon.
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OBJECTIVE: Although presence of ascites has been reported in patients with fulminant hepatic failure (FHF), spontaneous bacterial peritonitis (SBP) has not been studied in a large group of such patients. Hence, the present study was conducted to evaluate the prevalence and prognostic significance of ascites and SBP in FHF patients. METHODS: Two hundred ninety-eight consecutive patients (mean age 32.9+/-14.8 yr) with FHF were studied. There were 133 (44.6%) men and 165 (55.4%) women. Acute viral hepatitis accounted for 91.6% of the patients and were analyzed in the present study. RESULTS: Ascites was clinically detected in 79 (28.9%) patients. The patients with ascites were older (p = 0.005), had longer jaundice-encephalopathy interval (p<0.0000001), lesser grade of encephalopathy on admission (p = 0.0000043), and a lower incidence of raised intracranial pressure on admission (p = 0.0007). Patients with ascites had significantly lower serum albumin (p = 0.021), ALT (p = 0.0005), AST (p = 0.00017), and PT (p = 0.002) on admission than in patients without ascites. Multivariate logistic regression analysis showed that jaundice-encephalopathy interval (> or =14 days) and serum albumin (< or =2.5 g/dl) were the only independent predictors of ascites. SBP was detected in 14 (17.7%) patients (neutrocytic culture positive, 4; neutrocytic culture negative, 9; and monomicrobial bacterascites, 1). Escherichia coli was identified in three patients. Survival was no different between patients with and those without ascites and also between patients with and those without SBP. CONCLUSIONS: Ascites is a frequent accompaniment of FHF and is complicated by SBP. Jaundice-encephalopathy interval of 14 days or more and serum albumin (< or =2.5 g/dl) on admission predicts the development of ascites in these patients.
BACKGROUND: The postulated mechanisms of biliary abnormalities in extrahepatic portal venous obstruction (EHPVO) are either extrinsic compression by collaterals or ischemic injury due to venous thrombosis. If the former hypothesis is correct, then biliary changes should revert to normal after portasystemic shunt surgery. METHODS: Five patients with EHPVO who underwent portasystemic shunt surgery were studied. One of these patients had obstructive jaundice due to portal cavernoma. Endoscopic retrograde cholangiography (ERC) was performed before as well as after the shunt surgery. Doppler ultrasound and splenoportovenography were obtained to confirm the diagnosis of EHPVO as well as shunt patency. RESULTS: All patients had biliary abnormalities on pre-shunt ERC. The post-shunt ERC showed partial reversal of biliary abnormalities in 3 patients, complete reversal in 1 patient, and no reversal in 1 patient. Smooth strictures opened after shunt surgery and proximal dilatation disappeared in most patients. The indentations and caliber irregularities disappeared after shunt surgery, whereas angulations and ectasias of biliary ducts persisted. CONCLUSION: Shunt surgery results in regression of some of the biliary abnormalities and relieves biliary obstruction, suggesting that mechanical compression by collaterals is the mechanism behind biliary abnormalities in EHPVO. However, some biliary changes persist after shunt surgery signifying fixed obstruction due to ischemia or fibrous scarring. Thus, the two theories are not mutually exclusive.
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Liver biopsy rarely leads to complications in a non-cirrhotic liver. We describe here a case of a biliary cyst of the liver that developed after a liver biopsy. It was successfully treated with surgery.
BACKGROUND: Angiography has been the mainstay for diagnosis of Budd-Chiari syndrome even though other modalities are increasingly being used. We have evaluated our findings of duplex Doppler sonography (DDS) in patients with Budd-Chiari syndrome. METHODS: Duplex Doppler sonography was performed in 37 consecutive angiographically proven patients with Budd-Chiari syndrome. RESULTS: Real time ultrasonography showed abnormalities of right, middle and left hepatic veins (HV) in 21, 15 and 18 patients, respectively. Duplex Doppler sonography showed abnormal flow patterns in 37, 22 and 31 patients in the right, middle and left HV, respectively, thereby increasing the diagnostic yield by 40%. An abnormal waveform in one or more HV was present in all 37 patients. Uniphasic flow was the commonest abnormality and was seen in 22, nine and 14 patients, respectively, in the right, middle and left HV, while there was no flow in five, four and seven patients in the right, middle and left HV, respectively. Intrahepatic collaterals were seen in 35 of 37 patients (94.6%). Hepatopetal flow was found in the portal vein of 21 of 23 patients (91.3%), while flow was hepatofugal in one and portal vein thrombosis was found in another. CONCLUSION: Duplex Doppler sonography is a useful procedure which helps in the diagnosis of patients with Budd-Chiari syndrome.
BACKGROUND: Portal vein thrombosis, usually idiopathic, is the cause of portal hypertension in 46% of Indian patients, who present with a variceal bleed. The presence of lupus anticoagulant (LA) and antithrombin III deficiency have been reported to be associated with an increased tendency to venous thrombosis. METHODS AND RESULTS: We studied 30 patients with portal venous thrombosis diagnosed by ultrasound. Two patients were positive for a lupus anticoagulant and both had very prolonged partial thromboplastin time with kaolin. None of the patients had antithrombin III deficiency.
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Not much is known about the relationship between portal hemodynamics and the grades of cirrhosis. Using pulsed Doppler ultrasonography, we studied portal vein diameter, portal flow velocity, and portal blood flow rate in 37 patients with liver cirrhosis (11 Child's A, 13 Child's B, and 13 Child's C) and 10 healthy controls. There was no difference in the maximum inner diameter of the portal vein in cirrhotics and controls. However, there was a significant decrease in the portal flow velocity in patients with Child's C cirrhosis, as compared to controls and patients with Child's A and Child's B cirrhosis. The portal blood flow rate in Child's B and Child's C cirrhosis was also significantly less as compared to controls and patients with Child's A cirrhosis. Patients with ascites and encephalopathy had significantly lower portal flow velocities and blood flow rate as compared to those without ascites and encephalopathy, respectively. This study indicates that portal flow significantly decreased in cirrhotic patients with worsening Child's grade of cirrhosis.
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