Imaging Insights into EHPVO Induced Portal Biliopathy and its Grading: Retrospective Study Over A Decade at A Tertiary Care Hospital

Background and Aim: There is limited data on imaging features of extra hepatic portal venous obstruction (EHPVO) induced portal biliopathy. We describe a decade long experience of imaging spectrum of EHPVO induced portal biliopathy using MR/CT in a referral centre for liver diseases. Methods: Retrospective data of patients with primary EHPVO on contrast magnetic resonance imaging MRI/ computed tomography (CT) (n=120) and portal biliopathy (PB) on subsequent magnetic resonance cholangiopancreatography (MRCP) (n=80/120) between June 2009 - 2019 was collected. Categorisation of portal biliopathy was as per the Sarin classification and the corresponding, relevant imaging parameters were studied and analysed. Results: Sarin Type 1 biliopathy was present in 16.3 %, Type 2 in 13.8%, Type 3a in 8.8% and Type 3b in 61.3%patients. The median total serum bilirubin was 1.6 (0.9-3.4) mg/dl with a mean CBD diameter of 6.7 ± 2.9 mm. Bilobar and unilobar IHBRD were observed in 87.5% and 6.3% patients respectively. The mean CBD angle was 138.9 ± 18.8º. CBD showed smooth wall contours (10%), extrinsic indentations (83.8%) and smooth strictures (6.3%). The median CBD stricture length was 26 mm (1.25- 45 mm). Pre-stenotic dilatation was observed in 66.3% with stricture length >16 mm (sensitivity 81.1 % specificity 78%) predisposing to it. Statistically significant associations were tabulated according to the classification of PB. Conclusion: This study provides the decade long experience of imaging findings in EHPVO induced portal biliopathy according to its classification and its clinical implications.

Study of Family Clustering and PNPLA3 Gene Polymorphism in Pediatric Non Alcoholic Fatty Liver Disease

Objectives: To find association of pediatric NAFLD with metabolicrisk factors, and Patatin-like phospholipase domain-containingprotein 3 (PNPLA3) gene polymorphism.Design: Cross-sectional studySetting: Pediatric Hepatology unit of a tertiary care hospitalParticipants: Overweight/obese children (<18 years) with (69patients) or without (30 patients) NAFLD (ultrasonographybased), and their parents.Intervention: Metabolic screening, PNPLA3 gene polymorphism,and transient elastographyOutcome measure: Association of pediatric NAFLD with parentalmetabolic risk factors and PNPLA3 gene polymorphism.Results: In the NAFLD group, there was high parental incidenceof metabolic diseases, fatty liver (80%) and low high-densitylipoproteins levels (84%). Family history of NAFLD (in any parent),higher alanine aminotransferase levels and higher totalcholesterol levels in the child independently predicted possibilityof NAFLD, but similar results could not be replicated for PNPLA3gene polymorphism. Controlled attenuation parametermeasurement (by transient elastography) had high sensitivity andspecificity to diagnose steatosis.Conclusion: There is high familial incidence of metabolicdiseases in children with NAFLD. Controlled attenuationparameter can be useful as a non-invasive modality to screen fattyliver in children.

Steatosis in chronic hepatitis B: Prevalence and correlation with biochemical, histologic, viral, and metabolic parameters.

Background and Aims: Hepatic steatosis (HS) is highly prevalent in chronic hepatitis C and is an important variable predicting progression of histological injury, insulin resistance, and reduced response to antiviral therapy. There are limited data on HS in patients with chronic hepatitis B (CHB). This is relevant since response to current antiviral therapies for CHB is rather limited. We investigated the spectrum and predictors of HS in CHB patients. Materials and Methods: Liver biopsies of consecutive patients of chronic Hepatitis B Virus (HBV) infection were studied and were categorized as: Group I - hepatosteatosis (>5%) and Group II - no steatosis (£5%). Anthropometric, histological, biochemical, virological, and metabolic determinants were compared. Logistic regression analysis was applied to identify variables that were independently associated with the presence of steatosis. Results: Of the 350 patients, 118 (33.7%) liver biopsies showed steatosis (Group I); 65 (55.1%) had mild (6 to <25%) and 53 (44.9%) had moderate to severe steatosis (325%). Patients in group I, compared with group II, were older (35.5 ± 10.5 vs 27.9 ± 14.0 years, P < 0.01), predominantly male (M: F, 10.8: 1 vs 4.8: 1, P = 0.035), obese (75.0% vs 23.4%, P < 0.01), with higher body mass index (25.2 ± 4.8 vs 20.4 ± 3.5, P < 0.01), with higher triglycerides (138.8 ± 62.1 vs 88.0 ± 27.9, P = 0.02), with higher cholesterol (171.9 ± 43.5 vs 139.3 ± 37.6, P = 0.017), and with higher serum insulin (13.1 ± 9.1 vs 9.1 ± 6.0, P < .027) levels. HBV DNA level was significantly lower in group I than group II; however, HBV genotype did not influence HS. By multivariate regression analysis, only high serum triglyceride level was independent parameter associated with HS. Conclusions: Steatosis is seen in one-third cases with HBV-related chronic liver disease and is associated with host metabolic factors, especially serum triglyceride levels, whereas HBV DNA level negatively correlated with HS.

Comparison of clinical, biochemical and histological features of alcoholic steatohepatitis and non-alcoholic steatohepatitis in Asian Indian patients.

Background: Alcoholic steatohepatitis (ASH) and non-alcoholic steatohepatitis (NASH) are significant forms of liver disease and may progress to end-stage liver disease, cirrhosis and potentially malignant complications. The most difficult aspect of establishing a diagnosis of NASH is distinguishing it from ASH. Laboratory markers such as AST, ALT and GGT lack sufficient sensitivity and specificity. Aim: To study the clinical, biochemical and histological differences between non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH). Materials and Methods: Sixty histologically confirmed cases of non-alcoholic steatohepatitis and 38 cases of alcoholic steatohepatitis were included in the study. A modified form of scoring system proposed by Yip and Burt was used to grade histological features of NASH and ASH. Results: Mean age was 42.85 ± 12.36 years in ASH group and 35.07 ± 8.06 years for NASH group. Male: Female ratio was 37:1 in ASH and 4:1 in NASH. The mean ALT (P = 0.012), SAP (P = 0.003), serum bilirubin (P = 0.001), AST/ALT ratio (P = 0.03), steatosis (P < 0.001), ballooning degeneration of hepatocytes (P < 0.001), portal inflammation (P < 0.001), Mallory hyaline (P = 0.001), ductular proliferation and fibrosis (P < 0.001) showed a significant difference between ASH and NASH cases. Discussion: Older age, male sex, larger derangement of serum biochemistry, high serum bilirubin, AST/ALT > 1, more ballooning degeneration, portal inflammation, Mallory's hyaline, hepatocytic and ductular cholestasis, ductular proliferation and higher stage of fibrosis favors a diagnosis of ASH. Younger age, high ALT, AST/ALT < 1, higher grade of steatosis and absence of extensive neutrophilic portal inflammation favors a diagnosis of NASH.

Hepatic venous pressure gradient measurement: time to learn!

Portal hypertension is a clinical syndrome defined by a pathological increase in portal pressure. The development of cirrhosis of the liver is characterized by clinical manifestations related to portal hypertension like esophageal varices, ascites, bleeding, and encephalopathy. Direct measurement of portal pressure is invasive, inconvenient, and clinically impractical. Currently, the most commonly used parameter is the Hepatic Venous Pressure Gradient (HVPG), i.e., the difference between the wedged (WHVP) and the free hepatic venous pressures. HVPG represents the gradient between pressures in the portal vein and the intra-abdominal portion of inferior vena cava. When blood flow in a hepatic vein is stopped by a wedged catheter, the proximal static column of blood transmits the pressure from the preceding communicated vascular territory (hepatic sinusoids) to the catheter. Thus, WHVP reflects hepatic sinusoidal pressure and not the portal pressure itself. In the normal liver, due to pressure equilibration through interconnected sinusoids, wedged pressure is slightly lower than portal pressure, though this difference is clinically insignificant. In liver cirrhosis, the static column created by balloon inflation cannot be decompressed at the sinusoidal level due to disruption of the normal intersinusoidal communications; therefore, WHVP gives an accurate estimation of portal pressure in cirrhosis. The normal HVPG value is between 1 to 5 mmHg. Pressure higher than this defines the presence of portal hypertension, regardless of clinical evidence. HVPG >or= 10 mmHg (termed clinically significant portal hypertension) is predictive of the development of complications of cirrhosis, including death. HVPG above 12 mmHg is the threshold pressure for variceal rupture. The main advantages of HVPG are its simplicity, reproducibility, and safety. This review summarizes the technique of the HVPG measurement.

Distribution of hepatitis C virus genotypes in patients with chronic hepatitis C infection in India.

BACKGROUND & OBJECTIVES: Hepatitis C virus (HCV), an important cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma, shows a considerable genetic heterogeneity among hepatitis C virus isolates from all over the world. At least six main groups of sequence variants are recognized. The natural history of disease and response to treatment may be related to the genotype of HCV in a particular patient. Antigenic differences between genotypes also have implications for optimal design of serological sequencing and confirmatory assays for HCV. The present study was undertaken with the objective to find out various genotypes of hepatitis C virus prevalent in Indian patients with chronic hepatitis C infection. METHODS: Thirty six consecutive newly diagnosed patients with chronic hepatitis C infection were included in the study. HCV RNA was extracted from the serum by standard guanidinium thiocyanate method. Following reverse transcription and amplification, the HCV genotypes were determined by line probe assay (INNO-LiPA HCV II). RESULTS: Of the 36 patients, genotype 3 was found in 24 (66.6%). Of these 24 patients, 3a was seen in 5 patients (13.8%), 3b in two (5.5%) and mixed subtype 3a and 3b in 17 patients (47.2%). Genotype 1 was found in 5 patients (13.8%), with 1b in 1 and 1a in rest four cases. Two patients (5.5%) were infected with genotype 2 (subtype 2a and mixed subtype 2a, 2b respectively). One (2.7%) was infected with genotype 4 (4a). Mixed genotype infection was found in 4 patients (11.1%). INTERPRETATION & CONCLUSION: The present findings showed that genotype 3 of hepatitis C virus was the most prevalent genotype in patients with chronic hepatitis C in this part of India.