Evidence Of Liver Cirrhosis Research Articles

Sofosbuvir-Velpatasvir Full Dose in Chronic Hepatitis C in End-Stage Renal Disease: An Observational Study from a Himalayan Region

Background Treatment of chronic hepatitis C (CHC) in the setting of chronic kidney disease and end-stage renal disease (ESRD) is challenging. Objectives We planned to evaluate the efficacy and safety of full dose of combination of sofosbuvir-velpatasvir in the treatment of CHC in patients with ESRD or those on maintenance hemodialysis. Methods The prospective observational study was conducted in a tertiary care center in North India where all patients with chronic kidney disease (CKD) were assessed. Those with hepatitis C virus (HCV) antibody positivity underwent testing for HCV ribonucleic acid and were treated if eligible. Full dose of sofosbuvir-velpatasvir was administered daily for 12 weeks (or 24 weeks for decompensated liver disease). Results Of the 162 patients (mean age: 43.08 ± 12.08 years, 114 males), 125 were on regular hemodialysis. Twenty-four (15%) had evidence of liver cirrhosis, out of which four patients had evidence of decompensation. One hundred forty-two patients (87.6%) had an early virological response. Most patients, 160 (98.7%), obtained end of therapy viral clearance and sustained virological response at 12 weeks after therapy. Two patients died, and rest of the patients completed therapy. The adverse effects noticed were nausea (20%), vomiting (18%), headache (10%), and weakness (7%). Conclusion A combination of sofosbuvir and velpatasvir is effective and safe in treating CHC in the setting of CKD.

Regular at-home abdominal paracentesis via Tenckhoff catheter in patients with refractory congestive heart failure.

Peritoneal dialysis (PD) is increasingly used for the long-term management of refractory congestive heart failure (CHF). Patients with severe CHF and ascites were treated with regular at-home abdominal paracentesis via Tenckhoff catheter. We investigated the outcome of those patients, aiming to identify potential prognostic factors for longer survival. Patients with refractory CHF referred by cardiologists to the PD unit from years 2009 to 2019 and treated with regular at-home abdominal paracentesis via Tenckhoff catheter without peritoneal exchanges, were enrolled into this prospective observational study. From the total of 69 refractory CHF patients treated with PD, 18 (26%) were managed with regular at-home abdominal paracentesis via Tenckhoff catheter and improved without the need for peritoneal exchanges for fluid removal (no peripheral oedema or pulmonary congestion) or for solutes removal. Median survival of severe CHF patients treated with abdominal paracentesis was 13.5months (0-34months). Long-term survivors demonstrated significant improvement in the New York Heart Association (NYHA) functional class, improvement in kidney function and decrease in serum C-reactive protein (CRP) and Brain natriuretic peptide (BNP) compared with their baseline status. A subgroup of patients with shorter survival were more likely to have evidence of liver cirrhosis and significantly lower serum sodium compared with patients with longer survival. Refractory CHF patients with massive ascites could be successfully treated with regular at-home abdominal paracentesis via Tenckhoff catheter. This treatment provides a useful alternative to periodical percutaneous paracentesis on as-needed basis.

PORTAL HYPERTENSION IN OSLER-WEBER-RENDU SYNDROME: A CASE REPORT

Hereditary hemorrhagic telangiectasia or Osler-Weber-Rendu syndrome is a rare autosomal dominant vascular disorder characterized by epistaxis, mucocutaneous telangiectasias, and arteriovenous malformations affecting various organs and systems. The liver is a commonly involved organ (74% of patients with hereditary hemorrhagic telangiectasia), although symptomatic liver disease is quite infrequent. In symptomatic cases, clinical manifestations relate most commonly to the predominant type of vascular shunting present (arteriovenous, arterioportal, or portovenous). Clinically, liver disease can manifest as a high-output cardiac failure, portal hypertension, or biliary disease. Imaging plays an important role in diagnosis, characterization, and follow-up of liver involvement, with ultrasound, computed tomography, magnetic resonance imaging, and angiography being useful in this context. We present a case of patient with Osler-Weber-Rendu syndrome with portal hypertension without evidence of liver cirrhosis.

Screening and linkage to care for medical students with hepatitis B virus infection in Sierra Leone

PurposeHepatitis B virus (HBV) infection is considered a major public health concern for Sierra Leone. Although medical students are at increased occupational risk for HBV infection, little is known about the burden of HBV infection amongst medical students in Sierra Leone. MethodsAs part of a screening and vaccination campaign, a cross-sectional study on prevalence of HBV among medical students in Freetown was conducted in December 2019. Antigen point of care test was used for HBV screening and data on students' risk history and demographics were collected. Additionally, for students diagnosed positive with HBV, linkage to care and initial assessment data after diagnosis was collected from the HBV clinic they were linked to. ResultsOne hundred and fifty-seven medical students (77.3%) from year three to six were screened for HBV infection. Almost all students (98.1%) had never been vaccinated against HBV and more than half (56.7%) reported a history of needle stick injuries. The prevalence of HBV infection (Hepatitis B surface antigen (HBsAg) positivity) was 10.2% (n = 16). Among HBsAg positive students, 75% (n = 12) were successfully enrolled at chronic HBV clinic within three months of diagnosis. Only one student had evidence of liver cirrhosis and was started on treatment with Tenofovir diproxil fumarate. ConclusionThe prevalence of HBV infection is high among medical students in Sierra Leone. Despite the high prevalence, most of the students linked to care had no evidence of severe liver disease.

A rare case of infiltrative hepatocellular carcinoma presented with neck mass

AbstractInfiltrative hepatocellular carcinoma (HCC) has a poorer prognosis and is more difficult to diagnose compared to other HCC subtypes. The presented case is a man with metastatic infiltrative HCC presented with bilateral neck masses. This 57‐year‐old hepatitis B virus (HBV) carrier man had HBV infection under control with no evidence of liver cirrhosis. Initially, there was a slight elevation of alpha fetal protein (AFP). Abdominal CT showed an ill‐defined lesion at liver without triphasic character of HCC and multiple abdominal lymphadenopathies. Yet there was no portal vein thrombosis. Cholangiocarcinoma was first favored. Later on, bilateral neck masses were noted. Cervical mass biopsy showed positive HepPar1 by immunohistochemical (IHC) stain. Metastatic infiltrative HCC was diagnosed, and he started to receive sorafenib. The size of neck lymphadenopathy decreased after 3‐month therapy, but the AFP value remained stationary. Infiltrative HCC is hard to detect. We reported a rare infiltrative HCC case with atypical finding on image study and cervical lymph node metastasis in hope that it would bring a better understanding of the disease.

High prevalence of undiagnosed liver cirrhosis and advanced fibrosis in type 2 diabetic patients

Background. Patients with type 2 diabetes mellitus (T2DM) are at risk for developing end-stage liver disease due to nonalcoholic steatohepatitis (NASH), the aggressive form of non-alcoholic fatty liver disease (NAFLD). Data on prevalence of advanced fibrosis among T2DM patients is scarce. Aim. To evaluate prevalence of steatosis, advanced fibrosis and cirrhosis using non-invasive methods in T2DM patients.Material and methods. 145 consecutive T2DM patients (> 55 years-old) were prospectively recruited. Presence of cirrhosis and advanced fibrosis was evaluated by magnetic resonance imaging (MRI) and NAFLD fibrosis score (NFS) respectively. Exclusion criteria included significant alcohol consumption, markers of viral hepatitis infection or other liver diseases. Results are expressed in percentage or median (interquartile range).Results. 52.6% of patients were women, the median age was 60 years old (57-64), mean BMI was 29.6 ± 4.7 kg/m2 and diabetes duration was 7.6 ± 6.9 years. A high prevalence of liver steatosis (63.9%), advanced fibrosis assessed by NFS (12.8%) and evidence of liver cirrhosis in MRI (6.0%) was observed. In a multivariate analysis GGT > 82 IU/L (P = 0.004) and no alcohol intake (P = 0.032) were independently associated to advanced fibrosis.Conclusion. A high frequency of undiagnosed advanced fibrosis and cirrhosis was observed in non-selected T2DM patients. Screening of these conditions may be warranted in this patient population.

Gut Dysbiosis Associated With Hepatitis C Virus Infection.

Little is known about the effect of hepatitis C virus (HCV) infection on gut microbiota and the relationship between alteration of gut microbiota and chronic hepatitis C (CHC) progression. We performed a comparative study of gut microbiota composition between CHC patients and healthy individuals. Fecal samples from 166 CHC patients were compared with those from 23 healthy individuals; the gut microbiota community was analyzed using 16S ribosomal RNA gene sequencing. CHC patients were diagnosed with persistently normal serum alanine aminotransferase without evidence of liver cirrhosis (LC) (PNALT, n = 18), chronic hepatitis (CH, n = 84), LC (n = 40), and hepatocellular carcinoma in LC (n = 24). Compared with healthy individuals, bacterial diversity was lower in persons with HCV infection, with a decrease in the order Clostridiales and an increase in Streptococcus and Lactobacillus. Microbiota dysbiosis already appeared in the PNALT stage with the transient increase in Bacteroides and Enterobacteriaceae. Predicted metagenomics of microbial communities showed an increase in the urease gene mainly encoded by viridans streptococci during CHC progression, consistent with a significantly higher fecal pH in CH and LC patients than in healthy individuals or those in the PNALT stage. HCV infection is associated with gut dysbiosis, even in patients with mild liver disease. Additionally, overgrowth of viridans streptococci can account for hyperammonemia in CH and LC. Further studies would help to propose a novel treatment strategy because the gut microbiome can be therapeutically altered, potentially reducing the complications of chronic liver disease.

Bleeding Downhill Varices Associated With Central Venous Catheter-Related Thrombosis: An Emphasis on Management

Esophageal varices can be uphill or downhill. Downhill varices (DV) occur less frequently and are due to obstruction of the superior vena cava that may lead to downward venous flow via esophageal collaterals towards the portal vein and inferior vena cava. 55 year-old female with a history of non-Hodgkin's lymphoma, ovarian cancer, coronary artery disease s/p stents, Factor V Leiden deficiency, stroke, chronic superior vena cava (SVC) syndrome who was admitted for melena and fatigue x 3 weeks. Currently on aspirin, Plavix and warfarin. She presented with Hemoglobin 6.1 from baseline of 11.6, INR 4.5. Platelets 350. US abdomen showed fatty liver, patent portal vein, no suggestion of veno-occlusive disease, no ascites. CT abdomen pelvis showed diffuse esophageal varices likely from collateral supply due to chronic SVC occlusion, no evidence of liver cirrhosis. EGD showed 3 columns of downhill esophageal varices with high-risk stigmata extending throughout the esophagus 15 - 40 cm. No gastric varices. She has h/o chronic SVC syndrome due to history of thrombosis of subclavian vein from a port placed decades ago. She underwent endovascular stenting few years ago that appears occluded on CT a year ago. This was followed by unsuccessful attempt at endovascular intervention on her chronically occluded stents to right subclavian vein and SVC. Repeat EGD showed 4 columns of small varices, no banding. Followed in GI and hematology clinic & undergoing variceal surveillance. DV contribute only 0.1% of all esophageal variceal bleeding. The most common etiology of bleeding DV is a complication related to a venous catheter. The diagnosis of DV is reached at endoscopy. This is recognized as a separate entity from portal hypertension varices, since both the etiology and clinical management are very different. DV bleed very rarely when compared to uphill varices. Cornerstone of the management is directed to the underlying cause of vascular obstruction (stents or vascular bypass in surgical candidates) that will cure the clinical syndrome and also prevent its recurrence. When all the above measures fail to resolve the obstruction only palliative measures can be applied. Endoscopic treatment options include banding however associated with increased risk of bleeding or perforation in upper esophagus. In general, endoscopic surveillance is recommended; however, the optimal interval is unknown.

Clinical Presentation, Treatment Outcome and Predictors of Severity in Autoimmune Hepatitis: A Retrospective, Multicenter Experience

AIM: Autoimmune Hepatitis (AIH) is a chronic hepatitis of unknown etiology. It affects adults and children and can progress to cirrhosis. We aim to investigate the mode of presentation, predictors of severity and treatment outcome of AIH in Saudi patients. METHODS: This is a multicenter retrospective study that involved patients diagnosed with AIH from 3 tertiary hospitals. Clinical, biochemical, radiological and histopathological data were collected and treatment outcomes were reported. RESULTS: A total of 212 patients were included. Female: male ratio was 3:2 and the mean age was 36.2 ± 16.8 years while 50 patients (23.6%) were above age of 50. Abnormal liver function tests (LFTs) were found in (45%). Presentation was chronic in 37.7%, acute in 30.7%, with evidence of liver cirrhosis in 28.8% and with a fulminant disease in 2.8%. Antinuclear antibody (ANA) and Anti-smooth muscle antibody (ASMA) were negative in 65 (30.6%) and 74 (35%) patients respectively. Pre-treatment liver biopsies in 166 patients showed advanced fibrosis (stage 3 and 4) in 63.3%. On multivariate analysis, platelets, alanine transaminase (ALT) level and immunoglobulin G (IgG) level were predictors of fibrosis. Complete response was achieved in 74.5% while 9% had partial response and 16.5% had no response to treatment. CONCLUSION: The majority of AIH patients had advanced fibrosis at the time of diagnosis and liver cirrhosis was found in nearly one-third of cases. IgG, ALT, and platelet were predictors of advanced fibrosis. Complete response to treatment was achieved in two-third of patients. Relying on autoimmune markers for diagnosis can be misleading.

The use of AFP and DCP as serum biomarkers to differentiate between hepatocellular carcinoma and intrahepatic cholangiocarcinoma in non-cirrhotic livers.

e15162 Background: Differential diagnosis of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) can be challenging in patients without evidence of liver cirrhosis. Definitive diagnosis is based on tissue biopsy. We investigated if the use of serum biomarkers could help differentiate between these two types of malignancies, thereby avoiding the risks associated with biopsy. Methods: Patients with cholangiocarcinoma and HCC were recruited from Queen Elizabeth Hospital, Birmingham, UK; blood samples were collected at time of diagnosis. Two biomarkers, alpha-fetoprotein (AFP) and des-gamma-carboxy prothrombin (DCP) were measured in the serum samples from 56 patients with cholangiocarcinoma and 35 patients with HCC without evidence of liver cirrhosis. Of the 56 patients with cholangiocarcinoma, 17 were intrahepatic and 39 were extrahepatic. Results: 17 ICC and 35 HCC were included in the analysis. The levels of AFP and DCP were much higher in HCC as compared to ICC. The median AFP was 64.6 (IQR 10.9, 3564.2) in HCC as compared to 3 (IQR 2.4, 3.9) in ICC. Similarly, the median DCP was 215.41 (IQR 22.46, 692.53) in HCC as compared to 0.33 (IQR 0.16, 1.08) in ICC. Stepwise logistic regression was performed using both biomarkers. Log- DCP remained significant at 95% level in predicting HCC from ICC, giving an AUC of 0.96. Conclusions: In patients with a non-cirrhotic liver and radiological evidence of cancer, measurement of serum AFP and DCP level may help differentiate between HCC and ICC. In this study, DCP is the most useful discriminator between HCC and ICC. Further prospective studies should be done with larger sample sizes to validate the use of AFP and DCP as diagnostic biomarkers in this clinical setting.

Case of idiopathic portal hypertension complicated with autoimmune hepatitis

We report a case of idiopathic portal hypertension (IPH) complicated with autoimmune hepatitis. A 60-year-old woman was admitted to our hospital with esophageal and gastric varices in February 2010. Abdominal ultrasonography and computed tomography showed splenomegaly and collateral veins without evidence of liver cirrhosis. Laboratory examinations and liver biopsy indicated that the esophageal and gastric varices were caused by IPH. She underwent endoscopic injection sclerotherapy and partial splenic embolization. Two years after these therapies, laboratory examinations showed liver dysfunction with elevated levels of aspartate aminotransferase (180 IU/L), alanine aminotransferase (190 IU/L), γ-glutamyl transpeptidase (159 IU/L) and immunoglobulin G (2609 mg/dL). The titer of antinuclear antibodies was 1:320 and its pattern was homogeneous and speckled. Histological examination revealed plasma cell/lymphocyte infiltration and interface hepatitis in the portal tract. Based on these findings, a diagnosis of autoimmune hepatitis accompanied by IPH was made. After treatment with prednisolone (20 mg/day), liver functions were normalized immediately. Overlapping of IPH and AIH is extremely rare, but the present case is interesting considering the etiology of IPH because an autoimmune mechanism is thought to be involved in the pathogenesis of IPH.

Towards an easier pleurodesis: Ultrasound-guided iodopovidone sclerotherapy in cirrhotic patients with hepatic hydrothorax

Background and Aim: Hepatic hydrothorax is one of the complications encountered in end stage liver disease. Pleural drainage carries the risk of massive protein and electrolyte depletion as well as the risk of bleeding and hepatic encephalopathy. Pleurodesis following pleural aspiration decreases the chance of pleural effusion recurrence, and has been a widely used long-standing method of controlling recurrent pleural effusions. The aim of this study is to evaluate the effect of pleurodesis using ultrasound-guided iodopovidone sclerotherapy in hepatic hydrothorax. Patients and Methods: This prospective study included 56 patients with clinical, laboratory and radiological evidence of liver cirrhosis and symptomatic right sided hepatic hydrothorax. All patients were subjected to repeated thoracentesis. Ten ml of lidocaine 2% were injected in the pleural space followed by 20 ml of iodopovidone. The follow-up was done after 3 months. Results: The sclerotherapy procedure was successful in 40 out of 56 cases (71.4%), and the success rate was 66.7% in massive effusion and reached 80% in moderate effusion. Twenty eight patients (50%) had to repeat the procedure for a second time, sixteen of which (28.6%) failed despite the second trial and twelve cases (21.4%) showed no fluid reaccumulation. Conclusion: Ultrasound-guided iodopovidone sclerotherapy is an effective approach for a successful pleurodesis in hepatic hydrothorax.

Quantitative hepatic CT perfusion measurement: Comparison of Couinaud's hepatic segments with dual-source 128-slice CT

PurposeTo compare the quantitative liver computed tomography perfusion (CTP) differences among eight hepatic segments. Materials and methodsThis retrospective study was based on 72 acquired upper abdomen CTP scans for detecting suspected pancreas tumor. Patients with primary or metastatic liver tumor, any focal liver lesions except simple cyst (<3cm in diameter), history of liver operation or splenectomy, evidence of liver cirrhosis or invasion of portal vein were excluded. The final analysis included 50 patients (M:F=21:29, mean age=43.2 years, 15–76 years). Arterial liver perfusion (ALP), portal-venous perfusion (PVP), total hepatic perfusion (THP=ALP+PVP), and hepatic perfusion index (HPI) of each hepatic segment were calculated and compared by means of one-way analysis of variance (ANOVA) and the Bonferonni correction method. ResultsCompared to hepatic segments 5, 6, 7 and 8, segments 2 and 3 showed a tendency of higher ALPs, lower PVPs, and higher HPIs, most of which were statistically significant (p<0.05). Hepatic segments 1 and 4 had higher mean values of ALP and HPI and lower mean values of PVP than segments 5, 6, 7 and 8 as well, although no significant differences were detected except for ALP and HPI for liver segments 1 and 7 (p=0.001 and 0.035 respectively), and ALP for liver segments 1 and 5 (p=0.039). Higher ALP and HPI were showed in hepatic segment 3 compared to segment 4 (p=0.000 and 0.000 respectively). No significant differences were found for THP among eight segments. ConclusionsIntra-hepatic perfusion differences exist in normal hepatic parenchyma especially between lateral sector (segments 2 and 3) and right lobe (segments 5, 6, 7 and 8). This might have potential clinical significance in liver-perfusion-related protocol design and result analysis.

Disseminated Sarcoidosis Resulting in Portal Hypertension and Gastrointestinal Bleeding: A Rare Presentation

A 41-year-old man was evaluated for an upper gastrointestinal bleed. He was stabilized and an upper esophagogastroduodenoscopy revealed gastritis and esophageal varices. A computed tomography (CT) scan of the abdomen showed hepatosplenomegaly and moderate ascites. Analysis of the ascitic fluid was consistent with portal hypertension. A liver biopsy demonstrated noncaseating granuloma consistent with sarcoidosis, there was no evidence of liver cirrhosis on pathology. Portal hypertension associated with sarcoidosis is rare; after the first reported case in 1949, 35 other cases have been reported in the English literature, with only 16 patients presenting with portal hypertension without evidence of liver cirrhosis. Our patient is among the small group reported to have sarcoidosis-related portal hypertension without evidence of liver cirrhosis. The present case illustrates the importance of recognizing an uncommon manifestation of sarcoidosis

HBsAg Seroclearance in Chronic Hepatitis B

The long-term clinical course, including the development of hepatocellular carcinoma (HCC) after hepatic B surface antigen (HBsAg) seroclearance is not established. We discovered that the incidence of HCC and the risk factors for HCC in chronic hepatitis B (CHB) patients after HBsAg seroclearance. During 28 years, 96 CHB patients with HBsAg seroclearance were retrospectively reviewed. These patients continued to undergo HCC surveillance. The median follow-up time from initial visit was 166.5 months (range, 7 to 321 mo). The mean age at the initial visit and at the time of seroclearance was 39.2 ± 10.6 years and 46.4 ± 9.9 years, respectively. The mean age at the time of HBsAg seroclearance was significantly lower (P=0.03) in patients with spontaneous HBsAg seroclearance than patients with treatment-associated HBsAg seroclearance. During a median of 56 months (range, 7 to 238 mo) of follow-up after HBsAg seroclearance, 6 (6.5%) patients developed HCC. The mean age at the time of developing HCC was 55.8 ± 10.3 years. On univariate analysis, the evidence of liver cirrhosis from the time of HBsAg seroclearance and age more than 45 years at the time of HBsAg seroclearance were significant risk factors for HCC development. In multivariate analysis, the evidence of liver cirrhosis at HBsAg seroclearance was the only significant risk factor for HCC development. HCC can develop after HBsAg seroclearance in patients with known cirrhosis. Patients who achieved HBsAg seroclearance at older age (>45) may have undiagnosed cirrhosis and hence remain at risk for HCC. HCC surveillance should be carried out for both of those patient populations.

Acute Budd-Chiari Syndrome

1Division of Gastroenterology; 2Department of Laboratory Medicine; 3Department of Surgery, University of British Columbia, Vancouver, British Columbia Correspondence: Dr Eric M Yoshida, Division of Gastroenterology, Vancouver General Hospital, Diamond Health Care Centre, 5153-2775 Laurel Street, Vancouver, British Columbia V5Z 1M9. Telephone 604-875-5371, fax 604-875-5447, e-mail eric.yoshida@vch.ca Received for publication April 8, 2011. Accepted April 11, 2011 CASE PRESENTATION A 23-year-old woman presented to hospital with a two-week history of abdominal pain, nausea and increasing abdominal girth. Her medical history was significant only for migraines and oral contraceptive use. Laboratory values showed an alanine aminotransferase level of 155 U/L, an aspartate aminotransferase level of 85 U/L, an alkaline phosphatase level of 165 U/L, total bilirubin of 12 μmol/L (0.71 mg/dL), an albumin concentration of 27 g/L (2.7 g/dL) and an international normalized ratio of 1.2. An abdominal Doppler ultrasound and a computed tomography angiogram (Figure 1) demonstrated a nonocclusive, intrahepatic inferior vena cava (IVC) clot measuring 3.4 cm × 1.4 cm, as well as marked ascites. The patient subsequently began to develop congestive hepatopathy and was scheduled for emergency placement of a portocaval shunt to protect her liver function. Caudate lobectomy was required to expose the IVC for a polytetrafluoroethylene graft anastomosis. Pathology of the caudate lobe and random biopsies from the right and left lobes showed focal hepatic vein and central venous organizing thrombosis with concomitant sinusoidal dilation (Figure 2). The patient had a relatively uncomplicated postoperative recovery. Portocaval shuntogram and pressure measurements showed a widely patent shunt with no significant pressure gradient. Thrombophilia workup was negative for any identifiable intrinsic clotting disorder. DISCUSSION Budd-Chiari syndrome is caused by thrombosis of the hepatic veins and/or the thrombosis of the intrahepatic or suprahepatic IVC. While an underlying etiology such as malignancy, rheumatological disorder, myeloproliferative disease, inheritable coagulopathy, infection or hyperestrogen state can be identified in many cases, the etiology remains idiopathic in 16% to 35% of cases (1-3). Clinical presentations vary – ranging from acute or fulminant liver failure, to subacute (signs or symptoms for less than six months and no evidence of liver cirrhosis) to chronic (signs or symptoms for more than six months with evidence of portal hypertension and cirrhosis). The goals of therapy are to prevent the propagation of the clot, restore patency of thrombosed veins, decompress liver congestion and manage complications such as ascites and portal hypertension. For acute thrombosis, thrombolytic therapy or radiological procedures (eg, angioplasty, stenting or transjugular intrahepatic portosystemic shunts) can be considered; however, surgical decompression remains the mainstay of treatment. Surgical shunts commonly connect the portal venous system to the IVC, creating a low-pressure route for hepatic arterial blood to drain from the liver. In patients who underwent shunt surgery before development of cirrhosis and whose shunts remain patent, five-year survival rates of as high as 89% have been reported (4-6). Chronic Budd-Chiari syndrome is managed with anticoagulation and treatment of the complications of liver failure. Rarely, liver transplantation may be necessary. IMAGE OF THE MONTH

Spontaneous viral clearance of chronic HCV infection in Upper Egypt: A community-based study with a 10 year follow-up

Background and study aims Hepatitis C virus (HCV) infection is a global blood-borne disease with the highest prevalence in Egypt. The natural course of HCV infection is highly variable. The reason why the infection persists in some patients and resolves spontaneously in others is not known. The aim of this study was to detect the frequency of spontaneous clearance of chronic HCV infection in Upper Egypt and to determine the predictors of persistence of HCV infection. Patients and methods In 1997, a community-based study was performed in Sallam village in Upper Egypt. Out of the 329 patients who had positive HCV-RNA, 200 patients were included in this study, after excluding cirrhotic patients at the start of the study and those who had received specific treatment for HCV infection. These patients were followed up every six months prospectively starting from 2004 till 2007 by clinical, ultrasonographic, and laboratory examinations (liver functions, complete blood count, prothrombin time and concentration). Serum HCV-RNA was tested for at the end of the follow up period. Results After a 10-year follow-up, spontaneous clearance of chronic HCV infection was detected in 35 (17.5%) out of 200 patients. Most of clinical and laboratory abnormalities were detected in patients with HCV-RNA persistence than those who had cleared HCV-RNA. By ultrasonographic examination, normal liver echopattern was found in 30 (85.7%) cases with HCV-RNA clearance and in 75 (45.5%) patients who had HCV-RNA persistence. Evidence of liver cirrhosis was found only in 9 cases with HCV-RNA persistence (5.5%). Old age (>60 years) was the strongest predictor of persistence of HCV infection followed by obesity and history of blood transfusion. Conclusions Spontaneous clearance of chronic HCV infection could occur without any specific antiviral therapy in 17.5% of patients. Older age was the strongest predictor of persistence of HCV infection followed by obesity and infection by blood transfusion.

CONGENITAL HEPATIC FIBROSIS WITHOUT ANY SYMPTOMS AS DIAGNOSED BY LAPAROSCOPY

The present report represents the case of a 36-year-old woman with congenital hepatic fibrosis (CHF). She was admitted to our hospital because of gastric varices. She was asymptomatic and her liver function tests were within normal limits. Computed tomography showed hepatomegaly, splenomegaly and collateral circulation, but no evidence of liver cirrhosis. Real-time tissue elastography suggested severe fibrosis of the liver. Laparoscopy showed wide and discrete white markings on the surface of the liver and she was diagnosed with CHF based on the histological examination. The findings obtained from elastography and laparoscopy were useful for making the diagnosis of CHF.

Imatinib treatment for patients with advanced stage hepatocellular carcinoma: A multicenter phase II trial.

e14629 Background: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide with limited treatment options in advanced stages. The antitumor activity of systemic chemotherapies in patients with HCC has been disappointing. The aim of this study was to evaluate the safety and efficacy of imatinib, a tyrosine kinase inhibitor, in patients with advanced HCC. Methods: Patients with stage III and IVa/b HCCs without surgical and/or loco ablative therapeutic options and preserved liver function (CPC A/B) were eligible. The patients were treated with 400 mg imatinib daily for 12 months. Response was assessed by CT scan. Results: 22 patients (5 f, 16 m; mean age 67) were enrolled in this study. The causes of liver disease were mainly viral (5) and (non) alcoholic fatty liver disease (8). 15 patients presented with CPC A and 3 with B, 3 patients had no evidence of liver cirrhosis. 14 patients had had previous HCC-treatments, mainly resection or loco ablative therapies. Patients were treated with imatinib for a median time period of 9 (4-52) weeks; in 10 patients imatinib was discontinued due to tumor progression, in 4 due to the patients' decision, in 2 due to decompensated liver cirrhosis and in one due to pruritus; 4 patients received the drug for the intended 12 months. Median TTP was 12 (95%CI: 10-14) weeks. Two patients (HCC in noncirrhotic liver) had stable disease throughout the study period, one until discontinuation (pruritus) and the remaining 18 patients developed disease progression. The median overall survival was 7.4 (95%CI: 5.9-8.9) months. Complications due to decompensated liver cirrhosis were the causes of death in all patients. No severe adverse event related to imatinib was observed; the most common adverse events were nausea (10) and peripheral edema (8). In 4 patients imatinib dosage had to be reduced to 200 mg daily after 2, 4, 14 and 28 weeks of treatment because of nausea (3) and angioedema (1). Conclusions: The results of this multicenter study suggest that imatinib is well tolerated in the majority of HCC patients. The median TTP was 11 weeks which is comparable to other targeted therapies indicating that imatinib might be a promising candidate for further studies in the treatment of advanced HCC. No significant financial relationships to disclose.

Imatinib treatment for patients with advanced stage hepatocellular carcinoma: A multicenter phase II trial

Background: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide with limited treatment options in advanced stages. The antitumor activity of systemic chemotherapies in patients with HCC has been disappointing. The aim of this study was to evaluate the safety and efficacy of imatinib, a tyrosine kinase inhibitor, in patients with advanced HCC. Methods: Patients with stage III and IVa/b HCCs without surgical and/or loco ablative therapeutic options and preserved liver function (CPC A/B) were eligible. The patients were treated with 400mg imatinib daily for 12 months. Response was assessed by CT scan. Results: 22 patients (5 f, 16m; mean age 67, range 47–84 ys.) were enrolled in this study. The causes of liver disease were mainly viral (5) and (non) alcoholic fatty liver disease (8). 15 patients presented with CPC A and 3 with B, 3 patients had no evidence of liver cirrhosis. 14 patients had had previous HCC-treatments, mainly resection or loco ablative therapies (TACE, PEI). Patients were treated with imatinib for a median time period of 9 (4–52) weeks; in 10 patients imatinib was discontinued due to tumor progression, in 4 due to the patients' decision, in 2 due to decompensated liver cirrhosis and in one due to pruritus; 4 patients received the drug for the intended 12 months. Median TTP was 12 (95%CI: 10–14) weeks. Two patients (HCC in non-cirrhotic liver) had stable disease throughout the study period, one until discontinuation (pruritus) and the remaining 18 patients developed disease progression. The median overall survival was 7.4 (95%CI: 5.9–8.9) months. Complications due to decompensated liver cirrhosis were the causes of death in all patients. No severe adverse event related to imatinib was observed; the most common adverse events were nausea (10) and peripheral edema (8). In 4 patients imatinib dosage had to be reduced to 200mg daily after 2, 4, 14 and 28 weeks of treatment because of nausea (3) and angioedema (1). Conclusion: The results of this multicenter study suggest that imatinib is well tolerated in the majority of HCC patients. The median TTP was 11 weeks which is comparable to other targeted therapies indicating that imatinib might be a promising candidate for further studies in the treatment of advanced HCC.