Pancreatobiliary Lymphadenopathy: Etiology, Location, and Factors Predicting Good Yield of Endoscopic Ultrasound-guided Biopsy.

Introduction: Pancreatobiliary lymphadenopathy (PBL) may be due to a number of benign or malignant causes. Tissue sampling of these lymph nodes (LN) can be possible with the help of endoscopic ultrasound (EUS). Aim of this study was to identify the etiology of the PBL, morphology, and factors predicting good yield of biopsy with EUS. Materials and methods: All patients found to have pancreatobiliary lymph node (PBLN) enlargement (>10 mm) on abdominal imaging and referred for EUS-guided biopsy were included in this prospective observational study. The facility of rapid on-site evaluation (ROSE) was not available. Adequacy of the tissue specimen was assessed by the endoscopist with macroscopic on-site evaluation (MOSE) and then sent to histopathologist for final diagnosis. Factors predicting good yield of biopsy were then analyzed. Results: Of the total 87 patients with PBL, 54 (62.1%) were males. Mean age of the patients was 52.0 (±13.4) and range 18-80 years. The commonest locations of PBL were porta hepatis 37 (42.5%), peripancreatic 24 (27.6%), celiac 16 (18.4%), and others 10 (11.5%). Histological reports showed: neoplastic tissue in 34 (39.1%), non-neoplastic in 20 (23%), normal lymphoid tissue (27.6%) and suboptimal in 9 (10.3%). Among the 34 neoplastic causes, 26 had metastatic adenocarcinoma, 5 had lymphoma, and 3 had metastatic neuroendocrine tumors. Among the 20 non-neoplastic causes, 10 had tuberculosis, 4 had anthracosis, and 6 had other findings. Factors predicting good yield of biopsy were a PBLN size ≥12 mm and satisfactory MOSE on both univariate [PBLN (p = 0.005); MOSE (p < 0.0001)] and multivariate [PBLN (p = 0.011); MOSE (p < 0.0001)] analysis. Conclusion: The commonest etiology of PBLN enlargement was metastatic adenocarcinoma among the neoplastic causes and tuberculosis among the non-neoplastic causes. The most common PBLNs approached by EUS were in portahepatis and peripancreatic regions. A good biopsy yield can be predicted with PBLN size of ≥12 mm and a satisfactory MOSE. How to cite this article: Tasneem AA, Yaseen T, Laeeq SM, et al. Pancreatobiliary Lymphadenopathy: Etiology, Location, and Factors Predicting Good Yield of Endoscopic Ultrasound-guided Biopsy. Euroasian J Hepato-Gastroenterol 2024;14(1):40-43.

Cytomegalovirus-Associated Colitis as a Cause of Lower Gastrointestinal Bleeding in Kidney Transplant Recipients: A Single-Centered Study.

Introduction Cytomegalovirus (CMV) is the most common viral pathogen affecting patients undergoing solid organ transplantation. It is often the most important infection for patients who have undergone kidney transplantation. Clinical presentations of cytomegalovirus infection range from asymptomatic infection to organ-specific involvement. This study aimed to determine the frequency of cytomegalovirus-associated colitis in kidney transplant recipients (KTRs) presenting with lower gastrointestinal bleeding. Methods After the approval of the ethical review committee of the Sindh Institute of Urology and Transplantation (ERC-SIUT), this cross-sectional study was conducted at the Department of Hepatogastroenterology at the Sindh Institute of Urology and Transplantation from January 2021 to December 2021. All the KTRs (six months after the transplantation) of either gender and aged between 18 and 65 years, presenting with lower gastrointestinal (GI) bleeding as per the operational definition, were enrolled in the study. Those patients who were either unfit for the endoscopy or refused to give consent were excluded from the study. Colonic biopsies were reviewed by a consultant histopathologist for the features of CMV infection. Results A total of 95 renal transplant recipients of either gender or age above 18 to 65 years with lower GI bleeding were included in the study. Among them, 84 (88.4%) were males, while 11 (11.6%) were females. The mean age of the patients included in the study was 37±11 years. The most common presenting complaint was fresh bleeding per rectum, which was observed in 73 (76.8%). The most common findings observed on colonoscopy in KTRs with bleeding per rectum were colonic ulcers and erosions noted in 41 (43.1%) and 36 (37.3%) patients, respectively. On histopathology, CMV colitis was noted in 21 (22.1%) patients. On comparison of different baseline variables, the presence of fresh bleeding per rectum and the presence of both ulcers and erosions on colonoscopy were the factors significantly associated with CMV colitis in KTRs. Conclusion CMV colitis is a prevalent condition in KTRs, presenting with lower GI bleeding. Despite the significant occurrence, the levels of CMV viremia were not associated with CMV colitis, suggesting that diagnosis should rely on histopathological confirmation. Prophylaxis during periods of high immunosuppression is crucial to reducing the incidence of CMV infections and improving both graft function and patient survival.

Reinforcing the management of type 1 gastric esophageal varices.

Variceal bleed represents an important complication of cirrhosis, with its presence reflecting the severity of liver disease. Gastric varices, though less frequently seen than esophageal varices, present a distinct clinical challenge due to its higher intensity of bleeding and associated mortality. Based upon the Sarin classification, GOV1 is the most common subtype of gastric varices seen in clinical practice.

Ascitic Fluid Lactate Level as a Predictor of Mortality in Cirrhotic Patients Having Spontaneous Bacterial Peritonitis (SBP).

Introduction Limited studies are available for predicting mortality in patients with spontaneous bacterial peritonitis (SBP) based on ascitic fluid analysis. Recently, a proposition has been made regarding the role of ascitic fluid lactate as a better prognostic indicator of mortality in cirrhotic patients with SBP. Therefore, we aimed to evaluate the utility of ascitic fluid lactate in predicting mortality in cirrhotic patients with SBP. Methods This was a prospective, observational study that was conducted in the Hepato-Gastroenterology Department of Sindh Institute of Urology and Transplantation (SIUT), Karachi from 1 January 2022 to 31 December 2022. All the patients having liver cirrhosis with ascites, aged between 18 and 65 years, and presenting with fever and/or abdominal pain were recruited in the study in the first six months (i.e., from 1 January 2022 to 30 June 2022) and were followed for six more months for the outcome. However, those patients on dialysis or those with hepatocellular carcinoma, any other malignancy as per a history of solid organ transplant, a history of HIV infection, or those underlying systemic sepsis or infections other than SBP were excluded from the study. The presence or absence of SBP was confirmed by doing the ascitic fluid analysis. Ascitic fluid lactate levels were also requested in each patient. Mortality was assessed at one, two, three, and six months, respectively. All the data were analyzed using SPSS version 23.0. The area under the receiver operating curve (AUROC) was obtained for ascitic fluid lactate for predicting mortality in SBP. At an optimal cutoff, the diagnostic accuracy of ascitic fluid lactate was obtained. Results The total number of cirrhotic patients included in the study was 123. The majority of the patients belong to Child Turcotte Pugh (CTP) class C (n = 88; 71%). Two third of the patients (65.8%; n = 81) had viral hepatitis i.e., hepatitis B, D, and/or C, as the cause of cirrhosis. Overall mortality was observed in 51(41.5%) patients. Ascitic fluid lactate was significantly raised in patients with SBP than in patients with non-SBP (p = 0.004). The AUROC of ascitic fluid lactate was highest at three months (AUROC = 0.88) followed by six months (AUROC = 0.84), two months (AUROC = 0.804), and one month (AUROC=0.773). At an optimal cut-off of more than or equal to 22.4 mg/dl, ascitic fluid lactate had a sensitivity of 84.9%, specificity of 85.7%, positive predictive value (PPV) of 97.3%, negative predictive value of 42.8% with diagnostic accuracy of 85% in predicting overall mortality in patients with SBP. On sub-analysis, the diagnostic accuracy of ascitic fluid lactate was highest at six months followed by at three, two, and one month, respectively. Conclusion Ascitic fluid lactate showed a good diagnostic utility in predicting the overall mortality in patients with SBP with the best diagnostic accuracy in predicting long-term (six months) mortality. However, further studies are required to validate our results.

Etiologies Associated With Elevated Liver Enzymes After Renal Transplant.

OBJECTIVES: One of the most important causes of morbidity and mortality in renal transplant recipients is liver disease. Liver dysfunction is shown in 7% to 67% of kidney transplant recipients. Liver insufficiency accounts for death in up to 28% of kidney transplant recipients. We stratified various etiological factors responsible for elevated liver enzymes in kidney transplant recipients. MATERIALS AND METHODS: We enrolled all patients who fulfilled inclusion criteria. The principal investigator obtained and recorded demographic and clinical information via a standardized form. We reviewed clinical records of kidney recipients with hepatotoxicity during the course of illness, and we analyzed data with SPSS statistical software (version 22). Descriptive statistics were used for continuous and categorical variables. RESULTS: All recipients of living related renal transplants from January 2015 to December 2016 were included in the study (n = 496). We excluded 64 patients with positive serology for hepatitis B or hepatitis C before transplant. Of the remaining 432 patients, 74 (17.1%) had deranged liver enzymes. Forty-one patients (55.4%) had deranged liver enzymes 3 to 4 years after transplant, whereas 23 patients (31.1%) had deranged liver enzymes 4 years after transplant. Liver parenchymal biopsy was performed in 17 patients (23%) to evaluate the etiology. The most common cause of deranged liver enzymes was sepsis, which was seen in 21 patients (28.4%), followed by viral hepatitis, ie, cytomegalovirus hepatitis in 7 (9.5%) and hepatitis C in 6 (8.1%) patients. Other causes included antituberculosis treatment-induced liver injury, autoimmune hepatitis, sinusoidal obstruction syndrome, and nonalcoholic steatohepatitis, observed in 4 patients each (5.4%). CONCLUSION: The most common cause of deranged liver enzymes in patients who received living related renal transplants in our population was sepsis, which can have a substantial effect on graft survival.

Recurrence Rate of Early Hepatitis C Virus Infection After Renal Transplantation Following Successful Treatment of Patients on Dialysis With Direct-Acting Antiviral Agents.

OBJECTIVES: Recurrence of hepatitis C virus after organ transplant has dreadful complications. An excellent response has been shown with direct-acting antiviral agents in transplant recipients. Although a sustained virological response is considered as the virological cure, it requires patients to be on dialysis for 3 months more before undergoing renal transplant, thus increasing the risk of hepatitis C virus reinfection and associated complications. We aimed to determine hepatitis C virus recurrence in renal transplant recipients who had achieved endof-treatment response before transplant. MATERIALS AND METHODS: Per our institutional dialysis protocol, patients who do not achieve rapid virological response are treated with 6 months of direct-acting antiviral agents. All patients who achieve end-of-treatment response are then referred for renal transplant. Our study included kidney transplant recipients who were treated with directacting antiviral agents and had a hepatitis C virus polymerase chain reaction test 3 months after renal transplant. We obtained demographic and clinical data of patients and used SPSS version 20.0 for statistical analyses. RESULTS: Our study included 48 transplant recipients; most were males (81.1%) with mean age of 28.7 ± 9.4 years. All patients received sofosbuvir, daclatasvir, and ribavirin combination before transplant. Most patients (70%) received treatment for 3 months. The polymerase chain reaction test for hepatitis C virus was conducted after a mean of 8.3 ± 3.3 months posttransplant. Laboratory parameters showed total bilirubin of 3.6 ± 17.5 mg/day, alanine aminotransferase of 51.5 ± 80.2 IU/L, and gammaglutamyltransferase of 133.9 ± 220 IU/L. Two recipients (4.2%) had posttransplant recurrence of hepatitis C virus infection. CONCLUSIONS: To our knowledge, this study is the first to document excellent response of direct-acting antivirals in renal transplant recipients who had been referred early for transplant. Thus, dialysis patients can undergo transplant after achieving end-oftreatment response.

Management of Tacrolimus-Induced Toxicity With Normal Serum Levels After Liver Transplant.

Drug-induced liver injury after liver transplant occurs in 1.7% of patients. Tacrolimus is an effective immunosuppressant that is used to treat acute rejection. Although rare, it can cause toxicity, which is demonstrated by cholestatic liver injury. Here, we present a case of a young male patient who was diagnosed with Wilson disease, had penicillaminechelating therapy, and underwent living related liver transplant. Within 1 month posttransplant, he developed deranged, predominantly cholestatic pattern liver function tests. Laboratory parameters showed total bilirubin of 1.12 mg/ dL, alanine aminotransferase of 553 IU/L, gammaglutamyltransferase of 624 IU/L, and tacrolimus level of 10.2 ng/mL. After thorough evaluation, a liver biopsy was performed. Liver biopsy showed hepatocellular necrosis with centrilobular cholestasis without any evidence of graft rejection. However, with normal level of tacrolimus, the biopsy was suggestive of drug-induced liver injury. Thus, tacrolimus dose was reduced, resulting in improved liver function tests and patient discharge from the hospital. Tacrolimus is an effective immunosuppressant after liver transplant and has the ability to treat early acute rejection. The patient's liver biopsy showed hepatocellular necrosis with centrilobular cholestasis without any evidence of graft rejection. Cholestatic liver injury after tacrolimus usually resolves after dose reduction or by switching to another agent. With demonstrated tacrolimus-induced toxicity in liver transplant recipients, despite normal serum levels, transplant physicians should keep high index of suspicion regarding toxicity in the posttransplant setting.