Fibroprogression and Cirrhosis Occurring in Living Liver Donor: First Case Report.

Background: Limited dead donor pool paved the way for living liver donation so that waitlist mortality could be reduced. With over two decades of experience in the East as well as in the West, right lobe adult-to-adult living donor liver transplantation has become an established intervention. The short-term surgical outcomes, complications and health-related quality of life are well known. There is dearth of data on long-term health of remnant liver of donors, especially after a decade of donation. Case description: A 56-year-old lady who donated her right liver lobe 11 years back for her husband with end-stage liver disease. Recipient is doing well till date. She was incidentally found to have thrombocytopenia on follow-up. Her haematological evaluation was negative for blood dyscrasias. Further evaluation demonstrated biopsy-proven cirrhosis with endoscopic evidence of portal hypertension. Aetiological workup was done, which ruled out viral, autoimmune causes as well as Wilson's disease and hemochromatosis. This donor had gained weight post-donation with body mass index of 32.4 kg/m2 and dyslipidaemia. The final diagnosis of fibro progression due to non-alcoholic fatty liver disease was made. Conclusion: We report the first case of cirrhosis developing in a right lobe living liver donor. While selecting living liver donors, extensive evaluation is done to rule out all potential aetiologies remaining silent but later could lead on to chronic liver disease. Although all other aetiologies, which could induce inflammation and fibrosis, are ruled out at the time of donation, lifestyle liver disease, especially non-alcoholic fatty liver disease, can occur in remnant liver post-donation. This case underscores the importance of regular follow-up of liver donors.

Impact of sarcopenia on post-liver transplant morbidity and mortality in cirrhotic patients.

BACKGROUND: Modalities available for severity assessment and prediction of complications after liver transplant (LT) in cirrhotic patients are model for end-stage liver disease-sodium (MELD-Na) and Child-Turcotte-Pugh (CTP) scores. The limitation of these scores is the lack of assessment of nutritional and functional status. Sarcopenia is a newer modality, which is developed for objective assessment of nutritional status. The aim of this study is to analyze the significance of sarcopenia in predicting 1-year mortality and morbidity in post-LT patients. METHODS: In this retrospective study, patients who underwent LT for cirrhosis between January 2013 and December 2018 were included. A computerized tomography (CT) image was used to analyze the psoas muscle index at the L3 vertebra (L3-PMI), and sarcopenia was defined as the values belonging to the lowest quartile of L3-PMI. The effect of sarcopenia on mortality and morbidity in terms of requirement for mechanical ventilation, duration of hospital stay, and occurrence of infections was studied. RESULTS: Among the study population (n = 74), 71 were men and the mean age was 51 years. Sarcopenia was observed in 27% (n = 20). Fifteen recipients had mortality within 1 year after transplant. In our analysis, sarcopenia was significantly associated with 1-year mortality (sensitivity 60%, specificity 81%; positive predictive value [PPV] 45%; negative predictive value [NPV] 88%; and p-value 0.001). Duration of mechanical ventilation, total hospital stay, and occurrence of infection were not significantly associated with sarcopenia. Sarcopenia was found as an independent predictor of mortality on binary logistic regression. CONCLUSION: The preoperative sarcopenia index in cirrhotic patients can predict the risk of mortality in post-liver transplant patients.

Hepatitis B Reactivation in Liver Transplant Recipients With Hepatitis B Virus Core Antibody Positive Grafts: a Retrospective Study.

BACKGROUND: Liver grafts from hepatitis B core antibody (anti-HBc) positive donors increase the risk of hepatitis B virus (HBV) reactivation in recipients due to posttransplant immunosuppressive therapy. AIM AND OBJECTIVE: to study the HBV reactivation in liver transplant recipients with anti-HBc-positive donors. METHODS: This was a retrospective study. Liver transplant recipients who received grafts from anti-HBc-positive donors between January 2013 and December 2017 were included in analysis. Hospital records of all subjects for a 2-year posttransplantation period were studied to observe reactivation of hepatitis B. As per our institute protocol, prophylaxis for HBV was given to subjects with either positive hepatitis B surface antigens or hepatitis B surface antibody (anti-HBs) titre <100 mIU/ml, after transplantation with anti-HBc-positive donor grafts. Recipients with anti-HBs titre >100 mIU/mL were exempted from prophylaxis and kept on regular monitoring for HBV markers. RESULTS: Of 85 liver transplant recipients, 20 subjects who received anti-HBc-positive grafts were included in analysis. The mean age of the study population was 46 years (range 2-68 years). The most common aetiology of cirrhosis in our study population was cryptogenic followed by ethanol. Among the study population, 16 (80%) transplant recipients had anti-HBs titre less than 100 mu/ml and 4 (20%) subjects had anti-HBs > 100 miu/ml. HBV reactivation occurred in 6 (30%) subjects. Reactivation was seen even in those who received HBV prophylaxis, while none of the subjects with anti-HBs titre >100 miu/ml developed HBV reactivation despite absence of prophylaxis. CONCLUSION: HBV reactivation can occur even in the presence of target anti-HBs titre (i.e. >10 miu/ml) and HBV prophylaxis during postliver transplantation. However, HBV reactivation is not seen in recipients with anti-HBs titre of >100 miu/ml.

Prevalence and determinants of hepatopulmonary syndrome in decompensated chronic liver disease.

BACKGROUND: One of the severe complications of liver disease is hepatopulmonary syndrome (HPS). There is paucity in literature regarding the various factors associated with the development of HPS. This study was conducted to analyze the prevalence and determinants of HPS among patients with decompensated chronic liver disease (CLD). METHODS: This study was a cross-sectional-observational study conducted in a tertiary care center. Decompensated CLD patients admitted for pre-liver transplant workup were included in the study. Demographic data, clinical findings, and biochemical and hematologic parameters were collected. Pulse oximetry, arterial blood gas analysis, bubble contrast echocardiogram, diffusion capacity of the lungs for carbon monoxide (DLCO), and spirometry were done to get the needed parameters. All data were entered into a Microsoft Excel sheet and analyzed using the statistical software SPSS for Windows, version 22.0. RESULTS: Among 64 subjects, 58 were men (90.6%). Mean age was 54.5 years. HPS was present in 26 (40.6%) patients. Platypnea and orthodeoxia were present more often in HPS patients. DLCO was significantly impaired among patients with HPS. Portopulmonary hypertension was seen in 8 (12.5%) subjects with no difference between HPS and non-HPS patients. Subjects with HPS had more severe liver disease. A model for end-stage liver disease (MELD)-Na score > 19 was associated with HPS (sensitivity 73.08%, specificity 65.79%, PPV 59.4%, and NPV 78.1%). Multivariate analysis (binary logistic regression) revealed that a higher MELD-Na score, hepatic encephalopathy, and impaired DLCO were independently associated with HPS. CONCLUSIONS: HPS is associated with more severe liver disease (as per Child-Turcotte-Pugh [CTP] stage and MELD-Na score). There was no relation between HPS and causes of CLD. Higher MELD-Na score, hepatic encephalopathy, impaired DLCO, clubbing, and spider naevi were independently associated with HPS.