Preoperative Alpha-Fetoprotein and Radiological Total Tumor Diameter as Predictors of Hepatocellular Carcinoma Recurrence After Liver Transplantation.

BACKGROUND: Liver transplantation is a unique treatment opportunity for patients with chronic liver disease and hepatocellular carcinoma (HCC). Selection of HCC patients for transplantation was revolutionized by Milan-based criteria, but tumor recurrence and shortage of organs are still a major concern. Nowadays, additional preoperative tumor parameters can help to refine the graft allocation process. The objective of this study was to evaluate the prognostic value and cut-off points of pretransplant serum alpha-fetoprotein (AFP) levels and radiological tumor parameters on liver transplantation outcomes. METHODS: This is a single-team retrospective cohort of 162 consecutive deceased donor liver transplants (DDLT) with pathologically confirmed HCC. Pretransplant serum AFP levels and radiological tumor parameters were retrieved from a preoperative follow-up. Receiver-operating characteristics (ROC) curves were used to evaluate cut-off points for each outcome. Multivariate Cox regression model was used to assess the predictors of HCC relapse and recipient mortality. RESULTS: Twelve recipients (7.4%) had HCC recurrence after transplantation, with median survival time of 5.8 months. Pretransplant AFP ≥30 ng/mL (hazard ratio [HR]: 13.84, P = .003) and radiological total tumor diameter (TTD) ≥5 cm (HR: 12.89, P = .005) were independent predictors for HCC relapse. Moreover, pretransplant AFP ≥150 ng/mL was independently associated with recipient mortality (HR: 4.45, P = .003). CONCLUSIONS: Pretransplant AFP levels and radiological TTD were independently associated with HCC relapse and recipient mortality after DDLT, with different cut-off points predicting different outcomes. These findings may contribute to improving decision-making in the context of liver transplantation for HCC patients.

Liver Transplant and Active Ulcerative Colitis: A Case Report.

BACKGROUND: The association between ulcerative colitis (UC) and primary sclerosing cholangitis has been described for several years and can be classified as having a distinct disease phenotype from inflammatory bowel diseases (IBD). The simultaneous occurrence of decompensated liver disease requiring liver transplant and active IBD is a management challenge, considering that these patients may be at increased risk of infections, thromboembolic events, bleeding, and drug hepatotoxicity. CASE PRESENTATION: We describe a case of a 37-year-old patient with UC and sclerosing cholangitis presenting with severe decompensated rectocolitis complicated with thromboembolic phenomena and severe liver dysfunction who underwent liver transplant while using biological therapy to control bowel disease. CONCLUSIONS: This case highlights the evolution of sclerosing cholangitis to liver transplant in patients with decompensated UC. Despite the risk of recurrence, primary sclerosing cholangitis has excellent results after liver transplant. Despite the use of immunosuppression after liver transplant, biological therapy may be necessary to control IBD.

Progressive Familial Intrahepatic Cholestasis Type 2 and Recurrence After Liver Transplantation: A Case Report.

Progressive familial intrahepatic cholestasis type 2 (PFIC2) is a rare autosomal recessive disorder caused by mutations in the ABCB11 gene. Clinical manifestations include cholestasis with low γ-glutamyltransferase (GGT), hepatosplenomegaly, and severe pruritus. Liver transplantation is required for individuals with progressive liver disease or failure of the bypass procedure and has been considered curative. However, in the case of PFIC2, although bile salt excretory pump (BSEP) deficiency is a liver-specific condition rather than a systemic disease, evidence of recurrent BSEP disease has been shown in a small proportion of allografts. We describe an unusual case of a 21-year-old individual with PFIC2 and evidence of recurrent BSEP disease after liver transplantation, with clinical and laboratory improvement after pulse therapy with methylprednisolone for 3 days and adjustment of oral immunosuppression. This case report highlights the recurrence of PFIC2 in patients post liver transplant. It also emphasizes the importance of clinical suspicion, which should be considered in cases of posttransplant cholestasis in PFIC2 patients, especially those with low γ-glutamyltransferase (GGT) and without signs of acute graft rejection. Having knowledge of the condition favors a targeted diagnostic approach and contributes to early therapeutic management and a higher success rate.

Liver Transplantation After Acute Portal Vein Thrombosis: Case Report.

BACKGROUND: Portal vein thrombosis is a relatively frequent complication in patients with liver cirrhosis. Its detection and management are essential to avoid worsening portal hypertension or liver function complications. This complication can also negatively impact or even preclude liver transplant. CASE PRESENTATION: We report the case of a patient who presented with acute portal vein thrombosis, which allowed the diagnosis of liver cirrhosis and hepatocarcinoma within the Milan criteria. Chemical thrombolysis was performed with a mechanical aspiration of the thrombus, and in a second moment, the patient was submitted to a liver transplant. CONCLUSIONS: Advances in the therapeutic approach to portal vein thrombosis and surgical techniques have allowed the condition to no longer be an absolute contraindication to liver transplantation. Diagnosis in the acute phase is associated with greater therapeutic success, aiming to avoid the extension of thrombosis and achieve portal vein recanalization.

Transmission of cryptococcosis by liver transplantation: A case report and review of literature.

BACKGROUND: Cryptococcosis is a fungal infection caused by the yeast-like encapsulated basidiomycetous fungus of the Cryptococcus neoformans (C. neoformans) species complex. These fungi are ubiquitous in soil and bird droppings, and infection by them is an important global health concern, particularly in immunosuppressed patients, such as organ transplant recipients and those infected by the human immunodeficiency virus. The fungus usually enters the body through the respiratory tract, but extremely rare cases of infection acquired by transplantation of solid organs have been reported. CASE SUMMARY: We report a case of disseminated cryptococcosis in a liver transplant recipient, diagnosed 2 wk after the procedure. The patient initially presented with fever, hyponatremia and elevated transaminase levels, manifesting intense headache after a few days. Blood cultures were positive for C. neoformans. Liver biopsy showed numerous fungal elements surrounded by gelatinous matrix and sparse granulomatous formations. Magnetic resonance imaging of the brain showed multiple small lesions with low signal in T2, peripheric enhancement and edematous halo, diffuse through the parenchyma but more concentrated in the subcortical regions. Treatment with amphotericin B for 3 wk, followed by maintenance therapy with fluconazole, led to complete resolution of the symptoms. The recipients of both kidneys from the same donor also developed disseminated cryptococcosis, confirming the transplant as the source of infection. The organ donor lived in a rural area, surrounded by tropical rainforest, and had negative blood cultures prior to organ procurement. CONCLUSION: This case highlights the risk of transmission of fungal diseases, specifically of C. neoformans, through liver graft during liver transplantation.

Hypolactasia is associated with insulin resistance in nonalcoholic steatohepatitis.

AIM: To assess lactase gene (LCT)-13910C>T polymorphisms in Brazilian non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) patients in comparison with healthy controls. METHODS: This was a transverse observational clinical study with NAFLD patients who were followed at the Hepatology Outpatient Unit of the Hospital das Clínicas, São Paulo, Brazil. The polymorphism of lactase non-persistence/lactase persistence (LCT-13910C>T) was examined by PCR-restriction fragment length polymorphism technique in 102 liver biopsy-proven NAFLD patients (steatosis in 9 and NASH in 93) and compared to those of 501 unrelated healthy volunteers. Anthropometric, clinical, biochemical and liver histology data were analyzed. Continuous variables were compared using the t or Mann-Whitney tests, and categorical data were compared with the Fisher's exact test. Univariate logistic regression and multivariate logistic regression adjusted for gender and age were performed. RESULTS: No differences in the LCT-13910 genotype frequencies were noted between the NAFLD patients (66.67% of the patients with steatosis were CC, 33.33% were CT, and none were TT; 55.91% of the patients with NASH were CC, 39.78% were CT, and 4.3% were TT; P = 0.941) and the healthy controls (59.12% were CC, 35.67% were CT, and 5.21% were TT) or between the steatosis and NASH patients. That is, the distribution of the lactase non-persistence/lactase persistence polymorphism (LCT-13910C>T) in the patients with NAFLD was equal to that in the general population. In the NASH patients, the univariate analysis revealed that the lactase non-persistence (low lactase activity or hypolactasia) phenotype was associated with higher insulin levels (23.47 ± 15.94 µU/mL vs 15.8 ± 8.33 µU/mL, P = 0.027) and a higher frequency of insulin resistance (91.84% vs 72.22%, P = 0.02) compared with the lactase persistence phenotype. There were no associations between the LCT genotypes and diabetes (P = 0.651), dyslipidaemia (P = 0.328), hypertension (P = 0.507) or liver histology in these patients. Moreover, in the NASH patients, hypolactasia was an independent risk factor for insulin resistance even after adjusting for gender and age [OR = 5.0 (95%CI: 1.35-20; P = 0.017)]. CONCLUSION: The LCT-13910 genotype distribution in Brazilian NAFLD patients was the same as that of the general population, but hypolactasia increased the risk of insulin resistance in the NASH patients.