The first case of coronavirus disease 2019 (COVID-19) was diagnosed in December 2019 in Wuhan, China. Since then, this novel infectious disease, caused by the severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), has grown into a pandemic with over 330 million infected individuals worldwide, many of them with innate or acquired immunosuppression.Liver transplantation (LT) is offered as a curative therapy for end-stage liver disease as well as for acute liver failure cases. Advances in immunosuppressive therapy decreased the rates of acute and chronic graft rejection, significantly improving the quality of life.Liver transplant recipients are considered at particularly high risk for developing critical COVID-19 infection because of their chronic immunosuppressed state. Available data are heterogeneous, and the mortality rate is variably reported in the literature. There is controversy regarding whether their immunosuppressive status is a risk or a protective factor for developing severe respiratory disease. Moreover, the mechanism of action is still unclear.We report the clinical outcome of three liver transplant recipients who had COVID-19 pneumonia at different moments following liver transplantation. All patients received a standard immunosuppression regimen and specific antiviral therapy, requiring no invasive mechanical ventilation. They were discharged from the hospital with no long-term COVID-19 complications.

Objectives. We evaluated platelet counts in end-stage renal disease and chronic viral hepatitis. Materials and Methods. We studied 70 patients with end-stage renal disease and chronic viral hepatitis and compared them to a control group of 45 patients without hepatitis. Results. The presence of viral hepatitis was associated with a higher prevalence of thrombocytopenia. Correlations between age, C-reactive protein, liver stiffness measurement, and platelet count were observed. C-reactive protein levels > 10 mg/dl were associated with a lower risk of thrombocytopenia in patients with end-stage renal disease and chronic viral hepatitis, yet age > 60 years, dialysis vintage > 10 years, aspartate and alanine aminotransferase levels > 20 IU/L, albumin levels < 3.5 g/dl, and fibrosis stage ≥ 3 were not related. Conclusions. Chronic viral hepatitis leads to a higher prevalence of thrombocytopenia. Platelet counts in these patients begin to decrease significantly once liver fibrosis reaches stage III. Keywords  thrombocytopenia, end-stage renal disease, chronic viral hepatitis Highlights ✓ Thrombocytopenia is a common occurrence in patients with end-stage renal disease undergoing hemodialysis; ✓ Chronic viral hepatitis B or C in end-stage renal disease patients does not impact platelet counts, suggesting that the natural course of liver disease is slowed in subjects undergoing hemodialysis

Aim Our aim is to present the case of an Irish neonate who presented to our Paediatric Department with prolonged hyperbilirubinemia as a consequence of breast milk quality and Gilbert's Mutation (UGT1A1*28 mutation). Methods We describe the clinical features, course of illness and haematological findings, management and the challenges of same and in addition the outcome to date in our patient. Results An Irish male neonate of non-consanguineous union, with gestation of 36 weeks, unremarkable perinatal history, exclusively breast fed, first came to medical attention at third day of life with DCT-negative unconjugated hyperbilirubinemia requiring phototherapy for two days. He represented with increased bilirubin levels again 3 days later and again at two weeks of age, each time necessitating phototherapy. Systemic examination was normal. Thyroid & liver function tests, full blood count, urine culture, urine for cytomegalovirus and toxicology screen, lactate dehydrogenase were normal. He was fed exclusive expressed breast milk by bottle and was observed to have high volume intake of 275 ml/kg/day, with overfeeding resulting in vomiting. By 5 weeks of age, he had not regained his birthweight and had dropped from the 25-50 th to the 0.4 th centile. On further work up, his screen for Hereditary Spherocytosis was negative, haptoglobin was low <0.10 g/L, liver ultrasound scan was normal. His UGT1A1 enzyme levels were sent the results showed that he was heterozygote for UGT1A1*28 mutation, indicating carrier status for Gilbert's Syndrome.Breastfeeding was discontinued, and his weight and hyperbilirubinaemia improved dramatically. Conclusion Breast-feeding jaundice is traditionally considered as a consequence of inadequate supply, with breast-milk jaundice secondary to increased recirculation of bilirubin due to deconjugating breast-milk enzymes. This case was unusual in that supply was established to be adequate, rather the nutritional quality of the breast-milk was theorised to be suboptimal, secondary to severe social stressors affecting mother. This, in combination with Gilbert's syndrome status, resulted in moderate prolonged unconjugated hyperbilirubinaemia and failure to thrive in this infant.It may be helpful forPaediatricians to maintain an index of clinical suspicion for the mutation in children with refractory prolonged unconjugated hyperbilirubinemia. We rarely advocate breast-feeding discontinuation, however in this instance it resulted in dramatic clinical improvement of this infant's condition.

with tumor thrombus occupying the right atrium and portal vein in a patient with hereditary hemochromatosis and liver cirrhosis.

Chronic hepatitis C viral infection is an important cause of morbidity and mortality in patients with end-stage renal disease treated with hemodialysis. Liver fibrosis represents a main determinant of liver disease prognosis and clinical management, and its assessment by liver biopsy can decide treatment allocation. Although liver biopsy is the gold standard for staging liver fibrosis, it is an invasive procedure associated with complications that are more prevalent in patients with end-stage renal disease. FibroTest represents a surrogate marker of fibrosis which evaluates the levels of apolipoprotein A1, total bilirubin, haptoglobin, gamma-glutamyltransferase and α2-macroglobulin, generating a score that indicates the level of fibrosis. Discrepancies were observed in clinical practice between FibroTest score and histopathological findings. The aim of this study was to evaluate how hemodialysis influences the level of each FibroTest parameter and the final score. The systematic literature review conducted by us suggests that hemodialysis induces a reduction in apolipoprotein A1, haptoglobin and bilirubin levels, with an increase in gamma-glutamyltransferase and alpha-2-macroglobulin levels. In conclusion, hemodialysis modifies the levels of FibroTest parameters, suggesting that it may also have an impact on the accuracy of liver fibrosis assessment in hemodialysis patients.