The role of serum visfatin and vaspin in hepatocellular carcinoma in hepatitis C-related liver cirrhosis.

Aim of the study: To investigate the role of the novel adipokines visfatin and vaspin in hepatitis C virus (HCV)-cirrhotic patients with and without hepatocellular carcinoma (HCC) and their association with tumour characteristics and liver dysfunction. Material and methods: This case-control study was carried out between March 2021 and September 2021. Serum visfatin and vaspin were measured in 67 HCV-cirrhotic patients (37 had HCC, and 30 did not) and 20 healthy individuals using enzyme-linked immunosorbent assay (ELISA). Results: Serum visfatin and vaspin were substantially elevated in HCC patients compared to those without HCC and healthy controls (p = 0.001, < 0.0001, respectively) and significantly associated with hepatic dysfunction. At a cut-off value of 12.1 ng/ml, the sensitivity and specificity of the serum visfatin in detecting HCC were 67.6% and 83.3%, respectively. Serum vaspin at a cut-off value of 321 ng/dl had a sensitivity of 94.6% and specificity of 66.7%. In multivariate regression analysis, serum vaspin and albumin were independent risk factors for HCC development. Patients with Barcelona Clinic Liver Cancer (BCLC) stage D had significantly the highest serum levels of visfatin and vaspin (p = 0.03, 0.008, respectively). Conclusions: Serum visfatin and vaspin were substantially higher in HCC patients, associated with tumour stage, and might be considered as potential biomarkers of HCC, but this should be confirmed in larger independent cohorts of patients with liver cirrhosis. Serum vaspin and albumin were independent risk factors for HCC development. There was a substantial association between visfatin, vaspin, and the severity of the underlying liver dysfunction.

Serum copeptin is associated with major complications of liver cirrhosis and spontaneous bacterial peritonitis.

Aim of the study: We aimed to investigate the possible association between serum copeptin and complications of liver cirrhosis, including its potential role as a stress biomarker in spontaneous bacterial peritonitis (SBP). Material and methods: This cross-sectional study included 89 cirrhotic ascitic patients (37 with SBP and 52 without SBP) admitted to Sohag University Hospitals, Egypt, between June 2021 and February 2022. Serum copeptin was measured in all patients, and its association with SBP and other complications of liver cirrhosis was investigated. Results: Serum copeptin was significantly elevated in patients with SBP compared to those without SBP (p = 0.032) and significantly correlated with ascitic fluid study parameters, systemic inflammatory markers, and liver, renal, and circulatory functions. Serum copeptin and C-reactive protein (CRP) were independent risk factors for the presence of SBP. Serum copeptin detects SBP at a cut-off value of 9 pmol/l, with sensitivity and specificity of 73% and 64%, respectively. Serum copeptin was significantly associated with hepatic encephalopathy, gastrointestinal bleeding, hepatorenal syndrome, and larger amounts of ascites. Conclusions: Serum copeptin is an independent risk factor for the presence of SBP and significantly increased in patients presented with major complications of liver cirrhosis, demonstrating its ability to reflect circulatory dysfunction and systemic inflammation.

Unusual pattern of thrombotic events in young adult non-critically ill patients with COVID-19 may result from an undiagnosed inherited and acquired form of thrombophilia.

In 145 previously healthy non-critically ill young adults, coronavirus disease 2019 (COVID-19)-related symptoms, risk factors for thrombosis, coagulation and inflammatory parameters were compared, with 29 patients reporting unusual thrombotic events (UTEs) and 116 not having thrombotic events. The inflammatory indices, coagulation and prothrombotic platelet phenotype (PTPP) were significantly higher in patients with UTEs versus those without. Patients with UTEs were categorised according to detection of thrombophilic genes (TGs), coagulation and inflammatory markers to the non-TG and TG subcohort. A total of 38 UTEs were identified, which included splanchnic vein thrombosis (SVT; 11), stroke (six), cerebral vein thrombosis (five), thrombotic microangiopathy (four), limb ischaemia and inferior vena cava thrombosis (three each), ST-segment elevation myocardial infarction (two), superior vena cava thrombosis (two), upper limb deep venous thrombosis and retinal vein thrombosis, one each. We found a 55% prevalence of TGs mainly heterozygous coagulation factor II, thrombin (FII)-G20210A, Janus kinase 2 (JAK2)-V617F, protein-S, and antithrombin III deficiency with a high (76·9%) prevalence of venous UTEs, multiple vessels thrombosis, and recurrence rate among the TG versus non-TG subcohort. The presence of JAK2-V617F, and FII-G20210A mutations was linked with SVT. Thrombosis in the non-TG subcohort was associated with more haemorrhagic problems, thrombosis progression and a significantly higher level of inflammatory markers, PTPP, mean platelet volume, von Willebrand factor, and factor VIII, which remained high for up to 6 months, as well as elevated D-dimer. Acquired and inherited thrombophilia with endotheliopathy appeared to be a relevant mechanism to explain the occurrence of UTEs that are not correlated to COVID-19 severity.

Characteristics and predictors of short-term mortality in decompensated cirrhotic patients with acute-on-chronic liver failure.

Aim of the study: We aimed to investigate the characteristics of acute-on-chronic liver failure (ACLF) and factors associated with 28-day mortality in patients with ACLF. Material and methods: This prospective study included ACLF patients based on the European Association for the Study of the Liver-Chronic Liver Failure (EASL-CLIF) Consortium criteria, admitted between March 2021 and February 2022. We examined variables associated with 28-day mortality using multivariate Cox regression analysis. Results: Of 326 patients admitted with acute decompensation (AD) of cirrhosis, 109 (33.44%) patients were diagnosed with ACLF (mean age 63.61 ±11.15 years, 65.14% males). Of these, 26.61%, 35.78%, and 37.61% of patients were in ACLF grades 1, 2, and 3 respectively. HCV (80.73%) was the main aetiology of cirrhosis. Upper gastrointestinal bleeding (25.69%) was the most common trigger. Kidney failure (73.39%) was the most common organ failure. The 28-day mortality rate was 66.97%. Cox regression analysis revealed that the existence of 2 (HR = 6.99, 95% CI: 2.68-18.25, p < 0.0001) or ≥ 3 (HR = 9.34, 95% CI: 3.6-24.74, p < 0.0001) organ failures, hepatic encephalopathy (HR = 2.96, 95% CI: 1.27-6.94, p = 0.01), and elevated serum bilirubin (HR = 1.03, 95% CI: 1.00-1.06, p = 0.04) were independent predictors for 28-day mortality, while shifting blood pH to the normal range was associated with a decrease in the HR of ACLF mortality (HR = 0.03, 95% CI: 0.002-0.44, p = 0.01). Conclusions: ACLF has a very high 28-day mortality, which is associated with the existence of 2 or more organ failures, hepatic encephalopathy, elevated serum bilirubin, and low blood pH.

Acute human parvovirus B19 infection triggers immune-mediated transient bone marrow failure syndrome, extreme direct hyperbilirubinaemia and acute hepatitis in patients with hereditary haemolytic anaemias: multicentre prospective pathophysiological study.

A total of 244 patients with hereditary haemolytic anaemias (HHA) were screened for acute symptomatic human parvovirus B19 infection (HPV-B19) in a prospective study. To assess the risks associated with HPV-B19 infection, patients were classified into Group I and Group II according to presence or absence (symptoms, signs and specific serology) of acute HPV-B19 infection respectively. In all, 131 (53·7%) patients had ß-thalassaemia, 75 (30·7%) hereditary spherocytosis (HS), 27 (11·1%) sickle cell anaemia (SCA) and 11 (4·5%) glucose-6-phosphate dehydrogenase (G6PD) deficiency. Of 33 (13·5%) patients who presented with symptomatic HPV-B19 infection, 19 (57·5%) had HS, nine (27·3%) had ß-thalassaemia and five (15·2%) had SCA. In Group I, there were significant differences in the mean white blood cell, red blood cell and platelet counts, haemoglobin concentration, total bilirubin (TB), alanine aminotransferase, aspartate aminotransferase and serum creatinine (all P < 0·001) compared to Group II. In all, 27 (81·8%) patients had arthropathy and bone marrow failure (BMF); 13 (39·4%) had acute kidney injury (AKI), more in SCA (80%); and 12 (36·4%) patients had hepatitis, more in HS (66·8%). Five (15·2%) patients with HS had BMF, AKI, nervous system involvement and extreme hyperbilirubinaemia (TB range 26·3-84·7 mg/dl). Five (15·2%) patients had haemophagocytic syndrome. Two patients with HS combined with Type-I autoimmune hepatitis presented with transient BMF. Complete recovery or stabilisation was noted at 12 months in every patient except for one patient with SCA who died during the infection. HPV-B19 must be suspected and screened in patients with HHA with typical and atypical presentations with careful follow-up.