Hepatic Medicine : Evidence and Research最新文献

Background: Viral infections are the most common diseases. Of them, human immunodeficiency virus (HIV), hepatitis B viruses (HBV), and hepatitis C viruses (HCV) are common. When HBV or HCV becomes co-morbid with HIV, they lead to severe forms of a disease and rapid death.

Objective: This study aimed to determine the seroprevalence and associated factors of HBV and HCV among HIV-positive study participants.

Methods: A cross-sectional study was conducted among 81 individuals, and a non-randomized purposive sampling technique was used. From each study participant, sociodemographic and clinical data were gathered by using a pretested questionnaire and data collection sheet, respectively. Further, a venous blood sample was collected for viral load count, and HBV and HCV determination. To keep the quality of test results, commercially prepared quality control samples were used. The data were entered to EPI-Info version 7 and analyzed by using SPSS version 20. The descriptive data were summarized in percentages, median, and IQR. Logistic regression was analyzed to determine associated factors. To say the data were statistically significant, the p-values should be less than 0.05.

Results: A total of 81 study participants were included. Of them, 56.8% (46/81) and 67.9% (55/81) were female and urban residents, respectively. The prevalence of hepatitis co-infection was 21% (95% CI: 17%, 23%). Further, the prevalence of HBV/HIV and HCV/HIV was 13.5% (95% CI: 10.5%, 16.5%) and 8.6% (95% CI: 5.6%, 11.6%), respectively. Wise use of highly active antiretroviral therapy (HAART) 0.01 (0.00, 0.213) was a preventive factor to hepatitis infection.

Conclusion and recommendation: The HBV and HCV co-infection among HIV-positive patients was a significant public health concern. Also, having wise use of HAART can reduce exposure to hepatitis co-infection. Therefore, clear strategies on hepatitis screening and wise use of HAART to HIV would be critical.

The term porto-sinusoidal vascular disease (PSVD) has been recently proposed to replace the term idiopathic non-cirrhotic portal hypertension (INCPH) to describe patients with or without signs of portal hypertension and typical histological lesions involving the portal venules or sinusoids in the absence of cirrhosis. According to the new definition, the presence of known causes of liver disease as well as of portal vein thrombosis does not rule out PSVD. Therefore, the patients in whom the diagnosis of PSVD is possible are much more than the patients strictly fulfilling the diagnostic criteria for INCPH. In this setting, the clinical challenge for the hepatologist is to identify patients at risk of developing PSVD and to indicate liver biopsy to confirm the diagnosis. We describe some possible scenarios in which PSVD should always be suspected, and we provide some tools useful to reach the diagnosis of PSVD.

Intrahepatic cholangiocarcinoma (ICC) is one of the rarest and most aggressive types of cancer. The symptoms of ICC patients can be vague, leading to late diagnosis and dismal prognosis. In this review, we investigated the treatment options for ICC, as well as ways to overcome challenges in identifying and treating this disease. Imaging remains the gold standard to diagnose ICC. Patients are staged based on the tumor, nodes and metastases (TNM) staging system. Patients eligible for surgical resection should undergo surgery with curative intent with the goal of microscopically disease-free margins (R0 resection) along with lymphadenectomy. Minimal invasive surgery (MIS) and liver transplantation have recently been offered as possible ways to improve disease outcomes. ICC recurrence is relatively common and, thus, most patients will need to be treated with systemic therapy. Several clinical trials have recently investigated the use of neoadjuvant (NT) and adjuvant therapies for ICC. NT may offer an opportunity to downsize larger tumors and provide patients, initially ineligible for surgery, with an opportunity for resection. NT may also treat occult micro-metastatic disease, as well as define tumor biology prior to surgical resection, thereby decreasing the risk for early postoperative recurrence. Adjuvant systemic therapy may improve outcomes of patients with ICC following surgery. Ongoing clinical trials are investigating new targeted therapies that hold the hope of improving long-term outcomes of patients with ICC.

Primary biliary cholangitis (PBC), formerly known as primary biliary cirrhosis, is a chronic cholestatic immune-mediated liver disease characterized by injury to intrahepatic bile ducts that may ultimately progress to cirrhosis and liver failure and result in the need for liver transplant or death without treatment. Ursodeoxycholic acid (UDCA) and obeticholic acid (OCA) are approved therapies for PBC and are associated with a reduced risk of progression of disease, although patients may continue to experience significant symptoms of pruritus and fatigue independent of liver disease. The two most commonly reported symptoms among patients with PBC are fatigue and pruritus which may be debilitating, and negatively impact physical, mental, emotional, and social wellbeing. Intense symptom burden has been associated with depressive symptoms, cognitive defects, poor sleep schedules, and social isolation. This literature review explores the presence of anxiety and depressive symptoms in chronic liver disease, the impact of symptom burden on patients' wellbeing, and available pharmaceutical and natural therapies.

Background & aims: Hyponatremia is an important predictor of early death among cirrhotic patients in the orthotopic liver transplantation (OLT) waiting list. Evidence exists that prioritizing OLT waiting list according to the MELD score combined with plasma sodium concentration might prevent pre transplantation death. However, the evolution of plasma sodium concentrations during the perioperative period of OLT is not well known. We aimed to describe the evolution of perioperative sodium concentration during OLT and its relation to perioperative neurohormonal responses.

Methods: Twenty-seven consecutive cirrhotic patients who underwent OLT were prospectively included in the study over a period of 27 months. We studied the evolution of plasma sodium levels, the hemodynamics, the neurohormonal response and other biological markers during the perioperative period of OLT.

Results: Among study's population, four patients had hyponatremia before OLT, all with Child cirrhosis. In patients with hyponatremia, plasmatic sodium reached normal levels during surgery, and sodium levels remained within normal ranges 1 day, 7 days, as well as 6 months after surgery for all patients. Creatinine clearance was decreased significantly during the perioperative period, while creatinine and cystatin C levels increased significantly. Neutrophil gelatinase-associated lipocalin (NGAL) and vasopressin levels did not change significantly in this period. Plasma renin activity, concentrations of norepinephrine and brain natriuretic peptide varied significantly during the perioperative period.

Conclusion: In our study, plasmatic sodium concentrations among hyponatremic cirrhotic patients undergoing OLT seem to reach normal levels after OLT and remain stable six months after surgery providing more evidence for the importance of sodium levels in prioritization of liver transplant candidates. Further investigation of rapid correction and stabilization of sodium levels after OLT, as observed in our study, would be of interest in order to fully understand the mechanisms involved in cirrhosis-related hyponatremia, its prognostic value and clinical implications.

Histology remains essential for the diagnosis and management of many disorders affecting the liver. However, the biopsy procedure itself is associated with a low risk of harm to the patient and cost to the health services; samples may not be adequate and are subject to sampling variation. Furthermore, interpretation often depends on the skill of the pathologist. Increasingly, new techniques are becoming available that are altering the indications for liver biopsy. Many diseases of the liver can be diagnosed and managed using serological and radiological techniques; the degree of fibrosis and fat can often be assessed by serological or imaging techniques and the nature of space occupying lesions defined by serology, imaging and use of liquid biopsy. However, these techniques, too, are subject to limitations: sensitivity and specificity is not always adequate for diagnosis or management; some techniques are expensive and often also require expert interpretation. Although there may be less need for liver biopsy today, histology remains the gold standard as well as an essential tool for the diagnosis and management of many conditions, especially where there are multiple pathologies, or where a diagnosis cannot or has not been made by alternative approaches. Until less invasive techniques become more reliable and accessible, liver histology will remain a key investigation.

According to the Centers for Disease Control and Prevention, chronic liver disease and cirrhosis is the 11th leading cause of death in the United States. Common causes of chronic liver disease include alcohol, viral hepatitis, and non-alcoholic steatohepatitis (NASH). Inflammation is a critical driver in the progression of liver disease to liver fibrosis and ultimately cirrhosis. While the severity of chronic liver disease extends over a continuum, the management is more easily differentiated between compensated and decompensated cirrhosis. In this review, we discuss pathophysiology, clinical features and management of common complications of liver cirrhosis based on literature review and the current clinical practice guidelines of the American Association for the Study of Liver Diseases (AASLD).

Background: The SARS-CoV-2 virus may have direct or indirect effects on other human organs beyond the respiratory system and including the liver, via binding of the spike protein. This study investigated the potential direct interactions with the liver by comparing the binding of SARS-CoV-2 spike proteins to human AT2-like cells, primary human hepatocytes and immortalized hepatocyte-like hybrid cells. Receptors with binding specificity for SARS-CoV-2 spike protein on AT2 cells and hepatocytes were identified.

Methods: The specific binding of biotinylated spike and spike 1 proteins to undifferentiated human E12 MLPC (E12), E12 differentiated alveolar type 2 (AT2) cells, primary human hepatocytes (PHH) and E12 human hepatocyte-like hybrid cells (HLC) was studied by confocal microscopy. We investigated the expression of ACE-2, binding of biotinylated spike protein, biotinylated spike 1 and inhibition of binding by unlabeled spike protein, two neutralizing antibodies and an antibody directed against the hepatocyte asialoglycoprotein receptor 1 (ASGr1).

Results: E12 MLPC did not express ACE-2 and did not bind either of spike or spike 1 proteins. AT2-like cells expressed ACE-2 and bound both spike and spike 1. Both PHH and HLC did not express ACE-2 and did not bind spike 1 protein. However, both PHH and HLC actively bound the spike protein. Biotinylated spike protein binding was inhibited by unlabeled spike but not spike 1 protein on PHH and HLC. Two commercial neutralizing antibodies blocked the binding of the spike to PHH and HLC but only one blocked binding to AT2. An antibody to the hepatocyte ASGr1 blocked the binding of the spike protein to PHH and HLC.

Conclusion: The absence of ACE-2 receptors and inhibition of spike binding by an antibody to the ASGr1 on both PHH and HLC suggested that the spike protein interacts with the ASGr1. The differential antibody blocking of spike binding to AT2, PHH and HLC indicated that neutralizing activity of SARS-CoV-2 binding might involve additional mechanisms beyond RBD binding to ACE-2.

Portal hypertension is the main driver of complications in patients with advanced chronic liver disease (ACLD) and is defined by values of hepatic venous pressure gradient measurement (HVPG) >5 mmHg. Values of HVPG ≥10 mmHg determine the presence of clinically significant portal hypertension (CSPH), the main predictor of the risk of variceal bleeding, hepatic decompensation, and mortality. However, its measurement is invasive and requires high expertise, so its routine use outside third level centers or clinical trials is limited. In the last decades, several non-invasive tests (NITs) have been developed and validated for the diagnosis of portal hypertension. Among these, liver (LSM) and spleen stiffness measurement (SSM) are the most promising tools available, as they have been proven accurate to predict CSPH, high-risk esophageal varices, decompensation, and mortality in patients with ACLD. In the last Baveno VI Consensus proceedings, LSM evaluation was recommended for the first time for diagnosis of CSPH (LSM >20-25 kPa) and the screening of patients with a low probability of having high-risk varices (LSM <20 kPa and platelet count >150.000/mm³). In this review, we aimed to summarize the growing evidence supporting the use of non-invasive tests for the evaluation of portal hypertension in patients with chronic liver disease.