Editor-in-Chief, Deputy Editor 2017-2019

 

Editor-in-Chief:

Tom MOREELS

 

Deputy Editor:

Nicolas LANTHIER

 

 

Symposium: 14th BASL Winter Meeting, Zaventem, December 12, 2009



Hepatic encephalopathy


Price: €10,00

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome which can develop in the course of chronic and acute liver disease. It is characterized by cognitive and motoric deficits of varying severity. HE is functional in nature, potentially reversible and is thought to reflect the clinical manifestation of a low-grade cerebral edema, which exacerbates in response to ammonia and other precipitating factors, such as electrolyte disturbances, bleeding, infections, high protein diet, diuretics and sedatives. The action of these rather heterogeneous factors integrates at the level of oxidative/nitrosative stress and astrocyte swelling, which is associated with an oxidative/nitrosative stress response in the brain with consequences for signal transduction, neurotransmission, synaptic plasticity and oscillatory networks in the brain. Manifest HE is diagnosed on the basis of clinical symptoms according to the West Haven criteria, whereas diagnosis of minimal HE requires psychometric or neurophysiological testings. Here objective and reproducible measures to assess HE severity, such as critical flicker frequency or evoked potentials are superior to paper pencil tests. Identification and treatment of precipitating factors is the mainstay of HE therapy. Also intravenous ornithine aspartate, vegetable protein, oral branched chain amino acids, lactulose enemas and liver transplantation are considered to be effective. Whereas the efficacy of oral lactulose and non-resorbable antibiotics in the treatment of an acute HE attack is under debate, the beneficial effect of lactulose and rifaximin in the secondary HE prophylaxis has recently been established. (Acta gastro enterol. belg., 2010, 73, 457-464). [Product Details...]



Hepatitis B and hepatitis C virus and chronic kidney disease


Price: €10,00

The most common cause of liver disease in patients with chronic kidney disease (CKD) remains infection by hepatitis B virus (HBV) and/or hepatitis C virus (HCV). The adverse effects of HBV and/or HCV infections upon survival in patients with CKD have been repeatedly confirmed. An excess risk of death in HBsAg positive or anti-HCV antibody-positive patients may be at least partially attributed to chronic liver disease with its attendant complications. A negative impact of HCV infection on survival after renal transplantation has been linked to extrahepatic complications, including chronic glomerulonephritis, sepsis, chronic allograft nephropathy, post-transplantation diabetes mellitus, and abnormal metabolism of calcineurin-inhibitors. Transmission of HCV infection by grafts from HCV-infected donors has been unequivocally demonstrated. Registry analyses suggest that recipients of kidneys from anti-HCV antibody positive donors are at increased risk of mortality. Renal grafts from HCV-infected donors should be restricted to viremic anti-HCV positive recipients. Several drugs have been recently licensed for therapy of HBV infection but available data in patients with CKD is mostly limited to experience with lamivudine. The standard of care for hepatitis C infection in patients on regular dialysis is monotherapy with conventional interferon, according to recent guidelines. Only dire circumstances justify interferon use after renal transplantation. (Acta gastro enterol. belg., 2010, 73, 465-471). [Product Details...]


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