Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deficiency of apolipoprotein can be of genetic origin or due to diseases like advanced chronic liver disease. Deficiency of apolipoprotein A causes Tangier disease without any major hepatic involvement being reported. Deficiency of apolipoprotein B causes abetalipoproteinemia or familial hypobetalipoproteinemia; with hepatic involvement in the form of raised transaminases, fatty liver and cirrhosis. Advanced chronic liver disease itself can cause reduction of apolipoprotein A and apolipoprotein B levels and acanthocytosis. In patients with chronic liver disease of undetermined etiology, lipid profile and apolipoprotein levels should be obtained routinely. If it suggests apolipoprotein B deficiency, then liver biopsy can be avoided, as the etiology of chronic liver disease is established. Isolated deficiency of either apolipoprotein A or apolipoprotein B suggests etiology of chronic liver disease, while deficiency of both apolipoprotein A and apolipoprotein B is a manifestation of advanced chronic liver disease.
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PMID:Apolipoprotein deficiency and chronic liver disease. 1122 45

Advanced chronic liver disease (aCLD) represents a major public health concern. aCLD is more prevalent and severe in the elderly, carrying a higher risk of decompensation. We aimed at understanding how aging may impact on the pathophysiology of aCLD in aged rats and humans and secondly, at evaluating simvastatin as a therapeutic option in aged animals. aCLD was induced in young (1 month) and old (16 months) rats. A subgroup of aCLD-old animals received simvastatin (5 mg/kg) or vehicle (PBS) for 15 days. Hepatic and systemic hemodynamic, liver cells phenotype and hepatic fibrosis were evaluated. Additionally, the gene expression signature of cirrhosis was evaluated in a cohort of young and aged cirrhotic patients. Aged animals developed a more severe form of aCLD. Portal hypertension and liver fibrosis were exacerbated as a consequence of profound deregulations in the phenotype of the main hepatic cells: hepatocytes presented more extensive cell-death and poorer function, LSEC were further capillarized, HSC over-activated and macrophage infiltration was significantly increased. The gene expression signature of cirrhosis significantly differed comparing young and aged patients, indicating alterations in sinusoidal-protective pathways and confirming the pre-clinical observations. Simvastatin administration for 15-day to aged cirrhotic rats improved the hepatic sinusoidal milieu, leading to significant amelioration in portal hypertension. This study provides evidence that aCLD pathobiology is different in aged individuals. As the median age of patients with aCLD is increasing, we propose a real-life pre-clinical model to develop more reliable therapeutic strategies. Simvastatin effects in this model further demonstrate its translational potential.
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PMID:Aging Influences Hepatic Microvascular Biology and Liver Fibrosis in Advanced Chronic Liver Disease. 3144 Mar 76