Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical course of a 26 year old female patient with acute liver necrosis and coma due to hepatitis B is reported. The disturbances of conciousness had improved. The patient survived 41 days after the beginning of the coma and developed liver cell regeneration and an acute post-hepatitic liver cirrhosis. As a grave complication a septicemia with aspergillus was observed. The patient died because of gastro-intestinal hemorrhage. At autopsy there were no signs of brain edema. The treatment consisted in: daily infusions with coenzyme A, nicotinamid-adenin-dinucleotide, alpha lipoic acid and cocarboxylase to improve the metabolic disorders and the clinical picture; mannitol intravenously to prevent and to treat cerebral edema; 33 charcoal-hemoperfusions to remove toxic substances of acute liver failure. Treatment of the aspergillus infection with 5-fluorocytosine and amphotericine B and infusion of concentrated ascites led to a decompensation of liver functions. From this observation the following conclusions can be drawn: after an acute viral hepatic necrosis, new synthetic functions and improvements of the disturbed intermediary metabolism in regenerated liver-cells can eventually be seen only after twenty-four to thirty days. With systematically applicated mannitol infusions it is possible to treat cerebral edema effectively.
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PMID:Treatment of fulminant hepatic failure with infusions of Co-factors and mannitol and charcoal-hemoperfusions during Forty-one days. 50 61

The mortality rate of fulminant hepatic failure was high until liver transplantation was presented as a potential therapy. We encountered a patient with hyperacute fulminant hepatic failure due to hepatitis B virus infection. Living donor liver transplantation was planned but abandoned because her brain edema progressed too rapidly to complete the donor evaluation. The present case reveals the limitation of living donor liver transplantation as a treatment for hyperacute fulminant hepatic failure.
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PMID:Rapid progression of encephalopathy in a patient with hepatitis B infection. 2010 60

Previous studies have shown that patients with hepatitis B virus-related cirrhosis (HBV-RC) without overt hepatic encephalopathy (OHE) are associated with a varying degree of cognitive dysfunction. Several resting-state functional magnetic resonance imaging (fMRI) studies have been conducted to explore the neural correlates of such cognitive deficits, whereas little effort has been made to investigate the cortical integrity in cirrhotic patients without OHE. Here, using cortical thickness, surface area and local gyrification index (lGI), this study performed a comprehensive analysis on the cortical morphometry of patients with HBV-RC without OHE (HBV-RC-NOHE) vs. matched healthy controls. Compared with healthy controls, we found significantly increased cortical thickness in the bilateral lingual and parahippocampal gyrus, right posterior cingulate cortex, precuneus, peri-calcarine sulcus and fusiform gyrus in patient with HBV-RC-NOHE, which may closely relate to be the low-grade brain edema. Cortical gyrification analysis showed significantly increased lGI in the left superior and inferior parietal cortex as well as lateral occipital cortex, which was speculated to be associated with disruptions in white matter connectivity and sub-optimal intra-cortical organization. In addition, the mean cortical thickness/lGI of the regions with structural abnormalities was shown to be negatively correlated with psychometric hepatic encephalopathy score (PHES) of the patients with HBV-RC-NOHE. These morphological changes may serve as potential markers for the preclinical diagnosis and progression of HBV-RC-NOHE.
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PMID:Cortical signature of patients with HBV-related cirrhosis without overt hepatic encephalopathy: a morphometric analysis. 2610 7