Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case of sudden death caused by a rare complication of Crohn's disease. A 29-year-old man with Crohn's disease who had not taken medications regularly complained of nausea, vomiting, and abdominal pain for 2 days, and then died suddenly. Autopsy revealed protruding intestinal loops filled with gas, internal fistulas between fused loops of the terminal ileum, and complete obstruction of the fistulous tract. The histologic findings of transmural inflammation consisting of lymphocytic infiltration, accumulation of partially hyalinized collagen, and fibrosis in the skip areas from the ileum to the cecum were compatible with Crohn's disease. Furthermore, marked emaciation, atrophic change of the heart muscle, and diffuse fatty change of the liver were found. Although the patient died of obstructive ileus caused by a stricture produced by progression of Crohn's disease, he was severely affected by malnutrition which may have been fatal. This case not only illustrates that Crohn's disease can cause obstructive ileus and sudden death, but also makes the forensic pathologist realize the importance of suspecting the presence of an active inflammatory bowel disease in a patient with internal fistulas or malnutrition.
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PMID:Sudden death of a patient with Crohn's disease. 978 Jun 67

The pathogenesis of fatty liver disease remains largely unknown. Here, we assessed the importance of hepatic fat accumulation on the progression of hepatitis in zebrafish by liver specific expression of Hepatitis B virus X protein (HBx). Transgenic zebrafish lines, GBXs, which selectively express the GBx transgene (GFP-fused HBx gene) in liver, were established. GBX Liver phenotypes were evaluated by histopathology and molecular analysis of fatty acid (FA) metabolism-related genes expression. Most GBXs (66-81%) displayed obvious emaciation starting at 4 months old. Over 99% of the emaciated GBXs developed hepatic steatosis or steatohepatitis, which in turn led to liver hypoplasia. The liver histology of GBXs displayed steatosis, lobular inflammation, and balloon degeneration, similar to non-alcoholic steatohepatitis (NASH). Oil red O stain detected the accumulation of fatty droplets in GBXs. RT-PCR and Q-rt-PCR analysis revealed that GBx induced hepatic steatosis had significant increases in the expression of lipogenic genes, C/EBP-alpha, SREBP1, ChREBP and PPAR-gamma, which then activate key enzymes of the de novo FA synthesis, ACC1, FAS, SCD1, AGAPT, PAP and DGAT2. In addition, the steatohepatitic GBX liver progressed to liver degeneration and exhibited significant differential gene expression in apoptosis and stress. The GBX models exhibited both the genetic and functional factors involved in lipid accumulation and steatosis-associated liver injury. In addition, GBXs with transmissible NASH-like phenotypes provide a promising model for studying liver disease.
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PMID:Increase of hepatic fat accumulation by liver specific expression of Hepatitis B virus X protein in zebrafish. 2041 98