Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subacute hepatitis and liver failure occurred in a 40-yr-old woman following a 1-month course of treatment with the nonsteroidal anti-inflammatory drug bromfenac. Serologies for hepatitis A, B, and C were negative, as were antinuclear antibodies and ceruloplasmin. A transjugular liver biopsy demonstrated submassive hepatic necrosis. The clinical course was complicated by encephalopathy, fluid retention, and spontaneous bacterial peritonitis, prompting consideration for liver transplantation. With supportive measures, jaundice and fluid retention resolved over a 3-month period. We conclude that prolonged use of bromfenac was the etiological agent in this case, and that this drug can cause severe hepatotoxicity resulting in liver failure.
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PMID:Severe hepatotoxicity associated with bromfenac sodium. 1023 25

Infections in patients affected with liver cirrhosis are frequent, recurrent and associated to unfavorable outcome. They are facilitated by acquired and progressive defects on the innate immune and reticuloendothelial system that are aggravated by alcohol consumption. Infections in patients with cirrhosis are typically bacterial or viral in origin and have in most cases a stereotyped clinical presentation, although diagnosis may be difficult in some cases. Pneumonia, urinary tract infection, bacteremia and spontaneous bacterial peritonitis explain more than 90% of the cases. The latter requires a high clinical suspicion and a standardized diagnostic work up. Preventive strategies are important in the management of these patients and include chemoprophylaxis against spontaneous bacterial peritonitis in selected cases, vaccines against pneumococcal and influenza infections, and hepatitis A and B vaccine in susceptible patients. Due to limited seroconversion, active immunization should be applied as earlier as possible, before clinical deterioration ensues.
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PMID:[Diagnosis, management and prevention of infections in cirrhotic patients]. 1579 72

There is dispute about the cause of Beethoven's death; alcoholic cirrhosis, syphilis, infectious hepatitis, lead poisoning, sarcoidosis and Whipple's disease have all been proposed. In this article all primary source documents related to Beethoven's terminal illness and death are reviewed. The documents include his letters, the report of his physician Andreas Wawruch, his Conversation Books, the autopsy report, and a new toxicological report of his hair. His terminal illness was characterised by jaundice, ascites, ankle oedema and abdominal pain. The autopsy data indicate that Beethoven had cirrhosis of the liver, and probably also renal papillary necrosis, pancreatitis and possibly diabetes mellitus. His lifestyle for at least the final decade of his life indicated that he overindulged in alcohol in the form of wine. Alcohol was by far the most common cause of cirrhosis at that period. Toxicological analysis of his hair showed that the level of lead was elevated. During the eighteenth and early nineteenth centuries, lead was added illegally to inexpensive wines to sweeten and refresh them. These findings strongly suggest that liver failure secondary to alcoholic cirrhosis, associated with terminal spontaneous bacterial peritonitis, was the cause of death. This was complicated in the end stages by renal failure. If the presence of endogenous lead was verified by analysis of Beethoven's skeletal remains, it would suggest that the lead was derived from wine that he drank. Lead poisoning may account for some of his end-of-life symptoms. There is little clinical or autopsy evidence that Beethoven suffered from syphilis.
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PMID:Beethoven's terminal illness and death. 1721 30