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

Circulating autoantibodies against amyloid A protein (AA) were demonstrated by enzyme immunoassay in 18/62 patients with rheumatoid arthritis (RA) and in 9/27 patients with systemic lupus erythematosus (SLE). In the subset of RA patients who had developed amyloid, the frequency of antibodies to AA was lower than in those without amyloid (P less than 0.05). The antibody levels showed some variation in serial serum samples during follow-up (1-4 years) of patients with amyloidosis or SLE, but did not correlate with disease activity. In contrast to the patients with rheumatic diseases, patients with inflammatory bowel disease and acute bacterial peritonitis had antibody levels within the range of the healthy control subjects. The results show that autoantibodies to protein AA may occur in rheumatic diseases; their occurrence does not, however, identify subjects with tissue amyloid deposits. Absorption experiments suggest that the antibodies may be directed to circulating amyloid A protein.
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PMID:Antibodies to amyloid A protein in rheumatic diseases. 326 8

The pathophysiology of ascites in patients with cirrhosis is complex and includes increases in hepatic sinusoidal pressure, the formation of hepatic and splanchnic lymph, renal sodium retention, and hypoalbuminemia. However, the role of hypoalbuminemia in ascites formation is controversial. Evaluating ascites in hypoalbuminemic patients with nephrotic syndrome could add to our understanding of the role of hypoalbuminemia in ascites development. We conducted a retrospective analysis of 52 adults and 21 children with nephrotic syndrome who were hospitalized in the Hadassah University Hospital on Mount Scopus during 1981-1994. There was a significant difference in the prevalence of ascites between pediatric (52%) and adult patients (23%) (p = 0.024). Pediatric patients had lower serum albumin levels than adults (1.70 +/- 0.08 g/dl vs. 2.10 +/- 0.07 g/dl, p = 0.001). Adult patients with ascites had lower serum albumin levels than adult patients without ascites (1.80 +/- 0.13 g/dl vs. 2.20 +/- 0.07 g/dl, p = 0.01). This difference was not found in pediatric patients. Temporary fluctuations in liver enzymes (up to four times the upper limit of normal for transaminases) were evident in five patients from the pediatric group with ascites, whereas all pediatric patients without ascites had completely normal liver enzymes (p = 0.035). Among the 12 adult patients with ascites, seven had liver disease (three with cirrhosis and four with amyloidosis), and two had right-sided congestive heart failure. Among the 40 adult patients without ascites, only four had liver disease (amyloidosis). The plasma albumin levels of the patients with amyloidosis without ascites were higher than patients with amyloidosis with ascites (1.90 +/- 0.10 g/dl vs. 1.50 +/- 0.07 g/dl, p = 0.03). Two patients with nephrotic syndrome and ascites (one without liver disease) had episodes of spontaneous bacterial peritonitis. Ascites in nephrotic syndrome is more common in children than in adults. Although in most pediatric patients ascites formation is probably a common manifestation of the general fluid retention, in most adult patients with nephrotic syndrome ascites can be attributed to both hypoalbuminemia and the presence of liver disease or congestive heart failure, with increased hepatic sinusoidal pressure.
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PMID:Ascites in Nephrotic syndrome. Incidence, patients' characteristics, and complications. 877 92

We report this case of secondary amyloidosis associated with Castleman's disease. A 51-year-old man presented with systemic symptoms of generalized weakness, fatigue, unintended weight loss, anorexia and progressively worsening abdominal distension. On examination he was found to have an indurated right-sided submandibular mass and tense ascites. He was found to have multiorgan dysfunction with deranged liver function tests and renal failure. Ascitic fluid analysis revealed evidence of spontaneous bacterial peritonitis. Biopsy of the submandibular mass revealed angiofollicular lymph node hyperplasia consistent with a diagnosis of Castleman's disease. A subsequent liver biopsy showed extensive deposition of amyloid protein. Bone marrow biopsy also showed the presence of amyloid and increased kappa light chain-restricted plasma cells. The patient was not considered a candidate for chemotherapy or solid organ transplantation in view of active sepsis and poor physical condition. Secondary systemic amyloidosis complicating Castleman's disease is very rare. Untreated secondary systemic amyloidosis often has a rapidly fatal course, such as seen in our patient.
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PMID:Systemic Reactive Amyloidosis Associated with Castleman's Disease. 2434 20