Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated lupus, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension, encephalopathy, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
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PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33

Urea kinetic modelling (UKM) was used to assess adequacy of dialysis in 50 CAPD patients. Nutritional status was assessed from the measurement of visceral protein status (total protein, albumin, transferrin, immunoglobulins, complement), somatic protein status (anthropometry), and dietary intake (1 week weighed dietary inventory and normalized protein catabolic rate (NPCR) from UKM). Morbidity was assessed from the peritonitis and admission history. Mean Kt/V (corrected to x3 weekly dialysis) was 0.66 +/- 0.02. Dietary protein intake estimated from the NPCR (1.08 +/- 0.03 g kg-1 day-1) correlated well (r = 0.72, P < 0.001) with that estimated from the dietary inventory (1.10 +/- 0.04 g kg-1 day-1). There was a strong correlation between Kt/V and NPCR corrected for actual weight (r = 0.65, P < 0.001), but when NPCR was corrected for IBW this correlation was weaker (r = 0.35, P < 0.05). Patients were divided by Kt/V into two groups (> 0.65, n = 22 and < 0.65, n = 28). There were no significant differences in the indices of visceral protein status between the two groups. Weight, height, BMI, fat free mass and arm muscle area were significantly greater in the group Kt/V < 0.65. Residual renal function (creatinine clearance) was higher in the group Kt/V > 0.65 (3.8 +/- 0.7 versus 1.9 +/- 0.5 1/24 h, P < 0.05) and plasma creatinine less (913 +/- 51 versus 1265 +/- 51 mumol/l, P < 0.001). Hb, potassium, bicarbonate, phosphate, alkaline phosphatase, PTH, and blood pressure were not different. Neither was there any difference between the two groups in any of the indices of morbidity.
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PMID:Adequacy of dialysis and nutritional status in CAPD. 815 6