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The serum-ascites albumin difference is reported to be superior to ascitic total protein, ascitic-to-serum total protein ratio, lactic dehydrogenase, and ascitic-to-serum lactic dehydrogenase ratio in differentiating between ascites from liver disease and malignant ascites, S-A greater than 1.1 reflecting portal hypertension. We analyzed ascitic fluid from 46 consecutive patients with chronic liver disease, 28 patients with ascites associated with malignancy, 10 patients with right-sided heart failure, 4 patients with hypothyroidism, and 6 patients with miscellaneous causes of ascites to determine if this albumin difference is indeed a more valuable parameter. Analysis of our data confirms with a larger number of patients that the serum-ascites albumin difference is a more reliable indicator of transudative ascites, better termed portal hypertensive ascites. Malignant ascites without liver metastases had features of nonportal hypertensive ascites, and the serum-ascites albumin difference confirms this. The characteristics of malignant ascites associated with liver metastases, however, resemble those of the portal hypertensive ascites complicating liver disease. This new parameter is also helpful in distinguishing congestive heart failure with high protein ascites and portal hypertensive ascitic features from malignant ascites without liver metastases. Of particular note, myxedematous ascitic fluid, classically categorized as exudative, had an S-A greater than 1.1, indicating the possible role of portal hypertension in the development of ascites in these patients.
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The diagnosis of tuberculous ascites is often difficult because of the subtle clinical clues, poorly discriminative biochemical assays, delayed results of bacteriological studies and hazards of laparoscopy. Therefore, the role of ascites adenosine deaminase (ADA) activity and interferon-gamma (IFN-delta) level in distinguishing tuberculous from other causes of ascites was examined in 50 patients with ascites. Following bacteriologic culture, seventeen (34%) patients were found to have tuberculous ascites; nine (59.9%) of them had also schistosomal hepatic fibrosis (SHF). Therefore, 36% (9 out of 25) of all patients with SHF included in the study, had coexistent peritoneal tuberculosis despite the presence of transudative ascites and unrecognized clinical features. Ascites ADA activity was significantly higher in tuberculous than in other causes of ascites (P < 0.001) regardless of the presence of an underlying liver disease. A cut-off of 28 U/L reached a sensitivity of 94.4% and a specificity of 100%. A direct correlation was found between ascites ADA activity and total proteins in the tuberculous group (r = 0.613) and the only false-negative result occurred in a patient with SHF and low-ascites protein. Ascites IFN-delta level was also significantly higher in tuberculous ascites with or without SHF than in other causes of ascites (P < 0.05). A cut-off of 26 pg/ml reached a sensitivity of 81% and a specificity of 100%. There was no correlation between ascites ADA activity and IFN-delta level in the tuberculous group (r = 0.329). Based on the results of the present study, it can be concluded that tuberculous ascites should be considered as an important cause of ascites particularly in patients with underlying liver disease. Ascites ADA activity was more sensitive than ascites IFN-delta in diagnosing tuberculosis (TB). It has proved to be an easy, rapid, safe and reliable method for routine use in the early diagnosis of tuberculous ascites.
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Five percent of cirrhotic patients with ascites in our unit have grossly bloody fluid. Eleven of 32 randomly selected retrospective patients had hepatocellular carcinoma, one tuberculous peritonitis, seven prior trauma, and in 13 the bloody ascites was apparently spontaneous. Five prospectively encountered patients brought the number of cases of spontaneous bloody ascites available for review to 18. Three of these had sudden large intraperitoneal hemorrhages, and bloody ascites in the remaining 15 was incidentally noted at routine diagnostic paracentesis. Bleeding in the former three patients was from a retroperitoneal vein, spontaneous splenic rupture, and an unknown site, respectively. All patients required laparotomy and two died. Ascites red cells in the latter 15 patients may have been from a slowly leaking collateral vein or a hepatic lymphatic and required no treatment. However, the prognosis of these patients was significantly poorer than that of a control group of patients with similar liver tests and clear ascites.