Tumor necrosis factor-alpha, interleukin-6, and nitric oxide in sterile ascitic fluid and serum from patients with cirrhosis who subsequently develop ascitic fluid infection.

Ascitic fluid infection probably results from repeated episodes of bacteremia and seeding of ascitic fluid. The outcome of these episodes of colonization is probably a function of serum and ascitic fluid defense mechanisms and the virulence of the organism. Patients who develop spontaneous bacterial peritonitis may have serum and ascitic fluid characteristics that are different from those who do not develop infection. We prospectively collected serum and ascitic fluid specimens at the time of admission from patients with sterile cirrhotic ascites, and tested these specimens for interleukin-6, tumor necrosis factor-alpha, and nitric oxide and compared these results as well as other characteristics of patients who did not develop infection to those who did. An elevated baseline serum tumor necrosis factor-alpha as well as an increased proportion of polymorphonuclear leukocytes in sterile ascitic fluid from patients who subsequently developed infection probably represent a subclinical activation of defense mechanisms from prior silent colonizations with bacteria.

Small-diameter portacaval H-graft shunt: a paradigm shift back to surgical shunting in the management of variceal bleeding in patients with preserved liver function.

Small-diameter portacaval H-graft (SDPHG) shunts are partial portosystemic shunts that control variceal bleeding while preserving nutrient blood flow to the liver, minimizing postoperative encephalopathy and liver failure. Since July 1, 1997, we placed SDPHG shunts in 18 patients (age, 52.1 +/- 2.6 years; range, 35 to 72 years) with cirrhosis (Child's class A, B, and C in 6, 10, and 2 patients, respectively) and refractory variceal bleeding who were not candidates for transplantation. Ten procedures (55.6%) were urgent or emergent. SDPHG shunts effectively reduced the portacaval pressure gradient (18 +/- 3 v 5 +/- 2 mm Hg; P <.05). Surgical times (210 +/- 11 minutes), estimated blood losses (358.3 +/- 107.8 mL), transfusion requirements (0 transfusions in 10 patients; 55.6%; mean, 0.9 +/- 0.3 units), and postoperative hospitalization (7.7 +/- 1.0 days) were excellent. Surgical mortality (30 days) was 0%. During 14. 0 +/- 1.9 months (range, 1.1 to 29.1 months) of follow-up, 4 patients (22.2%) died, including both patients with Child's class C cirrhosis. The cumulative 1-year survival rate was 82.1% (Child's class A, B, and C, 83.3%, 90%, and 0%, respectively). Long-term survivors had significantly lower preoperative Child-Pugh scores compared with nonsurvivors (7.8 +/- 0.3 v 9.5 +/- 1.0; P <.05). Postoperative encephalopathy developed in 3 survivors (20%). Fifteen patients (83.3%) have not experienced rebleeding; shunt failure led to rebleeding in only 1 patient (5.6%). SDPHG shunt placement can be performed with low morbidity and surgical mortality. Nontransplantation candidates with Child's class A and B cirrhosis have excellent long-term survival with this safe, effective, and definitive treatment for refractory variceal bleeding.

Ascitic fluid adenosine deaminase insensitivity in detecting tuberculous peritonitis in the United States.

Tuberculous peritonitis, although common in Third World countries, remains an uncommon cause of ascites in the United States. Ascitic fluid adenosine deaminase (ADA) activity has been proposed as a useful diagnostic test. The aim of this retrospective study was to determine the clinical utility of ascitic fluid ADA activity in diagnosing tuberculous peritonitis in a U.S. patient population. A total of 368 ascitic fluid specimens from a well-characterized ascitic fluid bank, including tuberculous peritonitis (n = 7), tuberculous peritonitis in the setting of cirrhosis (n = 10), and consecutive specimens of widely varied etiologies (n = 351) were analyzed for ADA activity by ultraviolet spectrophotometry at 265 nm. The overall sensitivity of the ADA determination in diagnosing tuberculous peritonitis was only 58.8%, and the specificity was 95.4%. The accuracy of ADA determination (93.8%) compared favorably with that of the common ascitic fluid tests of white blood cell (WBC) count (>500/mm3), total protein (>2.5 g/dL), and combined WBC count and total protein (45.8%, 74.4%, and 81.3%, respectively). However, ADA was only 30% sensitive in detecting tuberculous peritonitis in the setting of cirrhosis, and cirrhosis was present in 59% of the tuberculous peritonitis patients in our population. In addition, malignancy-related ascites (13%) and bacterial peritonitis specimens (5.8%) occasionally yielded false-positive results. In conclusion, our results indicate that the ascitic fluid ADA activity has good accuracy but poor sensitivity and imperfect specificity in a U.S. patient population in which the prevalence of tuberculosis is low and underlying cirrhosis is common.