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Long-lasting NO overproduction in cirrhotic patients with spontaneous bacterial peritonitis

✍ Scribed by P N Bories; B Campillo; L Azaou; E Scherman


Publisher
John Wiley and Sons
Year
1997
Tongue
English
Weight
260 KB
Volume
25
Category
Article
ISSN
0270-9139

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✦ Synopsis


Nitric oxide production was studied in cirrhotic patients with spontaneous bacterial peritonitis (SBP) or with other infections. We followed up on the time course of serum nitrate levels in 51 hospitalized patients aged between 34 and 81 years. Four groups were defined: patients with SBP (group 1, n = 14), patients with bacteremia (group 2, n = 11), patients with urinary tract infection (group 3, n = 11) and patients in a stable clinical condition (group 4, n = 20). The four groups did not differ in terms of Pugh score (11 +/- 1, 10 +/- 1, 11 +/- 1, and 10 +/- 1, respectively). Serum nitrate levels averaged 31 +/- 2 micromol/L in group 4 (84 samples). On the day results of cytobacteriological examination were positive, mean serum nitrate levels were 75 +/- 17, 63 +/- 9, and 36 +/- 9 micromol/L, respectively, in groups 1 (17 cases), 2 (11 cases), and 3 (11 cases) (P < .001). The maximum nitrate values recorded during follow-up were higher in groups 1 (149 +/- 15 micromol/L) and 2 (112 +/- 11 micromol/L) than in group 3 (66 +/- 7 micromol/L; P < .001 and < .01, respectively). These maximum values were recorded in all groups approximately 2 weeks after the infection was diagnosed. The mean duration of NO overproduction, as defined by nitrate level (3)90 micromol/L, was 15 +/- 3 days in group 1 and 5 +/- 1 day in group 2. When the nitrate concentration was studied in serum and ascitic fluid sampled on the same day, it was found to be higher in ascitic fluid than in serum in eight cases of SBP in the period preceding the peak serum nitrate concentration (100 +/- 17 vs. 63 +/- 14 micromol/L; P < .001). Our data indicate that SBP in cirrhotic patients led to a long-lasting increased local production of NO. This overproduction may contribute to maintaining splanchnic vasodilation and thus worsen the hyperkinetic state in these patients.


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