Leukotrienes play a role in inflammation, and their participation in airway inflammation and bronchoconstriction in patients with severe asthma can be ameliorated by a new class of drugs known as leukotriene modulators. The role of leukotrienes in increasing vascular permeability in experimental peritonitis and in inducing chemotaxis of inflammatory cells has recently been documented. Steroids have been incriminated in the development of bacterial translocation in animal models in association with the suppression of mucosal immunity. The development of spontaneous bacterial peritonitis is recognized in cirrhotic patients with ascites and in those with nephrotic syndrome. The onset of bacterial peritonitis in the absence of these predisposing conditions or other underlying cause, such as perforated viscus, is termed 'primary bacterial peritonitis', and has never been described in asthmatic patients. We present an asthmatic patient who developed primary bacterial peritonitis while receiving a leukotriene modulator in combination with prednisolone therapy. The hypothesis that leukotriene receptor blockade might predispose to the development of primary bacterial peritonitis in patients receiving steroid therapy is discussed.

Leukotriene inhibitors in combination with steroids: potential role in the development of primary bacterial peritonitis.

Objective and design To evaluate the beneficial effects of exogenous NO and an inhibitor of the COX2, and their action levels in a model of SIRS/bacterial translocation (BT) induced by Zymosan A ® . Material and methods Ninety Wistar rats were submitted to different treatments, and after 12 h and 24 h they were anaesthetized in order to collect blood, mesenteric lymph nodes, and kidney for subsequent biochemical analyses and microbiological examinations. Treatments A nitric oxide donor, Molsidomine ® , was compared with a COX2 inhibitor, Celecoxib ® . Methods Zymosan A ® was administered to Wistar rats. The animals were divided into 6 groups: one group for survival study, Group (1) No manipulation (BASAL); Group (2) vehicle of Zymosan A ® given intraperitoneally (SHAM); Group I (control), with Zymosan A ® (0.6 g/kg) intraperitoneally; Group II (Molsidomine), with Molsidomine ® (4 mg/kg) through the penis dorsal vein, 30 min prior to administration of the Zy ® (0.6 g/kg); Group III (Celecoxib), with Celecoxib ® (400 mg/kg) orally through a stomach tube, 6 h prior to administration of the Zy (0.6 g/kg). Determinations The parameters survival, bacterial translocation, renal function, neutrophil accumulation, oxygen free radicals (OFR), detoxifying enzymes, and cytokines were measured at different times after Zymosan administration. Results The model established induced a mortality rate of 100% and generated BT and systemic inflammatory response syndrome (SIRS) in all samples. It also significantly increased all variables, with p p p ® showed a lower capacity for SIRS regulation. Conclusions The exogenous administration of NO prevented BT and controlled SIRS. Therefore these results suggest that Molsidomine could be used as a therapeutic strategy to protect against BT.

Comparative study of bacterial translocation control with nitric oxide donors and COX2 inhibitor

Following intraperitoneally (ip) applied treatment with 125 mg/mouse prednisolonum (PRD) no bacterial translocation (BT) was observed in mice The PRD treatment applied in combination with lymphotropic cytostatics as dianhydrogalactitol (30 mg/kg ip) or chlorpromazine (75 mg/kg ip) both causing BT, did not increase the mice's drug sensitivity to the used agents According to our results, PRD can be suitable for combined application with other immunosuppressive agents as it can increase immunosuppression without increase of side-effects such as those induced by bacterial translocation

Interaction of immunosuppressive drugs in mouse experiments with special regards to bacterial translocation.

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Interaction of immunosuppressive drugs in mouse experiments with special regards to bacterial translocation.