Case report of sclerosing encapsulating peritonitis secondary to tuberculosis

Sclerosing encapsulating peritonitis (SEP) is a visceral encapsulation syndrome of inflammatory origin, seen as an infrequent cause of intestinal obstruction in young patients. It is a condition characterised by complete encapsulation of small bowel loops by a fibrocollagenous membrane, leading to cocoon formation. Histologically, the membrane is composed mainly of organised fibrin, probably derived from the plasma exudation of peritoneal microvasculature. Clinical presentation is related to the development of altered gut motility, resulting in abdominal pain and features of intestinal obstruction. We here discussed about a young patient who presented with features of intestinal obstruction and diagnosed with SEP, secondary to abdominal tuberculosis and was then treated surgically. SEP as a cause of intestinal obstruction is a rare life threatening entity encountered in day to day practice. Definitive diagnosis of this condition is challenging in the pre-operative period and is usually missed and a high index of suspicion is required.

Ouabain Modulates Zymosan-Induced Peritonitis in Mice

Ouabain, a potent inhibitor of the Na+, K+-ATPase, was identified as an endogenous substance. Recently, ouabain was shown to affect various immunological processes. We have previously demonstrated the ability of ouabain to modulate inflammation, but little is known about the mechanisms involved. Thus, the aim of the present work is to evaluate the immune modulatory role of ouabain on zymosan-induced peritonitis in mice. Our results show that ouabain decreased plasma exudation (33%). After induction of inflammation, OUA treatment led to a 46% reduction in the total number of cells, as a reflex of a decrease of polymorphonuclear leukocytes, which does not appear to be due to cell death. Furthermore, OUA decreased TNF-α(57%) and IL-1β(58%) levels, without interfering with IL-6 and IL-10. Also,in vitroexperiments show that ouabain did not affect endocytic capacity. Moreover, electrophoretic mobility shift assay (EMSA) shows that zymosan treatment increased (85%) NF-κB binding activity and that ouabain reduced (30%) NF-κB binding activity induced by zymosan. Therefore, our data suggest that ouabain modulated acute inflammatory response, reducing the number of cells and cytokines levels in the peritoneal cavity, as well as NFκB activation, suggesting a new mode of action of this substance.

Hog barn dust extract increases macromolecular efflux from the hamster cheek pouch

The purpose of this study was to determine whether short-term exposure to an aqueous extract of hog barn dust increases macromolecular efflux from the intact hamster cheek pouch and, if so, to begin to determine the mechanism(s) underlying this response. By using intravital microscopy, we found that suffusion of hog barn dust extract onto the intact hamster cheek pouch for 60 min elicited a significant, concentration-dependent leaky site formation and increase in clearance of FITC-labeled dextran (molecular mass, 70 kDa). This response was significantly attenuated by suffusion of catalase (60 U/ml), but not by heat-inactivated catalase, and by pretreatment with dexamethasone (10 mg/kg iv) ( P < 0.05). Catalase had no significant effects on adenosine-induced increase in macromolecular efflux from the cheek pouch. Suffusion of hog barn dust extract had no significant effects on arteriolar diameter in the cheek pouch. Taken together, these data indicate that hog barn dust extract increases macromolecular efflux from the in situ hamster cheek pouch, in part, through local elaboration of reactive oxygen species that are inactivated by catalase. This response is specific and attenuated by corticosteroids. We suggest that plasma exudation plays an important role in the genesis of upper airway dysfunction evoked by short-term exposure to hog barn dust.