Pneumomediastinum as a complication of emphysematous cholecystitis: Case report

<p>Abstract</p> <p>Background</p> <p>Emphysematous cholecystitis is a variant of acute cholecystitis which is generally caused by gas-forming organisms. Emphysematous cholecystitis may cause gas spreading within the subcutaneous tissue, peritoneal cavity and retroperitoneum.</p> <p>Case presentation</p> <p>We present a case of emphysematous cholecystitis in a middle-aged diabetic patient who, postoperatively, presented edema in both flanks and left chest crepitation on palpation, associated with hemodynamic worsening. Computed tomography scan of the chest and abdomen revealed a large pneumomediastinum, pneumoretroperitoneum, gas in subcutaneous tissue and flank abscesses. In both blood and surgical wound exudate cultures, <it>Escherichia coli </it>was found.</p> <p>Conclusion</p> <p>Emphysematous cholecystitis should be considered as a possible cause of pneumomediastinum.</p

Interleukin-18 resistance in patients with obesity and type 2 diabetes mellitus.

Contains fulltext : 69672.pdf (publisher's version ) (Closed access)OBJECTIVE: Interleukin-18 (IL-18) has been recently demonstrated to improve experimental hyperphagia and insulin resistance. Paradoxically, concentrations of circulating IL-18 in obese subjects and in patients with type 2 diabetes are increased. The objective of this study is to provide an explanation for this paradox. DESIGN: We have hypothesized that cells from obese individuals or from patients with type 2 diabetes mellitus have a diminished response to stimulation with IL-18. IL-18 responsiveness was tested by stimulating blood monocytes of obese or diabetes patients with rIL-18 or microbial components. RESULTS: Obese individuals and patients with type 2 diabetes mellitus exhibit increased circulating concentrations of IL-18. More importantly, leukocytes isolated from obese or type 2 diabetes patients respond poorly after stimulation with IL-18, as reflected by defective interferon-gamma (IFN gamma) production. The defective response to IL-18 stimulation was accompanied by a 50% reduction in the expression of IL-18R alpha and beta chains. In addition, cells of patients with obesity and diabetes displayed an impaired release of IFN gamma after challenge with bacterial or fungal pathogens, which was due to defective IL-18-mediated signaling. CONCLUSION: Patients with obesity or type 2 diabetes mellitus are characterized by lower responses after stimulation with IL-18. This IL-18 resistance explains the association of obesity and diabetes with high IL-18 circulating concentrations, similar to hyperinsulinemia and hyperleptinemia. IL-18 resistance may represent an important mechanism of the increased susceptibility of these patients to a number of infections