Evaluation of Risk Factors for Rectus Sheath Hematoma.

Rectus sheath hematoma (RSH) develops due to rupture of epigastric arteries or the rectus muscle. Although RSH incidence rate is low, it poses a significant diagnostic dilemma. We evaluated the risk factors for RSH, its presentation, management, and outcomes for 115 patients hospitalized with confirmed RSH by computed tomography scan between January 2005 and June 2009. More than three-fourth (77.4%) of the patients were on anticoagulation therapy, 58.3% patients had chronic kidney disease (CKD) stage ≥3, 51.3% had abdominal injections, 41.7% were on steroids/immunosuppressant therapy, 37.4% had abdominal surgery/trauma, 33.9% had cough, femoral puncture was performed in 31.3% of patients, and 29.5% were on antiplatelet therapy. Rectus sheath hematoma was not an attributable cause in any of the 17 deaths. Mortality was significantly higher in patients with CKD stage ≥3 (P = .03) or who required transfusion (P = .007). Better understanding of RSH risk factors will facilitate early diagnoses and improve management.

Evidence that glutathione depletion is a mechanism responsible for the anti-inflammatory effects of ethyl pyruvate in cultured lipopolysaccharide-stimulated RAW 264.7 cells.

Ethyl pyruvate (EP), an effective scavenger of reactive oxygen species, is also an anti-inflammatory agent in a variety of in vivo and in vitro model systems. To gain a better understanding of the molecular basis for the anti-inflammatory effects of EP, we compared the pharmacological properties of EP andN-acetyl-l-cysteine (NAC), a well studied scavenger of reactive oxygen species and a precursor for the endogenous antioxidant glutathione (GSH). The studies were performed using RAW 264.7 murine macrophage-like cells that were stimulated with lipopolysaccharide (LPS). Although EP and NAC both inhibited LPS-induced nitric oxide and interleukin (IL)-6 secretion, the former compound was considerably more potent than the latter. EP markedly inhibited inducible nitric-oxide synthase, IL-6, and IL-10 mRNA induction, whereas the effects of NAC were minimal. EP inhibited LPS-induced nuclear factor-kappaB DNA binding to a much greater extent than did NAC. Both compounds inhibited LPS-induced lipid peroxidation, but the two compounds had qualitatively different effects on cellular levels of GSH. Although NAC increased GSH levels, EP had the opposite effect. The anti-inflammatory effects of EP were partially reversed when RAW 264.7 cells were treated with a cell-permeable GSH analog, glutathione ethyl ester. These data support the view that the anti-inflammatory effects of EP are mediated, at least in part, by the ability of EP to deplete cellular GSH stores. Moreover, the findings presented here suggest that an unusual combination of biochemical effects (inhibition of lipid peroxidation and GSH depletion) might account for the anti-inflammatory effects of EP.