Acute Onset of a Swollen Leg With Crepitus: A Complication With Rectal Perforation.

Crepitus happened into the soft tissue is indicated subcutaneous emphysema. Subcutaneous emphysema of leg without trauma was likely to diagnose gas gangrene or gas-forming myonecrosis (GFM) at emergency department (ED). On the other hand, abdominal fatal condition with gas from the gut may spread to the leg should be considered a different diagnosis. We report a case of critically ill patient who presented to the ED with initial features suggestive of necrotizing fasciitis with gas gangrene of left leg. Assessment and further intervention revealed subcutaneous emphysema of leg secondary to a perforation of rectum associated with previous anastomosis site for rectal cancer surgery. Subcutaneous emphysema of the leg rarely happened secondary to perforation of the gastrointestinal tract and has often created serious diagnostic problems which may lead to mortality. Consequently, prompt diagnosis and aggressive treatment is imperative. Physicians and surgeons should be aware of this condition that could be fatal but curable by early intervention.

Induction of intracellular heat-shock protein 72 prevents the development of vascular smooth muscle cell calcification.

AIMS: Vascular calcification (VC) is a significant contributor to cardiovascular mortality in patients with chronic kidney disease (CKD) and coronary artery disease (CAD). Osteo/chondrocytic transformation and simultaneous dedifferentiation of smooth muscle cells (SMCs) are important in the pathogenesis of VC. Heat-shock protein 72 (HSP72) is a cardioprotective inducible heat-shock protein that functions as a molecular chaperone. However, its role in the development of accelerated vascular dysfunction and calcification is largely unexplored. METHODS AND RESULTS: We describe for the first time marked reduction in HSP72 expression in arteries from patients with CKD and CAD, compared with healthy controls, in vivo. Induction of HSP72 by heat-shock treatment (HST) significantly prevented the development of calcification of human aortic smooth muscle cells (HA-SMCs), in vitro. These anti-calcific effects were abolished following treatment with both quercetin, an HST inhibitor, and HSP72 siRNA knockdown. Induction of HSP72 suppressed Cbfa-1-dependent osteo/chondrocytic transformation and stabilized SMC contractile phenotype through the myocardin-serum response factor (SRF) pathway. Co-immunoprecipitation studies demonstrated physical association between SRF and HSP72. Furthermore, organ culture of arteries from CKD and CAD patients showed that these arteries retained their ability to induce HSP72 following HST, despite initially reduced expression. CONCLUSION: Our study shows for the first time that intracellular HSP72 may function as a central regulator of molecular pathways involved in the development of VC. We suggest treatment strategies that up-regulate HSP72 as a new approach to inhibit VC.