During the infection, the patient's capillaries become engorged, and focal hemorrhages develop; ultimately, the systemic expansion of capillary leakage leads to retroperitoneal edema, which may affect the pancreas.[1] Potential mediators, which increase vascular permeability during the acute stage of HFRS, are tumor necrosis factor-alpha, interleukin-1 and interleukin-2, and nitric oxide.[18] Activation of inflammation mediators during the hypotensive stage of HFRS seems to be caused by an inflammatory cascade mediated by cytokines, immunocytes, and the complement system. This evidence concerns the gene TNF and infection.