[Sigmoid shaped ventricular septum causing hemodynamic deterioration during lumbar anesthesia: a case report].

A 73-year-old woman with a left femoral neck fracture underwent an operation for femoral caput replacement. Twenty-five minutes after induction of spinal anesthesia, ST depression emerged followed by shock. Although the ST depression indicated an ischemic event, Levine grade IV systolic murmur was noticed at the aortic valve area. Echocardiography revealed narrowing of the left ventricular outflow tract with a pressure gradient of 170 mmHg. Rapid fluid infusion (1,000 ml) stabilized her blood pressure and the patient recovered without adverse sequelae. Echocardiography and magnetic resonance imaging suggested the presence of sigmoid shaped ventricular septum rather than obstructive hypertrophic cardiomyopathy. There was no significant pressure gradient at rest. Sigmoid shaped ventricular septum is usually considered as a normal aging process and has little clinical importance, but several cases associated with outflow obstruction have been reported. As the patient had no abnormal findings on electrocardiography or chest radiography and had no abnormal symptom on physical examination, the sequelae were impossible to predict.

Involvement of IL-2/IL-2R system activation by parasite antigen in polyclonal expansion of CD4(+)25(+) HTLV-1-infected T-cells in human carriers of both HTLV-1 and S. stercoralis.

The intermediate state of HTLV-1 infection, often found in individuals dually infected with Strongyloides stercoralis (S. stercoralis) and HTLV-1, is assumed to be a preleukemic state of adult T-cell leukemia (ATL). To investigate the effects of S. stercoralis superinfection on the natural history of HTLV-1 infection, we characterized peripheral blood samples of these individuals in Okinawa, Japan, an endemic area for both HTLV-1 and S. stercoralis and we studied effects of the parasite antigen on T-cells. The dually infected individuals showed a significantly higher provirus load and an increase in CD4(+)25(+) T cell population, with a significant, positive correlation. This increase was attributable to polyclonal expansion of HTLV-1-infected cells, as demonstrated by inverse-long PCR analysis of the integration sites. S. stercoralis antigen activated the IL-2 promoter in reporter gene assays, induced production of IL-2 by PBMC in vitro, and supported growth of IL-2 dependent cell lines immortalized by HTLV-1 infection or the transduction of Tax. Taken collectively, these results indicate that S. stercoralis infection induces polyclonal expansion of HTLV-1-infected cells by activating the IL-2/IL-2R system in dually infected carriers, an event which may be a precipitating factor for ATL and inflammatory diseases.