Fever of unknown origin revealed to be primary splenic lymphoma: A rare case report with review of the literature.

Fever is a common clinical presentation of a number of diseases. A sustained unexplained fever >38.3°C lasting for >3 weeks without an established diagnosis despite intensive diagnostic evaluation is referred to as fever of unknown origin (FUO). FUO remains a clinical challenge for physicians, as it may be attributed to a wide range of disorders, mainly infections, malignancies, non-infectious inflammatory diseases and miscellaneous diseases. We herein report the case of a 59-year-old male patient who presented with prolonged unexplained fever and was found to have a diffusely enlarged hypermetabolic spleen, as shown on 18F-fluorodeoxyglucose positron emission tomography/computed tomography examination. Following splenectomy, histopathological examination revealed primary splenic lymphoma (PSL) of B-cell origin. The patient received 6 courses of systemic chemotherapy with rituximab, etoposide, cyclophosphamide, doxorubicin, vincristine and prednisone (R-ECHOP regimen) and responded well to treatment. Thus, in patients with FUO and splenomegaly, the possibility of PSL should be taken into consideration.

RTEF-1 protects against oxidative damage induced by H2O2 in human umbilical vein endothelial cells through Klotho activation.

Oxidative stress is a main risk factor of vascular aging, which may lead to age-associated diseases. Related transcriptional enhancer factor-1 (RTEF-1) has been suggested to regulate many genes expression which are involved in the endothelial angiogenesis and vasodilation. However, whether RTEF-1 has a direct role in anti-oxidation and what specific genes are involved in RTEF-1-driven anti-oxidation have not been elucidated. In this study, we found that overexpressing RTEF-1 in H2O2-treated human umbilical vein endothelial cells decreased senescence-associated-ß-galactosidase (SA-ß-gal)-positive cells and G0/G1 cells population. The expressions of p53 and p21 were decreased in H2O2-treated RTEF-1 o/e human umbilical vein endothelial cells. However, specific small interfering RNA of RTEF-1 totally reversed the anti-oxidation effect of RTEF-1 and inhibited RTEF-1-induced decreased p53 and p21 expressions. It demonstrated that RTEF-1 could protect cells from H2O2-induced oxidative damage. In addition, we demonstrated that RTEF-1 could up-regulate Klotho gene expression and activate its promoter. Furthermore, Klotho small interfering RNA significantly blocked RTEF-1-driven endothelial cell protection from H2O2-induced oxidative damage and increased p53 and p21 expressions. These results reveal that RTEF-1 is a potential anti-oxidation gene and can prevent H2O2-induced endothelial cell oxidative damage by activating Klotho.