Search

The May-Thurner syndrome is a well-known anatomical anomaly where the left common iliac vein (LCIV) is compressed between the right common iliac artery and the fifth vertebral body. This report describes the case of a "right-sided" May-Thurner syndrome where the right common iliac vein (RCIV) is compressed by the left common iliac artery in a patient with a left-sided inferior vena cava (IVC). A 26-year-old woman was admitted to our institution with acute edema of the right lower limb. The diagnosis of May-Thurner syndrome was done by CT scan and confirmed by phlebography. An endovascular treatment with stenting was carried out, with good patency and clinical result at 12-month follow-up. [ABSTRACT FROM AUTHOR]

Follicular helper T (TFH) cells are expanded in systemic lupus erythematosus, where they are required to produce high affinity autoantibodies. Eliminating TFH cells would, however compromise the production of protective antibodies against viral and bacterial pathogens. Here we show that inhibiting glucose metabolism results in a drastic reduction of the frequency and number of TFH cells in lupus-prone mice. However, this inhibition has little effect on the production of T-cell-dependent antibodies following immunization with an exogenous antigen or on the frequency of virus-specific TFH cells induced by infection with influenza. In contrast, glutaminolysis inhibition reduces both immunization-induced and autoimmune TFH cells and humoral responses. Solute transporter gene signature suggests different glucose and amino acid fluxes between autoimmune TFH cells and exogenous antigen-specific TFH cells. Thus, blocking glucose metabolism may provide an effective therapeutic approach to treat systemic autoimmunity by eliminating autoreactive TFH cells while preserving protective immunity against pathogens. T cell functions depend on distinct metabolic fluxes. Here the authors show different metabolic requirements of humoral responses to self versus microbial antigens: while glucose is dispensable for antiviral Tfh and antibody responses, it is essential to mount these responses against autoantigens. [ABSTRACT FROM AUTHOR]

A letter to the editor regarding acute decompensation of isovaleric acidemia induced by Graves' disease is presented.