However, increasing data with the tumor necrosis factor inhibitors suggest that these agents may also be acceptable options for the management of refractory vascular BD in daily practice.
Comparative study of corticosteroid monotherapy, and TNF inhibitors with or without corticosteroid in patients with refractory entero-Behcet's disease.
We report on the therapeutic use of anti-TNF monoclonal antibodies for BD-associated NVD and NVE in one pediatric patient (subcutaneous adalimumab) and one young man (intravenous infliximab).
A subgroup analysis arranged by the geographical regions showed HLA-A*26 is in fact associated with the onset of BD in Northeast Asia (OR = 2.11, 95% CI: 1.75-2.56), but not in the Middle East or in Europe.
Recurrent Myocardial Infarction Despite Normal C-reactive Protein in a Patient with Behcet's Disease and Compound Heterozygous Methylenetetrahydrofolate Reductase (MTHFR) Mutations (C677T and A1298C).
Further functional studies are required to research whether the variant of TNFAIP3 plays a part in the development of GPP or simply causes the Behçet's disease phenotype.
To our knowledge, this is the first analysis of KIR3DL1/S1 allelic variation in Behçet disease and may provide insight into the pathogenic role of <i>HLA-B*51</i> and its interaction with KIR3DL1/S1.
VDR gene polymorphisms may possibly have a role in the pathogenesis of BD through their effects on VDR expression and may be associated with the increased risk of several clinical findings.
Optimal coronary artery disease (CAD) therapy was commenced, and Behcet's disease treatment was intensified with the normalization of C-reactive protein.
However, no difference of CRP (P = 0.219) or ESR (P = 0.320) between AAD patients and controls was observed, and no correlation of CRP (R = -0.150, P = 0.377) or ESR (R = 0.067, P = 0.692) with ascending aortic diameter in total BD patients was discovered either.
T-cell-associated miRNA expression levels, miR-25, miR-106b, miR-326, and miR-93 were significantly upregulated, while miR-146a and miR-155 levels were lower in PBMCs of patients with BD when compared with the controls.
The education of the NK cells depending on the HLA, the balance of KIR3DL1/KIR3DL2 licensed NK cells and the different capacities of these receptors to eliminate pathogens could be involved in the etiopathogenesis of BD.