RESUMO
A horseshoe abscess is caused by infection that spreads between the flexor tendon sheath of the thumb or little finger through the radial and ulnar bursae through communication between the two and/or the space of Parona. We present a case of an 80-year-old woman with rheumatoid arthritis who presented with 6 months of right hand and wrist soft tissue swelling, initially treated as a rheumatoid arthritis flare. MRI demonstrates the horseshoe abscess and after surgical irrigation and debridement with synovectomy, cultures demonstrated infection with mycobacterium avium intracellulare (MAI). This case demonstrates the importance of MRI in diagnosing and evaluating the extent of hand infections and for considering mycobacterial organisms for appropriate treatment and antibiotic regimen.
Assuntos
Abscesso/diagnóstico por imagem , Mãos/diagnóstico por imagem , Infecção por Mycobacterium avium-intracellulare/diagnóstico por imagem , Abscesso/complicações , Idoso de 80 Anos ou mais , Antibacterianos , Artrite Reumatoide/complicações , Feminino , Humanos , Tenossinovite , Punho , Articulação do PunhoRESUMO
A central challenge for improving autoimmune therapy is preventing inflammatory pathology without inducing generalized immunosuppression. T helper 17 (TH17) cells, characterized by their production of interleukin-17, have emerged as important and broad mediators of autoimmunity. Here we show that the small molecule halofuginone (HF) selectively inhibits mouse and human TH17 differentiation by activating a cytoprotective signaling pathway, the amino acid starvation response (AAR). Inhibition of TH17 differentiation by HF is rescued by the addition of excess amino acids and is mimicked by AAR activation after selective amino acid depletion. HF also induces the AAR in vivo and protects mice from TH17-associated experimental autoimmune encephalomyelitis. These results indicate that the AAR pathway is a potent and selective regulator of inflammatory T cell differentiation in vivo.
