Among diagnostic progress over the last three years in internal medicine, 
Antisynthetase Syndrome is now more easily recognised with the diffusion of 
laboratory tests for research of antibodies against tRNA synthetases (Anti JO1, 
anti PL7, Anti PL12). In two third of cases, these antibodies are found despite 
absence of antinuclear antibodies. Hence, we have to search them specifically in 
patients with polyarthritis associated with myositis, cutaneous manifestations 
(Raynaud phenomenom and "mechanic'hands") and interstitial lung disease. 
Discovery of asymptomatic mutation in the L ferritin coding sequence help us to 
better understand the "unexplained" hyperferritinemia. Initially described by 
japonese gastroenterologists, auto immune pancreatitis in fact a part of a 
systemic sclerosing disease with a biochemical hallmark: in crease of a subclass 
of immunoglobulins G (IgG4). A new pediatric disease due to a deficiency of the 
interleukin1 receptor antagonist (multifocal aseptic osteitis, periostitis, 
stomatitis, disseminated pustulosis) help us to better understand unexplained 
auto inflammatory diseases. The therapeutic progress is primarily due to an 
explosion of biological therapies, particularly four of them very useful for 
internists (in an off label use) : Interleukin 1 inhibitors (anakinra, 
Canakinumab) to treat some auto inflammatory diseases (cryopirin associated 
periodic syndromes and deficency of interleukin 1 receptor antagonist), 
monoclonal antibody against interleukin 5 (mepolizumab) to treat some 
hypereosinophilic syndromes and Churg and Strauss angiitis, interleukin 6 
inhibitiors to treat multifocal Castleman's disease and adult Still disease, a 
monoclonal antibody against vascular endothelial growth factor (Bevacizumab) to 
treat hereditary hemorrhagic telangiectasia.