Do platelets trigger a CD40-dependent inflammatory response in the microvasculature of inflammatory bowel disease patients?
These results show that platelets can actively contribute to mucosal inflammation and represent a previously unrecognized component of IBD pathogenesis.
In subjects with known coronary atherosclerosis, low-degree inflammatory activity is not only increased in diabetic patients, but also increased with increasing HbA(1c) in non-diabetic individuals with HbA(1c) within the normal range, i.e., at a pre-diabetic level of glucose metabolism derangement.