In other non-HSCT settings, BOOP has been seen in association with infection, drugs, radiation therapy, and a number of connective tissue disorders [90]. It has also been shown that

the 2-year cumulative incidence of late-onset non-infectious pulmonary complications (LONIPC, including BO and BOOP) has been 10% in 438 patients undergoing HSCT. Moreover, the survival rate at 5 years has been significantly worse in affected subjects than in unaffected ones [91]. Graft versus host disease (GVHD) is a frequent and lethal complication PHA-848125 order of HSCT that limits the use of this important selleck screening library therapy. On the basis of pathophysiology and appearance, GVHD is classified in acute and chronic one [92]. Acute GVHD occurs prior to day 100 after transplant and it consists in an enhanced inflammatory/immune response, mediated by the competent donor’s lymphocytes, infused into the recipient, where they react against an environment perceived as a foreign one. The process is amplified through the tissue release of molecules which stimulate the donor’s lymphocytes. This apparently contradictory phenomenon is simply a physiological

reaction Loperamide of the damaged tissue to the disease which has led to the transplant therapy [93]. Acute GVHD presents clinical manifestations in the skin, i.e. maculopapular rash, which can spread throughout the body, dyskeratosis (in severe cases the skin may blister and ulcerate) [94], in the gastrointestinal

tract, i.e. diarrhea, emesis, anorexia, abdominal pain, mucosal ulceration with bleeding, Cobimetinib mouse luminal dilatation [95], and in the liver, i.e. same liver dysfunction of veno-occlusive disease, drug toxicity, viral infection, sepsis, or iron overload [96]. Chronic GVHD is the major cause of late non-relapse death following HCT [97]. However, chronic GVHD pathophysiology is not completely understood. Probably, thymus atrophy or dysfunction, which can develop after pharmacological preparation of transplant, play a major role in chronic GVHD manifestation. This fact leads to a peripheral tolerance decrease and to an increase in the number of autoreactive T lymphocytes. Autoreactive T lymphocytes lead to an interferon gamma mediated increase in the collagen deposition and fibrosis, a characteristic feature of chronic GVHD [97, 98]. The manifestations of chronic GVHD are protean and often of an autoimmune nature. Many districts are involved, i.e.