The answer to this issue is intervention at the molecular level. There are several current options that may be considered, but all have significant risks. Low-dose radiation postoperatively will initially inhibit fibrous tissue formation;

however, it has implications in terms of wound healing and may make any future surgeries more difficult with late accelerated fibrosis GDC 0199 and poor healing. Intra-articular steroids will inhibit fibrous tissue formation and will also reduce the host defences to infection, which, if it were to occur either through inoculation at the time of surgery or haematogenous seeding, would require further surgery and possibly implant removal. Were this necessary, it would invite recurrence of severe arthrofibrosis. A short course of oral steroids is more attractive than intra-articular steroids, but may not be adequate to reverse the selleck chemicals fibroplastic process. Namazi and co-investigators have studied arthrofibrosis of the knee in New Zealand White Rabbits by dividing the anterior cruciate ligament [22]. They were able to prevent the development of intra-articular scar by injecting botulinum toxin (Botox). They theorize that the mechanism of action is by inactivation of interlukin-1 which is a pro-inflammatory cytokine implicated in arthrofibrosis. Karen Lyons and co-investigators at the Orthopaedic Hospital Research Center at UCLA have developed a transgenic

mouse biochemical model of severe arthrofibrosis that seems analogous MCE to clinically severe cases that may allow us to develop other more effective therapies. Surgery releases connective tissue growth factor (CTGF), which stimulates fibroplasia. Antibodies against CTGF may inhibit arthrofibrosis. Haemophilic arthropathy is consistently associated with arthrofibrosis resulting in restricted motion of the involved joint. Early in the process, preservation of functional range of motion through prevention of recurrent bleeding and physical therapy is essential. In more advanced cases requiring surgery,

especially knee replacement, technical factors and aggressive rehabilitation are critical. Even then arthrofibrosis may recur. The ultimate solution in these severe cases lies in the realm of molecular biology. “
“Acquired haemophilia A is a rare bleeding disorder caused by autoantibodies against factor VIII (FVIII). There is a scarcity of acquired haemophilia A studies from Asian countries. The aim of this study was to evaluate clinical characteristics and outcomes of acquired haemophilia A among Asian populations. Data were collected from a retrospective case series and combined with a systematic review. The case series included all patients with acquired haemophilia A from 1999 to 2012 at Chiang Mai University Hospital. The systematic review searched MEDLINE and EMBASE databases for relevant keywords. A total of 111 patients were reviewed in this study (including 26 patients from the present series). There were 56 male (50.5%) and 55 female (49.5%) patients.