In a prospective study, 114 patients with 138 zone 2 flexor tendon injuries were treated over a three-year period. Early active mobilisation of the injured fingers was commenced within 48 hours of surgery. 98 patients (86%) were reviewed at least six months after operation. Using the grading system recommended by the American Society for Surgery of the Hand, the active range of motion recovered was graded excellent or good in 77% of digits, fair in 14% and poor in 9%. Dehisence of the repair occurred in 11 digits (9.4%) and in these an immediate re-repair followed by a similar programme of early active mobilisation resulted in an excellent or good outcome in seven digits.
Neurofibromatosis type 1 (NF1) is one of the most common neurogenetic diseases affecting adults and children. Neurofibromas are one of the most common of the protean manifestations of NF1. Plexiform neurofibromas, which will frequently cause cosmetic abnormalities, pain, and neurologic deficits, are composed of "neoplastic" Schwann cells accompanied by other participating cellular and noncellular components. There is increasing evidence that loss of NF1 expression in neoplastic Schwann cells is associated with elevated levels of activated RAS, supporting the notion that the NF1 gene product, neurofibromin, acts as a growth regulator by inhibiting ras growth-promoting activity. In addition, there is increasing evidence that other cooperating events, which may be under cytokine modulation, are important for neurofibroma development and growth. Treatment of plexiform neurofibromas has been empiric, with surgery being the primary option for those with progressive lesions causing a major degree of morbidity. The efficacy of alternative treatment approaches, including the use of antihistamines, maturation agents, and antiangiogenic drugs, has been questionable. More recently, biologic-based therapeutic approaches, using drugs that target the molecular genetic underpinnings of plexiform neurofibromas or cytokines believed important in tumor growth, have been initiated. Evaluation of such trials is hindered by the unpredictable natural history of plexiform neurofibromas and difficulties in determining objective response in tumors that are notoriously large and irregular in shape. Innovative neuroimaging techniques and the incorporation of quality-of-life scales may be helpful in evaluation of therapeutic interventions. The ability to design more rational therapies for NF1-associated neurofibromas is heavily predicated on an improved understanding of the molecular and cellular biology of the cells involved in neurofibroma formation and growth.
We treated 37 patients with chronic osteomyelitis of the tibia (25), femur (9), radius (2) and humerus (1) by a twostage technique, comprising radical debridement of all infected bone and soft tissue with the provision of softtissue cover, and delayed autogenous bone grafting when necessary. All patients were reviewed at an average of 49 months (12 to 121). Infection-free bone union was achieved in 34. No patient required amputation. Wide excision of all compromised tissue and the closure of bone within a healthy vascularised soft-tissue envelope are essential if infection is to be eradicated. The combined assessment and management of such patients by an orthopaedic surgeon and a plastic surgeon are advocated.
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