Patients should have severe active Crohns disease with a CDAI score of 300 or more, have not responded to immunomodulating drugs and corticosteroids, and for whom surgery is inappropriate. Since February 2015, it is also approved for the treatment of ulcerative colitis where other treatments have not worked.In Australia, infliximab is available through the PBS for Crohns disease treatment provided the patient has not responded to conventional treatment and has a severe case of the condition.Infliximab is available in the Republic of Ireland through the HSEs Medical Card and Drug Payment Scheme.Johnson & Johnson reported in its 2013 annual report, "Remicade (infliximab), accounted for approximately 9.4% of the Companys total revenues for fiscal 2013." References
External links
"Infliximab". Drug Information Portal. U.S. National Library of Medicine.
They often do not cause additional morbidity but may in up to one-half of patients. Neurocognitive impairment, attention-deficit hyperactivity disorder,  autism spectrum disorder and behavioral disorders are also commonly seen in patients with neurofibromatosis type 1. Epilepsy is seen in 4-7% of patients.Musculoskeletal system manifestations can develop in patients with neurofibromatosis type 1. Common findings include sphenoid wing dysplasia, osteopenia, osteoporosis, anterior chest wall deformities as well as scoliosis. Patients are at a much greater risk for fractures than the general population.Vascular abnormalities are also frequently encountered in patients with neurofibromatosis type 1. These may include renal artery stenosis, pulmonary artery stenosis, cerebral artery stenosis and aneurysms. Complications may include myocardial infarction and stroke. Relative to the general population the risk for certain types of cancer is increased significantly. For instance, the risk for brain tumors and breast cancer is increased by 5 times. Neurofibromatosis Type II
Neurofibromatosis type 2 is an autosomal dominant condition that affects approximately 1 in 35,000-40,000 people. It is caused by mutations in the NF2 gene on chromosome 22 which has a high penetrance though most patients do not present with symptoms until adulthood. Approximately half of patients have de novo mutations and as many as 59.7% are mosaic. Patients who present in childhood tend to have a more severe phenotype.Bilateral vestibular schwannomas are the most characteristic finding and in the vast majority of cases are benign. However, they are responsible for significant morbidity and are responsible for the most common presenting symptom of hearing loss in adults.