Everything You Learn About Ruxolitinib Is Incorrect

1q28 and 17.5?Mb duplication at 6p22.3p22.3. Both parents had normal karyotypes indicating that the translocation had arisen de novo. Thyroid function tests, structural/functional echocardiography, cranial and renal ultrasound scans and ophthalmological examination were normal. Hearing test was also within normal results. At the age of 14.5?months neurodevelopmental assessment (Bayley III) was performed.1 After adjustment for prematurity, the performance was within the expectations for age: Cognitive Composite Score 85 (percentile rank 16), Language Composite Score 103 (percentile rank 58) and Motor Composite Score 103 (percentile rank 58). Neurological examination was normal and there were no clinical concerns. The translocation did not have exact precedent in the medical literature. As with other X autosome translocations in females, its phenotypic impact may be ameliorated by non-random X inactivation. A small number of individuals have been reported with similar focal facial dermal dysplasias such as Setleis syndrome.2 The case does not establish a causal relationship, but reports a possible new association between this translocation and temporal skin folds. Learning points We report a child with bilateral temporal skin folds and with an unbalanced translocation with Crizotinib concentration breakpoints at Xq22.1 and 6p22.3, a possible novel association. Unbalanced translocation with breakpoints at Xq22.1 and 6p22.3 is not associated with impaired early neurodevelopmental outcome. Array comparative genomic hybridisation is the first line investigation for the detection of unbalanced chromosome translocations. Footnotes Competing interests: None. Patient consent: Obtained. Provenance and peer review: Not commissioned; externally peer reviewed.""Necrotising fasciitis is a rare yet extremely serious soft tissue infection, which if not diagnosed promptly can lead to rapid clinical deterioration and death. It is estimated that there are approximately 500 cases of necrotising fasciitis per year in the UK.1 The key to successful diagnosis is a low threshold of clinical suspicion of what may initially present with non-specific symptoms: pain, fever and malaise. Visible skin changes may only appear late, after 5?days or later. In the past, differential diagnoses have included haematoma, bursitis, phlebitis, sciatica, cellulitis, septic arthritis or deep venous thrombosis.2 We report an unusual addition to this list: a full-thickness burn. Rapid clinical deterioration invariably ensues with signs of septicaemia, areas of skin infarction and severe pain that may appear disproportionate to the initial clinical appearance. Once necrotising fasciitis is suspected, immediate plans for surgical exploration and debridement are imperative. In the interim, prompt fluid resuscitation, intensive care input and broad spectrum antibiotic therapy should be instated.