Towards an integrated clinical framework for patient with shoulder pain

Background: Shoulder pain (SP) represents a common musculoskeletal condition that requires physical therapy care. Along the years, the usual evaluation strategies based on clinical tests and diagnostic imaging has been challenged. Clinical tests appear unable to clearly identify the structures that generated pain and interpretation of diagnostic imaging is still controversial. The current patho-anatomical diagnostic categories have demonstrated poor reliability and seem inadequate for the SP treatment. Objectives: The present paper aims to (1) describe the different proposals of clinical approach to SP currently available in the literature; to (2) integrate these proposals in a single framework in order to help the management of SP. Conclusion: The proposed clinical framework, based on a bio-psychosocial vision of health, integrates symptoms characteristics, pain mechanisms and expectations, preferences and psychosocial factors of patients that may guide physiotherapist to make a diagnostic triage and to choose the right treatment for the individual patient

Case Report: A Novel Activating FLT3 Mutation in Acute Myeloid Leukemia

FMS-like tyrosine kinase 3 (FLT3) is among the most common driver genes recurrently mutated in acute myeloid leukemia (AML), accounting for approximately 30% of cases. Activating mutations of the FLT3 receptor include internal tandem duplications (ITD) that map to the auto-inhibitory juxtamembrane (JM) domain or point mutations within the tyrosine kinase domain (TKD). Several FLT3 tyrosine kinase inhibitors have been developed in the last few years, but midostaurin is currently the only one approved for the treatment of newly diagnosed patients harboring FLT3 mutations. Here we describe for the first time a novel in-frame deletion in exon 14 (JM domain) of the FLT3 gene, that we identified in a young woman with CBFb-MYH11-positive AML. We demonstrated that this novel FLT3 variant is pathogenic, since it is responsible for constitutive activation of FLT3 receptor. Finally, ex-vivo studies demonstrated that this novel mutation is sensitive to midostaurin