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Keywords:Bladder outlet obstruction (BOO) Men Lower urinary tract symptoms Diagnosis Urodynamics Noninvasive Systematic review Please visit www.eu-acme.org/ europeanurology to read and answer questions on-line. The EU-ACME credits will then be attributed automatically. AbstractContext: Several noninvasive tests have been developed for diagnosing bladder outlet obstruction (BOO) in men to avoid the burden and morbidity associated with invasive urodynamics. The diagnostic accuracy of these tests, however, remains uncertain. Objective: To systematically review available evidence regarding the diagnostic accuracy of noninvasive tests in diagnosing BOO in men with lower urinary tract symptoms (LUTS) using a pressure-flow study as the reference standard. Evidence acquisition: The EMBASE, MEDLINE, Cochrane Database of Systematic Reviews, Cochrane Central, Google Scholar, and WHO International Clinical Trials Registry Platform Search Portal databases were searched up to May 18, 2016. All studies reporting diagnostic accuracy for noninvasive tests for BOO or detrusor underactivity in men with LUTS compared to pressure-flow studies were included. Two reviewers independently screened all articles, searched the reference lists of retrieved articles, and performed the data extraction. The quality of evidence and risk of bias were assessed using the QUADAS-2 tool. Evidence synthesis: The search yielded 2774 potentially relevant reports. After screening titles and abstracts, 53 reports were retrieved for full-text screening, of which 42 (recruiting a total of 4444 patients) were eligible. Overall, the results were predominantly based on findings from nonrandomised experimental studies and, within the limits of such study designs, the quality of evidence was typically moderate across the literature. Differences in noninvasive test threshold values and variations in the urodynamic definition of BOO between studies limited the comparability of the data.

Myeloproliferative neoplasms with eosinophilia are commonly characterized by a normal karyotype and remain poorly defined at the molecular level. We therefore investigated 426 samples from patients with hypereosinophilia of unknown significance initially referred for screening of the FIP1L1-PDGFRA (FP) fusion gene also for KIT D816V and JAK2 V617F mutations. Overall, 86 (20%) patients tested positive: FP1 in 55 (12%), KIT D816V1 in 14 (3%), and JAK2 V617F1 in 17 (4%) patients, respectively. To gain better insight into clinical characteristics, we compared these cases with 31 additional and well-characterized KIT D816V1 eosinophilia-associated systemic mastocytosis (SM-eo) patients enrolled within the "German Registry on Disorders of Eosinophils and Mast cells." Significant differences included younger age, male predominance, and higher eosinophil counts for FP1 cases while abdominal lymphadenopathy, ascites, and serum tryptase levels >100 lg/l were characteristic for those with KIT D816V. Leukocytes, hemoglobin, and splenomegaly did not differ significantly. A median of three additional mutations, most frequently TET2 and SRSF2, were identified in 12/13 KIT D816V1 SM-eo patients with available material indicating a more complex molecular pathogenesis. Median survival was not reached for FP1 cases but was only 26 and 41 months for KIT D816V1 SM and JAK2 V617F1 MPN-eo, respectively. Eosinophilia of 2 3 10 9 /l was identified as discriminator for inferior survival in KIT D816V1 and/or JAK2 V617F1 patients (median survival 20 months vs. not reached, P 5 0.002). Thus, there is a clear prognostic and therapeutic rationale for detection of KIT D816V and JAK2 V617F in the diagnostic work up of eosinophilia.