The seasonal distribution of immune thrombotic thrombocytopenic purpura is influenced by geography: Epidemiologic findings from a multi-center analysis of 719 disease episodes.

Prior studies have suggested that immune thrombotic thrombocytopenic purpura (iTTP) may display seasonal variation; however, methodologic limitations and sample sizes have diminished the ability to perform a rigorous assessment. This 5-year retrospective study assessed the epidemiology of iTTP and determined whether it displays a seasonal pattern. Patients with both initial and relapsed iTTP (defined as a disintegrin and metalloprotease with thrombospondin type motifs 13 activity <10%) from 24 tertiary centers in Australia, Canada, France, Greece, Italy, Spain, and the US were included. Seasons were defined as: Northern Hemisphere-winter (December-February); spring (March-May); summer (June-August); autumn (September-November) and Southern Hemisphere-winter (June-August); spring (September-November); summer (December-February); autumn (March-May). Additional outcomes included the mean temperature in months with and without an iTTP episode at each site. A total of 583 patients experienced 719 iTTP episodes. The observed proportion of iTTP episodes during the winter was significantly greater than expected if equally distributed across seasons (28.5%, 205/719, 25.3%-31.9%; p = .03). Distance from the equator and mean temperature deviation both positively correlated with the proportion of iTTP episodes during winter. Acute iTTP episodes were associated with the winter season and colder temperatures, with a second peak during summer. Occurrence during winter was most pronounced at sites further from the equator and/or with greater annual temperature deviations. Understanding the etiologies underlying seasonal patterns of disease may assist in discovery and development of future preventative therapies and inform models for resource utilization.

Comparability of Beckman Coulter Cardiac Troponin I Assays.

OBJECTIVE: Cardiac troponin I (cTnI) is one of the most sensitive and specific biomarkers of myocardial injury. The rise and/or fall of cardiac troponins above the 99th percentile of the upper reference limit (URL) is required in the assessment of acute myocardial infarction. METHODS: We analyzed the variation between the Beckman Coulter contemporary cTnI AccuTnI+3 assay and high sensitivity cTnI (hs-cTnI) assay tested on DXI 800 using 424 patient specimens with troponin levels ranging from 0-16754 ng/L. We also analyzed the concordance of the same assay hs-cTnI on different Beckman Coulter instruments Access 2 and DXI 800 using 115 patient specimens with troponin levels ranging from 2-100466 ng/L. RESULTS: The between-method comparison of AccuTnI+3 and hs-cTnI on DXI 800 showed a good correlation with the slope of 1.003, correlation coefficient (CC) of 0.9590, and bias of -40.65 (-5.16%). However, comparison of AccuTnI+3 and hs-cTnI in 103 patients with troponin less than 20 ng/L, the 99th percentile of the URL for male, showed the slope of 1.325, CC of 0.7462, and bias of 1.91 (21.53%). The within-method comparison of hs-cTnI on Access 2 and DXI 800 showed the slope was 1.130 with CC of 0.9915, and bias of 840.4 (10.6%). Further examination of the results revealed that hs-cTnI levels were more comparable at levels less than 200 ng/L, with a slope of 1.069, CC of 0.9951, and bias of 2.3 (6.2%). CONCLUSION: These data indicate that contemporary cTnI AccuTnI+3 results above the 99th percentile URL are comparable with hs-cTnI results if both are tested on DXI 800, and hs-cTnI results tested on Access 2 and DXI 800 are comparable at levels less than 200 ng/L. Therefore, to use the Beckman Coulter cTnI assay properly, we suggest the laboratory report cardiac troponins with the assay and instrument names to reduce confusion during results comparison.