ABSTRACT
OBJECTIVES: To retrospectively investigate whether a case-by-case combination of the Prostate Imaging Reporting and Data System version 2.1 (PI-RADS) with the Likert score improves the diagnostic performance of mpMRI for clinically significant prostate cancer (csPCa), especially by reducing false-positives. METHODS: One hundred men received mpMRI between January 2020 and April 2021, followed by prostate biopsy. Reader 1 (R1) and reader 2 (R2) (experience of > 3000 and < 200 mpMRI readings) independently reviewed mpMRIs with the PI-RADS version 2.1. After unveiling clinical information, they were free to add (or not) a Likert score to upgrade or downgrade or reinforce the level of suspicion of the PI-RADS category attributed to the index lesion or, rather, identify a new index lesion. We calculated sensitivity, specificity, and predictive values of R1/R2 in detecting csPCa when biopsying PI-RADS ≥ 3 index-lesions (strategy 1) versus PI-RADS ≥ 3 or Likert ≥ 3 index-lesions (strategy 2), with decision curve analysis to assess the net benefit. In strategy 2, the Likert score was considered dominant in determining biopsy decisions. RESULTS: csPCa prevalence was 38%. R1/R2 used combined PI-RADS and Likert categorization in 28%/18% of examinations relying mainly on clinical features such as prostate specific antigen level and digital rectal examination than imaging findings. The specificity/positive predictive values were 66.1/63.1% for R1 (95%CI 52.9-77.6/54.5-70.9) and 50.0/51.6% (95%CI 37.0-63.0/35.5-72.4%) for R2 in the case of PI-RADS-based readings, and 74.2/69.2% for R1 (95%CI 61.5-84.5/59.4-77.5%) and 56.6/54.2% (95%CI 43.3-69.0/37.1-76.6%) for R2 in the case of combined PI-RADS/Likert readings. Sensitivity/negative predictive values were unaffected. Strategy 2 achieved greater net benefit as a trigger of biopsy for R1 only. CONCLUSION: Case-by-case combination of the PI-RADS version 2.1 with Likert score translated into a mild but measurable impact in reducing the false-positives of PI-RADS categorization, though greater net benefit in reducing unnecessary biopsies was found in the experienced reader only.
ABSTRACT
BACKGROUND: COVID-19 patients carry an increased rate of thrombosis. It is controversial to which extent thrombi in the pulmonary arterial tree really contribute to disease severity with hypoxemia secondary to microvascular/lung parenchymal damage with viral alveolitis considered to play the main role in critical disease. OBJECTIVES: The primary objective was to compare post-mortem lung disease from fatal COVID-19 pneumonia in patients with macroscopically evident pulmonary arterial tree thrombosis and patients without, by characterizing the immunohistochemical nature of thrombi, and by comparing clinical and laboratory features of these patients with other COVID-19 patients who died but without evidence of pulmonary arterial thrombosis (controls). PATIENTS AND METHODS: 13 COVID-19 pneumonia cases (mean age ± standard deviation: 74 ± 6.5 years) with macroscopically visible pulmonary arterial thrombosis were compared to 14 controls. Hematoxylin and Eosin stained slides were reviewed choosing those with visible pulmonary thrombi which were further characterized by immunohistochemistry, in particular for the inflammatory infiltrates. Ante mortem serum markers relevant to pulmonary embolism were evaluated in both groups. RESULTS: Twenty arterial thrombi (5 cases with multiple thrombi) were selected for study and were composed by white blood cells (WBC) [median, IQR range: 10 % (5-12.25)], mainly neutrophils [58 % (35.2-64.5)]. Cases with thrombosis showed significantly higher levels of platelet count [median, IQR range: 195000/mmc (157750-274,500) vs 143,500 (113000-175,250), p = 0.011], LDH [854 U/L (731-1315) vs 539 (391.5-660), p = 0.003] at admission, and D-dimer at ICU transfer [25,072 FEU (6951-50,531) vs 1024 (620-5501), p = 0.003]. CONCLUSIONS: Immunothrombotically driven arterial thrombi in COVID-19 patients are associated with D-Dimer and LDH elevations, thus linking inflammation, coagulopathy and organ damage in fatal COVID-19.