Multi-center clinical evaluation of the Panther Fusion SARS-CoV-2/Flu A/B/RSV assay in nasopharyngeal swab specimens from symptomatic individuals.

The symptomology is overlapping for respiratory infections due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), influenza A/B viruses, and respiratory syncytial virus (RSV). Accurate detection is essential for proper medical management decisions. This study evaluated the clinical performance of the Panther Fusion SARS-CoV-2/Flu A/B/RSV assay in nasopharyngeal swab (NPS) specimens from individuals of all ages with signs and symptoms of respiratory infection consistent with COVID-19, influenza, or RSV. Retrospective known-positive and prospectively obtained residual NPS specimens were collected during two respiratory seasons in the USA. Clinical performance was established by comparing Panther Fusion SARS-CoV-2/Flu assay results to a three-molecular assay composite comparator interpretation for SARS-CoV-2 and to the FDA-cleared Panther Fusion Flu A/B/RSV assay results for all non-SARS-CoV-2 targets. A total of 1,900 prospective and 95 retrospective NPS specimens were included in the analyses. The overall prevalence in prospectively obtained specimens was 20.7% for SARS-CoV-2, 6.7% for influenza A, and 0.7% for RSV; all influenza B-positive specimens were retrospective specimens. The positive percent agreement of the Panther Fusion assay was 96.9% (378/390) for SARS-CoV-2, 98.0% (121/123) for influenza A virus, 95.2% (20/21) for influenza B virus, and 96.6% (57/59) for RSV. The negative percent agreement was ≥98.5% for all target viruses. Specimens with discordant Panther Fusion SARS/Flu/RSV assay results all had cycle threshold values of ≥32.4 (by comparator or by Panther Fusion SARS/Flu/RSV assay). Only five co-infections were detected in the study specimens. The Panther Fusion SARS-CoV-2/Flu/RSV assay provides highly sensitive and specific detection of SARS-CoV-2, influenza A virus, influenza B virus, and RSV in NPS specimens.

Relationship of main pulmonary artery diameter to pulmonary arterial pressure in scleroderma patients with and without interstitial fibrosis.

OBJECTIVE: This study aimed to determine the relationship between main pulmonary artery diameter (MPAD) and pulmonary hypertension (PH) in scleroderma patients with and without interstitial lung disease. METHODS: We retrospectively reviewed 48 subjects with scleroderma who underwent a chest computed tomography (CT) and right heart catheterization with 6 months of each other. Patients were divided into 2 groups based on the absence or presence of interstitial lung disease on chest CT. Subset analysis was performed based on available pulmonary function tests and divided into groups by forced vital capacity (FVC). Computed tomographic scans were scored for extent of fibrosis and ground glass opacity. Pulmonary artery and ascending aorta measurements were obtained by 2 independent observers. Univariate and multivariate models were used to evaluate the correlation between MPAD and mean pulmonary artery pressure (mPAP) measured by right heart catheterization. Receiver operating characteristic analysis was performed for diagnostic accuracy of the MPAD measurement in predicting PH. RESULTS: Strong correlations between mPAP and MPAD were found in this study regardless of the presence or absence of mild to moderate interstitial fibrosis on chest CT. When dividing patients based on FVC, the correlation between mPAP and MPAD was substantially attenuated. An MPAD value of 30.8 mm yielded the highest sensitivity and specificity at 81.3% and 87.5%, respectively. CONCLUSIONS: In scleroderma patients, an enlarged main pulmonary artery (>30 mm) predicts PH even in the presence of mild to moderate fibrosis although the relationship may be attenuated in the presence of a low % FVC.

Non-Nodal CD5-Negative Mantle Cell Lymphoma with Secondary TP53 Deletion.

Mantle cell lymphoma is a non-Hodgkin lymphoproliferative neoplasm with several clinical and morphologic variants linked, primarily, through genetic derangement of the cyclin D1 locus. Aberrant phenotypes have been described, though prognostic data in such cohorts are limited due to a paucity of cases. We report a case of mantle cell lymphoma with non-nodal clinical presentation, aberrant loss of CD5 expression, and concomitant cytogenetic deletion of 17p. While non-nodal disease is often associated with an improved prognosis in mantle cell lymphoma, this 67-year-old patient experienced a more challenging clinical course with a poor initial response to chemotherapy. Therefore, this case may represent a type of non-nodal mantle cell lymphoma with a prognosis similar to that of classical cases due to the additional phenotypic and genetic alterations found in this patient.

PML-RARA Fusion Transcripts Detectable 8 Months prior to Promyelocytic Blast Crisis in Chronic Myeloid Leukemia.

Promyelocytic blast crisis arising from chronic myeloid leukemia (CML) is rare. We present a 40-year-old male who developed promyelocytic blast crisis 17 months after CML diagnosis, confirmed by the presence of the t(15;17) and t(9;22) translocations in the leukemic cells. Preserved nucleic acids from routine BCR-ABL1 testing provided a unique opportunity to evaluate clonal progression over time. Retrospective analysis demonstrated PML-RARA fusion transcripts were first detectable 8 months prior to blast crisis presentation. A review of 21 cases of promyelocytic blasts crisis published in the literature reveals a male predominance with earlier age at onset as compared to females. Interestingly, TKI therapy during chronic phase did not impact the time interval between diagnosis and promyelocytic blast crisis. Treatment with standard acute promyelocytic leukemia regimens provides more favorable outcomes with complete molecular remission. Although rare, it is important to consider a promyelocytic blast crisis when evaluating for transformation of CML due to its effective treatment with specific therapies.