ArticleAmerican journal of clinical pathology2026
Hypereosinophilia of persistent/unknown cause: a bone marrow-based study integrating WHO-HAEM5 criteria and myeloid next-generation sequencing.
Article in American journal of clinical pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
objectivesHypereosinophilia (HE), defined as an absolute eosinophil count (AEC) ≥1.5 × 109/L, poses diagnostic challenges when distinguishing clonal myeloid neoplasms from idiopathic HE/hypereosinophilic syndrome, particularly under WHO-HAEM5 criteria. We characterized patients with HE of persistent/unknown cause (HEPU) undergoing bone marrow (BM) evaluation to refine diagnostic classification.
methodsWe identified 307 BM biopsy specimens (2015-2023) mentioning "eosinophilia." Patients with defined reactive or clonal etiologies were classified as group 2 (known etiology, n = 269). The remaining patients constituted group 1 (HEPU, n = 38). We reviewed clinical data, morphology, cytogenetics/fluorescence in situ hybridization (FISH), and myeloid next-generation sequencing (NGS), assigning final diagnoses via the fifth edition of the World Health Organization Classification of Haematolymphoid Tumours (WHO-HAEM5) criteria and the 2022 International Consensus Classification (ICC).
resultsCompared to group 2, patients with HEPU were younger (median 48 vs 62 years; P = .004) and exhibited higher initial AECs (2.8 vs 0.6 × 109/L; P < .001). Comprehensive workup reclassified the HEPU cohort (n = 38) into the idiopathic spectrum (36.8%), reactive eosinophilia (28.9%), clonal disorders including myeloid and lymphoid neoplasms (28.9%), and mixed reactive vs idiopathic (5.3%) categories. While cytogenetics/FISH were largely noncontributory (detecting FIP1L1::PDGFRA in 2 cases), myeloid NGS detected mutations in 47% (7/15) of tested patients with HEPU, involving genes such as TP53, BCOR, SF3B1, and TET2.
conclusionsIntegrated clinicopathologic and molecular assessment reclassified most HEPU cases as reactive or clonal, with only 39% remaining idiopathic. Myeloid NGS frequently identifies clonal variants critical for refining HE classification, although results require cautious interpretation within the WHO-HAEM5 and ICC 2022 context.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.