{"title":"A fatal posterior-fossa chloroma masquerading as tuberculous meningitis after peripartum BCR-ABL1 inhibitor cessation - a case report","authors":"Bhvika Zutshi, Sandeep Garg, Praveen Bharti, Amit Kumar, Annesha Chakraborty, Saarthak Miglani, Ajay Kumar Meena, Arpit Singh Chahal, Sankha Sekhar Ghosh","doi":"10.1016/j.lrr.2026.100607","DOIUrl":null,"url":null,"abstract":"<div><div>Intracranial myeloid sarcoma complicating chronic myeloid leukemia (CML) is exceptional; when its cerebrospinal-fluid profile simultaneously mimics tuberculous meningitis (TBM), the diagnostic trap becomes fatal. A 27-year-old postpartum woman with Ph⁺ CML, initially presenting in B-cell acute lymphoblastic leukemia lymphoid blast crisis, developed rapidly progressive posterior-fossa syndrome following peripartum tyrosine kinase inhibitor (TKI) discontinuation. CSF revealed lymphocyte-predominant pleocytosis, hypoglycorrhachia, hyperproteinorachia, and adenosine deaminase 33 U/L, with negative CBNAAT, malignant cytology, and flow cytometry; BCR-ABL1 P210 registered an International Scale of 49.196%. Contrast-enhanced MRI demonstrated a dural-based, homogeneously enhancing, diffusion-restricting cerebellopontine mass with pachymeningeal involvement, consistent with granulocytic sarcoma. Death from tonsillar herniation occurred within one week, before tissue confirmation. Three imperatives emerge: CSF adenosine deaminase elevation lacks specificity for TBM in hematological malignancy; Ph⁺ CML can undergo myeloid CNS relapse following peripartum TKI cessation; and a posterior-fossa dural mass in leukemia demands urgent tissue diagnosis.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"26 ","pages":"Article 100607"},"PeriodicalIF":0.8000,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Leukemia Research Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2213048926000476","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/9/12 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"HEMATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Intracranial myeloid sarcoma complicating chronic myeloid leukemia (CML) is exceptional; when its cerebrospinal-fluid profile simultaneously mimics tuberculous meningitis (TBM), the diagnostic trap becomes fatal. A 27-year-old postpartum woman with Ph⁺ CML, initially presenting in B-cell acute lymphoblastic leukemia lymphoid blast crisis, developed rapidly progressive posterior-fossa syndrome following peripartum tyrosine kinase inhibitor (TKI) discontinuation. CSF revealed lymphocyte-predominant pleocytosis, hypoglycorrhachia, hyperproteinorachia, and adenosine deaminase 33 U/L, with negative CBNAAT, malignant cytology, and flow cytometry; BCR-ABL1 P210 registered an International Scale of 49.196%. Contrast-enhanced MRI demonstrated a dural-based, homogeneously enhancing, diffusion-restricting cerebellopontine mass with pachymeningeal involvement, consistent with granulocytic sarcoma. Death from tonsillar herniation occurred within one week, before tissue confirmation. Three imperatives emerge: CSF adenosine deaminase elevation lacks specificity for TBM in hematological malignancy; Ph⁺ CML can undergo myeloid CNS relapse following peripartum TKI cessation; and a posterior-fossa dural mass in leukemia demands urgent tissue diagnosis.