Jayesh Menon, Tyler Rehbein, Patrick Reagan, Carla Casulo
{"title":"Paraneoplastic Motor Neuropathy in Nodular Sclerosis Hodgkin's Lymphoma: Case Report.","authors":"Jayesh Menon, Tyler Rehbein, Patrick Reagan, Carla Casulo","doi":"10.1155/crh/9468544","DOIUrl":"https://doi.org/10.1155/crh/9468544","url":null,"abstract":"<p><p>Paraneoplastic neurological syndromes (PNS) are an uncommon complication of malignancy, characterized by autoantibody generation against neuronal structures, causing a spectrum of neurological syndromes affecting the central, peripheral, and/or autonomic nervous systems. PNS in lymphoma is exceedingly rare and there is limited evidence on the features, incidence, and severity of these neurological sequelae secondary to malignancy. Here, we report on a case of isolated diffuse motor neuropathy secondary to underlying nodular-sclerosis classical Hodgkin's lymphoma (cHL) in a 71-year-old male. This patient initially presented to the hospital with 3 months of progressive generalized weakness, weight loss, gait instability, and a rash. A broad workup revealed evidence of diffuse lymphadenopathy, which was characterized as nodular-sclerosis cHL on biopsy. Concurrent neurological workup demonstrated generalized axonal motor neuropathy on nerve conduction studies with negative serologies for a panel of paraneoplastic autoantibodies, but positive Asialo-GM1 titers, a marker of autoimmune myopathy. The patient was initiated on doxorubicin, vinblastine, and dacarbazine (AVD) for their lymphoma and received two doses of IVIg for their motor neuropathy, which did not reoccur. The patient was transitioned to brentuximab + nivolumab for 4 cycles, followed by nivolumab + AVD for 6 cycles with a complete response and no evidence of disease. Asialo-GM1-associated isolated diffuse motor neuropathy in Hodgkin's lymphoma has not been previously reported in the literature. In this case report, we review the 2021 updated diagnostic criteria for the diagnosis of paraneoplastic neurological syndromes in the context of this patient presentation to highlight an instance where these guidelines do not fully capture the wide spectrum of PNS.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"9468544"},"PeriodicalIF":0.7,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13130846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147822211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Diffuse Alveolar Hemorrhage as the Initial Manifestation of Acute Myelomonocytic Leukemia.","authors":"Samyukta Varma, Abdullah Al Twal","doi":"10.1155/crh/3835062","DOIUrl":"https://doi.org/10.1155/crh/3835062","url":null,"abstract":"<p><p>Diffuse alveolar hemorrhage (DAH) is a rare but life-threatening condition caused by the accumulation of red blood cells in the alveolar spaces, leading to respiratory failure. While DAH has been reported in patients with acute myeloid leukemia (AML) following chemotherapy, its occurrence as an initial manifestation of AML is uncommon. We present the case of a 31-year-old female with no known hematologic history who presented with hemoptysis and dyspnea. Her leukocyte count was 28.2 × 10<sup>9</sup>/L with 83% monocytic predominance. The patient underwent diagnostic bronchoscopy, which confirmed DAH. Bone marrow biopsy revealed AML with monocytic differentiation. Flow cytometry showed a positive inversion 16, and FLT3 mutation was negative. The patient was treated with induction chemotherapy (7 + 3 regimen: daunorubicin and cytarabine), but her condition deteriorated, and she eventually succumbed to respiratory failure. This case highlights the importance of considering hematologic malignancy in the differential diagnosis of DAH, particularly in the absence of other identifiable causes.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"3835062"},"PeriodicalIF":0.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147785177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Guido Pelaez, Behram Suha Yildiz, Mert Candan, Mohammad Ismail, Francesca Vacca, Marianna B Ruzinova, Samuel Ballentine, Kathleen Byrnes, Armin Ghobadi
{"title":"Development of Colonic Polyposis in a Woman With Chronic Myeloid Leukemia Treated With Dasatinib.","authors":"Guido Pelaez, Behram Suha Yildiz, Mert Candan, Mohammad Ismail, Francesca Vacca, Marianna B Ruzinova, Samuel Ballentine, Kathleen Byrnes, Armin Ghobadi","doi":"10.1155/crh/4605635","DOIUrl":"https://doi.org/10.1155/crh/4605635","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic myeloid leukemia (CML) is a hematopoietic malignancy driven by constitutive tyrosine kinase activity. Dasatinib, a second-generation (2G) tyrosine kinase inhibitor (TKI), is a preferred treatment due to its superior, durable, and rapid response rates. While dasatinib has known gastrointestinal (GI) side effects, colonic polyposis is a rare complication, not well described in the literature.</p><p><strong>Case presentation: </strong>Upon routine colonoscopy, a 66-year-old woman with chronic-phase CML was incidentally discovered to have asymptomatic colonic polyposis after 11 months of dasatinib therapy. Histopathology revealed reactive inflammatory changes without evidence of dysplasia or neoplasia. The polyposis resolved completely after cessation of dasatinib.</p><p><strong>Conclusion: </strong>The mechanism behind dasatinib-induced polyposis is unclear. We hypothesize a role of dasatinib's differential inhibition of multiple kinase pathways, regulatory T cells, and STAT5 signaling in the intestinal epithelium, causing an unregulated inflammatory state. This case underscores the need for awareness of this rare adverse effect and further research into its pathogenesis.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"4605635"},"PeriodicalIF":0.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147785218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Liping Yang, Zhimei Zhou, Xiaoyuan Qu, Lili Jing, Juanjuan Liu, Li Chen, Linfeng Ma
{"title":"A Rare Case Report of Immunoglobulin D Subtype Multiple Myeloma Complicated With Hyperlipidemia.","authors":"Liping Yang, Zhimei Zhou, Xiaoyuan Qu, Lili Jing, Juanjuan Liu, Li Chen, Linfeng Ma","doi":"10.1155/crh/9065226","DOIUrl":"10.1155/crh/9065226","url":null,"abstract":"<p><p>Multiple myeloma is a plasma cell malignancy characterized by complex heterogeneous cytogenetic abnormalities. In most cases, patients suffering from multiple myeloma typically display normal or decreased blood lipid concentrations. We herein present a case of immunoglobulin (Ig) D-λ subtype multiple myeloma with concurrent hyperlipidemia. This patient presented with elevated lipid levels upon lenalidomide, bortezomib, and dexamethasone (RVD) chemotherapy with triglycerides of 4.12 mmol/L (reference range: 0.4-1.7 mmol/L), total cholesterol of 6.71 mmol/L (reference range: 3.12-5.72 mmol/L), low-density lipoprotein cholesterol of 4.29 mmol/L (reference range: 1.04-1.96 mmol/L), and lipoprotein(a) of 582 mg/L (reference range: 0-300 mg/L), which showed typical symptoms of hyperlipidemia. After chemotherapy cycles, the elevated lipid indicators were gradually decreased (or close) to normal levels without any antihyperlipidemia drug or therapy. This report analyzed a rare hyperlipidemic multiple myeloma case and may provide insights into the safety and guidance of the procedure for clinical diagnosis and treatment.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"9065226"},"PeriodicalIF":0.7,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147724331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Amanda Rohner, Annatina Sarah Schnegg-Kaufmann, Yara Banz, Piet Rosenstock
{"title":"Pernicious Anemia Resulting in Intramedullary Hemolysis, Masking Underlying Polycythemia Vera and Mild Alpha-Thalassemia-A Case Report.","authors":"Amanda Rohner, Annatina Sarah Schnegg-Kaufmann, Yara Banz, Piet Rosenstock","doi":"10.1155/crh/8353795","DOIUrl":"https://doi.org/10.1155/crh/8353795","url":null,"abstract":"<p><strong>Background: </strong>Vitamin B12 deficiency can cause severe intramedullary hemolysis and cytopenias. Myeloproliferative neoplasms (MPNs), particularly polycythemia vera (PV), are typically characterized by hyperproliferation but may remain undetected when masked by concomitant deficiencies.</p><p><strong>Case presentation: </strong>A 48-year-old woman presented with fatigue, weight loss, and pancytopenia. Laboratory tests showed severe macrocytic anemia, hemolysis, and markedly reduced vitamin B12 levels. Gastroscopy and antibody testing confirmed autoimmune atrophic gastritis with pernicious anemia. Bone marrow biopsy revealed hypercellularity, panmyelosis, and myelofibrosis (MF-2), initially interpreted as reactive. After vitamin B12 supplementation, cytopenias resolved; however, follow-up demonstrated polycythemia, leukocytosis, and thrombocytosis. Molecular analysis identified a JAK2 V617F mutation (variant allele fraction 40%), confirming PV with progression toward myelofibrosis. The patient was treated with phlebotomy, low-dose aspirin, and hydroxyurea, alongside continued vitamin B12 replacement. In addition, mild alpha-thalassemia was diagnosed in the course of an increasingly microcytic hypochromic blood count.</p><p><strong>Conclusion: </strong>Severe vitamin B12 deficiency may mask an underlying MPN, as well as other hematologic disorders like alpha-thalassemia. Close follow-up after hematologic recovery is essential to avoid delayed diagnosis of coexisting hematologic malignancies and disorders. This case presents a combination of complex and extremely rare hematological scenarios, where various hematological disorders exert conflicting influences on red blood cell indices, making diagnosis challenging.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"8353795"},"PeriodicalIF":0.7,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13081683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147700211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Matthew Sawyer, Nishkala Neela, Avery Pennywell, Vasanthan Kuppuswamy, Dale Okorodudu
{"title":"A Curious Case of HLH: A Case Report of Hemophagocytic Lymphohistiocytosis Secondary to Atezolizumab.","authors":"Matthew Sawyer, Nishkala Neela, Avery Pennywell, Vasanthan Kuppuswamy, Dale Okorodudu","doi":"10.1155/crh/7839972","DOIUrl":"https://doi.org/10.1155/crh/7839972","url":null,"abstract":"<p><p>A 65-year-old man presented to the hospital with multiorgan failure in the setting of recently being started on atezolizumab for his small cell lung cancer. His main clinical findings were white blood cell count of 18.9 K/μL (48% neutrophils, 32% lymphocytes, 15% monocytes, and 0% eosinophils), creatinine of 10.3 mg/dL (increased from a baseline of 1.5), transaminitis with AST of 1365 and ALT of 388, total bilirubin of 2.3, a lactic acid above 11 (the upper detectable limit of our analyzer), and a serum bicarbonate of 2.8. Imaging was only notable for splenomegaly. Upon presentation, he was intubated for airway protection and admitted to the intensive care unit. Over 3 days, he was treated for severe septic shock with multiple blood pressure medications, antibiotics, continuous renal replacement therapy (CRRT), and stress dose steroids. On Day 4, his CRRT machine began clotting with a yellow, lipidic film, leading us to consider HLH. His ferritin and triglycerides were largely elevated, and hemolysis labs showed destruction of cells, making HLH the leading diagnosis. He was started on high-dose steroids while the full interleukin panel was pending. The IL-2 soluble receptor came back elevated, confirming the diagnosis of HLH. Before this panel returned, he received one dose of tocilizumab with high-dose steroids before dying. This case is unique as it is the fourth documented case of secondary HLH due to the immune checkpoint inhibitor, atezolizumab. This presentation of HLH was also difficult due to the lack of fever, hepatomegaly, and cytopenias commonly seen as the presenting symptoms in HLH. Prompt initiation of treatment for HLH is critical, and due to this challenging presentation, this patient did not receive steroids and tocilizumab until Days 4 and 5, respectively.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"7839972"},"PeriodicalIF":0.7,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13082213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147700225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Satomi Hiya, Joseph Tripodi, John Mascarenhas, Alina Dulau Florea, Vesna Najfeld
{"title":"Acute Myeloid Leukemia, Myelodysplasia-Related (AML-MR), With del(5q) and Double Minutes Containing Chromosomal Segment 11q24 Leading to Amplification and Expression of FLI1.","authors":"Satomi Hiya, Joseph Tripodi, John Mascarenhas, Alina Dulau Florea, Vesna Najfeld","doi":"10.1155/crh/2250750","DOIUrl":"https://doi.org/10.1155/crh/2250750","url":null,"abstract":"<p><p>Double minutes (dmins), a form of extrachromosomal DNA (ecDNA), represent a rare cytogenomic event in myeloid neoplasms and are most commonly associated with amplification of oncogenes such as <i>MYC</i> or <i>KMT2A</i>. Dmins derived from the 11q24 region that exclude <i>KMT2A</i> are exceedingly uncommon, and their pathogenic significance remains poorly understood. We report a 74-year-old female initially diagnosed with myelodysplastic syndrome (MDS) with isolated del(5) (q13q33) and mutations in <i>TP53</i> and <i>SF3B1</i>. After eight years and treatment with lenalidomide with excellent clinical response, she developed progressive cytopenias and transformation to acute myeloid leukemia, myelodysplasia-related (AML-MR). Cytogenomic analysis at the time of leukemic transformation revealed del(5) (q13q33) in all 20 metaphase cells analyzed and loss of the <i>EGR1</i> (5q31.2) gene in 94% of interphase nuclei by fluorescence in situ hybridization (FISH). Notably, 18 of 20 metaphase cells also harbored dmins, ranging from 2 to 22 copies per cell. Array-based comparative genomic hybridization and single nucleotide polymorphism array (array-CGH + SNP) identified a 5.57 Mb amplification of chromosome 11q24.2-q25 encompassing at least 40 genes, including <i>FLI1</i> and <i>ETS1</i> but excluding <i>KMT2A</i>. Metaphase FISH confirmed localization of the amplified 11q24 segment within the dmins, and immunohistochemistry demonstrated nuclear FLI1 expression in myeloblasts. The patient was treated with combination azacitidine and venetoclax and an investigational immunotherapy within a clinical trial. This case represents the third reported instance of dmins derived from the 11q24 region involving <i>FLI1</i> and <i>ETS1</i> and the first identified in the context of AML evolved from del(5q) MDS. Dmins in myeloid neoplasms have been linked to genomic instability, clonal evolution, and therapeutic resistance. Amplification and expression of <i>FLI1</i> in blasts, a hematopoietic transcription factor implicated in leukemogenesis and poor prognosis in AML, suggest a potential pathogenic role for 11q24-derived dmins in disease progression. Our findings expand the spectrum of dmin-associated oncogenic amplifications in myeloid neoplasms and highlight <i>FLI1</i> and <i>ETS1</i> as recurrent targets of 11q24-derived ecDNA amplification. Recognition of such rare events underscores the importance of integrative cytogenomic profiling for uncovering novel mechanisms of leukemic transformation and potential therapeutic targets.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"2250750"},"PeriodicalIF":0.7,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147692894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jennifer Priessnitz, Ali Hariri, Yuliya Levkiavska, Kyle E Bonner, Stephen I Fisher, Joshua M Sill
{"title":"Aggressive Natural Killer Cell Leukemia: A Rare and Rapidly Progressive Hematologic Malignancy-Case Report and Literature Review.","authors":"Jennifer Priessnitz, Ali Hariri, Yuliya Levkiavska, Kyle E Bonner, Stephen I Fisher, Joshua M Sill","doi":"10.1155/crh/7796972","DOIUrl":"https://doi.org/10.1155/crh/7796972","url":null,"abstract":"<p><p>Aggressive natural killer cell leukemia (ANKL) is a rare, fulminant hematologic malignancy characterized by neoplastic proliferation of mature NK cells. It is frequently associated with Epstein-Barr virus (EBV) infection, although EBV-negative cases have also been reported. While typically observed in young to middle-aged adults of East Asian descent, increasing recognition has led to identification of ANKL across diverse age groups and ethnicities. The disease is defined by a rapid clinical course and poor prognosis, underscoring the importance of early diagnosis and effective treatment. We present a case of a 71-year-old Caucasian male who developed fever, altered mental status, hepatosplenomegaly, pancytopenia, and hemophagocytic lymphohistiocytosis (HLH) and who was ultimately diagnosed with ANKL. Although he demonstrated initial clinical improvement with chemotherapy, relapse of the ANKL ensued a few months later, and he ultimately succumbed to progressive disease. A review of current literature is provided, focusing on molecular pathogenesis and emerging therapeutic strategies.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"7796972"},"PeriodicalIF":0.7,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Valentina Rago, Valeria Brogna, Fabrizio Cavalca, Matteo Faltoni, Antonio Maria Alviano, Carlo Gambacorti-Passerini, Elena Maria Elli
{"title":"An Uncommon Presentation of Sweet's Syndrome in Primary Myelofibrosis.","authors":"Valentina Rago, Valeria Brogna, Fabrizio Cavalca, Matteo Faltoni, Antonio Maria Alviano, Carlo Gambacorti-Passerini, Elena Maria Elli","doi":"10.1155/crh/4413111","DOIUrl":"https://doi.org/10.1155/crh/4413111","url":null,"abstract":"<p><p>Sweet's syndrome (SS) is a rare neutrophilic dermatosis often associated with hematologic malignancies. Due to its infectious mimicry, diagnosis is frequently delayed. We report a case of primary myelofibrosis initially treated for suspected cellulitis, which progressed to necrotic lesions and refractory fever despite broad-spectrum antibiotics. A skin biopsy confirmed neutrophilic vasculitis consistent with SS. Prompt treatment with corticosteroids followed by ruxolitinib achieved rapid resolution by suppressing the underlying cytokine storm.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"4413111"},"PeriodicalIF":0.7,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Maryam Ghazizadeh, Matin Ghazizadeh, Mohammad Moini
{"title":"Aplastic Anemia Proceeding to Thymoma: A Rare Co-Occurrence-A Case Report and Review Article.","authors":"Maryam Ghazizadeh, Matin Ghazizadeh, Mohammad Moini","doi":"10.1155/crh/6971236","DOIUrl":"https://doi.org/10.1155/crh/6971236","url":null,"abstract":"<p><strong>Background: </strong>Malignant thymoma is a rare tumor associated with various paraneoplastic syndromes, such as myasthenia gravis, pure red cell aplasia, and hypogammaglobulinemia. Aplastic anemia (AA) is an uncommon complication of thymoma that may occur during the disease or after thymoma resection. We report a case presented with AA before the thymoma.</p><p><strong>Case: </strong>We report the case of a 34-year-old man with thymoma who developed AA before the detection of the tumor. Although pancytopenia did not improve after thymectomy, prolonged immunosuppressive therapy led to complete resolution of AA. The patient has no recurrence during a 42-month follow-up period.</p><p><strong>Conclusion: </strong>AA may precede the detection of thymoma and represent its initial clinical manifestation. So, thymoma should be considered a rare cause, along with other more common etiologies of AA. Patients with AA and thymoma require prolonged immunosuppressive therapy after surgery.</p>","PeriodicalId":46307,"journal":{"name":"Case Reports in Hematology","volume":"2026 ","pages":"6971236"},"PeriodicalIF":0.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13045276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147624154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}