Hematology Reports

Drug-induced agranulocytosis is a rare but life-threatening adverse reaction associated with numerous non-chemotherapy drugs. Management relies on immediate drug withdrawal, infection control, and, in selected patients, administration of granulocyte-colony stimulating factor (G-CSF). This review summarizes current knowledge on the determinants of epidemiology, clinical presentation, hematologic and biologic features, comorbidities, and outcomes influencing the decision to introduce G-CSF in drug-induced agranulocytosis. Evidence from observational studies and meta-analyses suggests that G-CSF shortens neutropenia duration and hospitalization, although its impact on mortality remains uncertain. The decision to use G-CSF should consider initial neutrophil count, presence of severe infection or sepsis, age, and comorbidities. Despite the accumulated experience, randomized controlled trials are still lacking, and treatment algorithms remain empirical.

Primary effusion-based lymphomas are uncommon and may pose significant diagnostic challenges. Fluid overload-associated large B-cell lymphoma is a recently recognized entity in the 5th edition of the World Health Organization Classification of Hematolymphoid Tumors and should be included in the differential diagnosis of effusion-based lymphomas, particularly in elderly immunocompetent patients with conditions that predispose to fluid overload. Background and Clinical Significance: We report a case of fluid overload-associated large B-cell lymphoma to add to the limited literature and highlight distinguishing features from other primary effusion lymphomas. Case Presentation: A 77-year-old male with end-stage renal disease on hemodialysis and heart failure with reduced ejection fraction was admitted for respiratory failure and found to have a right-sided pleural effusion. Two pleural fluid specimens examined several weeks apart revealed sheets of large atypical lymphoid cells positive for CD20, Pax-5, CD79a, CD45, MUM1, BCL2, BCL6 (weak) and negative for TTF1, CD68, MOC31, BER EP4, WT1, Calretinin, CD3, CD138, CD30, and cMYC. Human Herpesvirus-8 and Epstein–Barr virus were negative. Staging showed a few mildly fluorodeoxyglucose-avid mediastinal lymph nodes which were benign. Ultimately, the patient was diagnosed with fluid overload-associated large B-cell lymphoma and treated with rituximab, cyclophosphamide, vincristine sulfate, and prednisone, but passed away three months after diagnosis. Conclusions: Fluid overload-associated large B-cell lymphoma is a new and important diagnostic consideration in effusion-based lymphomas. It may be mistaken for other conditions such as primary effusion lymphoma or other diffuse large B-cell lymphomas. The presence of a Human Herpesvirus-8-negative effusion-based lymphoma in an elderly immunocompetent patient without nodal or tissue involvement should prompt consideration of fluid overload-associated large B-cell lymphoma.

Background and Clinical Significance: Acute promyelocytic leukemia (APL) is a rapidly progressive subtype of acute myeloid leukemia defined by PML::RARA fusion and characterized by life-threatening coagulopathy. Because the disease typically follows an aggressive course, immediate treatment is essential once APL is suspected. This case report describes an atypical de novo presentation marked by indolent progression rather than the expected aggressive trajectory. Case Presentation: A 37-year-old female exhibited gradually declining white blood cell and neutrophil counts over the course of a year, followed by unexplained pancytopenia with severe neutropenia (0.1 × 10⁹/L). Evaluation for nutritional deficiencies and autoimmune disease was unrevealing aside from a positive ANA without clinical features of autoimmunity. Bone-marrow biopsy demonstrated morphologic and flow cytometric findings suggestive of APL, low-level t(15;17), PML::RARA fusion, and concomitant TP53 loss and ETV6 mutation. Despite the indolent clinical presentation and low disease burden, the molecular and cytogenetic findings confirmed the diagnosis of classical APL with TP53 loss and ETV6 mutation. Induction therapy with all-trans-retinoic acid and arsenic trioxide resulted in hematologic remission. Conclusions: This case highlights an unusually indolent form of de novo APL not previously documented in the literature, expanding the recognized clinical spectrum of the disease. The findings emphasize the importance of still considering severe diagnoses, such as APL, when presentations deviate from classical patterns. Atypical clinical trajectories should prompt careful assessment of marrow morphology and immunophenotypic features. Continued characterization of such cases may refine diagnostic criteria and direct individualized approaches to therapy.