454 Gelatinous Transformation of Bone Marrow “Serous Atrophy” Combined with Advanced Collagen Fibrosis: A Case of Postpolycythemic Myelofibrosis in Patient on Janus Kinase Inhibitor

Introduction/Objective Gelatinous transformation of bone marrow (serous atrophy) is a non-neoplastic marrow condition characterized by gelatinous extracellular material deposition composed of hyaluronic acid-rich mucopolysaccharide, fat cell atrophy, and associated marrow hypoplasia, disrupting hematopoiesis. It is seen in severe malnutrition, advanced malignancy, sepsis, HIV, and post-chemotherapy, as in tyrosine kinase inhibitor therapy (imatinib). It typically presents with cytopenia. We report a case of serous atrophy with grade 3 collagen fibrosis in a patient with post polycythemic myelofibrosis on 12 years of ruxolitinib therapy, a JAK1/2 (Janus Kinase) inhibitor. Methods/Case Report A 77-year-old woman with JAK2-positive polycythemia vera diagnosed 28 years ago progressed to secondary myelofibrosis after 16 years, with massive splenomegaly. She was treated with oral ruxolitinib for 12 years. Due to worsening cytopenias and painful splenomegaly, therapy was switched to momelotinib, a JAK inhibitor that also targets Activin A receptor (ACVR1). The patient subsequently developed leukocytosis (>20 × 109/L), prompting bone marrow biopsy which revealed marked hypocellularity, serous atrophy, with loss of trilineage hematopoiesis, and extensive collagen and reticulin fibrosis (highlighted with Masson trichrome and reticulin stains). The gelatinous material is positive for Alcian blue. Results NA Conclusion Ruxolitinib is an FDA-approved therapy for intermediate- and high-risk myelofibrosis, including postpolycythemic progression. Anemia and thrombocytopenia are frequent adverse events in advanced myelofibrosis, which are usually managed by dose adjustment or temporary interruption. Gelatinous transformation of the bone marrow, when coexisting with advanced myelofibrosis, may further complicate the clinical course. Serous atrophy may manifest as poor hematologic response to ruxolitinib dose modifications and may signal disease progression.