ABSTRACT
Thalassemia is known to induce extramedullary hematopoiesis (EMH), which is a compensatory mechanism in which the body forms blood cells outside the bone marrow. While EMH typically affects organs such as the spleen and liver, there are rare instances where it leads to spinal cord compression (SCC) in the epidural space. A 31-year-old male patient with transfusion-dependent beta thalassemia presented with numbness and bilateral limb weakness due to EMH. Neurological examination revealed increased tone in both legs, reduced power, loss of crude touch and pain sensation, and increased deep tendon reflexes. Magnetic resonance imaging (MRI) indicated a lobulated soft tissue structure in the posterior dural intrathecal space causing SCC. Laminectomy of the T2-T8 vertebrae was done, after which the lesion was identified and completely removed. Post-surgery, significant neurological improvements were observed in both motor and sensory functions. Thalassemia patients presenting with symptoms of SCC should be investigated for the presence of epidural EMH. Treatment options include decompressive surgery, blood transfusions, hydroxyurea, and radiotherapy.
ABSTRACT
Antithrombin (AT) deficiency and antiphospholipid syndrome (APS) are distinct but potentially overlapping disorders with significant implications for thrombosis. We present a case of a 28-year-old male with hereditary AT deficiency who subsequently developed primary APS. Despite the challenges of overlapping symptoms and anticoagulation therapy, a careful diagnostic approach revealed the coexistence of these rare conditions. The patient was successfully managed with long-term anticoagulation, hydroxychloroquine, and other supportive measures. This case underscores the importance of comprehensive laboratory testing, especially when managing patients with pre-existing anticoagulation needs.
