Abstract A099: Pulmonary thromboembolism secondary to iron deficiency anemia: A case study
Authors: Khan Aliya M , Toustsoglou Maria , Philippeaux Sandy , Del sol David , Hepgur Mehmet 
Published: September 2024

Introduction: Pulmonary thromboembolism (PTE) is a significant clinical issue associated with high morbidity and mortality. Risk factors for thromboembolic events include immobilization, myocardial infarction, cerebrovascular accident, surgery, and trauma. Iron deficiency anemia (IDA) can cause reactive thrombocytosis, increasing thromboembolic risk. This study presents a 30-year-old female admitted for PTE, possibly secondary to IDA. Case Presentation: A 30-year-old female with IDA and heavy menstrual bleeding presented with right-sided chest pain and shortness of breath. Her pain, exacerbated by inspiration, and relieved by leaning forward, had worsened over four days. She also reported dizziness and agonal breathing. On arrival, her vitals included a blood pressure of 95/62 mmHg, heart rate of 110 bpm, respiratory rate of 22 breaths/min, and a temperature of 37°C. Physical examination revealed tachycardia, tachypnea, and diminished breath sounds in the right lower lung field. Laboratory tests showed a hemoglobin level of 4.6 g/dL and a platelet count of 745 × 10^9/L, low ferritin, low serum Iron, and high total iron-binding capacity (TIBC). A CT pulmonary angiogram revealed a wedge-shaped infarct in the right lower lobe, consistent with pulmonary embolism. CT abdomen/pelvis showed a thrombus in the right iliac vein, indicative of deep vein thrombosis. The echocardiogram showed left ventricular ejection fraction &gt;55% with no right chamber strain. A pelvic ultrasound revealed no significant pathology. Treatment included heparin and blood transfusions, increasing hemoglobin to 9.0 g/dL. Hemolytic workup including prothrombin gene abnormalities, Factor V Leiden mutation, and protein C activity was negative. However, Protein S activity was low, and PTT-la positive, implying that the patient may be positive for lupus anticoagulant, later ruled out by serial antibody tests.Subsequently, the patient was discharged home on Eliquis and Ferrous sulfate with outpatient hematology follow-up. Discussion: The association between venous thromboembolism and IDA can be explained by several mechanisms. One study suggests that iron deficiency causes hypercoagulability through reactive thrombocytosis, increased oxidative stress, and altered blood viscosity. Another hypothesis is that the hyperdynamic state in anemic patients leads to vascular endothelial injury due to shear forces. This case highlights the importance of considering IDA as a potential risk factor for thromboembolism, especially in patients without other evident prothrombotic conditions. Conclusion: Iron deficiency may be an underestimated risk factor for thromboembolic events. This case underscores the need for a comprehensive workup for VTE that includes assessing for IDA. Iron replacement therapy could serve as an effective preventive strategy in patients with a history of IDA and those at risk for thromboembolism. Further research is warranted to explore the mechanisms linking IDA with increased thrombotic risk and to establish appropriate preventive measures.

Citation Format: Aliya M Khan, Maria Toustsoglou, Sandy Philippeaux, David Del sol, Mehmet Hepgur. Pulmonary thromboembolism secondary to iron deficiency anemia: A case study [abstract]. In: Proceedings of the 17th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2024 Sep 21-24; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2024;33(9 Suppl):Abstract nr A099.