Incidence of Venous Thromboembolism in Patients with Different Classes of Obesity in Comparison to Inherited Thrombophilias

Introduction: Obesity is a significant risk factor for venous thromboembolism (VTE). It is linked to physical inactivity, increased intra-abdominal pressure, chronic inflammation, impaired fibrinolysis and high fibrinogen levels leading to a prothrombotic state and increasing the risk of VTE. For provoked VTE, anticoagulation is typically recommended for 3-6 months if the provoking factor can be resolved. Unprovoked and recurrent VTE may necessitate lifelong anticoagulation. Individuals with VTE and inherited homozygous thrombophilias may need indefinite anticoagulation. Obesity as the sole risk factor, traditionally does not impact the duration of anticoagulation for VTE treatment. More research is needed to accurately estimate the VTE risk associated with different classes of obesity and to compare the incidence of VTE with obesity to the risk of VTE with inherited thrombophilias.

Methods: A cohort study was conducted using data from the Cerner Health Facts database. Patients with ICD 9 or ICD 10 codes for BMI were stratified into underweight (BMI<19), average weight (19-24.9), overweight (BMI 25-29.9), class I obesity (30-34.9), class II obesity (35-39.9) and class III severe obesity (>40). Patients with inherited thrombophilias (Factor V Leiden, prothrombin gene mutation, antithrombin deficiency, protein S deficiency and protein C deficiency) were identified using ICD 9 code and ICD 10 codes. We identified diagnosis of VTE among overweight patients, those with different classes of obesity and patients with inherited thrombophilias. The incidence of VTE was calculated using deep vein thrombosis (DVT) and pulmonary embolism (PE) ICD 9 and ICD 10 codes. Patients with BMI>30 among those with inherited thrombophilias were excluded. Chi-square analysis was used to test for statistical significance.

Results: 372,594 patients were identified from the database. 1,034 patients had inherited thrombophilias with a BMI<30. 45,298 patients were overweight and after excluding patients with inherited thrombophilias, the number of overweight patients was 44,264. 91,937 patients had class I obesity, 77,049 patients had class II obesity and 136,244 patients had class III obesity. The incidence of VTE in overweight patients was 9.51% (4208/44264). The incidence of VTE in class I obesity was 9.12% (8382/91937), followed by 11.01% (8485/77049) in patients with class II obesity, followed by 14.38% (19587/136244) in patients with class III obesity. The incidence of VTE in patients with inherited thrombophilias was 14.31% (148/1034). Chi-square analysis revealed statistical significance with DF=4, X=1793.0966, p<0.001.

Conclusion: The incidence of VTE (DVT/PE) was notably higher in obese patients compared to overweight patients. Moreover, the risk of VTE increased with higher classes of obesity, with class III obesity showing the highest incidence followed by class II and class I. Notably, patients with class III obesity had a VTE incidence similar to those with inherited thrombophilias in our study indicating that severe obesity may possess a risk equivalent to inherited thrombophilias for developing VTE. These findings emphasize the importance of surveillance, education, and counseling for patients with severe obesity who develop VTE, as with those with inherited thrombophilias. Patients with weaker inherited heterozygous states have no significant impact on the duration of anticoagulation. Class III obesity may be a risk factor that could affect the duration of anticoagulation, but more studies are needed. Our study limitations include its retrospective nature and the use of ICD codes. The use of the same ICD codes for heterozygous and homozygous inherited thrombophilia states precluded a direct comparison between severe class III obesity and homozygous inherited thrombophilia states.

No relevant conflicts of interest to declare.