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  • These cancer related pro inflammatory

    2020-08-06

    These cancer-related pro-inflammatory states are known to cause
    Table 3
    Adjustment models for association of statin, aspirin use and venous thromboembolism risk.
    Adjustment model
    Demographics alone
    Demographics and
    Demographics,
    Demographics,
    Demographics,
    comorbidity
    comorbidity, and tumor
    comorbidity, tumor factors,
    comorbidity, tumor factors,
    factors
    and treatment type
    and treatment type, and
    survival events
    Characteristic
    Adjusted-HR P-value
    Adjusted-HR P-value Adjusted-HR P-value
    Adjusted-HR P-value
    Adjusted-HR P-value
    Statin
    Yes
    ASA
    Yes
    Cox proportional hazard regression models for P-values. Significant P-values are emboldened. Demographics included age (every quartile), race/ethnicity (Asian versus non-Asian), and obesity (b30.0, 30–34.9, 35.0–39.9, and ≥40.0). Comorbidities included hypertension (yes versus no), PSB 1115 (yes versus no), and hypercholesterolemia (yes versus no). Tumor factors included histology (type I versus type II), cancer stage (I–II versus III–IV), and CA-125 (b35 versus ≥35 IU/L). Treatment factors included hysterectomy (none, minimally-in-vasive, and laparotomy) and chemotherapy use (yes versus no). Survival events included endometrial cancer recurrence (yes versus no). Country type was not entered in the model be-cause of concern for multicollinearity for race. Abbreviations: HR, hazard ratio; CI, confidence interval; and ASA, aspirin.
    Joint effects of statin and aspirin use on venous thromboembolism risk.
    Adjustment model Demographics alone
    Demographics and
    Demographics,
    Demographics,
    Demographics,
    comorbidity
    comorbidity, and tumor comorbidity, tumor factors,
    comorbidity, tumor factors,
    factors
    and treatment type
    treatment type, and
    survival events
    Characteristic Adjusted-HR P-value*
    Adjusted-HR P-value*
    Adjusted-HR P-value* Adjusted-HR P-value*
    Adjusted-HR P-value*
    Statin alone
    ASA alone
    Both
    Cox proportional hazard regression models for venous thromboembolism risk. *P-values represent interaction. Significant P-values are emboldened. Demographics included age (every quartile), race/ethnicity (Asian versus non-Asian), and obesity (b30.0, 30–34.9, 35.0–39.9, and ≥40.0). Comorbidities included hypertension (yes versus no), diabetes mellitus (yes versus no), and hypercholesterolemia (yes versus no). Tumor factors included histology (type I versus type II), cancer stage (I–II versus III–IV), and CA-125 (b35 versus ≥35 IU/L). Treatment factors included hysterectomy (none, minimally-invasive, and laparotomy) and chemotherapy use (yes versus no). Survival events included endometrial cancer recurrence (yes versus no). Coun-try type was not entered in the model because of concern for multicollinearity for race. Abbreviations: HR, hazard ratio; CI, confidence interval; and ASA, aspirin.
    aspirin may reduce the inflammatory milieu as a whole and reduce the risk of VTE. Indeed, our study found that obese women (representing in-flammatory status in excess adiposity) or type II tumor histology/recur-rent disease (representing inflammatory status from aggressive tumor behavior) benefitted from statin use to reduce VTE risk.
    Another biological mechanism may include the anti-tumor effects of statins and aspirin. In endometrial cancer, VTE is strongly associated with recurrent disease [6]. Agents that might reduce cancer recurrence may indirectly reduce the risk of VTE. Recent clinical data have shown that statins and aspirin may be protective against disease progression in endometrial cancer [15,16]. However, these studies did not examine VTE, and this association remains understudied.
    Our results showed that type of statin also affects VTE incidence in endometrial cancer. Specifically, simvastatin demonstrated the largest reduction of VTE risk compared to other statins (Table 4). Our findings are consistent with a recent large-scale population-based prospective study in that simvastatin significantly reduced VTE risk whereas other higher potency statins did not as shown in a general population [25]. However, possibility for a lack of adequate sample size may be a con-cern. That is, rosuvastatin and fluvastatin uses were suggestive for de-creased VTE risk but it did not quite reach statistical significance in their study. Whether different statin types exert different anti-inflammatory or -tumor effects resulting in altered VTE risk in endome-trial cancer would be of interest and further study is warranted.