IMPORTANCE Enoxaparin sodium is widely used for deep vein thrombosis (DVT) prophylaxis, yet DVT rates remain high in the trauma and general surgery populations. Missed doses during hospitalization are common. OBJECTIVE To determine if missed doses of enoxaparin correlate with DVT formation. DESIGN, SETTING, AND PARTICIPANTS Data were prospectively collected among 202 trauma and general surgery patients admitted to a level I trauma center. MAIN OUTCOMES AND MEASURES Deep vein thrombosis screening was performed using a rigorous standardized protocol. RESULTS The overall incidence of DVT was 15.8%. In total, 58.9% of patients missed at least 1 dose of enoxaparin. The DVTs occurred in 23.5% of patients who missed at least 1 dose and in 4.8% of patients who did not (P < .01). On univariate analysis, the need for mechanical ventilation (71.8% vs 44.1%), the performance of more than 1 operation (59.3% vs 40.0%), and male sex (75% vs 56%) were associated with DVT formation (P < .05 for all). A bivariate logistic regression was then performed, which revealed age 50 years or older and interrupted enoxaparin therapy as the only independent risk factors for DVT formation. The DVT rate did not differ between trauma and general surgery populations or in patients receiving once-daily vs twice-daily dosing regimens. CONCLUSIONS AND RELEVANCE Interrupted enoxaparin therapy and age 50 years or older are associated with DVT formation among trauma and general surgery patients. Missed doses occur commonly and are the only identified risk factor for DVT that can be ameliorated by physicians. Efforts to minimize interrupted enoxaparin prophylaxis in patients at risk for DVT should be optimized.

3-Iodothyronamine (T(1)AM) and 3,3',5-triiodothyroacetic acid (Triac) are bioactive metabolites of the hormone thyroxine (T-4). In the present study, the ability of T(1)AM and 3,3',5-triiodothyronamine (T(3)AM) to be metabolized to 3-iodothyroacetic acid (TA(1)) and Triac, respectively, was investigated Both T(1)AM and T(3)AM were converted to their respective iodinated thyroacetic acid analogues in both cell and tissue extracts. This conversion could be significantly inhibited with the monamine oxidase (MAO) and semicarbazide-sensitive amine oxidase (SSAO) inhibitor iproniazid. TA, was found to be present in trace quantities in human serum and in substantial levels in serum from T(1)AM-treated rats. These results demonstrate that iodothyronamines ore substrates for amine oxidases and that this metabolism may be the source of the corresponding endogenous arylacetic acid products Triac and TA(1).

There is great interest lately in the availability of analytical methods for quantification of 3-iodothyronamine from blood and tissues. To date, no validated method for determination of 3-iodothyronamine from biological matrices has been described. Detailed in this report is an LC–MS/MS method that permits accurate and reproducible quantification of pharmacological concentrations of 3-iodothyronamine from rat serum, with a 0.0008M lower limit of quantification. Endogenous 3-iodothyronamine was observed from rodent and human serum (0.2mL) at the method limit of detection. In summary, the LC–MS/MS method enables quantification of circulating 3-iodothyronamine to allow examination of a relationship with biological activity.