Upper Extremity Deep Venous Thrombosis Risk Factors, Associated Morbidity and Mortality in Trauma Patients.

BACKGROUND: The literature on upper extremity deep venous thrombosis (UEDVT) is not as abundant as that on lower extremities. This study aimed to identify the risk factors for UEDVT, associated mortality and morbidity in trauma patients and the impact of pharmacological prophylaxis therein. METHODS: A 3-year retrospective review of patients admitted to a Level 1 trauma center was conducted. Patients aged 18 years or older who had experienced a traumatic event and had undergone an upper extremity ultrasound (UEUS) were included in the study. Multiple logistic regression was used to identify independent risk factors that contributed to UEDVT. RESULTS: A total of 6,607 patients were admitted due to traumatic injuries during the study period, of whom 5.6% (373) had at least one UEUS during their hospitalization. Fifty-six (15%) were diagnosed with an UEDVT, as well as three non-fatal pulmonary emboli (PE) and four (7.1%) deaths, p = 0.03. Pharmacological prophylaxis with low-molecular-weight heparin (LMWH) or unfractionated heparin showed a protective effect against UEDVT; among the patients positive for UEDVT, 14 of 186 patients (7.5%) received LMWH, while 42 of 195 (21.5%) did not receive LMWH (p < 0.001). Multiple logistic regression revealed that the presence of upper extremity fractures, peripherally inserted central catheter (PICC) lines, and traumatic brain injury (TBI) were independent risk factors for UEDVT. CONCLUSIONS: UEDVT are associated with a higher mortality. The presence of upper extremity fractures, PICC lines, and TBI were independent risk factors for UEDVTs. Further, pharmacological prophylaxis reduces the risk of UEDVT.

Bile acids regulate intestinal cell proliferation by modulating EGFR and FXR signaling.

Bile acids (BAs) are synthesized in the liver and secreted into the intestine. In the lumen, enteric bacteria metabolize BAs from conjugated, primary forms into more toxic unconjugated, secondary metabolites. Secondary BAs can be injurious to the intestine and may contribute to disease. The epidermal growth factor receptor (EGFR) and the nuclear farnesoid X receptor (FXR) are known to interact with BAs. In this study we examined the effects of BAs on intestinal epithelial cell proliferation and investigated the possible roles for EGFR and FXR in these effects. We report that taurine-conjugated cholic acid (TCA) induced proliferation, while its unconjugated secondary counterpart deoxycholic acid (DCA) inhibited proliferation. TCA stimulated phosphorylation of Src, EGFR, and ERK 1/2. Pharmacological blockade of any of these pathways or genetic ablation of EGFR abrogated TCA-stimulated proliferation. Interestingly, Src or EGFR inhibitors eliminated TCA-induced phosphorylation of both molecules, suggesting that their activation is interdependent. In contrast to TCA, DCA exposure diminished EGFR phosphorylation, and pharmacological or siRNA blockade of FXR abolished DCA-induced inhibition of proliferation. Taken together, these results suggest that TCA induces intestinal cell proliferation via Src, EGFR, and ERK activation. In contrast, DCA inhibits proliferation via an FXR-dependent mechanism that may include downstream inactivation of the EGFR/Src/ERK pathway. Since elevated secondary BA levels are the result of specific bacterial modification, this may provide a mechanism through which an altered microbiota contributes to normal or abnormal intestinal epithelial cell proliferation.