Pharmacomechanical Catheter-Directed Thrombolysis for Deep-Vein Thrombosis.

BACKGROUND: The post-thrombotic syndrome frequently develops in patients with proximal deep-vein thrombosis despite treatment with anticoagulant therapy. Pharmacomechanical catheter-directed thrombolysis (hereafter "pharmacomechanical thrombolysis") rapidly removes thrombus and is hypothesized to reduce the risk of the post-thrombotic syndrome. METHODS: We randomly assigned 692 patients with acute proximal deep-vein thrombosis to receive either anticoagulation alone (control group) or anticoagulation plus pharmacomechanical thrombolysis (catheter-mediated or device-mediated intrathrombus delivery of recombinant tissue plasminogen activator and thrombus aspiration or maceration, with or without stenting). The primary outcome was development of the post-thrombotic syndrome between 6 and 24 months of follow-up. RESULTS: Between 6 and 24 months, there was no significant between-group difference in the percentage of patients with the post-thrombotic syndrome (47% in the pharmacomechanical-thrombolysis group and 48% in the control group; risk ratio, 0.96; 95% confidence interval [CI], 0.82 to 1.11; P=0.56). Pharmacomechanical thrombolysis led to more major bleeding events within 10 days (1.7% vs. 0.3% of patients, P=0.049), but no significant difference in recurrent venous thromboembolism was seen over the 24-month follow-up period (12% in the pharmacomechanical-thrombolysis group and 8% in the control group, P=0.09). Moderate-to-severe post-thrombotic syndrome occurred in 18% of patients in the pharmacomechanical-thrombolysis group versus 24% of those in the control group (risk ratio, 0.73; 95% CI, 0.54 to 0.98; P=0.04). Severity scores for the post-thrombotic syndrome were lower in the pharmacomechanical-thrombolysis group than in the control group at 6, 12, 18, and 24 months of follow-up (P<0.01 for the comparison of the Villalta scores at each time point), but the improvement in quality of life from baseline to 24 months did not differ significantly between the treatment groups. CONCLUSIONS: Among patients with acute proximal deep-vein thrombosis, the addition of pharmacomechanical catheter-directed thrombolysis to anticoagulation did not result in a lower risk of the post-thrombotic syndrome but did result in a higher risk of major bleeding. (Funded by the National Heart, Lung, and Blood Institute and others; ATTRACT ClinicalTrials.gov number, NCT00790335 .).

Gastric bypass does not influence olfactory function in obese patients.

Morbidly obese individuals have altered sense of taste and smell. Gastric bypass (GBP) alters taste but olfactory function has not been evaluated. Changes in these senses may influence dietary preferences following GBP. Our aim was to evaluate the effect of abdominal operation, specifically GBP, and weight loss on olfactory function. Fifty-five persons undergoing GBP and cholecystectomy and 40 persons undergoing cholecystectomy (CC) alone were administered the Cross Cultural Smell Identification Test (CC-SIT) preoperatively and 2 and 6 weeks postoperatively. Patients undergoing GBP underwent further tests at 3, 6, 9, and 12 months. Body mass index (BMI) was also assessed. Mean BMI was significantly greater preoperatively in the GBP group (50.6 ± 8.0 vs. 30.6 ± 7.3 kg/m(2), p < 0.05). Significantly more GBP patients had abnormal CC-SIT results preoperatively (12.7% vs. 5.0%). There were no significant differences in percentage of abnormal tests at 2 and 6 weeks within groups but remained lower in CC patients (2 weeks, GBP 6.2% vs. CC 5.7%; 6 weeks, GBP 9.8% vs. CC 3.2%, p < .05). BMI decreased in the GBP group at 12 months (50.6 ± 8.0 preoperatively to 31.9 ± 6.9 p < 0.05). Absolute olfactory dysfunction (AOD) was present at each interval up to 12 months after GBP. Only 22% of patients with AOD remained obese. GBP does not appear to influence olfactory function. AOD present in morbidly obese persons is not affected by weight loss. These findings support that olfactory dysfunction may be a contributing factor to the development of obesity.

Genetic determination of susceptibility to estrogen-induced mammary cancer in the ACI rat: mapping of Emca1 and Emca2 to chromosomes 5 and 18.

Hormonal, genetic, and environmental factors play major roles in the complex etiology of breast cancer. When treated continuously with 17beta-estradiol (E2), the ACI rat exhibits a genetically conferred propensity to develop mammary cancer. The susceptibility of the ACI rat to E2-induced mammary cancer appears to segregate as an incompletely dominant trait in crosses to the resistant Copenhagen (COP) strain. In both (ACI x COP)F(2) and (COP x ACI)F(2) populations, we find strong evidence for a major genetic determinant of susceptibility to E2-induced mammary cancer on distal rat chromosome 5. Our data are most consistent with a model in which the ACI allele of this locus, termed Emca1 (estrogen-induced mammary cancer 1), acts in an incompletely dominant manner to increase both tumor incidence and tumor multiplicity as well as to reduce tumor latency in these populations. We also find evidence suggestive of a second locus, Emca2, on chromosome 18 in the (ACI x COP)F(2) population. The ACI allele of Emca2 acts in a dominant manner to increase incidence and decrease latency. Together, Emca1 and Emca2 act independently to modify susceptibility to E2-induced mammary cancer.