Search tips
Search criteria

Results 1-15 (15)

Clipboard (0)

Select a Filter Below

more »
Year of Publication
Document Types
1.  A Pharmacogenetic versus a Clinical Algorithm for Warfarin Dosing 
The New England journal of medicine  2013;369(24):2283-2293.
The clinical utility of genotype-guided (pharmacogenetically based) dosing of warfarin has been tested only in small clinical trials or observational studies, with equivocal results.
We randomly assigned 1015 patients to receive doses of warfarin during the first 5 days of therapy that were determined according to a dosing algorithm that included both clinical variables and genotype data or to one that included clinical variables only. All patients and clinicians were unaware of the dose of warfarin during the first 4 weeks of therapy. The primary outcome was the percentage of time that the international normalized ratio (INR) was in the therapeutic range from day 4 or 5 through day 28 of therapy.
At 4 weeks, the mean percentage of time in the therapeutic range was 45.2% in the genotype-guided group and 45.4% in the clinically guided group (adjusted mean difference, [genotype-guided group minus clinically guided group], −0.2; 95% confidence interval, −3.4 to 3.1; P=0.91). There also was no significant between-group difference among patients with a predicted dose difference between the two algorithms of 1 mg per day or more. There was, however, a significant interaction between dosing strategy and race (P=0.003). Among black patients, the mean percentage of time in the therapeutic range was less in the genotype-guided group than in the clinically guided group. The rates of the combined outcome of any INR of 4 or more, major bleeding, or thromboembolism did not differ significantly according to dosing strategy.
Genotype-guided dosing of warfarin did not improve anticoagulation control during the first 4 weeks of therapy. (Funded by the National Heart, Lung, and Blood Institute and others; COAG number, NCT00839657.)
PMCID: PMC3942158  PMID: 24251361
2.  Health Benefits of Gastric Bypass Surgery after 6 Years 
Extreme obesity is associated with health and cardiovascular disease risks. Although gastric bypass surgery induces rapid weight loss and ameliorates many of these risks in the short term, long-term outcomes are uncertain.
To examine the association of Roux-en-Y gastric bypass (RYGB) with weight loss, diabetes mellitus, and other health risks 6 years after surgery.
Design, Setting, and Participants
A prospective Utah-based study conducted between July 2000 and June 2011 of 1156 severely obese (body mass index [BMI] ≥35) participants aged 18–72 years (82% women; mean BMI 45.9; 95% CI, 31.2–60.6) who sought and received RYGB surgery (n=418), sought but did not have surgery (n=417; control group 1), or were randomly selected from a population-based sample not seeking weight loss surgery (n=321; control group 2).
Main Outcome Measures
Weight loss, diabetes, hypertension, dyslipidemia, and health-related quality of life were compared between participants having RYGB surgery and control participants using propensity score adjustment.
Six years after surgery, patients who received RYGB surgery (with 92.6% follow-up) lost 27.7% (95% CI, 26.6%–28.9%) of their initial body weight compared with 0.2% (95% CI, -1.1% to 1.4%) gain in control group 1 and 0% (95% CI, −1.2 to 1.2%) in control group 2. Weight loss maintenance was superior in patients who received RYGB surgery, with 94% (95% CI, 92%–96%) and 76% (95% CI, 72%–81%) of patients receiving RYGB surgery maintaining at least 20% weight loss 2 and 6 years after surgery, respectively. Diabetes remission rates 6 years after surgery were 62% (95% CI, 49%–75%) in the RYGB surgery group, 8% (95% CI, 0%–16%) in control group 1, and 6% (95% CI, 0%–13%) in control group 2, with remission odds ratios (ORs) of 16.5 (95% CI, 4.7–57.6; P<.001) vs control group 1 and 21.5 (95% CI, 5.4–85.6; P<.001) vs control group 2. The incidence of diabetes throughout the course of the study was reduced after RYGB surgery (2%; 95% CI, 0%–4%; versus 17%; 95% CI, 10%–24%; OR, 0.11; 95% CI, 0.04–0.34 compared with control group 1 and 15%; 95% CI, 9%–21%; OR, 0.21; 95% CI, 0.06–0.67 compared with control group 2; both P<.001). The numbers of participants with bariatric surgery-related hospitalizations were 33 (7.9%), 13 (3.9%), and 6 (2.0%) for RYGB surgery group and 2 control groups, respectively.
Among severely obese patients, compared with nonsurgical control patients, the use of RYGB surgery was associated with higher rates of diabetes remission and lower risk of cardiovascular and other health outcomes over 6 years.
PMCID: PMC3744888  PMID: 22990271
3.  Favorable Changes in Cardiac Geometry and Function Following Gastric Bypass Surgery 
The objective of this study was to test the hypothesis that gastric bypass surgery (GBS) would favorably impact cardiac remodeling and function.
GBS is increasingly used to treat severe obesity, but there are limited outcome data.
We prospectively studied 423 severely obese patients undergoing GBS and a reference group of severely obese subjects that did not have surgery (n = 733).
At a 2-year follow up, GBS subjects had a large reduction in body mass index compared with the reference group (−15.4 ± 7.2 kg/m2 vs. −0.03 ± 4.0 kg/m2; p < 0.0001), as well as significant reductions in waist circumference, systolic blood pressure, heart rate, triglycerides, low-density lipoprotein cholesterol, and insulin resistance. High-density lipoprotein cholesterol increased. The GBS group had reductions in left ventricular (LV) mass index and right ventricular (RV) cavity area. Left atrial volume did not change in GBS but increased in reference subjects. In conjunction with reduced chamber sizes, GBS subjects also had increased LV midwall fractional shortening and RV fractional area change. In multivariable analysis, age, change in body mass index, severity of nocturnal hypoxemia, E/E', and sex were independently associated with LV mass index, whereas surgical status, change in waist circumference, and change in insulin resistance were not.
Marked weight loss in patients undergoing GBS was associated with reverse cardiac remodeling and improved LV and RV function. These data support the use of bariatric surgery to prevent cardiovascular complications in severe obesity.
PMCID: PMC3713780  PMID: 21292133
bariatric surgery; cardiac remodeling; diabetes; echocardiography; hypertension; left atrial volume; left ventricular hypertrophy; myocardial contraction; obesity
4.  Prospective Comparison of Three Enoxaparin Dosing Regimens to Achieve Target Anti-Factor Xa Levels in Hospitalized, Medically-Ill Patients with Extreme Obesity 
American Journal of Hematology  2012;87(7):740-743.
Enoxaparin is commonly used to prevent venous thromboembolism (VTE) [1, 2] but has not been well-studied in patients with extreme obesity, a population at high risk for VTE. We prospectively compared three enoxaparin dosing regimens for the achievement of goal peak anti-Factor Xa levels in medically-ill patients (n=31) with extreme obesity (body mass index (BMI) ≥ 40 kg/m2). Patients were assigned to receive fixed-dose (FD) enoxaparin 40mg daily (QDay, n=11), weight-based, lower-dose (LD) enoxaparin 0.4 mg/kg QDay (n=9), or weight-based, higher-dose (HD) enoxaparin 0.5 mg/kg QDay(n=11). The average BMI and weight of the entire cohort was 62.1 kg/m2 (range 40.5-82.4) and 176 kg (range 115-256 kg) and did not differ between groups. Peak anti-Factor Xa levels were significantly higher in the HD group compared to either LD or FD groups. Patients in the HD group achieved target anti-Factor Xa levels more frequently than the LD and FD groups (p<0.05). Peak anti-Factor Xa levels did not correlate with age, weight, BMI, or creatinine clearance, demonstrating the predictability of weight-based enoxaparin dosing. There were no adverse events (e.g. bleeding, thrombosis, thrombocytopenia). To our knowledge, this is the first prospective comparative study demonstrating that in extremely obese, medically-ill patients enoxaparin 0.5 mg/kg QDay is superior to fixed-dose and lower-dose enoxaparin for the achievement of target anti-Factor Xa levels.
PMCID: PMC3385867  PMID: 22565589
5.  Drug-Induced Thrombocytopenia for the Hospitalist Physician with a Focus on Heparin-lnduced Thrombocytopenia 
Hospital practice (1995)  2010;38(2):19-28.
Acute thrombocytopenia occurs commonly in hospitalized patients. For most, the etiology of an acutely declining platelet count is obvious and includes sepsis with disseminated intravascular coagulation, large-volume crystalloid infusion, or the administration of cytotoxic therapies, such as chemotherapeutic agents. For others, however, the etiology may be less apparent. In these cases, drug-induced thrombocytopenia (DIT), including heparin-induced thrombocytopenia (HIT), must be a diagnostic consideration. The approach to the hospitalized patient with thrombocytopenia, without an obvious cause, includes a careful medication history to identify potential culprits, such as glycoprotein IIb/IIIa inhibitors, vancomycin, linezolid, β-lactam antibiotics, quinine, antiepileptic drugs, or heparin/low-molecular-weight heparin. Usually, discontinuation of the offending medication is all that is necessary for resolution of thrombocytopenia. Heparin-induced thrombocytopenia, however, is an exception to this general rule given its unique pathogenesis and propensity for thrombotic complications and death. Differentiating between HIT and DIT due to nonheparin medications may prove challenging. Through a careful clinical assessment, consideration of the pre-test probability for HIT, and the thoughtful application of laboratory testing, HIT can be accurately diagnosed. Because patients with HIT have a high risk of thrombosis and bleeding is uncommon, the prompt initiation of an alternative anticoagulant (eg, a direct thrombin inhibitor) is warranted in these patients.
PMCID: PMC3682781  PMID: 20469610
drug-induced thrombocytopenia; heparin-induced thrombocytopenia; thrombocytopenia; thrombosis; platelet; heparin
6.  Genetics InFormatics Trial (GIFT) of Warfarin to Prevent Deep Vein Thrombosis (DVT): Rationale and Study Design 
The pharmacogenomics journal  2011;12(5):417-424.
The risk of venous thromboembolism (VTE) is higher after total hip or knee replacement surgery than after almost any other surgical procedure; warfarin sodium is commonly prescribed to reduce this peri-operative risk. Warfarin has a narrow therapeutic window with high inter-individual dose variability and can cause hemorrhage. The Genetics-InFormatics Trial (GIFT) of Warfarin to Prevent Deep Vein Thrombosis (DVT) is a 2×2 factorial-design, randomized controlled trial designed to compare the safety and effectiveness of warfarin-dosing strategies. GIFT will answer two questions: (1) Does pharmacogenetic (PGx) dosing reduce the rate of adverse events in orthopedic patients; and (2) Is a lower target International Normalized Ratio (INR) non-inferior to a higher target INR in orthopedic participants? The composite primary endpoint of the trial is symptomatic and asymptomatic VTE (identified on screening ultrasonography), major hemorrhage, INR ≥ 4, and death.
PMCID: PMC3175019  PMID: 21606949
pharmacogenetics; warfarin; randomized controlled trial; dosing algorithm
7.  18F-FDG PET in the Evaluation of Acuity of Deep Vein Thrombosis 
Clinical nuclear medicine  2012;37(12):1139-1145.
18F-FDG PET has been used for vascular disease, but its role in deep vein thrombosis (DVT) remains prospectively unexplored.
Patients and Methods
Whole-body 18F-FDG PET/CT scans were performed in patients 1 to 10 weeks after onset of symptomatic DVT (n = 12) and in control subjects without DVT (n = 24). The metabolic activity (SUVmax) of thrombosed and contralateral nonthrombosed vein segments was determined. The sensitivity and specificity of 18F-FDG PET/CT for the diagnosis of DVT were determined by receiver operating characteristic curve analyses. In 2 patients with DVT, changes in the metabolic activity of thrombosed vein segments in serial 18F-FDG PET scans.
The metabolic activity in thrombosed veins [SUVmax, 2.41 (0.75)] was visually appreciable and significantly higher than in nonthrombosed veins in either the contralateral extremity of patients with DVT [SUVmax, 1.09 (0.25), P = 0.007] or control subjects [1.21 (0.22), P < 001]. The area under the receiver operating characteristic curve for SUVmax was 0.9773 (P < 001), indicating excellent accuracy. An SUVmax threshold of greater than 1.645 was 87.5% sensitive and 100% specific for DVT. Metabolic activity in thrombosed veins correlated significantly with time from DVT symptom onset (decrease in SUVmax of 0.02/d, P < 0.05). Best-fit-line analyses suggested that approximately 84 to 91 days after acute DVT, the maximum metabolic activity of thrombosed veins would return to normal levels.
18F-FDG PET/CT is accurate for detecting acute symptomatic, proximal DVT. Metabolic activity in thrombosed veins decreases with time, suggesting that 18F-FDG PET may be helpful in assessing the age of the clot.
PMCID: PMC3564643  PMID: 23154470
duplex ultrasonography; deep vein thrombosis; 18F-FDG PET/CT; sensitivity; specificity; diagnosis; FDG; venothromboembolic disease
8.  Prospective Pilot Trial of PerMIT Versus Standard Anticoagulation Service Management of Patients Initiating Oral Anticoagulation 
Thrombosis and haemostasis  2012;108(3):561-569.
We performed a randomized pilot trial of PerMIT, a novel decision support tool for genotype-based warfarin initiation and maintenance dosing, to assess its efficacy for improving warfarin management. We prospectively studied 26 subjects to compare PerMIT-guided management with routine anticoagulation service management. CYP2C9 and VKORC1 genotype results for 13 subjects randomly assigned to the PerMIT arm were recorded within 24 h of enrollment. To aid in INR interpretation, PerMIT calculates estimated loading and maintenance doses based on a patient’s genetic and clinical characteristics and displays calculated S-warfarin plasma concentrations based on planned or administered dosages. In comparison to control subjects, patients in the PerMIT study arm demonstrated a 3.6-day decrease in the time to reach a stabilized INR within the target therapeutic range (4.7 vs. 8.3 days, p = 0.015); a 12.8% increase in time spent within the therapeutic interval over the first 25 days of therapy (64.3% vs. 55.3%, p = 0.180); and a 32.9% decrease in the frequency of warfarin dose adjustments per INR measurement (38.3% vs. 57.1%, p = 0.007). Serial measurements of plasma S-warfarin concentrations were also obtained to prospectively evaluate the accuracy of the pharmacokinetic model during induction therapy. The PerMIT S-warfarin plasma concentration model estimated 62.8% of concentrations within 0.15 mg/L. These pilot data suggest that the PerMIT method and its incorporation of genotype/phenotype information may help practitioners increase the safety, efficacy, and efficiency of warfarin therapeutic management.
Clinical Trials Registration Unique identifier: NCT00993200
PMCID: PMC3434319  PMID: 22836303
anticoagulation; warfarin; pharmacogenetics; algorithm; clinical trial
9.  Pharmacogenetic Warfarin Dose Refinements Remain Significantly Influenced by Genetic Factors after One Week of Therapy 
Thrombosis and Haemostasis  2011;107(2):232-240.
By guiding initial warfarin dose, pharmacogenetic (PGx) algorithms may improve the safety of warfarin initiation. However, once INR response is known, the contribution of PGx to dose refinements is uncertain. This study sought to develop and validate clinical and PGx dosing algorithms for warfarin dose refinement on days 6–11 after therapy initiation.
Materials and Methods
An international sample of 2,022 patients at 13 medical centers on 3 continents provided clinical, INR, and genetic data at treatment days 6–11 to predict therapeutic warfarin dose. Independent derivation and retrospective validation samples were composed by randomly dividing the population (80%/20%). Prior warfarin doses were weighted by their expected effect on S-warfarin concentrations using an exponential-decay pharmacokinetic model. The INR divided by that “effective” dose constituted a treatment response index.
Treatment response index, age, amiodarone, body surface area, warfarin indication, and target INR were associated with dose in the derivation sample. A clinical algorithm based on these factors was remarkably accurate: in the retrospective validation cohort its R2 was 61.2% and median absolute error (MAE) was 5.0 mg/week. Accuracy and safety was confirmed in a prospective cohort (N=43). CYP2C9 variants and VKORC1-1639 G→A were significant dose predictors in both the derivation and validation samples. In the retrospective validation cohort, the PGx algorithm had: R2= 69.1% (P<0.05 vs. clinical algorithm), MAE= 4.7 mg/week.
A pharmacogenetic warfarin dose-refinement algorithm based on clinical, INR, and genetic factors can explain at least 69.1% of therapeutic warfarin dose variability after about one week of therapy.
PMCID: PMC3292349  PMID: 22186998
warfarin; VKORC1; CYP2C9; pharmacogenetic
10.  A pilot study utilizing whole body 18 F-FDG-PET/CT as a comprehensive screening strategy for occult malignancy in patients with unprovoked venous thromboembolism☆ 
Thrombosis Research  2011;129(1):22-27.
Approximately 7-10% of patients with unprovoked VTE will be diagnosed with cancer within 12 months. Although cancer screening has been proposed in these patients, the optimal strategy remains unclear. In a pilot study, we prospectively investigated the use of FDG-PET/CT to screen for occult malignancy in 40 patients with unprovoked VTE.
Patients were initially screened for occult malignancy with a focused history, physical, and laboratory evaluation. Patients underwent whole body FDG-PET/CT and were followed for up to two years for a new diagnosis of cancer. The total costs of using FDG-PET/CT as a comprehensive screening strategy were determined using 2010 Medicare reimbursement rates.
Completion of FDG-PET/CT imaging was feasible and identified abnormal findings requiring additional evaluations in 62.5% of patients. Occult malignancy was evident in only one patient (cancer incidence 2.5%) and FDG-PET/CT imaging excluded malignancy in the remainder of patients. No patients with a negative FDG-PET/CT were diagnosed with malignancy during an average (±SD) follow-up of 449 (±311) days. The use of FDG-PET/CT to screen for occult malignancy added $59,151 in total costs ($1,479 per patient). The majority of these costs were due to the cost of the FDG-PET/CT ($1,162 per patient or 78.5% of total per-patient costs).
FDG-PET/CT may have utility for excluding occult malignancy in patients with unprovoked VTE. The costs of this comprehensive screening strategy were comparable to other screening approaches. Larger studies are needed to further evaluate the utility and cost-effectiveness of FDG-PET/CT as a cancer screening strategy in patients with unprovoked VTE.
PMCID: PMC3277867  PMID: 21802118
Cancer Screening; FDG-PET/CT; Occult Malignancy; Venous Thromboembolism; Cost Effectiveness; Early Detection of Cancer
11.  Prevention of venous thromboembolism in obesity 
Venous thromboembolism (VTE) is a significant cause of morbidity and mortality in hospitalized patients. Where appropriate, evidence-based methods of prophylaxis are implemented and the burden of VTE can be reduced substantially. Obesity, including morbid obesity, is associated with a high risk of VTE and, unfortunately, fixed doses of US FDA-approved anticoagulant regimens, including unfractionated heparins, low-molecular-weight heparins and factor Xa inhibitors, may not provide optimal VTE prophylaxis in these patients. Although the data are still limited, a rapidly growing body of literature and cumulative evidence suggests that anticoagulant dose adjustments in morbidly obese patients may optimize pharmacodynamic activity and reduce VTE risk. With the prevalence of morbid obesity continuing to rise, more high-quality clinical data are needed to better understand the pathobiology of VTE in obesity and provide effective, yet safe, prevention strategies.
PMCID: PMC3245959  PMID: 21108553
deep vein thrombosis; fondaparinux; low-molecular-weight heparin; morbid obesity; pulmonary embolism; special populations; venous thromboembolism prophylaxis
12.  Azathioprine-Induced Warfarin Resistance 
The Annals of pharmacotherapy  2008;42(7):1118-1123.
To describe a case of azathioprine-induced warfarin resistance, present a literature review on warfarin–azathioprine interactions, and provide recommendations on appropriate management of this clinically significant interaction.
A 29-year-old female with Cogan’s syndrome experienced thrombosis of the left internal carotid artery. She was treated with an average weekly warfarin dose of 39 mg (5.5 mg daily) prior to beginning azathioprine therapy. Three weeks following initiation of azathioprine 150 mg daily, the international normalized ratio (INR) decreased from 1.9 (prior to the medication change) to 1.0 without any change in the warfarin dose or other relevant factors. Over several weeks, the patient’s warfarin dose was titrated up to 112 mg weekly (16 mg daily) to achieve an INR of 2.5 (a 188%, or 2.9-fold dose increase). Because of elevated liver enzyme levels, the azathioprine dosage was decreased to 100 mg daily. Within 2 weeks following that decrease, warfarin requirements decreased to 105 mg weekly (15 mg daily).
Azathioprine was the probable causative agent of warfarin resistance according to the Naranjo probability scale, and a possible causative agent according to the Drug Interaction Probability Scale. A literature search (PubMed, 1966–December 2007) revealed 8 case reports of this drug interaction and 2 cases involving a similar effect with 6-mercaptopurine, the active metabolite of azathioprine. The exact mechanism of the interaction remains unknown. Previously published case reports point to a rapid onset and offset of the warfarin–azathioprine interaction and a dose-dependent increase of at least 2.5-fold in warfarin dose requirement with the initiation of azathioprine 75–200 mg daily.
This case report and several others point toward azathioprine as a clinically significant inducer of warfarin resistance. Providers should anticipate the need for higher warfarin doses, warfarin dose adjustment, and close INR monitoring in patients receiving azathioprine or its active metabolite, 6-mercaptopurine.
PMCID: PMC3245963  PMID: 18505911
anticoagulation; azathioprine; 6-mercaptopurine; warfarin
13.  Weight-based dosing of enoxaparin for VTE prophylaxis in morbidly obese, medically-Ill patients 
Thrombosis research  2009;125(3):220-223.
In clinical trials, fixed-dose enoxaparin (40 mg once daily) reduces the risk of venous thromboembolism (VTE) in medically-ill patients. However, morbidly obese patients were under-represented in these trials and using fixed-dose enoxaparin in obese patients may be inadequate. We completed a pharmacokinetic study in morbidly obese, medically-ill patients to determine if weight-based dosing of enoxaparin for VTE prophylaxis was feasible, without excessive levels of anticoagulation, as determined by peak anti-Xa levels.
Materials and Methods
Twenty eight morbidly obese (BMI≥35 kg/m2) patients were enrolled and completed the study protocol. Enoxaparin 0.5 mg/kg was administered once daily subcutaneously and peak anti-Xa levels were measured approximately 4–6 hours after the enoxaparin dose.
Results and Conclusions
Overall, 46% of patients were female, the average age (±SD) was 54 (±11) years, and the average weight and BMI were 135.6 kg (±25.3) and 48.1 kg/m2 (±11.1), respectively. The average daily dose of enoxaparin was 67 mg (±12). The average peak anti-Xa level was 0.25 (SD±0.11, range 0.08 to 0.59) units/mL. Peak anti-Xa levels did not significantly correlate with weight or BMI. There were no bleeding events, symptomatic VTE, or significant thrombocytopenia.
In morbidly obese, medically-ill patients, use of weight-based enoxaparin dosed at 0.5 mg/kg once daily is feasible and results in peak anti-Xa levels within or near recommended range for thromboprophylaxis, without any evidence of excessive anti-Xa activity. These data suggest that this weight-based regimen may be more effective than standard fixed-dose enoxaparin. Clinical outcome studies are warranted to determine the clinical safety and efficacy of this regimen.
PMCID: PMC3245965  PMID: 19272635
Low-molecular weight heparin; Medically-Ill; Obesity; Pharmacokinetics; Prophylaxis; Venous Thromboembolism
14.  Physician Alerts to Prevent Symptomatic Venous Thromboembolism in Hospitalized Patients 
Circulation  2009;119(16):2196-2201.
Venous thromboembolism (VTE) prophylaxis remains underutilized among hospitalized patients. We designed and carried out a large multicenter randomized controlled trial to test the hypothesis that an alert from a hospital staff member to the Attending Physician will reduce the rate of symptomatic VTE among high-risk patients not receiving prophylaxis.
Methods and Results
We enrolled patients using a validated point score system to detect hospitalized patients at high risk for symptomatic VTE who were not receiving prophylaxis. 2,493 patients (82% on Medical Services) from 25 study sites were randomized to the intervention group (n=1,238), in which the responsible physician was alerted by another hospital staff member, versus the control group (n=1,255), in which no alert was issued. The primary end point was symptomatic, objectively confirmed VTE within 90 days. Patients whose physicians were alerted were more than twice as likely to receive VTE prophylaxis as controls (46.0% versus 20.6%, p<0.0001). The symptomatic VTE rate was lower in the intervention group (2.7% versus 3.4%; hazard ratio, 0.79; 95% confidence interval, 0.50 to 1.25), but the difference did not achieve statistical significance. The rate of major bleeding at 30 days in the alert group was similar to the control group (2.1% versus 2.3%, p=0.68).
A strategy of direct staff member to physician notification increases prophylaxis utilization and leads toward reducing the rate of symptomatic VTE in hospitalized patients. However, VTE prophylaxis continues to be underutilized even after physician notification, especially among Medical Service patients.
PMCID: PMC2901546  PMID: 19364975
Deep vein thrombosis; Prevention; Prophylaxis; Pulmonary embolism; Venous thromboembolism
15.  Health Outcomes of Gastric Bypass Patients Compared to Nonsurgical, Nonintervened Severely Obese 
Obesity (Silver Spring, Md.)  2009;18(1):121-130.
Favorable health outcomes at 2 years postbariatric surgery have been reported. With exception of the Swedish Obesity Subjects (SOS) study, these studies have been surgical case series, comparison of surgery types, or surgery patients compared to subjects enrolled in planned nonsurgical intervention. This study measured gastric bypass effectiveness when compared to two separate severely obese groups not participating in designed weight-loss intervention. Three groups of severely obese subjects (N = 1,156, BMI ≥ 35 kg/m2) were studied: gastric bypass subjects (n = 420), subjects seeking gastric bypass but did not have surgery (n = 415), and population-based subjects not seeking surgery (n = 321). Participants were studied at baseline and 2 years. Quantitative outcome measures as well as prevalence, incidence, and resolution rates of categorical health outcome variables were determined. All quantitative variables (BMI, blood pressure, lipids, diabetes-related variables, resting metabolic rate (RMR), sleep apnea, and health-related quality of life) improved significantly in the gastric bypass group compared with each comparative group (all P < 0.0001, except for diastolic blood pressure and the short form (SF-36) health survey mental component score at P < 0.01). Diabetes, dyslipidemia, and hypertension resolved much more frequently in the gastric bypass group than in the comparative groups (all P < 0.001). In the surgical group, beneficial changes of almost all quantitative variables correlated significantly with the decrease in BMI. We conclude that Roux-en-Y gastric bypass surgery when compared to severely obese groups not enrolled in planned weight-loss intervention was highly effective for weight loss, improved health-related quality of life, and resolution of major obesity-associated complications measured at 2 years.
PMCID: PMC2864142  PMID: 19498344

Results 1-15 (15)