Context Estrogen therapy is thought to promote gallstone formation and cholecystitis but most data derive from observational studies rather than randomized trials.Objective To determine the effect of estrogen therapy in healthy postmenopausal women on gallbladder disease outcomes.Design, Setting, and Participants Two randomized, double-blind, placebocontrolled trials conducted at 40 US clinical centers. The volunteer sample was 22579 community-dwelling women aged 50 to 79 years without prior cholecystectomy.Intervention Women with hysterectomy were randomized to 0.625 mg/d of conjugated equine estrogens (CEE) or placebo (n=8376). Women without hysterectomy were randomized to estrogen plus progestin (E+P), given as CEE plus 2.5 mg/d of medroxyprogesterone acetate (n=14203). Main Outcome MeasuresParticipants reported hospitalizations for gallbladder diseases and gallbladder-related procedures, with events ascertained through medical record review. Cox proportional hazards regression was used to assess hazard ratios (HRs) and 95% confidence intervals (CIs) using intention-to-treat and time-to-event methods. ResultsThe CEE and the E+P groups were similar to their respective placebo groups at baseline. The mean follow-up times were 7.1 years and 5.6 years for the CEE and the E+P trials, respectively. The annual incidence rate for any gallbladder event was 78 events per 10000 person-years for the CEE group (vs 47/10000 person-years for placebo) and 55 per 10000 person-years for E+P (vs 35/10000 person-years for placebo). Both trials showed greater risk of any gallbladder disease or surgery with estrogen

The magnitude and patterns of CAM use among elders lend considerable importance to this field in public health policy making and suggest a need for further epidemiological research and ongoing awareness efforts for both patients and providers.

Objective. To determine the effect of hormone therapy on arthroplasty rates.Methods. We examined data from the Women's Health Initiative placebo-controlled, double-blind, randomized trials. Community-dwelling women ages 50-79 years were enrolled at 40 US clinics. Women with prior arthroplasty were excluded, yielding a sample size of 26,321 subjects. Women who had had hysterectomies (n ‫؍‬ 10,272) were randomly assigned to receive 0.625 mg/day conjugated equine estrogens (n ‫؍‬ 5,076), or placebo (n ‫؍‬ 5,196), with a mean followup of 7.1 years. Those who had not had hysterectomies (n ‫؍‬ 16,049) were randomly assigned to receive estrogen plus progestin (n ‫؍‬ 8,240), given as 0.625 mg/day conjugated equine estrogens plus 2.5 mg/day medroxyprogesterone acetate, or placebo (n ‫؍‬ 7,809), with a mean followup of 5.6 years. Participants reported hospitalizations, and arthroplasties were identified by procedure codes. Arthroplasties due to hip fracture were censored. Cox proportional hazards regression was used to assess hazard ratios (HRs) and 95% confidence intervals (95% CIs) using intent-to-treat methods and outcome of time to first procedure.Results. In the estrogen-alone trial, women receiving hormone therapy had significantly lower rates of any

Background Current biomarkers in ulcerative colitis (UC) are limited by their performance, cost and limited availability in daily practice. This study examined alterations in the leukocyte profiles as biomarkers of UC activity including the effects of age, gender and medications. Methods Case control study that included 110 UC subjects, 75 subjects with C. difficile infection, and 75 non-inflammatory bowel disease (IBD) subjects, randomly selected from a single institution IBD database. Mean values of neutrophils (N), lymphocytes (L), monocytes (M) and their ratios were compared between groups. ROC curve analyses assessed the performance of each biomarker in discriminating disease states. Subgroup analyses examined leukocytes profiles with endoscopic activity. Results Elevated monocyte counts and decreased L/M values significantly differed between subjects with active UC and UC in remission and performed better than other leukocyte profiles. A monocyte count of 483 and L/M ratio of 3.1 were 60% sensitive and had a specificity of 61% and 53% respectively for active UC. Monocyte count > 860 and L/M value < 1.6 had a 75% positive predictive value for UC activity. Those markers also correlated with endoscopically active disease. L/M and N/L values performed best at differentiating active UC from non-IBD controls, while N/L and neutrophil values performed best at differentiating from C. diff controls. Conclusion Monocytosis and a low L/M ratio might be effective, readily available and low cost biomarkers to identify disease activity in UC patients. N/L values were more effective at distinguishing active UC patients from patients without IBD and those with C. diff infection.

Studies considering the association between total cholesterol and noncardiovascular mortality, particularly from respiratory disease, yield inconclusive findings. To explore this question, the relation of lipids to pulmonary function, specifically forced expiratory volume in 1 second (FEV(1)), was investigated in the Third National Health and Nutrition Examination Survey. Conducted in the United States in 1988-1994 among adults aged> or =17 years, this survey measured serum lipids, FEV(1), and confounding factors including smoking and antioxidants. Multiple linear regression analysis explored the relation of FEV(1)/height(2) to low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, and their respective apolipoproteins (apo) B and A-I. A standard deviation increase in HDL cholesterol or apo A-I was associated with an FEV(1) increase of 43 ml (95% confidence interval (CI): 30, 56) or 29 ml (95% CI: 11, 47), respectively, for an average-height adult. A standard deviation increase in LDL cholesterol or apo B was associated with an FEV(1) decrease of -24 ml (95% CI: -43, -5) or -53 ml (95% CI: -74, -32), respectively, adjusted for serum antioxidant status. The lipid subfractions were differentially associated with FEV(1) consistent with the possibility that LDL cholesterol contributes to endogenous oxidative burden while HDL cholesterol attenuates inflammatory tissue damage. Whether these associations are causal remains to be determined.