Karen L. Lifford
Harvard University
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Publication
Featured researches published by Karen L. Lifford.
Journal of the American Geriatrics Society | 2005
Karen L. Lifford; Gary C. Curhan; Frank B. Hu; Robert L. Barbieri; Francine Grodstein
Objectives: To evaluate the association between type 2 diabetes mellitus (DM) and development of urinary incontinence in women.
Obstetrics & Gynecology | 2004
Francine Grodstein; Karen L. Lifford; Neil M. Resnick; Gary C. Curhan
OBJECTIVE: To better understand associations between postmenopausal hormone therapy and the development of urinary incontinence. METHODS: Postmenopausal hormone use was assessed via biennial mailed questionnaires beginning in 1976 among Nurses’ Health Study participants. In 1996, 39,436 postmenopausal women aged 50–75 years reported no leaking of urine and were followed-up for 4 years to identify incident cases of incontinence. We used logistic regression to estimate multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CIs) for the relation of postmenopausal hormone use from 1976 to 1996 to the development of incontinence from 1996 to 2000. RESULTS: We identified 5,060 incident cases of occasional (leaking urine 1–3 times/month) and 2,495 cases of frequent incontinence (leaking at least weekly) for average yearly incidence rates of 3.2% and 1.6%, respectively. The risk of incontinence was elevated among women taking postmenopausal hormones compared with women who had never taken hormones (oral estrogen: RR 1.54, 95% CI 1.44, 1.65; transdermal estrogen: RR 1.68, 95% CI 1.41, 2.00; oral estrogen with progestin: RR 1.34, 95% CI 1.24, 1.44; transdermal estrogen with progestin: RR 1.46, 95% CI 1.16, 1.84). There was little risk after the cessation of hormones (RR 1.14, 95% CI 1.06, 1.23) and a decreasing risk of incontinence with increasing time since last hormone use; 10 years after stopping hormones, the risk was identical in women who had and had never taken hormone therapy (RR 1.02, 95% CI 0.91, 1.14). CONCLUSION: Postmenopausal hormone therapy appears to increase risk of developing urinary incontinence. This risk does not vary by route of administration, type of hormones, or dose taken, but is diminished upon cessation of use. LEVEL OF EVIDENCE: II-2
Journal of the American Geriatrics Society | 2008
Karen L. Lifford; Mary K. Townsend; Gary C. Curhan; Neil M. Resnick; Francine Grodstein
OBJECTIVES: To examine the epidemiology of urinary incontinence (UI) in older women.
Obstetrics & Gynecology | 2009
Rebecca H. Allen; Garrett M. Fitzmaurice; Karen L. Lifford; Morana Lasic; Alisa B. Goldberg
OBJECTIVE: To test the equivalency of oral sedation and intravenous sedation for pain control in first-trimester surgical abortion. METHODS: Women undergoing suction curettage at less than 13 weeks of gestation were randomly assigned to oral sedation, 10 mg of oxycodone and 1 mg of lorazepam, or intravenous sedation, 100 micrograms fentanyl and 2 mg midazolam. All patients received 800 mg of preoperative ibuprofen and a 20-mL paracervical block with 1% lidocaine. The primary outcome was intraoperative pain as measured on a 21-point verbal rating scale that had a range from 0 to 100 (0=no pain and 100=worst pain ever) with an equivalence margin for the treatment group comparison of ±10. RESULTS: Of 130 women, 65 were randomly assigned to oral sedation and 65 to intravenous sedation. The groups differed at baseline by age and preoperative ratings of depression, stress, and anxiety; however, when adjusted for these differences, the primary results were unaffected. Mean intraoperative pain scores, controlling for age and preoperative depression, stress, and anxiety, were 61.2 for oral sedation and 36.3 for intravenous sedation (mean difference 24.9, 95% confidence interval 15.9–33.9). Other findings included no difference in postoperative adverse effects and less satisfaction with pain control with oral sedation compared with intravenous sedation. CONCLUSION: Oral sedation, as studied, is not equivalent to intravenous sedation for pain control during first-trimester surgical abortion. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, www.clinicaltrials.gov, NCT00337792 LEVEL OF EVIDENCE: I
Urologic Clinics of North America | 2002
Karen L. Lifford; Robert L. Barbieri
Chronic pelvic pain is difficult to diagnose and to treat [81] because of the multiple and often overlapping causes [82]. A systematic approach aids in the thorough evaluation and appropriate therapy. At the initial visit(s), a thorough history should be taken and complete physical examination performed. Screening for co-existing conditions, such as depression, narcotic dependency, and physical, sexual, or emotional abuse is crucial so these issues may be addressed immediately while additional causes for pelvic pain are evaluated. The relative likelihood of gastrointestinal, urologic, musculoskeletal, or gynecologic etiology must be considered to guide a more thorough initial evaluation. With gynecologic chronic pelvic pain, differentiation between hormonally responsive and nonresponsive conditions is helpful for diagnosis and treatment. Therapy can then be instituted or an appropriate referral made.
American Journal of Obstetrics and Gynecology | 2006
Kim N. Danforth; Mary K. Townsend; Karen L. Lifford; Gary C. Curhan; Neil M. Resnick; Francine Grodstein
American Journal of Obstetrics and Gynecology | 2003
Francine Grodstein; Ruth C. Fretts; Karen L. Lifford; Neil M. Resnick; Gary C. Curhan
Obstetrics & Gynecology | 2007
Kim N. Danforth; Aparna D. Shah; Mary K. Townsend; Karen L. Lifford; Gary C. Curhan; Neil M. Resnick; Francine Grodstein
American Journal of Obstetrics and Gynecology | 2007
Mary K. Townsend; Kim N. Danforth; Karen L. Lifford; Bernard Rosner; Gary C. Curhan; Neil M. Resnick; Francine Grodstein
Contraception | 2006
Rebecca H. Allen; Divya Kumar; Garrett M. Fitzmaurice; Karen L. Lifford; Alisa B. Goldberg