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• W2006243555 abstract "Body mass index is predictive of sonographic endometrial stripe thickness, which in turn is predictive of endometrial hyperplasia in patients with polycystic ovary syndrome. For every 1-mm increase in endometrial stripe, the odds ratio of hyperplasia increased by 1.48 (95% confidence interval, 1.04–2.10). Body mass index is predictive of sonographic endometrial stripe thickness, which in turn is predictive of endometrial hyperplasia in patients with polycystic ovary syndrome. For every 1-mm increase in endometrial stripe, the odds ratio of hyperplasia increased by 1.48 (95% confidence interval, 1.04–2.10). Polycystic ovary syndrome (PCOS) affects 5%–10% of reproductive-age women, and its associated chronic anovulation increases the risk for endometrial hyperplasia and malignancy (1Elliott J.L. Hosford S.L. Demopoulos R.I. Perloe M. Sills E.S. Endometrial adenocarcinoma and polycystic ovary syndrome: risk factors, management, and prognosis.South Med J. 2001; 94: 529-531PubMed Google Scholar, 2Hardiman P. Pillay O.C. Atiomo W. Polycystic ovary syndrome and endometrial carcinoma.Lancet. 2003; 361: 1810-1812Abstract Full Text Full Text PDF PubMed Scopus (292) Google Scholar). We sought to clarify hyperplasia predictors in premenopausal patients with PCOS, because prior studies regarding this particular population and topic are sparse and inconsistent (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar, 4Peri N. Levine D. Sonographic evaluation of the endometrium in patients with a history or an appearance of polycystic ovarian syndrome.J Ultrasound Med. 2007; 26: 55-58PubMed Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). This was an institutional review board–approved retrospective chart review of patients with PCOS, as defined by the 2003 Rotterdam criteria (6Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop GroupRevised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS).Hum Reprod. 2004; 19: 41-47Crossref PubMed Scopus (4412) Google Scholar), who had undergone a transvaginal ultrasound and endometrial biopsy with sufficient tissue for diagnosis from January 2000 to April 2006 at the Reproductive Endocrinology Clinic at the University of Cincinnati. Physicians performed the biopsy using the Pipelle curette (Cooper-Surgical) for the following clinical indications: sonographic endometrial stripe (ES) thickness of ≥9 mm (based on nonpublished internal observations of endometrial hyperplasia at this threshold), patient history of irregular bleeding, or >12 months of amenorrhea. The primary aim of this study was to determine clinical and screening characteristics associated with benign vs. hyperplasia/adenocarcinoma histology. Benign histology included proliferative, secretory, and disordered proliferative. Continuous variables were analyzed using Student’s t test and categoric variables with Fisher’s exact test. Linear regression was used to determine the effect of body mass index (BMI) on ES, whereas logistic regression predicted effects of BMI and ES on hyperplasia/adenocarcinoma. A receiver operating characteristic (ROC) curve was then constructed for ES and hyperplasia/adenocarcinoma. A stepwise discriminant analysis was used to identify the prediction equation that would allow for the largest separation of the hyperplasia vs. nonhyperplasia groups. Cases were categorized into these groups on the basis of their clustering around the centroid, or multivariate equivalent of the mean. Significance was assessed at two-tailed P<.05 (SPSS 17). Thirty-three women having a first-time biopsy with documented ES measurement by ultrasound were included. Hyperplasia was noted in 10 of 33, indicating 30% hyperplasia prevalence. Of those 10, 6 patients had simple hyperplasia without atypia, 2 complex without atypia, 2 complex with atypia, and none adenocarcinoma. Hyperplasia patients were treated with 12 weeks of either oral contraceptives or daily norethindrone acetate, followed by repeat biopsy. Four of 10 were lost to follow-up having simple (2Hardiman P. Pillay O.C. Atiomo W. Polycystic ovary syndrome and endometrial carcinoma.Lancet. 2003; 361: 1810-1812Abstract Full Text Full Text PDF PubMed Scopus (292) Google Scholar), complex without (1Elliott J.L. Hosford S.L. Demopoulos R.I. Perloe M. Sills E.S. Endometrial adenocarcinoma and polycystic ovary syndrome: risk factors, management, and prognosis.South Med J. 2001; 94: 529-531PubMed Google Scholar), and complex with atypical (1Elliott J.L. Hosford S.L. Demopoulos R.I. Perloe M. Sills E.S. Endometrial adenocarcinoma and polycystic ovary syndrome: risk factors, management, and prognosis.South Med J. 2001; 94: 529-531PubMed Google Scholar) hyperplasia. Second biopsies were negative for hyperplasia in 5 of 6 women and complex without atypia in 1, who went on to have a third biopsy showing adenocarcinoma. Because of the low frequency of complex histologies and lack of hyperplasia on second biopsies, statistics were performed only for first biopsies, and analyses did not separate the hyperplasia histologies. The 33 women were mostly Caucasian, with mean ± SD age of 30.1 ± 5.4 years, gravida 1, nulliparous, and experienced 3.9 ± 4.0 months between menses. Serum total T was 66.8 ± 37.9 ng/dL and DHEAS 151.0 ± 86.3 μg/dL. Hirsutism was present in 71%, acne in 17%, and sonographic evidence of polycystic ovaries in 88%. Patients with hyperplasia (n = 10) and nonhyperplasia (n = 23) were not significantly different in terms of age, gravidity, parity, number of months between menses, sonographic polycystic ovary morphology, hirsutism, oligomenorrhea, blood pressure, or serum levels of androgens, TSH, PRL, or FSH. No differences were noted with use of combined oral contraceptives, progestins, or insulin sensitizers. Fewer than five patients with hyperplasia had a history of diabetes, hypertension, tobacco use, alcohol use, endometriosis, hypothyroidism, depression, or asthma, so these variables were not statistically evaluated. Patients with hyperplasia had significantly higher BMI compared with those without (44.9 ± 7.3 vs. 36.5 ± 6.6 kg/m2, respectively, P=.007). Endometrial stripe was also thicker in hyperplasia (14.7 ± 5.8 mm; range, 9.4–30.2 mm) vs. nonhyperplasia (9.3 ± 4.1 mm; range, 2.2–17.2 mm) (P=.005). Linear regression indicated that for every 1 unit increase in BMI, ES increased by 0.52 mm (P=.007). Forward stepwise logistic regression modeling dropped BMI and indicated that for every 1-mm increase in ES, the odds ratio of hyperplasia increased by 1.48 (95% confidence interval, 1.04–2.10). Area under the curve using ROC analysis was 0.81 (95% confidence interval, 0.67–0.97); ES of ≥9.35 mm had 100% sensitivity and 56% specificity for hyperplasia (Fig. 1). This cutoff was the lower limit of the ES range described above for hyperplasia. For the stepwise discriminant analysis, group classification was determined from the identified prediction equation (predicted hyperplasia = 2.13 × ES − 2.329). The discriminant function was statistically significant (Wilkes λ = 0.770, P<.006). Sensitivity (82%) and specificity (53%) were consistent across the initial analysis and the cross-validation (sensitivity 82%, specificity 47%) analyses. On the basis of the group centroids (hyperplasia group 0.803; nonhyperplasia group −0.349), cases were classified into a predicted group. The ES value of 12 mm was the point at which cases were classified into the hyperplasia group, indicating that misclassification accounts for the low specificity noted in this study. The calculated positive and negative predictive values for an ES cutoff of 9.35 mm were 50% and 100%, respectively. In the United States endometrial cancer is the most common malignancy of female reproductive organs, and 12% of cases are diagnosed in women aged <50 years (7Soliman P.T. Oh J.C. Schmeler K.M. Sun C.C. Slomovitz B.M. Gershenson D.M. et al.Risk factors for young premenopausal women with endometrial cancer.Obstet Gynecol. 2005; 105: 575-580Crossref PubMed Scopus (258) Google Scholar). Risks of cancer include irregular cycles, hypertension, polycystic ovaries, obesity, nulliparity, and diabetes (5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar, 7Soliman P.T. Oh J.C. Schmeler K.M. Sun C.C. Slomovitz B.M. Gershenson D.M. et al.Risk factors for young premenopausal women with endometrial cancer.Obstet Gynecol. 2005; 105: 575-580Crossref PubMed Scopus (258) Google Scholar, 8Pillay O.C. Te Fong L.F. Crow J.C. Benjamin E. Mould T. Atiomo W. et al.The association between polycystic ovaries and endometrial cancer.Hum Reprod. 2006; 21: 924-929Crossref PubMed Scopus (101) Google Scholar). It is hypothesized that chronic inflammation such as that observed with unopposed estrogens, anovulation, and PCOS may be involved in the pathogenesis of endometrial cancer (9Modugno F. Ness R.B. Chen C. Weiss N.S. Inflammation and endometrial cancer: a hypothesis.Cancer Epidemiol Biomarkers Prev. 2005; 14: 2840-2847Crossref PubMed Scopus (197) Google Scholar). Endometrial hyperplasia may precede or occur concurrently with carcinoma (5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar, 10Lacey Jr., J.V. Sherman M.E. Rush B.B. Ronnett B.M. Ioffe O.B. Duggan M.A. et al.Absolute risk of endometrial carcinoma during 20-year follow-up among women with endometrial hyperplasia.J Clin Oncol. 2010; 28: 788-792Crossref PubMed Scopus (168) Google Scholar). Our sample of young premenopausal obese patients with PCOS had a 30% rate of endometrial hyperplasia by biopsy, within the reported range of 12%–49% (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar, 4Peri N. Levine D. Sonographic evaluation of the endometrium in patients with a history or an appearance of polycystic ovarian syndrome.J Ultrasound Med. 2007; 26: 55-58PubMed Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). Consistent with others, we noted that simple hyperplasia predominates, but complex and atypical histologies do occur (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar, 4Peri N. Levine D. Sonographic evaluation of the endometrium in patients with a history or an appearance of polycystic ovarian syndrome.J Ultrasound Med. 2007; 26: 55-58PubMed Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). Atypia obviously raises the most concern, with 27.5% risk of progression to carcinoma over 20 years (10Lacey Jr., J.V. Sherman M.E. Rush B.B. Ronnett B.M. Ioffe O.B. Duggan M.A. et al.Absolute risk of endometrial carcinoma during 20-year follow-up among women with endometrial hyperplasia.J Clin Oncol. 2010; 28: 788-792Crossref PubMed Scopus (168) Google Scholar). However, 4.6% of nonatypical hyperplasia progress to carcinoma, which is three times higher than in the general population (10Lacey Jr., J.V. Sherman M.E. Rush B.B. Ronnett B.M. Ioffe O.B. Duggan M.A. et al.Absolute risk of endometrial carcinoma during 20-year follow-up among women with endometrial hyperplasia.J Clin Oncol. 2010; 28: 788-792Crossref PubMed Scopus (168) Google Scholar). We found that hyperplasia was associated with more severe obesity than nonhyperplasia, but BMI was not predictive of histology, which echoed other reports (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). Similar to prior studies, we also did not find hyperplasia to be associated with age, hormonal contraceptive use, blood pressure, or parity (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). Our study did not indicate an association with intermenstrual interval and hyperplasia, but prior studies with longer durations of amenorrhea show conflicting results (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). Polycystic ovary syndrome is an independent risk factor for ES thickening (11Iatrakis G. Tsionis C. Adonakis G. Stoikidou M. Anthouli-Anagnostopoulou F. Parava M. et al.Polycystic ovarian syndrome, insulin resistance and thickness of the endometrium.Eur J Obstet Gynecol Reprod Biol. 2006; 127: 218-221Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar). We found that BMI also was a predictor of ES, in contrast to others (11Iatrakis G. Tsionis C. Adonakis G. Stoikidou M. Anthouli-Anagnostopoulou F. Parava M. et al.Polycystic ovarian syndrome, insulin resistance and thickness of the endometrium.Eur J Obstet Gynecol Reprod Biol. 2006; 127: 218-221Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar). Insulin resistance has also been reported as an independent risk factor for thickened ES (11Iatrakis G. Tsionis C. Adonakis G. Stoikidou M. Anthouli-Anagnostopoulou F. Parava M. et al.Polycystic ovarian syndrome, insulin resistance and thickness of the endometrium.Eur J Obstet Gynecol Reprod Biol. 2006; 127: 218-221Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar), but we found no effect of insulin sensitizer use. In our study, only ES thickness was predictive of hyperplasia, with prior studies conflicting as to ES usefulness in patients with PCOS (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). We found that for every 1-mm increase in ES, the odds ratio of hyperplasia increased by 1.48. Previously, 7 mm was suggested as a cutoff with 100% sensitivity and 27.8% specificity for hyperplasia in patients with PCOS (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar). We found that a higher cutoff of 9.35 mm in patients with PCOS had comparable sensitivity (100%), negative predictive value (100%), and positive predictive value (50%) but superior specificity (56%). Selection bias is a notable limitation. Setting an a priori cutoff of 9 mm in this retrospective study limits extrapolation of the ROC curve for lower cutoffs. Our study was somewhat smaller than but comparable in design to a previous report (3Cheung A.P. Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.Obstet Gynecol. 2001; 98: 325-331Crossref PubMed Scopus (80) Google Scholar), but a bigger sample would have allowed analysis for specific hyperplasia histologies, follow-up biopsies, and influence of tobacco and alcohol use. We also did not evaluate endometrial pattern or echogenicity, but the impact of these is controversial (4Peri N. Levine D. Sonographic evaluation of the endometrium in patients with a history or an appearance of polycystic ovarian syndrome.J Ultrasound Med. 2007; 26: 55-58PubMed Google Scholar, 5Tingthanatikul Y. Choktanasiri W. Rochanawutanon M. Weerakeit S. Prevalence and clinical predictors of endometrial hyperplasia in anovulatory women presenting with amenorrhea.Gynecol Endocrinol. 2006; 22: 101-105Crossref PubMed Scopus (24) Google Scholar). Although most of our sample was hyperandrogenic and anovulatory, we did not specifically analyze different PCOS phenotypes (6Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop GroupRevised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS).Hum Reprod. 2004; 19: 41-47Crossref PubMed Scopus (4412) Google Scholar), which may have affected the results (7Soliman P.T. Oh J.C. Schmeler K.M. Sun C.C. Slomovitz B.M. Gershenson D.M. et al.Risk factors for young premenopausal women with endometrial cancer.Obstet Gynecol. 2005; 105: 575-580Crossref PubMed Scopus (258) Google Scholar). The findings also may not be valid in nonobese, non-Caucasian populations. It is also possible that blind Pipelle sampling may have missed pathology within a polyp, although the detection rate of overall pathologies in premenopausal women is nearly 95% compared with hysterectomy (12Ozdemir S. Celik C. Gezginc K. Kiresi D. Esen H. Evaluation of endometrial thickness with transvaginal ultrasonography and histopathology in premenopausal women with abnormal vaginal bleeding.Arch Gynecol Obstet. 2009; 282: 395-399Crossref PubMed Scopus (24) Google Scholar). Our reported specificity is an improvement from prior investigators, but certainly a future objective would be identifying a constellation of factors that would further improve specificity and decrease the chance of unnecessary biopsies. In conclusion, we suggest routine ultrasound screening with biopsy at an ES of 9.35 mm to detect endometrial hyperplasia in obese patients with PCOS." @default.
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• W2006243555 title "Endometrial thickness predicts endometrial hyperplasia in patients with polycystic ovary syndrome" @default.
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