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PubMed2000

Problems in the differential diagnosis of endometrial hyperplasia and carcinoma.

The differential diagnosis of endometrial hyperplasia and well-differentiated endometrioid adenocarcinoma is complicated not only by the resemblance of these lesions to each other, but also by their tendency to be overdiagnosed (particularly hyperplasia) on the background of polyps, endometritis, artifacts, and even normally cycling endometrium. Atypical hyperplasia may also be overdiagnosed when epithelial metaplastic changes occur in simple or complex hyperplasia without atypia. Low-grade adenocarcinomas are best recognized by architectural evidence of stromal invasion, usually in the form of stromal disappearance, desmoplasia, necrosis, or combinations of these findings between adjacent glands. Endometrioid adenocarcinomas are usually Type 1 cancers associated with manifestations of endogenous or exogenous hyperestrogenic stimulation and a favorable prognosis. Subtypes include adenocarcinomas with squamous differentiation and secretory, ciliated cell and villoglandular variants. Rules and pitfalls in the grading of endometrioid adenocarcinomas and the estimation and reporting of myometrial invasion are presented.

Carcinoma, Endometrioid↗
PubMed1994

Incidence of endometrial hyperplasia in postmenopausal women taking conjugated estrogens (Premarin) with medroxyprogesterone acetate or conjugated estrogens alone. The Menopause Study Group.

OBJECTIVE: We evaluated four oral combinations of conjugated estrogens (Premarin) and medroxyprogesterone acetate in preventing endometrial hyperplasia, which can occur with conjugated estrogens alone. STUDY DESIGN: This was a 1-year prospective, double-blind, randomized, multicenter study in 1724 postmenopausal women. All five groups took conjugated estrogens (0.625 mg) daily. The respective medroxyprogesterone acetate dosages were 2.5 and 5.0 mg daily (groups A and B) and 5.0 and 10.0 mg for 14 days per 28-day cycle (groups C and D). RESULTS: Among the 1385 patients with valid biopsy data, endometrial hyperplasia developed in 20% in the conjugated estrogens-treated group and < or = 1% in each of the four conjugated estrogens/medroxyprogesterone acetate-treated groups. The incidence of endometrial hyperplasia did not differ significantly between any of the conjugated estrogens/medroxyprogesterone acetate regimens. However, none of the patients receiving the two higher medroxyprogesterone acetate dosages (groups B and D) had endometrial hyperplasia. CONCLUSION: The endometrial hyperplasia incidence was significantly lower in women treated with conjugated estrogens and medroxyprogesterone acetate than in women treated with conjugated estrogens alone.

Aged↗
PubMed1989

[Endometrial hyperplasia in the province of Trieste].

1103 cases of endometrial hyperplasia were diagnosed between January 1, 1978 and December 31, 1987 at the Department of Anatomy and Pathological Histology of the University of Trieste. Of these, 58% were cases of cystic glandular hyperplasia, 38% of adenomatous hyperplasia and 4% of atypical hyperplasia. Subdividing the period examined into two five-year periods, it was found that the rate of incidence of endometrial hyperplasias was more than doubled, this increase having been caused above all by cases of cystic hyperplasia. Distribution by age classes of subjects suffering from different hyperplastic forms suggests that cystic glandular hyperplasia is not a precursor of the adenomatous form, whereas the latter and atypical hyperplasia might constitute a continuous spectrum of potentially precancerous lesions.

Adolescent↗
PubMed2005

Histopathologic behavior of endometrial hyperplasia during tamoxifen therapy for breast cancer.

OBJECTIVE: The purpose of the present study is to prospectively evaluate the effects of tamoxifen on the pathological behavior of endometrial hyperplasias without atypia, diagnosed before the start of adjuvant endocrine therapy, in menopausal patients suffering from breast cancer. METHODS: Twenty-six patients suffering from estrogen-receptor positive breast cancer and candidate to receive adjuvant tamoxifen, were found to be affected by endometrial hyperplasias before the start of endocrine therapy. All women showed a baseline endometrial stripe, measured by transvaginal ultrasonography, thicker than 4 mm and the diagnosis of endometrial hyperplasia was made by hysteroscopy and endometrial biopsy. Two patients showing complex atypical hyperplasia underwent vaginal hysterectomy, whereas the remaining 24 patients, suffering from endometrial hyperplasia without atypia, were followed on a yearly basis during the period of tamoxifen intake, by hysteroscopy and endometrial biopsy. RESULTS: Baseline histopathology showed simple and complex hyperplasia in 20 and in 4 patients, respectively. The median follow-up period was 38 months; in particular, all patients underwent endometrial assessment after 12 months, while 22, 16, 10 and 4 patients were followed-up after 24, 36, 48 and 60 months of tamoxifen therapy, respectively. Progression from complex hyperplasia to complex atypical hyperplasia (1 patient) and from complex and simple hyperplasia to adenocarcinomas (2 patients) was found within 24 months of tamoxifen intake in 3 patients (12.5%). In 2 patients (8.3%), a progression from simple to complex hyperplasia was detected within 36 months of tamoxifen treatment. In 13 patients (54.1%), stable histology of simple or complex hyperplasia was found, whereas 6 patients (25.0%), with focal hyperplasia harbored in an endometrial polyp, showed a normalization of endometrial histology after polyp resection. CONCLUSIONS: Endometrial hyperplasias without atypia diagnosed before endocrine therapy for breast cancer in menopausal patients show an early and high progression-rate to atypical lesions under tamoxifen influence.

Antineoplastic Agents, Hormonal↗
PubMed1995

Morphologic hysteroscopic criteria suggestive of endometrial hyperplasia.

OBJECTIVES: To evaluate the morphologic hysteroscopic criteria leading to a diagnosis of endometrial hyperplasia and compare their accuracy with that of histology. METHODS: A total of 95 hysteroscopic examinations were evaluated. Of these, 37 had a histologic diagnosis of normal endometrium and the remaining 58 of simple or complex endometrial hyperplasia. We compared the morphologic hysteroscopic criteria for the two groups using Pearson's chi-squared and Fisher's exact test. RESULTS: Only the presence of endometrial glands presenting a cystic pattern at hysteroscopy gave statistically significant results (P < 0.05), with low sensitivity (15.79%), high specificity (97.29%) and a relative risk of 6.75. With a prevalence of endometrial hyperplasia of 22.97% in a population of women with metrorrhagia, the positive predictive value was 63.53% and the negative predictive value was 79.40%. CONCLUSION: Additional, prospective studies are needed to determine the real value of the diagnostic morphologic parameters under consideration.

Adult↗
PubMed2003

Treatment of atypical endometrial hyperplasia with an insulin-sensitizing agent.

Endometrial cancer and hyperplasia have long been associated with diabetes. Hyperinsulinemia may have a direct mitogenic effect on the endometrium and may inhibit the effect of progestogen therapy. This case report describes the treatment of a patient with atypical endometrial hyperplasia with an insulin-sensitizing agent. A 37-year-old patient presented after failed treatment of endometrial hyperplasia with progestogen therapy. One month after initiating metformin therapy the patient's endometrial biopsy demonstrated proliferative endometrium. This patient's atypical endometrial hyperplasia regressed after the initiation of treatment with an insulin-sensitizing agent. This relatively new class of drugs may provide an adjunct to the therapy of endometrial hyperplasia.

Administration, Oral↗
PubMed2002

Atypical complex endometrial hyperplasia treated with the GyneLase system.

A 47-year-old premenopausal, para 1, gravida 1 woman complained of menometrorrhagia. She had no risk factors for endometrial hyperplasia or cancer, and office endometrial biopsy indicated focal, nonatypical endometrial hyperplasia. Seven months later the patient was scheduled for hysteroscopic endometrial resection. Instead she was treated by hysteroscopy, curettage, and the GyneLase system. The curetting indicated atypical, complex endometrial hyperplasia. The woman refused hysterectomy and salpingo-oophorectomy and adjunctive therapy with progesterone. She agreed to close surveillance and further treatment if she had any vaginal bleeding. At 13 months she remains amenorrheic, the endometrial echo is 2 mm, and follicle-stimulating hormone level is 63 IU/L. Based on the patient's amenorrhea and ultrasound uterine measurement, it is tempting to assume that GyneLase treatment may have cured her atypical hyperplasia. However, at this time, we have no evidence to substantiate this assumption.

Curettage↗
PubMed2000

Hormone replacement therapy in postmenopausal women: endometrial hyperplasia and irregular bleeding.

BACKGROUND: The decline in circulating oestrogen around the time of the menopause often induces unacceptable symptoms that affect the health and well being of women. Hormone replacement therapy (both unopposed oestrogen and oestrogen and progestogen combinations) is an effective treatment for these symptoms. In women with an intact uterus, unopposed oestrogen may induce endometrial stimulation and increase the risk of endometrial hyperplasia and carcinoma. The addition of progestogen reduces this risk but may cause unacceptable symptoms, bleeding and spotting which can affect adherence to therapy. OBJECTIVES: The objective of this review is to assess which hormone replacement therapy regimens provide effective protection against the development of endometrial hyperplasia and/or carcinoma with a low rate of abnormal vaginal bleeding. SEARCH STRATEGY: Electronic searches for relevant randomised controlled trials of the Cochrane Menstrual Disorders and Subfertility Group Register of Trials, MEDLINE, EMBASE, PsychLIT, Current Contents, Biological Abstracts, Social Sciences Index and CINAHL were performed. Attempts were also made to identify trials from citation lists of review articles and drug companies were contacted for unpublished data. In most cases, the corresponding author of each included trial was contacted for additional information. SELECTION CRITERIA: The inclusion criteria were randomised comparisons of unopposed oestrogen therapy, combined continuous oestrogen-progestogen therapy and sequential oestrogen-progestogen therapy with each other and placebo administered over a minimum treatment period of six months. Trials had to assess which regimen was the most protective against the development of endometrial hyperplasia/carcinoma and/or caused the lowest rate of irregular bleeding. DATA COLLECTION AND ANALYSIS: Twenty three RCTs were identified and five were excluded. The reviewers assessed the eighteen included studies for quality, extracted the data independently and odds ratios for dichotomous outcomes were estimated. Outcomes analysed included frequency of endometrial hyperplasia or carcinoma, frequency of irregular bleeding and unscheduled biopsies or dilation and curettage, and adherence to therapy. MAIN RESULTS: Unopposed moderate or high dose oestrogen therapy was associated with a significant increase in rates of endometrial hyperplasia with increasing rates at longer duration of treatment and follow up. Odds ratios ranged from 5.4 (1. 4-20.9) for 6 months of treatment to 16.0 (9.3-27.5) for 36 months of treatment with moderate dose oestrogen (in the PEPI trial, 62% of those who took moderate dose oestrogen had some form of hyperplasia at 36 months compared to 2% of those who took placebo). Irregular bleeding and non adherence to treatment were also significantly more likely under these unopposed oestrogen regimens with greater effects with higher dose therapy. There was no evidence of increased hyperplasia rates, however, with low dose oestrogen. The addition of progestogens, either in continuous combined or sequential regimens, helped to prevent the development of endometrial hyperplasia and improved adherence to therapy (odds ratios of 3.7 for sequential therapy and 6.0 for continuous therapy). Irregular bleeding, however, was more likely under a continuous than a sequential oestrogen-progestogen regimen (OR = 2.3, 95% CI 2.1-2.5) but at longer duration of treatment, continuous therapy was more protective than sequential therapy in preventing endometrial hyperplasia (OR = 0.3, 95% CI 0.1-0.97). There was evidence of a higher incidence of hyperplasia under long cycle sequential therapy (progestogen given every 3 months) compared to monthly sequential therapy (progestogen given every month). No increase in endometrial cancer was seen in any of the treatment groups during the limited duration (maximum of 3 years) of these trials. (ABSTRACT TRUNCATED)

Endometrial Hyperplasia↗
PubMed1983

Endometrial hyperplasia and neoplasia. Cytologic screening with the Endopap endometrial sampler.

A new endometrial sampling device, the Endopap, was tested in a series of 851 patients. This sampler is of simple design, without moving parts, inexpensive and easy to use. Cellular samples proved adequate in 90% of the cases, usually with very abundant material. Endometrial cancer shed atypical cells in all 20 cases studied. However, only about half the patients with adenomatous hyperplasia were correctly identified by the endometrial sample. This fact seems to reflect the lack of adequate morphologic criteria for the recognition of endometrial hyperplasia; this situation prevails with all types of endometrial cell samplers.

Adenocarcinoma↗
PubMed1996

Use of computerized morphometric analyses of endometrial hyperplasias in the prediction of coexistent cancer.

OBJECTIVE: Our purpose was to determine whether computerized morphometric analysis is predictive of coexistent cancer in uteri that show endometrial hyperplasia in curettings or biopsy specimens. STUDY DESIGN: Forty-five patients with endometrial hyperplasia and 10 patients with well-differentiated cancers diagnosed from curettings or biopsy specimens and treated by hysterectomy at Thomas Jefferson University Hospital between 1989 and 1993 were identified from the pathology department archives. Curettings were analyzed by computerized morphometric analysis at the Free University Hospital in Amsterdam. Pathologists performing the morphometric analyses were blinded to the pathologic diagnoses obtained by examining the hysterectomy specimens. The histopathologic classification of the hysterectomy specimens were used as the end point. RESULTS: Twelve of 45 patients with endometrial hyperplasia (26.7%) by preoperative histopathologic classification showed coexistent carcinoma at hysterectomy. All instances of carcinoma occurred in patients with atypical hyperplasia. Sensitivity of morphometric analysis to predict carcinoma was 100%, with a specificity of 88.5%. The positive predictive value was 83.3%, and the negative predictive value was 100%. A blinded reanalysis of the quantitative analysis in 16 patients showed good reproducibility of this technique (r = 0.93). CONCLUSIONS: Morphometric analysis is useful for predicting which patients with endometrial hyperplasia have coexistent carcinomas. Computerized morphometric analysis may be useful in therapeutic decision making for complex atypical hyperplasia.

Aged↗
PubMed1986

Risk factors for adenomatous endometrial hyperplasia: a case-control study.

A population-based case-control study of histologically confirmed endometrial neoplasia was conducted in Toronto, Canada, between 1977 and 1978. Pathologic slide review resulted in classification of patients to diagnostic categories of endometrial carcinoma, endometrial carcinoma in situ, and endometrial hyperplasia. This report concerns the subset of patients classified as having adenomatous endometrial hyperplasia. Two age-matched neighborhood controls were selected for each case, and analyses included only those case-control sets in which the case and at least one control were concordant on menopausal status. Among postmenopausal women (87 cases and 151 controls), noncontraceptive estrogen use was a statistically significant risk factor (adjusted odds ratio (OR) = 6.7), as was heavy body weight relative to height (Quetelet index) (adjusted OR = 3.2). Long-term (5+ years) estrogen use conferred an estimated relative risk of more than 20, but use of oral contraceptives did not alter risk significantly. Among premenopausal women (62 cases and 97 controls), a high Quetelet index appeared to be a significant protective factor, even when adjusted for oral contraceptive use (adjusted OR = 0.2). While oral contraceptive use was not associated with a change in risk, long duration of use was highly, but statistically not significantly, protective against hyperplasia. The data for pre- and postmenopausal women indicate that both endogenous and exogenous estrogen exposure are important factors in the etiology of adenomatous endometrial hyperplasia.

Adult↗
PubMedDate not supplied

Spontaneous endometrial hyperplasia. A 5 year follow-up of 82 patients after high-dose gestagen treatment.

Endometrial hyperplasia was proposed as a predecessor to endometrial carcinoma already at the end of the 19th century. However, there have been different opinions regarding this view. The treatment also varies, but generally cyclic progesterone at a dose of 10 mg a day is used. In order to investigate whether endometrial hyperplasia is a premalignant state and also whether a high-dose gestagen treatment would cure a high proportion of these patients, a prospective randomised study was started in 1982. We now present the 5 year follow-up consisting of 82 patients treated with high-dose gestagen. In this study 19 out of 82 patients had hysterectomies (2 due to hyperplasia and 11 due to bleeding), almost the same frequency as in a previous report with patients followed-up with abrasio only, but now mainly due to bleeding problems. In summary, no carcinoma developed and the hyperplasia was cured with 500 mg MPA i.m. twice weekly for three months. However, the bleeding problems, though almost always only spotting, remained, leading to a frequency of hysterectomy that was still too high. We find latter clinical problem an enigma. Further studies are therefore in progress in our group which try to identify other treatment modalities for those patients with bleeding problems or who redeveloped hyperplasia after abrasio, in order to avoid hysterectomies.

Atrophy↗
PubMedDate not supplied

Soy protein isolate with isoflavones does not prevent estradiol-induced endometrial hyperplasia in postmenopausal women: a pilot trial.

OBJECTIVE: To test the hypothesis that soy protein isolate (SPI) with isoflavones opposes the proliferative effects of exogenous estradiol (E2) on the endometrium after menopause. DESIGN: Thirty-nine postmenopausal women were randomized to receive daily for 6 months either 0.5 mg E2 + placebo, 1.0 mg E2 + placebo, 0.5 mg E2 + 25 g SPI with 120 mg isoflavones, or 1.0 mg E2 + 25 g SPI with 120 mg isoflavones. Primary outcome measures were endometrial histology, ultrasound endometrial thickness, and Ki67 staining quantification, a marker of cellular proliferation. Secondary outcome measures were serum lipids and markers of bone resorption. RESULTS: Endometrial hyperplasia, endometrial stromal and epithelial cellular proliferation, and sonographically measured endometrial thickness were similarly affected in all groups. SPI did not lessen the beneficial effects of E2 on lipids and markers of bone resorption. CONCLUSION: In this pilot study, SPI with isoflavones did not protect the endometrium from E2-induced hyperplasia in postmenopausal women. If higher, long-term doses of isoflavone supplementation are found to be safe for postmenopausal women, then future studies combining E2 with isoflavones may be feasible as an alternative to traditional hormone replacement therapy.

Bone Remodeling↗
PubMedDate not supplied

Loss of heterozygosity alterations associated with progesterone therapy in endometrial hyperplasia and adenocarcinoma.

Loss of heterozygosity (LOH) was analyzed in four patients with endometrial hyperplasia (EH) with atypia (two patients) and without atypia (two patients) and in five patients with endometrial adenocarcinoma (EAC) to clarify the clinicopathologic relationship between genetic alterations and hormone therapy. Each patient was initially administered high-dose medroxyprogesterone acetate (MPA) as a uterine-sparing treatment. The five microsatellite markers used to analyze LOH were at chromosomal loci 8p22.1, 8p21, 8p21.3, 8p22, and 8p22. DNA was extracted from paraffin-embedded sections before, during, and after MPA therapy using laser capture microdissection. As a result, LOH was more frequently detected after MPA therapy (overall ratios were 16, 17, and 29% before, during, and after MPA therapy, respectively). LOH is more easily detected in EH loci than in EAC loci before MPA. For EAC, initial LOH detection on chromosome 8 may be related to an incomplete response to MPA, but negative LOH does not guarantee a favorable treatment outcome. For EH or atypical endometrial hyperplasia, it is unknown whether LOH alteration associated with MPA therapy is related to atypia of the disease.

Adenocarcinoma↗
PubMed2000

Apoptosis may be an early event of progestin therapy for endometrial hyperplasia.

OBJECTIVE: The aim of this study was to investigate the role of apoptosis during progestin therapy for the treatment of endometrial hyperplasia. METHODS: Pre- and posttreatment paraffin-embedded endometrial tissue samples from 19 women with endometrial hyperplasia were examined for changes in glandular cellularity and apoptotic activity related to the administration of progestins. Twelve patients were successfully treated with progestin therapy and 7 patients failed treatment. Glandular cellularity was assessed based on calculating the average number of cells per gland obtained on histologic examination of hematoxylin and eosin stained tissue sections. Apoptotic activity was assessed on the same tissue sections by counting the average number of apoptotic cells per 10 high power fields (hpf) using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The effects of progesterone on apoptotic activity in a low-grade endometrial adenocarcinoma cell line (Ishikawa cells) was also examined using an ELISA cell death detection kit. RESULTS: Glandular cellularity significantly decreased with progestin therapy in both treatment outcome groups. The reduction in cells per gland was significantly greater in the group of successfully treated cases compared to the treatment failures (P = 0.005). However, within the successfully treated group, in situ detection of apoptotic cells using the TUNEL assay showed no statistical difference between pre- and posttreatment endometrial samples. Interestingly, a significant decrease in apoptosis was found in posttreatment samples of the group with persistent hyperplasia. The average number of apoptotic cells detected in 10 hpf was reduced from 7.9 prior to treatment to 3.1 after progestin therapy (P = 0.03). In the progesterone-treated Ishikawa cell line, an increase in apoptotic activity started at 24 h, reached a peak at 48 h, and continued up to 72 h of hormone treatment. At 48 h, apoptotic activity was 42.6% greater than in the untreated control (P = 0.04). By 72 h of progesterone treatment, apoptosis was 37.2% greater in the treated cells compared to the noninoculated cells (P = 0.04). CONCLUSIONS: Progestin-induced apoptosis may occur during the early period of treatment for endometrial hyperplasia. Compared to the fully responsive group, persistent endometrial hyperplasia may have intrinsically different molecular mechanisms in response to progestin therapy.

Adult↗
PubMed2005

Aromatase inhibitor anastrozole for treating endometrial hyperplasia in obese postmenopausal women.

This is a preliminary study investigating the efficacy of aromatase inhibitor anastrozole in treating endometrial hyperplasia in obese postmenopausal women. We administered anastrozole for 12 months to 11 obese postmenopausal women with high operative risk, in order to treat endometrial hyperplasia (four simple, five complex and two atypical). Endometrial thickness in all cases and histology too in the two cases with atypia, revealed atrophical endometrium during treatment and additional mean follow-up of 10.2 months. The safety and tolerance profile was satisfactory. Anastrozole appears to be an interesting new modality for the treatment of endometrial hyperplasia in obese postmenopausal women.

Aged↗
PubMed2004

Coexisting endometrial cancer in patients with a preoperative diagnosis of atypical endometrial hyperplasia.

AIM: To investigate the possibility of coexisting endometrial cancer (EC) in patients with atypical endometrial hyperplasia (AEH). METHODS: Forty-six consecutive women who underwent hysterectomy for AEH were analyzed. RESULTS: Final histopathological evaluation of hysterectomy specimens revealed EC in 11 patients (23.9%). Preoperative diagnosis of AEH was established by pipelle biopsy in eight patients and curettage was performed in the remaining patients. Of the patients with pipelle biopsy, two had a diagnosis of EC (25%), whereas nine women who underwent curettage, were further diagnosed as having EC (23.7%) (P > 0.05). Four (13.3%) of 30 women who had frozen sections at hysterectomy, were diagnosed with EC. Diagnosis of EC was missed in two patients (50%) at frozen section. In contrast, seven of 16 women (43.7%) who did not have frozen section, had EC. CONCLUSION: A relatively high incidence of EC is seen in patients with a diagnosis of AEH. Diagnostic results of pipelle biopsy and curettage were comparable. Frozen sections of hysterectomy specimens does not guarantee to exclude the possibility of EC, especially in patients with no myometrial invasion.

Biopsy↗
PubMedDate not supplied

Accuracy of hysteroscopic diagnosis of endometrial hyperplasia: a retrospective study of 323 patients.

STUDY OBJECTIVE: To evaluate the diagnostic accuracy of hysteroscopic view in endometrial hyperplasia. DESIGN: Retrospective study (Canadian Task Force classification II-2). SETTING: Public hospital in northern Italy. PATIENTS: Three hundred twenty-three patients suffering from endometrial hyperplasia out of 2251 women (1119 premenopausal and 1132 postmenopausal) who underwent office-based hysteroscopy from January 1996 through May 2004. INTERVENTION: Review of 2251 outpatient hysteroscopies carried out with 5- to 6-mm sheathed hysteroscopes and accomplished with blind or hysteroscopically targeted endometrial biopsies. MEASUREMENTS AND MAIN RESULTS: The pathologic report was considered the reference test. Hysteroscopic detection of focal or extensive endometrial thickening, irregular vascular network, architectural distortion and crowding of gland openings, and gland cyst formation were considered endoscopic features consistent with hyperplasia. Overall sensitivity, specificity, negative predictive values (NPV), and positive predictive values (PPV) of hysteroscopy in order to foresee a diagnosis of hyperplasia were calculated. These figures were calculated both in premenopausal and postmenopausal patients. Histopathology yielded a diagnosis of simple, complex, and atypical hyperplasia in 247, 51, and 25 patients, respectively. Hysteroscopy foresaw hyperplasia in 38.4% of patients with simple hyperplasia and in 58.9% of patients with complex or atypical hyperplasia. Normal hysteroscopic findings underestimated simple hyperplasia in 34 patients (13.7%) and complex or atypical hyperplasias in 1 patient (1.3%) (p <.01). To predict the diagnosis of hyperplasia, hysteroscopy showed an overall sensitivity, specificity, NPV, and PPV of 63.7%, 91.7%, 91.3%, and 64.7%, respectively. Among premenopausal patients, hyperplasia was diagnosed in 134 women (11.9%); in this group, hysteroscopy showed sensitivity, specificity, NPV, and PPV of 65.6%, 88.5%%, 93.5%, and 50.5%, respectively. In postmenopausal patients, we found endometrial hyperplasia in 189 women (16.6%); sensitivity, specificity, NPV, and PPV of hysteroscopic view to anticipate hyperplasia were 61.6%, 95.2%, 89.3%, and 79.4%, respectively. A significantly better PPV to foresee hyperplasia was found in postmenopausal women compared with premenopausal patients (p <.01). CONCLUSIONS: Current hysteroscopic criteria suggesting endometrial hyperplasia are inaccurate; in order to exclude hyperplasia, a pathologic assessment is warranted in all hysteroscopies showing an irregularly lined or thick endometrium.

Adult↗