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PubMed1994

Low-risk endometrial hyperplasia: hysteroscopy and histologic evaluation after treatment with LH-RH analogue.

Endometrial hyperplasia is an endometrial pathologic condition often found at perimenopausal age. Abnormal uterine bleeding (A.U.B.) is the most frequent symptom of endometrial hyperplasia. The combination of hysteroscopy and endometrial biopsy is the most suitable approach for the diagnosis of endometrial hyperplasia in symptomatic patients. We have studied endometrial modifications due to LHRH-analogue in 75 patients with AUB and with a hysteroscopic and histologic picture of low-risk endometrial hyperplasia. LHRH analogue is a valid treatment for all estrogen induced pathologies, because of its suppressive action on hypothalamic-hypophysary gonadotropins. The administration of LHRH for 4 months induced an improvement of the menstrual cycle within the first month of treatment in 53.3% of cases. At the end of treatment 100% of the patients were in amenorrhea. The hysteroscopic follow-up at 3 months showed an endometrial thinning with a tendency to hypoatrophy of the mucosa in 72% of cases. Three months after the end of treatment 20 patient had regular menstrual cycles and hysteroscopic and a histologic picture of normal endometrium. Only 30 patients had persistent amenorrhea with a consequent hysteroscopic and histologic picture of endometrial hypoatrophy. The use of LHRH analogue seems to have a great impact on the management of estrogen-dependent gynaecological benign diseases.

Adult↗

PubMed2003

Endometrial hyperplasia with secretory changes.

OBJECTIVE: Secretory changes in endometrial hyperplasia are uncommon. The aim of this study is to review the morphologic and clinical findings of 24 cases of endometrial hyperplasia with secretory changes. METHODS: In 24 patients diagnosed with endometrial hyperplasia with secretory changes during 6 years, clinical characteristics such as menopausal status and hormone treatment were correlated with morphological features. A matched age control group of 24 women with conventional endometrial hyperplasia was used to compare the hormonal effect. RESULTS: Nineteen patients were premenopausal. Nine women showed simple hyperplasia without atypia and 15 complex hyperplasia, 7 of them with atypia. Seventeen women were under hormonal treatment at the time of diagnosis, 10 of them with progestins. In 7 patients endometrial adenocarcinoma could be seen, 5 coexisting with endometrial hyperplasia with secretory changes and in 2 appearing after 1 and 4 months. In control group only 2 patients were undergoing progestin hormonal treatment. CONCLUSIONS: Secretory changes can be found in hyperplastic endometrium, particularly in premenopausal women under hormonal treatment with progestins, with the risk of misdiagnosis.

Adult↗

PubMedDate not supplied

Cancer history and loss of MSH2 and MLH1 protein expression in patients with endometrial hyperplasia.

In order to evaluate the hereditary background of endometrial hyperplasia patients in relation to protein expression of DNA mismatch repair genes, we evaluated 69 patients with endometrial hyperplasia and 18 patients with normal endometrium having both a personal and family history of cancer (two hereditary nonpolypoid colorectal cancer (HNPCC) patients). We obtained personal and family histories of cancer for all patients. MSH2 and MLH1 protein expression was investigated by immunohistochemical methods. In the endometrial hyperplasia patients, 11 had personal histories and 40 had family histories of cancer. Among the 11 endometrial hyperplasia patients with a personal history of cancer, most cancers were breast or colorectal cancers (82%). In the 40 patients with a family history of cancer, colorectal cancer (33%) was the most frequent. The incidence of loss of expression of MSH2 and/or MLH1 protein in endometrial hyperplasia patients with personal (64%) or family (40%) histories was significantly higher than that in patients without such history (no personal: 21% and no family: 10%; P = 0.0035 and 0.0065). No protein loss was detected in any of the cases with normal endometrium having either a personal or family history of cancer. Our results suggest that a portion of endometrial hyperplasia cases having a personal or family history of cancer may belong to HNPCC, and that in these cases, abnormality of the mismatch repair system may be an early event in endometrial carcinogenesis.

Adaptor Proteins, Signal Transducing↗

PubMed2001

Accuracy of outpatient endometrial biopsy in the diagnosis of endometrial hyperplasia.

BACKGROUND: To determine the accuracy of outpatient endometrial biopsy in diagnosing endometrial hyperplasia in women with abnormal uterine bleeding. DESIGN: Systematic quantitative review of published medical literature. DATA SOURCES: Relevant papers were identified through electronic scanning of MEDLINE (1980-1999) and EMBASE (1980-1999), manual searching of bibliography of known primary and review articles and contact with manufacturers. REVIEW METHODS: Studies were selected if accuracy of outpatient endometrial biopsy, in women with abnormal pre or postmenopausal uterine bleeding, was estimated compared to a reference standard, which was endometrial histology obtained by tissue sampling under anesthesia. Quality assessment and data extraction were performed in duplicate. Diagnostic accuracy was determined by pooled likelihood ratios (LR) for positive and negative test results for endometrial hyperplasia. RESULTS: There were 881 subjects in 8 diagnostic evaluations reported in 6 primary studies. Postmenopausal women represented 25% of the participants studied. There were 43 patients in whom outpatient sampling was inadequate. A positive test result on outpatient biopsy diagnosed endometrial hyperplasia with a pooled LR of 12.0 (95% CI 7.8-18.6) while a negative test result had a pooled LR of 0.2 (95% CI 0.1-0.3). With a positive test result, the posttest probability of endometrial hyperplasia was 57.7% (95% CI 41.1%-72.7%) while it was 2.2% (95% CI 0.9%-4.1%) with a negative test. CONCLUSION: Outpatient endometrial biopsy has modest accuracy in diagnosing endometrial hyperplasia. Therefore, additional endometrial assessment should be undertaken, especially if symptoms persist or intrauterine structural abnormalities are suspected.

Ambulatory Care↗

PubMed2002

[Endometrial hyperplasias resistant to progestins: alternatives to traditional treatments].

Endometrial hyperplasias are mainly regarded as a response to unopposed endogenous estrogenic stimulation and concern 12% of perimenopausal women. They are usually diagnosed because of irregular bleeding. They are divided into two categories based on the presence or absence of cytological atypia and further classified as simple or complex according to the extent of architectural abnormalities. Endometrial hyperplasias with cytological atypia are classically treated by hysterectomy. Endometrial hyperplasias without cytological atypia are classically treated by progestins. The bad observance (25% spontaneously stopping), the 30% recurrence rate after stopping progestin and the 12-53% resistance rate to treatment lead to propose a second-line therapy after endocrinological check-up, exploration of haemostasis, pelvic ultrasonography, hysteroscopy and endometrial biopsies. Standard treatments include uterine curettage which is not very effective and hysterectomy. Medical alternatives (gonadotropin-releasing hormone agonists, levonorgestrel-releasing intrauterine device) and surgical alternatives (endometrial resection, thermal balloon endometrial ablation) were developed to avoid treating functional pathology radically. These conservative procedures correct 80% of endometrial hyperplasia symptoms with a low rate of lateral effects. However, these results need to be confirmed by long-term studies. Some economical, legal or material factors can also limit carrying out the procedures. Clinical trials need to be performed to better define the place of medical and surgical alternatives to hysterectomy in the treatment of endometrial hyperplasias resistant to progestins.

Drug Resistance↗

PubMed2001

Optimal management of endometrial hyperplasia.

The optimal management of endometrial hyperplasia is the subject of considerable debate. In this chapter the development of our current classification of endometrial hyperplasias is outlined in some detail in order to give an understanding of the complexity of the problem of determining the malignant potential of the hyperplasia which is the central issue in determining optimal treatment. While hysterectomy is still the definitive treatment for older women with hyperplasia, conservative therapy is perfectly acceptable in a defined group of younger women who are closely monitored.

Contraceptives, Oral, Combined↗

PubMed2002

Clonal analysis and mutations in the PTEN and the K-ras genes in endometrial hyperplasia.

The patterns of X chromosome inactivation and mutations of PTEN and K-ras were evaluated in cases of endometrial hyperplasia to determine the presence of potentially premalignant neoplastic versus polyclonal benign cell populations. Endometrial glandular epithelial cells were collected by laser capture microdissection, and genomic DNAs were extracted. Following treatment with the methylation sensitive restriction endonuclease Hha I, polymerase chain reaction amplification was performed targeting a highly polymorphic short tandem repeat of the human androgen receptor gene (HUMARA). PTEN and K-ras gene mutations were evaluated by analysis of single-strand conformation polymorphism. Two pathologists performed histologic diagnosis of the lesions independently. Monoclonal composition was demonstrated in 13 of 15 (87%) endometrial hyperplasias with atypia and 17 of 31 (55%) complex hyperplasias without atypia. Cytological atypia is significantly associated with the clonal status of the endometrial hyperplasia (13/15 vs 17/31, P = 0.049). In contrast, all 14 normal endometrial tissue samples were polyclonal. PTEN gene mutations were detected in 4 of 13 (30%) monoclonal endometrial hyperplasias with atypia and 2 of 17 (12%) monoclonal endometrial hyperplasias without atypia but were not detected in polyclonal endometrial hyperplasias, with or without atypia. K-ras gene mutations were present in 3 of 13 (23%) monoclonal endometrial hyperplasias with atypia but not in 2 cases of polyclonal endometrial hyperplasia with atypia or in 26 cases of endometrial hyperplasia without atypia. K-ras mutation is thus significantly more frequently found in endometrial hyperplasias with atypia than those without atypia (3/15 vs 0/31, P = 0.030). This study indicates that most cases of endometrial hyperplasia with atypia and a high proportion of cases of endometrial hyperplasias without atypia originate from a single progenitor cell, possibly as a result of genetic alterations, rather than as a result of benign reactive processes.

Cell Transformation, Neoplastic↗

PubMed2004

Treatment of endometrial hyperplasia with a danazol-releasing intrauterine device: a prospective study.

The purpose of the present study was to assess the effect of a danazol-releasing intrauterine device (D-IUD) in the treatment of endometrial hyperplasia. Twenty patients with endometrial hyperplasia including 14 with simple endometrial hyperplasia and 2 with complex endometrial hyperplasia (group A), and 4 with atypical endometrial hyperplasia (group B) were enrolled in the prospective study between August 1999 and December 2003. During and just after the treatment, improvement was seen in all patients. Simple or complex endometrial hyperplasia (group A) demonstrated regression to a normal secretory endometrium (38% of group A), pseudodecidual stromal change (31%) and glandular atrophy (25%), and miscellaneous change (inflammation, necrosis, etc.) (38%). Atypical hyperplasia (group B) demonstrated regression to a normal secretory endometrium (25% of group B), pseudodecidual stromal change (75%), glandular atrophy (50%) and miscellaneous change (granulation) (25%). In group A, 2 women conceived after completion of the treatment. The recurrence rate in patients with endometrial hyperplasia (groups A and B) in the follow- up was 20% and acceptable as compared with other studies. The pretreatment menstrual interval patterns of the patients were maintained peri- and post-treatment. These data indicate that D-IUD therapy might be a novel and effective method for the treatment of endometrial hyperplasia.

Adult↗

PubMed2003

P53 expression in spontaneous and estradiol-induced endometrial hyperplasia during menopause.

OBJECTIVE: To determine the percentage of endometrial hyperplasia positive for p53 expression in both spontaneously occurring cases or following the use of unopposed estradiol. METHODS: Fifty-four postmenopausal patients with endometrial hyperplasia diagnosed by endometrial biopsy and hysteroscopy were recruited to this study. Thirty-three patients had used unopposed estradiol for periods of time from 1 to 3 years. P53 expression was detected in paraffin-embedded endometrial specimens by immunohistochemical methods. RESULTS: The percentage of endometrial hyperplasia positive for p53 expression was significantly greater in spontaneously occurring hyperplasia than in cases induced by the unopposed use of estradiol. CONCLUSION: Endometrial hyperplasia caused by the unopposed use of estradiol during menopause probably harbors fewer genomic errors than those cases occurring spontaneously.

Aged↗

PubMed2001

Ultrasound and menstrual history in predicting endometrial hyperplasia in polycystic ovary syndrome.

OBJECTIVE: To assess the role of endometrial thickness on vaginal ultrasound assessment and menstrual history in predicting endometrial hyperplasia in women with polycystic ovary syndrome (PCOS) who presented with infertility due to anovulation. METHODS: This was a prospective study in a university referral-based fertility and endocrine clinic. Fifty-six women with PCOS presenting with infertility due to anovulation underwent both vaginal ultrasound assessments and endometrial biopsies. The main outcome measures were the predictive value of sonographic endometrial thickness (primary objective) and the menstrual history with other clinical characteristics (secondary objective) for proliferative endometrium and endometrial hyperplasia in logistic regression analysis. Their predictive value was further examined by receiver operating characteristic curve analysis. RESULTS: Thirty-six PCOS patients (64.3%) had proliferative endometrium and 20 (35.7%) had endometrial hyperplasia. Five of the latter (25%) had cytologic atypia. Endometrial thickness less than 7 mm or intermenstrual interval less than 3 months (corresponding to more than four menstrual periods yearly) was associated with proliferative endometrium only. The endometrial thickness correlated positively with endometrial hyperplasia (P =.018) and, together with the average intermenstrual interval, were significant predictors of endometrial hyperplasia (P <.001). CONCLUSION: These findings point to the usefulness of obtaining a detailed menstrual history in women with PCOS by identifying those at increased risk of endometrial hyperplasia and who require an endometrial biopsy. The endometrial thickness corroborates this clinical impression and is particularly useful when the menstrual history is uncertain. Endometrial hyperplasia in this population is effectively excluded when the endometrial thickness is less than 7 mm.

Adult↗

PubMed1984

The use and disuse of morphometry in the diagnosis of endometrial hyperplasia and carcinoma.

Endometrial adenomatous hyperplasia, and the different grades of endometrial carcinoma form a continuous spectrum of morphologic deviations. The reproducibility and consistency of the assessment of these microscopical patterns is a historical problem ("nicht Karzinom - aber besser hinaus"). Lack of objective criteria is the major cause of this. Computer-aided morphometric analysis has revealed the diagnostic significance of several quantitative microscopical features. Using these in a multivariate combination, a highly reproducible and objective classifier has been developed. Selection of the significant areas by skilled gynaecopathologists is essential for the useful application of this algorythm. Especially in cases of doubt, this classification rule can be of decisive importance. Routine application in diagnostic gynaecopathology of this selective type of morphometry over a period of four years has regularly corrected the original subjective histopathological grade. In a case of a young patient with an unsuspected sexcord tumor of the ovary with annular tubules, the erroneous diagnosis of endometrial carcinoma was corrected by the application of morphometry into adenomatous hyperplasia. An excision of the ovarian tumor was performed, and slowly the morphologic pattern of the subsequent microcurettings revealed a more and more normal microscopical pattern, with eventually signs of secretion. Other studies have shown, that morphometrical analysis of adenomatous hyperplasias can predict the majority of those patients, who will develop frank carcinoma in their later course. Finally, objective histopathological grading of carcinomas reveals the superior quality of morphometry above subjective qualitative methods. Prevention of under- or overtreatment with radiotherapy can therefore be the result of routine diagnostic morphometry.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis, Differential↗

PubMed2000

Comparison of endometrial carcinoma coexisting with and without endometrial hyperplasia.

OBJECTIVE: It has been reported that endometrial carcinoma has two pathogenic types; one with and the other without endometrial hyperplasia. The present study was done to clarify whether this was true in our series of a large number of Japanese patients. METHODS: Three hundred and twenty-eight patients with endometrial carcinoma were classified into two groups, one coexisting endometrial hyperplasia (group 1; 182 cases) and the other having normal endometrium without endometrial hyperplasia (group 2; 107 cases). The clinical and pathological observations of the two groups were compared. RESULTS: The ages of the patients were significantly lower in group 1 (30-83; mean 50.7) than in group 2 (34-81; mean, 57.2). The incidence of the carcinoma with invasion limited to less than 1/3 of the myometrium, with surgical stage I, lower grade endometrioid type and higher levels of progesterone receptor, and without lymph node metastasis were significantly higher in group 1 than in group 2. The cumulative survival rate for stage I was also significantly higher in group 1 patients. CONCLUSION: A significant difference was found between groups 1 and 2 in age distribution, degree of progress and pathological observations. Stage I patients in the former group had a better prognostic than the latter.

Adult↗

PubMedDate not supplied

Differential diagnosis of endometrial hyperplasia and carcinoma by computerized image cytometry of cell proliferation, apoptosis and Bcl-2 expression.

BACKGROUND: The differential diagnosis between atypical endometrial hyperplasia and endometrial carcinoma is often difficult and based on controversial criteria. Cell kinetic parameters may be helpful. DESIGN: Cell proliferation, apoptosis and Bcl-2 expression were evaluated in benign endometrium, non atypical and atypical endometrial hyperplasia and endometrial carcinoma. The results were compared by one way analysis of variance and Bonferroni T tests. RESULTS: Cell proliferation was significantly higher (p < 0.01) in endometrial adenocarcinoma (25.6 percent) than in atypical hyperplasia (17.1 percent) and non-atypical hyperplasia (7.5 percent) of the endometrium. Apoptosis was observed in 12.3 percent of endometrial adenocarcinomas and less frequently in atypical hyperplasia (7.4 percent) and non-atypical hyperplasia of the endometrium (5.8 percent). Bcl-2 expression was significantly lower (p < 0.002) in endometrial adenocarcinoma (1.7 percent) than in atypical hyperplasia (4.2 percent) and non-atypical hyperplasia (5.3 percent) of the endometrium. In benign endometrium, cell proliferation and Bcl-2 expression were significantly higher during the proliferative phase while the rate of apoptosis was significantly higher during the secretory phase. CONCLUSIONS: Our data suggests that cell proliferation, apoptosis and Bcl-2 expression could be helpful when distinguishing endometrial carcinoma from non-atypical or atypical endometrial hyperplasia.

Adult↗

PubMedDate not supplied

[Mastopathy and endometrial hyperplasia--coexistence, relationships].

Samples of endometrium were examined histologically in 161 female patients with endometrial hyperplasia or mastopathy. Moreover, LH, FSH, prolactin, testosterone, and dehydroepiandrosterone sulphate levels were assayed in 51 patients. Mastopathy was found in 36.8% of patients with endometrial hyperplasia. An estimate risk of mastopathy within 13 years following a diagnosis of endometrial hyperplasia is 33%. Endometrial hyperplasia accompanied mastopathy in 24.8% of cases, and an estimated risk of endometrial hyperplasia within 21 years following a diagnosis of mastopathy is 37%. Hormonal status of patients with endometrial hyperplasia-mastopathy is similar to that in patients with endometrial and breast cancer. The authors suggest that both endometrial hyperplasia and mastopathy should be considered markers of the risk of uterine and breast cancer.

Adolescent↗

PubMedDate not supplied

High rate of endometrial hyperplasia in renal transplanted women.

UNLABELLED: A high rate of endometrial hyperplasia, an estrogen-dependent premalignant lesion of the endometrium, has been observed among female kidney allograft recipients. The aim of the study was to evaluate the incidence of endometrial abnormalities among renal transplanted women with abnormal uterine bleedings. MATERIAL AND METHODS: A retrospective analysis compared 45 renal transplanted women who underwent dilatation and curettage for abnormal uterine bleeding between January 1999 and September 2004 with 90 consecutive, nontransplanted, control patients who underwent dilatation and curettage for the same reason in 2004. RESULTS: Thirty-one cases (69%) of endometrial hyperplasia and one case (2%) of endometrial cancer were detected among the renal allograft recipients. The majority of transplant patients (28 cases, 62%) developed endometrial hyperplasia without atypia successfully treated with progestagens. There were 29 cases (32%) of hyperplasia without atypia, 2 cases (1%) of atypical hyperplasia, and 4 cases (4%) of endometrial cancer in the control group. CONCLUSIONS: Renal transplanted women seem to have an extremely high risk of endometrial hyperplasia. The majority of cases may be successfully treated with progestagens. Immunocompromised renal graft recipients, however, show other risk factors for carcinogenesis. Thus, frequent clinical surveillance should be recommended in this group of patients, also because there is conflicting evidence with regard to the risk of progression to carcinoma among untreated patients.

Adult↗

PubMed1985

The behavior of endometrial hyperplasia. A long-term study of "untreated" hyperplasia in 170 patients.

Endometrial curettings from 170 patients with all grades of endometrial hyperplasia, who did not undergo a hysterectomy for at least 1 year were evaluated in order to correlate the histopathologic features with behavior. Follow-up ranged from 1 to 26.7 years (mean, 13.4 years). Cytologic and architectural alterations were analyzed separately in order to assess their respective roles in predicting the likelihood of progression to carcinoma. Classification of proliferative lesions based solely on the presence of cytologic atypia revealed that atypia was a discriminant factor. Proliferations lacking cytologic atypia were designated hyperplasia and those displaying atypia were designated atypical hyperplasia. Only 2 (1.6%) of 122 patients with hyperplasia progressed to carcinoma compared with 11 (23%) of women with atypical hyperplasia (P = 0.001). Subclassification of the two forms of hyperplasia (those with cytologic atypia and those without) was performed using the degree of architectural abnormalities. Hyperplasia and atypical hyperplasia displaying marked glandular complexity and crowding producing a back-to-back appearance were designated complex hyperplasia (CH) and complex atypical hyperplasia (CAH), respectively. Hyperplasia and atypical hyperplasia with lesser degrees of glandular complexity and crowding were designated simple hyperplasia (SH) and simple atypical hyperplasia (SAH), respectively. Progression to carcinoma occurred in 1 (1%) of 93 patients with SH, in 1 (3%) of 29 patients with CH, in 1 (8%) of the patients with SAH, and in 10 (29%) of the patients with CAH. The differences between the four subgroups suggest a trend but are not statistically significant. The findings in this study provide a rationale for classifying noninvasive endometrial proliferations primarily on the basis of cytologic atypia since this is the most useful criterion in predicting the likelihood of progression to carcinoma. In addition, the presence of concommitant architectural alterations appears to identify a particularly high-risk subgroup.

Adenocarcinoma↗

PubMed1997

[Endometrial hyperplasia and carcinoma in situ].

Endometrial hyperplasias--both simple and adenomatous are presented, as well as the differences between them and the endometrial carcinoma. The concept of endometrial carcinoma in situ (ESIS) and the criteria for invasiveness by the malignancies of the uterine corpus are discussed. Illustrations for various cases with ESIS are provided and the clinical behaviour by ESIS is discussed.

Adenocarcinoma↗

PubMed1976

The relation of adenomyosis uteri to coexistent endometrial carcinoma and endometrial hyperplasia.

The relation of adenomyosis uteri to endometrial carcinoma and endometrial hyperplasia has been the subject of only a few studies. These investigations have resulted in opposing conclusions on the association between the conditions. In this study of a 10-year period, all cases were retrieved from the surgical pathology laboratory files of adenomyosis uteri with either simultaneous endometrial carcinoma or endometrial hyperplasia. A control population was selected from patients who underwent hysterectomy for mechanical problems related to the uterus. Adenomyosis was found in association with endometrial carcinoma in 19.4% of 175 cases and in association with endometrial hyperplasia in 20.5% of 254 cases. The control series of 203 patients had a 16.7% incidence of adenomyosis. Statistical analysis showed no association between these conditions.

Adenocarcinoma↗