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PubMed1995

Angiogenesis in endometrial hyperplasia and stage I endometrial carcinoma.

OBJECTIVE: To evaluate angiogenesis in endometrial hyperplasia and stage I endometrial carcinoma, and to investigate the relationship between angiogenesis and tumor grade and depth of invasion. METHODS: Three groups of patients were analyzed: control patients who underwent hysterectomy for benign conditions (n = 19), patients with endometrial hyperplasia (n = 24), and patients with stage I endometrial carcinoma (n = 34). All hysterectomy specimens were stained immunohistochemically for factor VIII-related antigen as a sensitive and specific marker for vascular endothelium. Areas close to the deepest myometrial invasion or those with the highest grade of endometrial hyperplasia and the highest angiogenic intensity were selected. Three fields (x 400) were selected for each slide, and the mean microvessel count was calculated. Statistical analysis included Mann-Whitney U test or Kruskal-Wallis analysis of variance and Dunn post hoc procedure. P < .05 was considered significant. RESULTS: A significant difference was found between the microvessel count of controls versus the group with complex endometrial hyperplasia (median 21, range 16-80, versus median 38, range 20-130; P < .05). Microvessel counts of complex endometrial hyperplasia were significantly higher than those of simple hyperplasia (median 25, range 16-42; P < .05) and significantly lower than counts of endometrial carcinoma (median 77.5, range 19-189; P < .05). Microvessel counts in complex hyperplasia were not significantly different than those of noninvasive stage I endometrial carcinoma (median 38, range 20-130, versus median 44, range 19-119; P = .5). In cases of stage I endometrial carcinoma, a higher number of microvessels was noted in specimens with myometrial invasion than in those without myometrial invasion (median 44, range 19-119, versus median 83, range 19-189; P < .01). A higher number of microvessels was noted in cases with grade 2 than in those with grade 1, stage I endometrial carcinoma (median 44, range 19-98, versus median 96, range 63-189; P < .001). CONCLUSION: Complex endometrial hyperplasia and endometrial carcinoma are angiogenic. Furthermore, in stage I endometrial carcinoma, greater depth of invasion and higher tumor grade are directly correlated with angiogenic intensity.

Endometrial Hyperplasia↗

PubMed2005

Treatment of non-atypic endometrial hyperplasia using thermal balloon endometrial ablation therapy.

BACKGROUND/AIM: Traditionally endometrial hyperplasias have been treated with progestins. Unfortunately, quite often hyperplasias are resistant to treatment, or they recur after therapy. The aim of the study was to compare traditional progestin administration with thermal balloon endometrial ablation in the treatment of non-atypic endometrial hyperplasia. METHODS: Women with endometrial hyperplasia (n = 34) were randomized in a 1:1 allocation ratio. Endometrial biopsy samples were taken 6 and 12 months after the treatment; if any signs of hyperplasia were detected, hysterectomy was performed. In addition, the hospital records were checked in September 2003 to observe for any later hysterectomy. Main outcome measures were recovery from hyperplasia and avoidance of hysterectomy. RESULTS: In patients treated with thermal ablation, the hyperplasias persisted at 6 or 12 months in 4 out of 17 patients, whereas the rate was 6 out of 17 patients in the progestin therapy group. According to patient records, 1 further patient treated with thermal ablation and 3 further patients treated with progestin were hysterectomized after the last visit. A total of 14 of the 34 patients (41%) have been hysterectomized so far. CONCLUSIONS: These preliminary results suggest that thermal balloon endometrial ablation therapy seems to be as effective as traditional progestin administration in the treatment of non-atypic endometrial hyperplasia. The hysterectomy rate during the follow-up period was, however, considerably high, and, therefore, hysterectomy might be considered even a first-choice treatment for endometrial hyperplasias.

Adult↗

PubMedDate not supplied

Endometrial hyperplasia: value of endometrial thickness in ultrasonographic diagnosis and clinical significance.

The records of 90 patients with histologically proven endometrial hyperplasia (EH) were reviewed retrospectively. Eleven of these patients had pelvic ultrasound examinations available. These were compared to the pelvic ultrasound examinations of 19 patients with a histologically normal endometrium, available in 126 consecutive patients seen over the same period of time. Patients with EH had a mean endometrial thickness of 18.8 mm (range 8 mm to 45 mm) vs 5.4 mm (range 2 mm to 10 mm) in the control group. This difference in thickness was statistically significant (p much less than .01). The specificity and sensitivity of endometrial thickness in the diagnosis of EH were 100% and 81%, respectively, when 10 mm was taken as the upper limit of normal. Ultrasonographically demonstrable endometrial characteristics can differentiate EH from normal endometrium in a great majority of cases. The clinicopathological significance of EH is discussed.

Adult↗

PubMed2002

Cyclical change of hMSH2 protein expression in normal endometrium during the menstrual cycle and its overexpression in endometrial hyperplasia and sporadic endometrial carcinoma.

BACKGROUND: The role of hMSH2 protein, one of the major DNA repair proteins, until now, had not been elucidated in terms of normal endometrial function during the menstrual cycle. The current study was designed to address this issue and to determine whether the expression of hMSH2 is altered in the course of endometrial carcinogenesis. METHODS: Immunohistochemical reactivity with a monoclonal antibody against the hMSH2 protein was examined in endometrial tissue specimens from 45 patients with normal endometrium, 51 patients with endometrial hyperplasia, and 27 patients with endometrial carcinoma. Immunohistochemical expression of proliferating cell nuclear antigen (PCNA) also was studied in the same samples as a measure of the proliferative activity and was compared with hMSH2 expression in each sample. RESULTS: The functional layer of normal endometrium displayed cyclic changes in hMSH2 protein expression during the menstrual cycle, showing positive expression in the proliferative phase and becoming weak to negative in the secretory phase. This expression pattern was similar to that of PCNA. Sixty-three percent of endometrial carcinomas showed strong positivity for both hMSH2 and PCNA expression, and 7.4% had an intensity of hMSH2 protein expression similar to that found in normal proliferative endometrial glandular cells. There was only 1 sample (3.7%) that was completely negative for hMSH2 expression, and 26% of samples were weakly positive for PCNA and hMSH2 protein. All simple hyperplasias and the majority of complex and atypical hyperplasias showed positive immunoreactivity for hMSH2 and PCNA. CONCLUSIONS: This study demonstrates that hMSH2 protein expression changes during the menstrual cycle in parallel with proliferative activity. In most patients with sporadic endometrial carcinoma, the expression of hMSH2 protein is consistent with PCNA expression. In contrast, loss of hMSH2 expression is observed rarely in patients with sporadic endometrial carcinoma.

Adult↗

PubMedDate not supplied

[Endometrial hyperplasia predicts a better prognosis in endometrial carcinoma].

AIM: To evaluate the significance of the associated Endometrial Hyperplasia in Endometrial Carcinoma. STUDY DESIGN: 93 hysterectomy specimens for endometrial carcinoma were histologically reviewed on paraffin sections stained H&E and tricromic VG. RESULTS: 45 cases were associated with endometrial hyperplasia; 48 cases without endometrial hyperplasia were: 35 cases with the entire endometrial cavity occupied by carcinoma, 11 associated with endometrial atrophy and 2 with normal proliferative endometrium. In this second group, 37 cases (77%) were in advanced stages. A correlation was found between the presence of Endometrial Hyperplasia and the degree of differentiation, the FIGO stage of the carcinoma, and the age of the patient. CONCLUSIONS: Endometrial Carcinomas associated with Endometrial Hyperplasia involve younger women and have lower aggressivity than those without hyperplasia. Endometrial Hyperplasia may demonstrate a favorable prognosis in Endometrial Carcinomas.

Carcinoma, Endometrioid↗

PubMedDate not supplied

Resectoscopic surgery may be an alternative to hysterectomy in high-risk women with atypical endometrial hyperplasia.

STUDY OBJECTIVE: Endometrial hyperplasia is found in 2% to 10% of women with abnormal uterine bleeding (AUB). Up to 43% of patients with cytologic atypia harbor coexisting adenocarcinoma, and approximately 20% to 52% of atypical hyperplasias, if untreated, progress to cancer. The objective of this study was to estimate the incidence of atypical endometrial hyperplasia encountered during routine resectoscopic surgery in women with AUB and to evaluate the role of resectoscopic surgery in the management of women with AUB and atypical endometrial hyperplasia who refused and/or were at high risk for hysterectomy. DESIGN: Prospective cohort study (Canadian Task Force classification II-3). SETTING: University-affiliated teaching hospital. PATIENTS: From January 1990 through December 2005, the senior author (GAV) performed primary resectoscopic surgery in 3401 women with AUB. Among these, there were 22 women with atypical (17 complex, 5 simple) endometrial hyperplasia. INTERVENTIONS: All women underwent hysteroscopic evaluation and partial (n = 3) or complete (n = 19) endometrial electrocoagulation and/or resection. Subsequently, 6 women had hysterectomy and bilateral salpingo-oophorectomy (BSO). MEASUREMENTS AND MAIN RESULTS: The median (range) for age, parity, and body mass index were 55 years (24-78 years), 2 (0-4), and 30.1 kg/m2 (22.5-52.2 kg/m2), respectively. Among the 3401 women, there were 22 cases of atypical endometrial hyperplasia, 12 of which were incidentally diagnosed at the time of hysteroscopy (complex 10, simple 2, incidence 0.35%). After hysteroscopic diagnosis or confirmation of diagnosis, 6 women underwent hysterectomy and BSO. Of the remaining 16 women, followed for a median of 5 years (range 1.5-12 years), 1 was lost to follow-up, 1 had only a biopsy to preserve fertility, 1 died from lung cancer after 4 years, and 1 died from colon cancer after 5 years. One patient developed endometrial cancer after 10.5 years with postmenopausal bleeding. She remains alive and well 3.5 years after hysterectomy and BSO. The remaining 11 patients are amenorrheic at a median follow-up of 6 years (range 1.5-12 years). CONCLUSIONS: Resectoscopic surgery in 3391 women with AUB detected 12 incidental cases of atypical endometrial hyperplasia (incidence 0.35%). Skillful resectoscopic surgery may be an alternative to hysterectomy in women with AUB and atypical endometrial hyperplasia, who refuse or are at high-risk for hysterectomy and who are compliant with regular and long-term follow-up.

Adult↗

PubMed1987

Gross and histological characterization of endometrial tissues from SLA miniature pigs with cystic endometrial hyperplasia.

Cystic endometrial hyperplasia (CEH) is a uterine disorder characterized by the formation of large numbers of cysts in the endometrium. The purpose of this study was to examine and characterize cell types in the endometrium associated with the cysts and uterine glands. No apparent histological differences between CEH-involved and normal uterine columnar epithelium were found. Endometrial glands in CEH-involved and normal uteri were lined with simple or ciliated columnar epithelial cells and surrounded by lamellar connective tissue. The cyst epithelium appeared to be stretched obliquely and compressed so that both the cells and nuclei were horizontally oriented relative to the cyst lumen and were surrounded by lamellar connective tissue. Electron microgaphs revealed an abnormally high number of mitochondria in the cystic cells as compared to normal glandular cells. In conclusion, CEH is characterized by the formation of cysts which develop from the uterine glandular tissue. Epithelial cells lining the glands appeared to be distorted, possibly in response to internal pressure from increased volume due to high metabolic activity, and/or no uterine luminal opening.

Animals↗

PubMed2003

Lectin binding patterns in normal canine endometrium and in bitches with pyometra and cystic endometrial hyperplasia.

Cystic endometrial hyperplasia (CEH) and pyometra in the bitch are dioestral syndromes, supposed to be caused by hormonal disturbances and changes in endometrial steroid hormone receptor levels. Histologically, the endometria show cystic dilated glands and, if bacteria succeed in invading the uterus, pyometra may develop in the following metoestrus. In this study, lectin histochemistry was performed on paraffin sections to compare carbohydrate expression of uterine glands and surface epithelium in healthy dogs and in dogs with CEH and pyometra. Lectin binding is a useful tool to identify glycoconjugates, especially of the glycocalyx, which has essential functions in the endometrium during reproduction. Uterine tissue was obtained from 18 healthy bitches in metoestrus or anoestrus and 18 bitches with a clinical diagnosis of CEH or pyometra. Normal endometria showed cycle-dependent changes in SBA, PNA, HPA and UEA binding during metoestrus and anoestrus. LCA did not show cycle-dependent changes and WGA bound to Golgi regions in the apical parts of surface epithelial cells only in metoestrous. Endometria with inflammatory alterations lost cycle-specific lectin binding patterns and, with increasing severity of pathological changes, showed a marked decrease in binding intensity to the glandular and surface epithelial glycocalyx and secretions. In dogs with CEH, unaltered glands with generally strong lectin binding to the glycocoalyx and Golgi regions were found adjacent to altered glands. The decrease of lectin binding in pyometra cases is supposed to be a result of glandular exhaustion after cystic hyperplasia. In addition, bacterial adhesion to sugar residues on the uterine surface epithelium might impede lectin binding.

Animals↗

PubMed1997

Endometrial hyperplasia and the risk of endometrial carcinoma.

OBJECTIVES: To determine the incidence of endometrial carcinoma in endometrial hyperplasia and try to identify those patients at greatest risk. METHODS: We conducted a retrospective study of 116 patients who had simple, complex or mixed (simple with focal complex) endometrial hyperplasia with or without atypia, from January 1991 to December 1994. RESULTS: Twenty-nine patients had endometrial hyperplasia with atypia and 87 without atypia. Incidence of endometrial carcinoma was 27.6% in those with atypia; and 3.4% in those without atypia. All were stage I (A or B) adenocarcinomas. Polycystic Ovary Disease and subfertility were found significantly in the cases with cytological atypia; however, they were not significant in the cases with carcinoma. No significant historical differences that could predict carcinoma were found.

Adenocarcinoma↗

PubMed2004

Endometrial hyperplasia: a review.

UNLABELLED: Endometrial hyperplasia is a precursor to the most common gynecologic cancer diagnosed in women: endometrial cancer of endometrioid histology. It is most often diagnosed in postmenopausal women, but women at any age with unopposed estrogen from any source are at an increased risk for developing endometrial hyperplasia. Hyperplasia with cytologic atypia represents the greatest risk for progression to endometrial carcinoma and the presence of concomitant carcinoma in women with endometrial hyperplasia. Abnormal uterine bleeding is the most common presenting symptom of endometrial hyperplasia. Specific Pap smear findings and endometrial thickness per ultrasound could also suggest the diagnosis. Unopposed estrogen in women taking hormone replacement therapy increases the risk of endometrial hyperplasia. Tamoxifen has demonstrated its efficacy in treating women at risk for breast cancer, but it increases the risk of endometrial hyperplasia. The choice of treatment for endometrial hyperplasia is dependent on patient age, the presence of cytologic atypia, the desire for future childbearing, and surgical risk. Endometrial hyperplasia without atypia responds well to progestins. However, women with atypical hyperplasia should be treated with hysterectomy unless other factors preclude surgery. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians. LEARNING OBJECTIVES: After completion of this article, the reader should be able to describe the definition and classification of endometrial hyperplasia, to outline the clinical features of a patient with endometrial hyperplasia, to point out the natural history of endometrial hyperplasia, and to summarize the diagnostic options for patients with endometrial hyperplasia.

Algorithms↗

PubMed2002

[Endometrial hyperplasia--hysteroscopy findings].

Endometrial hyperplasia is considered to be a frequent cause of metrorrhagia. Traditionally diagnosis of this pathology was made on specimens obtained by uterine curettage or after hysterectomy performed for benign diseases. Recently, hysteroscopy has enabled to offer suggestive images of this pathology, in fact it allows to visualize directly the uterine cavity and to perform guided biopsies on the endometrial mucosa. The aim of this study is to evaluate the reliability of the hysteroscopy procedures in the diagnosis of the endometrial hyperplasia. 479 panoramic hysteroscopies were performed in a four-year period for different indications and we found endometrial hyperplasia in 129 patients. We compared the results with the histological findings. On the base be able the possible diagnose and the follow-up procedure for endometrial hyperplasia.

Endometrial Hyperplasia↗

PubMed1998

Concomitant endometrial hyperplasia in patients with endometrial carcinoma.

OBJECTIVES: The aim of this study was to compare the histopathologic features and prognosis of patients with endometrial carcinoma with and without concomitant hyperplasia. METHODS: Histologic slides of the surgical specimens of 214 consecutive patients who underwent surgery as primary treatment for endometrial carcinoma from 1985 through 1991 were reviewed. RESULTS: Ninety-two of the 214 patients (43%) with endometrial carcinoma had concomitant endometrial hyperplasia. Patients with endometrial carcinoma with hyperplasia were significantly younger than those without hyperplasia (mean age 62 +/- 10 vs 65 +/- 9 years, P < 0.05). Carcinomas associated with hyperplasia were better differentiated and of lower surgical stage. By univariate analysis the frequency of recurrence was significantly lower (4% vs 17%, P < 0.004) and the estimated 5-year survival rate significantly higher (96% vs 85%, P < 0.01) in patients with endometrial carcinoma with concomitant hyperplasia. However, in multivariate analysis the presence of endometrial hyperplasia was not an independent prognostic factor and the 5-year survival rates of patients with or without hyperplasia did not differ significantly in any surgical stage. CONCLUSION: The presence or absence of concomitant endometrial hyperplasia is strongly correlated with the surgical stage of endometrial carcinoma.

Adenocarcinoma↗

PubMed2005

[Pathohistological changes characteristic for endometrial hyperplasia].

Peculiarities of endometrial hyperplasia during monophase menstrual cycle have been investigated. 52 patients of premenopause and menopause period (age 35-52 years old) have been investigated using uterus scrape analysis. Histostereometric and morphometric methods have been used for the study. The analyses of the obtained results has shown that: 1. The endometrial hyperplasia accompanies the shortened and prolonged persistency of follicles in a monophase menstrual cycle. Therefore when making the pathohistological diagnosis, the pathogenetic aspects should be indicated; 2. Endometrial hyperplasia is not a separate nosological phenomenon and effectiveness of its therapy strongly depends on the condition of ovary and hormone systems.

Adult↗

PubMed1987

Immunohistochemical localization of placental proteins and tumor-associated antigens in endometrial cancer and endometrial hyperplasia.

As to endometrial cancer and endometrial hyperplasia, this study represents the localizations of the placental proteins and the tumor-associated antigens by both immunohistochemical light microscopy (ILM) and immunoelectron microscopy (IEM). The reagents examined include human placental lactogen (HPL), placental alkaline phosphatase (PAP), pregnancy-associated plasma protein A (PAPP-A), pregnancy-specific beta 1-glycoprotein (SP1), alpha 1-anti-trypsin (alpha-AT), and tissue polypeptide antigen (TPA). The tumor cells stained for HPL are localized and the SP1-positive cancer cells are almost entirely restricted to an infiltrating front. alpha-AT is shown in both tumor cells with marked cellular atypism and ones in deeply infiltrating foci. The immunoreactive frequency for the above six reagents in endometrial cancer is higher than that in endometrial hyperplasia. In endometrial cancer, the high frequency of an immunoreaction is confirmed in TPA (p less than 0.05). The combined stainings, i.e. either for TPA and SP1 or for TPA and PAPP-A, are efficient immunohistochemical screening methods to use in diagnosing endometrial cancer in the biopsied specimens (p less than 0.05).

Adenoma↗

PubMed2006

[Endometrial hyperplasia: A review].

Endometrial hyperplasias can be 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. They are usually diagnosed because of irregular bleeding in perimenopause. Hysteroscopy with a biopsy gives a more accurate diagnosis than transvaginal ultrasonography, sonohysterography, or blind curettage. Endometrial hyperplasias with no cytological atypia, regarded as a response to unopposed endogenous estrogenic stimulation, are normally treated with progestins. The intra-uterine route (levonorgestrel intra-uterine system) is more effective and better tolerated than the oral route. Either conservative surgery (endometrial resection, thermal ablation) or radical surgery (hysterectomy) in the case of other genital diseases is performed on women who did not respond to medical treatment. Endometrial hyperplasias with cytological atypia, considered as intra-epithelial neoplasias, are traditionally treated by hysterectomy. The absence of management protocols in the literature offers various treatment options and indications. Gonadotropin-releasing hormone agonists, danazol, or aromatase inhibitor are effective, but have adverse effects and are expensive. Endometrial ablation can be performed as a first line therapy in women suffering from bleeding related to hyperplasia without cytological atypia. Medical treatment may be offered to young women suffered from hyperplasias with cytological atypia and desiring pregnancy.

Biopsy↗

PubMed1982

The endometrial hyperplasias and their relationship to endometrial neoplasia.

The various forms of endometrial hyperplasia are classified and a description given of their pathology and of their inter-relationships. The nosological status of endometrial adenocarcinoma in situ and the histological differentiation between hyperplasia with severe cellular atypia and endometrial adenocarcinoma are discussed. The aetiology and pathogenesis of the various endometrial hyperplasias are considered and grounds are given for the belief that glandular hyperplasia with cellular atypia is a form of intraendometrial neoplasia. A new terminology, based on the biological nature of the various endometrial abnormalities, is proposed and a plea is made for the introduction of the term 'intraendometrial neoplasia' to encompass all forms of endometrial glandular hyperplasia with cellular atypia and intraendometrial adenocarcinoma.

Adenocarcinoma↗

PubMed2005

Endometrial cancer in patients with preoperative diagnosis of atypical endometrial hyperplasia.

OBJECTIVE: Atypical endometrial hyperplasia (AEH) has been associated with the presence of concomitant endometrial carcinoma (EC). The aim of this study is to examine the frequency of coexisting endometrial carcinoma when atypical endometrium hyperplasia was found upon biopsy. We also evaluated the influence of preoperative diagnostic techniques (pipelle and dilation and curettage (D&C)), and the value of transvaginal ultrasound in detecting unexpected tumor invasion. STUDY DESIGN: Between January 1992 and December 2003, at the Department of Obstetrics and Gynecology, University of Parma, and Policlinico S. Matteo, Pavia, 70 consecutive patients subjected to total hysterectomy with a histological diagnosis of AEH were retrospectively selected. 52/70 patients underwent vaginal hysterectomy, with bilateral salpingo-oophorectomy (BSO) whereas 18/70 had abdominal hysterectomy with BSO within 8 weeks since the diagnosis of AEH. RESULTS: We found in 30 of the 70 patients with atypical endometrial hyperplasia in the biopsy coexisting endometrial carcinoma (43%). No differences in diagnostic accuracy between the pipelle method and D&C were found. CONCLUSION: Transvaginal ultrasound was not a feasible method for predicting EC. After a follow-up of an average of 5 years there was, neither in the abdominal operated patients nor in the vaginal operated patients, a recurrence of disease.

Adult↗

PubMed1990

Pathophysiology and management of endometrial hyperplasia and carcinoma.

Endometrial cancer is currently the commonest pelvic malignancy affecting American women, most of whom share the same pathophysiologic basis, that is, unopposed estrogenic stimulation. The initial result of hyperestrogenism is the development of endometrial hyperplasia, which is reversible in most cases by appropriate hormonal therapy. Persistent stimulation eventually leads to atypical hyperplasia with nuclear atypia and invasive carcinoma. Because there is no cost-effective screening method for the detection of endometrial hyperplasia and carcinoma, it is essential to survey the high-risk population with appropriate diagnostic techniques. After diagnosis, therapy should be individualized based on pathologic findings (cell type and histologic grade) and extent of disease (International Federation of Gynaecologists and Obstetricians stage, depth of myometrial invasion, and pelvic and para-aortic lymph node status). Recent studies suggest that sex hormone receptors and nuclear DNA ploidy patterns provide useful prognostic information independent of histologic grade.

Adenocarcinoma↗