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Endometrial Hyperplasia

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Endometrial Hyperplasia

One of the most controversial subjects in gynecology for the past several decades has been the definition biologic activity and treatment of "endometrial hyperplasia " For many years it has been suggested that these hyperplasias represent part of the spectrum of the endometrium that is a continuum of what essentially begins as benign changes that may become adenocarcinoma These conclusions were based on prospective studies initially reported by Gusberg and Kaplan in 1963 Earlier Gusberg had defined morphologically adenomatous hyperplasia and suggested that it is a precursor of endometrial carcinoma In their 1963 report Gusberg and Kaplan studied 191 patients with adenomatous hyperplasia diagnosed from 1934 to 1954 Ninety of these had immediate hysterectomy, with 20% noted to have a coexisting carcinoma and an additional 13% with borderline lesions Of the remaining 101 patients, eight (11 8%) subsequently developed endometrial cancer with a mean follow-up of 5 3 years They concluded that the risk for a patient with adenomatous hyperplasia was significantly greater than for a woman without hyperplasia and suggested that at ten years, the cumulative risk for cancer was 30% Unfortunately over the years many terms have been applied to this entity, resulting in different implications as to the malignant potential, which has contributed to wholesale confusion


There has recently been a challenge to the continuum concept Kurman's (in Washington) and Ferenczy's (in Montreal) groups have extensively studied this condition and have come to similar conclusions They concluded that there appears to be two separate and biologically unrelated diseases of the endometrium—hyperplasia and neoplasia— and the important feature that distinguishes one from the other is cytologic atypia. Both groups have developed new definitions, and they are essentially in agreement Kurman categorizes simple hyperplasia as a benign proliferation with an increase in the number of endometrial glands. The glands may be dilated, as has previously been described as cystic hyperplasia ("Swiss cheese"), or there may be greater crowding of the glands and irregular outlines (commonly referred to as "adenomatous hyperplasia") .Back-to-back crowding and cytologic atypia is not present. Complex hyperplasia is noted by a complex growth pattern and back-to-back crowding. Again, cellular atypia is not present. Although Ferenczy recognizes these two patterns, he has preferred to include both under the umbrella of endometrial hyperplasia (EH). These patterns are believed to be variations of normal preovulatory or proliferative endometrium. As such they have essentially no malignant potential.

On the other hand atypical hyperplasia denotes a proliferation of glands in which varying degrees of nuclear atypia and loss of polarity are present (cytologic atypia). These aberrant lesions may have enlargement and pleomorphism of the nuclei, aneu-ploidy DNA, and macronucleoli Kurman divides cellular atypia into mild and moderate, with moderate atypia showing a greater degree of cellular pleomorphism. If a complex pattern is not present, he designates these lesions ‘simple atypical hyperplasia’. When marked back-to-back crowding is present with cytologic atypia, "complex atypical hyperplasia" is the diagnosis. Stratification of glandular epithelial cells as well as mitotic activity can be found with any form of hyperplasia. Ferenczy combines these two entities and has labeled them "endometrial intraepithelial hyperplasia (EIH) ". Both groups believe that these are cancer precursors, whereas the simple or complex hyperplasias (EH) are not. Kurman and Ferenczy followed a total of 255 patients from one to 26 years (mean of 13 4 years and seven years, respectively) and found that only two of 187 (1%) with hyperplasia progressed to cancer, whereas 16 of 68 (23 5%) with atypical hyperplasia (EIH) progressed to cancer Kurman's data suggested that there was a greater chance of developing cancer if complex atypical hyperplasia was present, compared with simple atypical hyperplasia (29% versus 8%), but this difference was not statistically significant

It is well recognized that hyperplasias may be associated with or be difficult to distinguish from endometrial carcinoma. Gusberg and Kaplan treated 90 hyperplasia patients with immediate hysterectomy, and 20% were found to have a coexisting carcinoma. Other authors have noted similar findings In patients with atypical hyperplasia diagnosed with an endometrial biopsy, a dilation and curettage (D & C) should probably be done to rule out a coexisting adenocarcinoma. It has been suggested that if gland epithelium is present in the stroma (stromal invasion) of the curetting specimens, even if the diagnosis is hyperplasia, there is a significant chance that the uterus may harbor an endometrial cancer.

^ Patient Profile

It is well recognized that in these patients hyperplasia may be related to unopposed estrogen, either endogenous or exogenous. These alterations can occur at any age, with a significant number (two-thirds or more) occurring before age 50. At least in Kurman's data, older patients did not have an increased chance of having an atypical hyperplasia. Abnormal bleeding is the most common symptom, although hyperplasia can be encountered in the amenorrheic patient and at the time of endometrial biopsy as part of an infertility workup. What causes the abnormal bleeding is unknown, although there has been considerable speculation as to the mechanism. The degree of frequency of bleeding has no bearing on the extent of the hyperplasia. Anovulation has been noted in many patients with hyperplasia and, as mentioned, may be identified during an infertility evaluation. Many of Kurman's patients were nulliparous at the time of diagnosis and several were found to have a history of polycystic ovarian disease. Hyperplasia has also been associated with granulosa cell tumors, ovarian thecomas, and adrenal corticohyperplasia, as well as with unopposed estrogen replacement therapy. Because hyperplasia and adenocarcinoma have been associated with estrogen replacement therapy, the current recommendation is to add a progestin to the estrogen in those women with utero in situ. A fair number of patients are obese, and in some instances considerably so. All of these associated medical conditions have one thing in common—unopposed estrogen.


In many patients therapy other than the diagnostic procedure (D & C) is unnecessary. More than one-third of Kurman's patients had a D & C as the only treatment and had no subsequent problems, thereby allowing the investigators to assume that the D & C had in fact been therapeutic (mean follow-up 17.8 years). This was true for both the simple and the atypical hyperplasias. Additionally, patients with recurrent Weeding were retreated with a curettage, but two of 24 patients did go on to develop adenocarcinomas, indicating that these patients are at apparent increased risk. Ferenczy noted a similar experience. As previously mentioned, particularly in those with atypical hyperplasia (EIH), a formal D & C should be done to make sure there is not a coexisting adenocarcinoma. Also, in patients with stromal invasion on endometrial biopsies or D & C, there is an increased risk of having an unidentified carcinoma. In patients whose fertility desires have been satisfied, hysterectomy appears indicated.

If a patient is on unopposed estrogen, either stopping the estrogen or adding the progestin may alleviate the hyperplasia, particularly if only simple hyperplasia is present. The use of ten to 12 days of progestin at the end of the cycle will, in many instances, revert the hyperplasia back to a normal endometrium. This combined therapy can be used for three to six months and the endometrium resam-pled. If hyperplasia continues to be present, the estrogen can be stopped with continued cyclic progestin, or progestin can be given continuously for several weeks. Particularly in the menstruating patient, cyclic or continuous progestin can be successful. Continuous progestin with increasing doses to make the patient amenorrheic has been particularly successful in the recalcitrant patient.

In the perimenopausal or postmenopausal patient, particularly if atypical hyperplasia is present, hysterectomy is recommended unless there are medical contraindications. Because of the increased incidence of coexisting adenocarcinoma and the likelihood of subsequent development of adenocarcinoma in these patients, surgery certainly is justified.

^ Endometrial Polyps

Endometrial polyps are sessile or pedunculated projections of the endometrium. They develop as solitary or multiple soft tumors, frequently composed of hyperplastic endometrium. Diffuse endometrial hyperplasia may consist of multiple polypoid projections. The cause of most endometrial polyps is best explained as similar to that of endometrial hyperplasia.

Most polyps are asymptomatic, and it is difficult to determine which symptoms actually are due to endometrial polyps, since they are frequently associated with leiomyomas of the uterus and endometrial hyperplasia. Polyps are often an incidental discovery at the time of curettage or hysterectomy. When symptoms do exist the clinical picture is one of nonspecific abnormal uterine bleeding. Endometrial polyps occasionally cause postmenopausal bleeding. It is not clear that polyps bear any relation to endometrial cancer, except possibly those found in postmenopausal women.


Endometrial polyps are common, but their exact incidence is not known. These lesions are found in patients ranging in age from 12 to 81 years, although they are most prevalent in women between the ages of 30 and 59.


Polyps vary in size from a local elevation of the endometrium to a growth filling the endometrial cavity. They may be sessile or pedunculated. Most arise in the fundus or cornua of the uterus, but they may protrude through the cervix. These are usually firmer and less red than cervical polyps. In most cases the polyp is made up of endometrium similar to that seen in the basalis and does not show secretory changes. Less than one-third of the polyps contain functional endometrium, similar histologically to the endometrium from which they arise. Polyps frequently show a microscopic picture of cystic hyperplasia; less commonly they show one of adenomatous hyperplasia. The tip of the polyp may be necrotic and inflamed, particularly if it is long and protrudes into the cervix. Squamous metaplasia of the lining surface has been observed.

Diagnosis and Treatment

The diagnosis is usually established at the time of curettage or hysterectomy. Occasionally a polyp may protrude through the cervical os and be mistaken for a cervical polyp. Polyps produce a depression in the outline of the uterine cavity that may be detected by hysterosalpingography. They are often missed at curettage unless the curettage is accompanied by the insertion of a grasping instrument in the uterine cavity. For this reason no curettage should be considered complete unless a polyp forceps is introduced before and after the actual curetting.

Endometrial polyps are benign, although carcinoma of the endometrium coexists with them in about 10% of postmenopausal women. The carcinoma, however, is usually not in the polyp. Thus polyps require no special treatment other than removal, although in postmenopausal women there must be a curettage of the endometrium.


Endometrial Hyperplasia iconTheme of №1 Compensatory and adaptive processes: hypertrophy, hyperplasia

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