Histopathological evaluation of Endometrium hyperplasia and it’s correlation with the clinical parameters in a tertiary care hospital

Introduction: Abnormal uterine bleeding is a common clinical presentation in the perimenopausal age group its biopsy serves as an excellent clue to the underlying disease. The presentation may vary according to the type of endometrial hyperplasia and their correlation helps in the proper management of the patients complain.

To analyze the histopathological patterns of endometrial hyperplasia as well as to correlate endometrial hyperplasia with the clinical parameters.

It is a retrospective study and included one year data. A total of 125 cases that underwent hysterectomies or endometrial biopsies for abnormal uterine bleeding were recorded with their clinical history. For all cases the histopathology slides were re-evaluated and results were recorded. Epidemiological variables were analyzed by cross tabulation to assess their relationship.

Out of 125 cases 53 cases had endometrial hyperplasia, 24 cases were having simple hyperplasia followed by 14 cases with simple hyperplasia without atypia, 9 cases with complex hyperplasia with atypia followed by 6 cases with complex hyperplasia without atypia. 30 to 50 years age group commonly had endometrial hyperplasia & menorrhagia was the common clinical complain in our patients.

In all the females coming to OPD with abnormal uterine bleeding clinical correlation should be properly made with biopsy report of the patient for the proper management of the condition, which avoids landing up of the patient into further complication.

Endometrium biopsies & hysterectomies specimen for any abnormal bleeding are commonly received in the department of pathology. Their diagnosis made on the light microscopy is quite helpful in planning the treatment for the patient since in most of the patients who are having endometrial hyperplasia with atypia are prone to develop endometrial carcinoma. Endometrium is constantly engaged in the dynamics of shedding & regrowth during active reproductive life, it is controlled by rise & fall of pituitary hormones .Alterations in the fine tuning mechanism may result in a spectrum of disturbances & endometrial hyperplasia is most important among them. Arising Endometrial hyperplasia often preceeds the development of endometrial carcinoma. More recently, studies have found that the risk of endometrial hyperplasia is associated with increasing body mass index & nulliparity.[1] In addition to this increasing obesity, anovulatory cycles & exogenous hormones are associated with endometrial & endometrial carcinoma both. The role of unopposed estrogen has been supported by many studies since high levels of estrogen has been found in the patients with endometrial carcinoma.[2], [3] Endometrial hyperplasia is defined as a proliferation of glands of irregular size & shape with an associated increase in gland to stroma ratio compared with proliferative endometrium. The process is generally diffuse but it may be focal also. The WHO classification, presently the most widely used, is a four –tier classification system takes into the account both cytologic & architectural abnormalities.[4] In the past the terms “adenomatous hyperplasia “ & “atypical hyperplasia “were used to denote proliferative lesions of the endometrium with varying degrees of architectural complexity & cytological atypia[5], [6], [7], [8], [9] in addition, the term “carcinoma in situ” was proposed to describe small lesions, with or without glandular crowding, having the cytologic features of carcinoma but lacking invasion.[7], [9], [10] We used WHO Classification in our study. In addition, a more recent epidemiologic study added further support for this simplified classification by showing that the only lesions that significantly increased the relative risk of carcinoma with atypical hyperplasia.[11] WHO classification of endometrial hyperplasia Hyperplasia without atypia, Simple hyperplasia without atypia, Complex hyperplasia without atypia. Atypical hyperplasia, Simple (atypical hyperplasia), Complex atypical hyperplasia. Patients with endometrial hyperplasia typically have abnormal bleeding. Occasionally the lesion is detected by endometrial biopsy performed during the course of infertility workup or before the start of hormonal therapy in post menopausal females. Hyperplasia usually appears as a result of unopposed estrogen use. And so most patients have a history of either persistent anovulation or exogenous unopposed estrogen usage. Though anovulation occurs at menarche & perimenopausal women, hyperplasia is not usually found in young women. Aims & Objectives To study the Histopathological patterns of endometrial hyperplasia. To correlate endometrial hyperplasia with clinical parameters.

This is a hospital based study done in the department of pathology at a tertiary care hospital. Study was conducted on 125 cases of endometrial hyperplasia which were re-evaluated and their relevant clinical details like menstrual history including age of menarche, date of last menstrual period, number of children, any history of abortions, age of menopause if occurred, any history of taking HRT and were recorded. Histological typing of endometrial hyperplasia by re-evaluating them under light microscopy & typing was done depending on the criteria used in WHO classification.

| S. No. | Histopathology | No. of cases | % | | 1. | Endometrial hyperplasia | 53 | 42.4 | | 2. | Proliferative phase | 21 | 16.8 | | 3. | Secretory phase | 26 | 20.8 | | 4. | Hormonal effects | 12 | 9.6 | | 5. | Atrophic endometrium | 09 | 7.2 | | 6. | Irregular shedding with endometritis | 04 | 3.2 | | Total | | 125 | 100 | | S. No. | Type of hyperplasia | No. of cases | % | | 1. | Simple hyperplasia | 24 | 45.2 | | 2. | Complex hyperplasia | 06 | 11.3 | | 3. | Simple hyperplasia with atypia | 14 | 26.4 | | 4. | Complex hyperplasia with atypia | 09 | 17 | | Total | | 53 | 100 | | S. No. | Age of the patient | Total | % | | 1. | 21-30yrs | 02 | 4% | | 2. | 31-40yrs | 22 | 42% | | 3. | 41-50yrs | 21 | 39% | | 4. | > 50yrs | 08 | 15% | | | | 53 | | | S. No. | Clinical complains | No. of cases with Endometrial Hyperplasia | % | | 1 | Menorrhagia | 88 | 70 | | 2 | Post menopausal bleed | 17 | 14 | | 3 | Continuous bleed | 18 | 15 | | 4. | Others | 02 | 1 |

Endometrial hyperplasia is the most common gynaecological disorder, it is due to unopposed estrogen stimulation. Endometrial assessment is performed to diagnose malignant & premalignant conditions & to evaluate the hormonal influences on the endometrium. In this study a total of 125 cases were assessed. In our study 53 cases presented with endometrial hyperplasia followed by secretory phase, then proliferative phase, 9cases presented with atrophic endometrium & four of them had irregular shedding with endometritis. Out of 53 patients 24 (45%) patients presented with simple hyperplasia, 14 patients had simple hyperplasia without atypia, 9 presented with complex hyperplasia without atypia followed by 6 patients having complex hyperplasia without atypia. The peak incidence of endometrial hyperplasia was noted in 3rd and 4th decade followed by 5th decade with only 2 patients lying in the age group of 21 to 30 years. Gusberg & Kaplan [12] in their study (1963) of 191 cases the peak incidence of endometrial hyperplasia was noted in 4th decade followed by 5th decade. The most common clinical complain in our study was menorrhagia followed by continuous bleeding, post menopausal bleeding in 17 patients our results were in concordance with the studies of Takreem et al. Takreem et al [13] also found out that menorrhagia is the commonest complain in endometrial hyperplasia (53.3%) which is in concordance with our study that is 66.6%.

It is very important to know the histopathological pattern of endometrium especially the hyperplasia going in them and their correlation with clinical parameters .Since early and proper recognition of these conditions helps in the proper management, treatment avoid landing up of the patients into further complications. Conflict of Interest The authors declare that there are no conflicts of interest in this paper. Source of Funding None.

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