Abnormal uterine bleeding is bleeding from the uterine corpus that departs from a woman’s normal pattern in volume, duration, regularity or frequency. The term itself used to mean different things to different clinicians, which is why the International Federation of Gynecology and Obstetrics settled the nomenclature and introduced the PALM-COEIN system — polyp, adenomyosis, leiomyoma, malignancy and hyperplasia on the structural side, and coagulopathy, ovulatory dysfunction, endometrial, iatrogenic and not-yet-classified on the non-structural side [1]. FIGO later paired that causal system with a second system describing the bleeding pattern itself, and estimated that AUB affects more than half of reproductive-aged women and girls at some point [2]. Community data support how common it is: a cross-sectional survey of 1,200 reproductive-age women reported AUB in 36.5%, with heavy menstrual bleeding the predominant pattern [3]. The cost of that bleeding is not just gynaecological. Women with AUB score markedly lower on health-related quality of life than women without it — a mean of 56.3 against 69.5 in one case-control study — and report significantly more sexual distress [4]. Heavy menstrual bleeding is now recognised by the World Health Organization as a risk factor for anaemia, affects an estimated 4–63% of menstruating women worldwide depending on the population studied, and has been costed at roughly USD 1,692 per woman per year in lost work [5]. In India, national anaemia programmes still do not treat heavy bleeding as a target, which is a gap worth naming. Sorting out why a woman is bleeding starts with her age and menstrual history, because the differential shifts sharply across the reproductive span. Up to 14% of women have irregular or excessively heavy periods, and the split between anovulatory and ovulatory bleeding largely determines what the endometrium will look like under the microscope. Chronic anovulation leaves the endometrium under prolonged unopposed oestrogen, which is precisely the setting in which hyperplasia and carcinoma develop; polycystic ovary syndrome, uncontrolled diabetes, thyroid disease and hyperprolactinaemia all feed into it [6]. Ovulatory heavy bleeding works differently, through defective endometrial vasoconstriction and failure of vascular haemostatic plug formation rather than through hormonal excess [7]. At tissue level, progesterone withdrawal in a non-fertile cycle lowers stromal tissue factor and plasminogen activator inhibitor-1 and raises matrix metalloproteinase activity to produce controlled menstrual shedding; in anovulation, none of that ordered sequence happens, and the endometrium is left non-haemostatic, proteolytic and heavily vascular [8]. Endometrial sampling remains the investigation that answers the question. Current evidence-based guidance recommends biopsy for any postmenopausal woman with uterine bleeding, for younger women with AUB who carry risk factors for endometrial carcinoma, and for non-obese women with unopposed hyperoestrogenism [9]. What the pathologist then faces is genuinely difficult. Fragmented specimens, exogenous hormones, overlapping architectural criteria and benign mimics make the separation of a real precancer from a look-alike one of the harder calls in diagnostic pathology, and the 2020 WHO classification tightened rather than simplified that task [10]. Studies from Indian centres describing this spectrum exist, but most report age bands and diagnostic categories differently, which makes pooling hard. We set out to document the histopathological spectrum of endometrial biopsies received from women with AUB at our centre, to quantify the functional-versus-organic split, and to describe how the dominant pattern changes between reproductive, perimenopausal and postmenopausal women.

Study design and setting. This was a hospital-based, cross-sectional observational study carried out in the Department of Pathology at Gujarat Adani Institute of Medical Sciences and G. K. General Hospital, Bhuj — a tertiary care teaching hospital in Kachchh district, Gujarat. Specimens were received from the Department of Obstetrics and Gynaecology. Study period. July 2022 to May 2024 (23 months). Inclusion criteria. Endometrial biopsies and curettings from women presenting with abnormal uterine bleeding, irrespective of age. Exclusion criteria. Specimens with inadequate, scanty or crushed material that did not permit a confident diagnosis; specimens in which a gestational cause was established. Sample size calculation. The size was fixed using the formula for a single proportion, n = Z²pq/d². Doraiswami et al. reported disordered proliferative endometrium — the commonest pathological pattern irrespective of age in their series of 409 endometrial lesions — in 20.5% of cases [11]. Taking p = 0.205, q = 0.795, Z = 1.96 for 95% confidence and an absolute precision d = 8.5%, the minimum required sample worked out to 87. We analysed 95 adequate specimens, which clears that minimum. Specimen handling. Tissue was fixed in 10% neutral buffered formalin for 12–24 hours, processed through graded alcohols and xylene, embedded in paraffin, and sectioned at 4–5 µm on a rotary microtome. Sections were stained with haematoxylin and eosin and examined under light microscopy. Deeper levels were cut where the initial sections were equivocal. Sampling was by dilatation and curettage or Pipelle aspiration as decided by the treating gynaecologist; the two techniques agree closely, with reported concordance of 97.6% and a kappa of 0.948 between Pipelle and conventional curettage in women aged 35 years and above [12]. Reporting and categorisation. Diagnoses were assigned according to the 2020 WHO Classification of Female Genital Tumours and standard criteria for cyclical and non-cyclical endometrium. Findings were then grouped as functional (proliferative phase, secretory phase, disordered proliferative endometrium, luteal phase defect, atrophic endometrium, exogenous progestin effect) or organic (endometrial polyp, chronic endometritis, hyperplasia with or without atypia, carcinoma). Age was analysed both in decade bands and in three clinical groups: reproductive (18–40 years), perimenopausal (41–50 years) and postmenopausal (≥51 years). Every slide was reviewed independently by two pathologists, and discordant cases were resolved on a double-headed microscope. Statistical analysis. Data were entered in Microsoft Excel and analysed as frequencies and percentages. Categorical comparisons across age groups were tested with Pearson’s chi-square test; Fisher’s exact test was substituted where expected cell counts fell below 5. A two-sided p < 0.05 was taken as significant. Ethics. The study was approved by the Institutional Ethics Committee, and the requirement for individual consent was waived for the retrospective use of archived diagnostic material. No identifying patient information appears in this report.

Ninety-five adequate endometrial specimens from women with AUB were analysed. Ages spanned 21 to 80 years. The 41–50-year band contributed the largest single share, 40 of 95 women (42.11%), followed by the 31–40 band with 24 women (25.26%). Only 4 women (4.21%) were above 60 years [Table 1]. Table 1: Age-wise distribution of endometrial biopsies in abnormal uterine bleeding (n = 95) Age group (years) Frequency Percentage 21 – 30 15 15.79 31 – 40 24 25.26 41 – 50 40 42.11 51 – 60 12 12.63 61 – 70 2 2.11 71 – 80 2 2.11 Total 95 100.00 Table 2: Distribution of histomorphological patterns of endometrium in abnormal uterine bleeding (n = 95) Histopathological diagnosis Frequency Percentage Disordered proliferative endometrium 23 24.21 Proliferative phase 22 23.16 Secretory phase 18 18.95 Endometrial hyperplasia without atypia 7 7.37 Endometrial carcinoma 7 7.37 Endometrial polyp 5 5.26 Exogenous progestin (pill) effect 4 4.21 Luteal phase defect 3 3.16 Atrophic endometrium 3 3.16 Endometrial hyperplasia with atypia 2 2.11 Chronic endometritis 1 1.05 Total 95 100.00 Disordered proliferative endometrium was the commonest histomorphological pattern, present in 23 cases (24.21%). Proliferative phase endometrium followed with 22 cases (23.16%) and secretory phase endometrium with 18 (18.95%). These three cyclical or near-cyclical patterns together made up two-thirds of the series. Among the organic lesions, endometrial polyp accounted for 5 cases (5.26%) and chronic endometritis for a single case (1.05%). Four women (4.21%) showed exogenous progestin effect [Table 2]. Grouped by cause, functional patterns explained 73 cases (76.84%) and organic lesions 22 cases (23.16%) [Table 4]. Endometrial hyperplasia was diagnosed in 9 women (9.47%) — 7 without atypia (7.37%) and 2 with atypia (2.11%). Endometrial carcinoma was reported in 7 women (7.37%). Table 3: Histomorphological pattern of endometrium across clinical age groups (n = 95) Histopathological diagnosis Reproductive age (18–40 y) n = 39 Perimenopausal age (41–50 y) n = 40 Postmenopausal age (≥51 y) n = 16 Total Proliferative phase 6 14 2 22 Secretory phase 15 2 1 18 Disordered proliferative endometrium 9 12 2 23 Endometrial hyperplasia without atypia 2 4 1 7 Endometrial hyperplasia with atypia 0 2 0 2 Endometrial carcinoma 0 0 7 7 Endometrial polyp 4 1 0 5 Exogenous progestin (pill) effect 0 3 1 4 Luteal phase defect 2 1 0 3 Atrophic endometrium 1 1 1 3 Chronic endometritis 0 0 1 1 Total 39 40 16 95 Age changed the picture substantially [Table 3]. Thirty-nine women (41.05%) fell in the reproductive group, 40 (42.11%) in the perimenopausal group and 16 (16.84%) in the postmenopausal group. Secretory phase endometrium was the commonest finding among reproductive-age women, in 15 of 39 (38.46%), with disordered proliferative endometrium next at 9 (23.08%). In the perimenopausal group proliferative endometrium came out on top, in 14 of 40 women (35.00%), with disordered proliferative endometrium at 12 (30.00%). Among postmenopausal women the commonest single diagnosis was endometrial carcinoma, in 7 of 16 (43.75%) — every carcinoma in the series sat in this group, and not one was seen below 51 years. Both cases of atypical hyperplasia were perimenopausal, and all 5 endometrial polyps came from women aged 50 or below. The functional-to-organic ratio differed significantly across the three age groups: organic lesions accounted for 6 of 39 reproductive-age women, 7 of 40 perimenopausal women and 9 of 16 postmenopausal women (χ² = 11.89, df = 2, p = 0.003). Carcinoma was confined entirely to the postmenopausal group (7/16 versus 0/79 in the other two groups combined; Fisher’s exact test, p < 0.001). Table 4: Functional versus organic causes of abnormal uterine bleeding (n = 95) Category Diagnoses included Frequency Percentage Functional Disordered proliferative endometrium, proliferative phase, secretory phase, luteal phase defect, atrophic endometrium, exogenous progestin effect 73 76.84 Organic Endometrial hyperplasia with and without atypia, endometrial carcinoma, endometrial polyp, chronic endometritis 22 23.16 Total 95 100.00 Representative morphology is shown in Figures 1–4.

Two findings from this series are worth sitting with. Disordered proliferative endometrium was the most frequent pattern at 24.21%, and every one of the seven carcinomas came from a postmenopausal woman. The first figure sits comfortably within the published range. A three-year retrospective study of 850 adequate endometrial samples reported disordered proliferative endometrium as the commonest functional cause at 27.7%, with proliferative endometrium next at 18.2% and functional causes accounting for 73.9% of all cases — almost exactly the 76.84% we found [13]. A Nepalese series of 403 biopsies put disordered proliferative endometrium at 13.4%, lower than ours, though their cohort included a larger proportion of normal cycling endometrium [14]. The consistency of the functional-versus-organic ratio across centres is the more interesting point: roughly three in four women with AUB who reach a pathology laboratory do not have a structural lesion, which has direct bearing on how quickly hysterectomy should be offered. Disordered proliferative endometrium is a perimenopausal phenomenon, driven by anovulatory cycles and asynchronous growth of the functional layer under unopposed oestrogen, and it also shows up in women taking exogenous oestrogen. Our peak in the 41–50 year band, 42.11% of the whole series, matches a study of 160 endometrial biopsies from Puducherry where the maximum number of samples also came from the 41–50 year group [15]. In the perimenopausal group specifically, proliferative endometrium was our commonest pattern at 35.00%, which lines up almost exactly with the 35.22% reported by Damle et al. in perimenopausal women above 40 years [16]. A study of 103 hysterectomies for perimenopausal AUB from Assam found 67.97% of patients between 40 and 45 years, a narrower peak than ours but in the same decade [17]. Hyperplasia in our cohort ran at 9.47%. That is close to the 10.92% reported from Kathmandu [14] and higher than the 5% seen in a Karachi series of 241 endometrial samples [18]. Comparisons here need care, because centres differ in whether they report simple and complex hyperplasia separately and in whether atypical hyperplasia is counted as hyperplasia or as a precancer. Our own split — 7 without atypia against 2 with atypia — matters clinically far more than the combined figure, and we come back to why. Carcinoma was diagnosed in 7.37% of our cases, which is on the higher side, and it made up 43.75% of all postmenopausal biopsies. A Jordanian review of 3,233 patients with AUB found malignant lesions in 42 women, the majority above 50 years [19]. The Karachi series reported carcinoma in 2% overall but 9% of postmenopausal women [18]. A retrospective study of 307 peri- and postmenopausal women correlating histology with transvaginal endometrial thickness found endometrial thickness above 11 mm strongly associated with hyperplasia and malignancy, and recommended sampling at that threshold in perimenopausal women and above 5 mm after menopause [20]. Our relatively high carcinoma rate almost certainly reflects referral pattern rather than true community incidence — a tertiary pathology laboratory in a district with limited local gynaecological services receives a selected, symptomatic and older population. Anyone reading this figure as a population estimate would be reading it wrongly. The distribution across the three clinical groups was the expected one, and it is the practical takeaway. Secretory endometrium led the reproductive group at 38.46%, which suggests ovulatory dysfunctional bleeding rather than structural disease in these younger women; a Ugandan cross-sectional study of women with AUB similarly found proliferative endometrium (38.9%) and simple hyperplasia without atypia (20.4%) as leading patterns in a young cohort with a mean age of 32.7 years [21]. Whether proliferative and disordered proliferative endometrium are biologically distinct entities in anovulatory AUB is less settled than the morphology suggests — immunoprofiling of CD4, CD8, CD56 and CD68 in 73 women found no significant difference in immune cell infiltration between the two [22]. The separation, for now, remains a morphological and clinical one rather than an immunological one. Which brings the discussion back to hyperplasia and why the atypia call is the one that counts. The long-term data are unambiguous. Kurman and colleagues followed 170 women with untreated hyperplasia for a mean of 13.4 years and found progression to carcinoma in 2 of 122 women without atypia (1.6%), against 11 of 48 with atypical hyperplasia (23%) [23]. Both of our atypical cases were perimenopausal, in the same window where unopposed oestrogen exposure is longest. Atypical hyperplasia, now termed endometrial intraepithelial neoplasia, is the direct precursor of endometrioid adenocarcinoma, and chronic unopposed oestrogen exposure remains its dominant risk factor. Management diverges completely — surveillance or progestin for hyperplasia without atypia, and a serious conversation about hysterectomy for atypical hyperplasia, modified by the woman’s wish to preserve fertility [24]. A pathology report that says only “endometrial hyperplasia” without addressing atypia has not finished its job. The postmenopausal findings deserve a final comment. All seven of our carcinomas were postmenopausal, and none appeared below 51 years. A recent series of 35 women with postmenopausal bleeding found benign disease in 74.3%, with atrophic endometrium the commonest finding at 28.6%, but premalignant or malignant lesions in a combined 25.7% — and critically, no premalignant or malignant lesion at all when endometrial thickness was 4 mm or less [25]. Postmenopausal bleeding is common, mostly benign, and occasionally the first sign of cancer. Those three facts are not in tension; they simply mean the tissue has to be looked at. Limitations. The sample of 95 is modest, and it came from a single centre, so the proportions here should not be generalised. The postmenopausal subgroup in particular held only 16 women, so the 43.75% carcinoma rate within it rests on 7 cases and carries a wide confidence interval. Small biopsy specimens carry a known risk of undersampling a focal lesion, and hysterectomy follow-up was not available for every woman diagnosed with hyperplasia or carcinoma, so biopsy-to-hysterectomy concordance could not be calculated. Immunohistochemistry and molecular classification were not applied, which limits what can be said about the carcinomas beyond morphology. A prospective study with radiological correlation and hysterectomy follow-up would answer the questions this one raises.

Endometrial biopsy in AUB yields a wide range of diagnoses, and in this cohort most of them were functional rather than structural. Disordered proliferative endometrium at 24.21% points to anovulation as the main mechanism in perimenopausal women, while the clustering of all seven carcinomas after menopause makes the case for sampling any woman who bleeds after her periods have stopped. The value of the report lies less in naming the pattern than in getting the atypia question right, because that single distinction separates a woman who can be managed with a progestin from one who needs an oncological referral.

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