Endometrial Hyperplasia: Causes & Treatment

Endometrial hyperplasia, a condition primarily evaluated and managed by gynecologists, is characterized by the disordered proliferation of endometrium, often stemming from hormonal imbalances. The American College of Obstetricians and Gynecologists (ACOG) provides guidelines for diagnosis and treatment, emphasizing the importance of accurate endometrial sampling techniques such as dilation and curettage (D&C) or hysteroscopy with biopsy. This abnormal growth of the uterine lining is frequently linked to excessive estrogen exposure without sufficient progesterone, a relationship extensively studied by researchers like Dr. Robert J. Kurman, known for his contributions to understanding endometrial pathology. Early detection and appropriate intervention are critical to prevent progression to endometrial cancer, reinforcing the need for comprehensive awareness and management strategies.

Endometrial hyperplasia, at its core, represents an aberration of the normal endometrial growth process. It is characterized by an abnormal proliferation of the endometrium, the inner lining of the uterus. This seemingly simple definition belies a complex condition with varying degrees of severity and potential for significant health consequences.

Defining Endometrial Hyperplasia

At a cellular level, endometrial hyperplasia involves an increase in the number of endometrial cells. This proliferation is often driven by hormonal imbalances, particularly an excess of estrogen relative to progesterone.

This hormonal imbalance disrupts the carefully orchestrated processes of endometrial growth and shedding that define the normal menstrual cycle. The result is an overgrowth of the endometrial lining, leading to a range of symptoms and potential complications.

The Importance of Early Detection and Management

The significance of understanding endometrial hyperplasia lies in the opportunity for early detection and effective management. Left unaddressed, endometrial hyperplasia can progress to endometrial cancer, a serious and potentially life-threatening condition.

Therefore, recognizing the risk factors, understanding the diagnostic procedures, and implementing appropriate treatment strategies are paramount in mitigating the potential adverse outcomes associated with this condition.

Timely intervention can often prevent progression to more advanced stages, preserving both the patient's health and quality of life.

Disordered Endometrial Proliferation: The Central Issue

The disordered proliferation of the endometrium is the central pathological feature of endometrial hyperplasia. Understanding the mechanisms driving this abnormal growth is crucial for developing targeted therapies and preventative strategies.

This uncontrolled proliferation can lead to a variety of clinical manifestations, including abnormal uterine bleeding, prolonged menstrual periods, and spotting between periods.

Furthermore, the cellular changes associated with hyperplasia can range from mild to severe, with the presence of atypia (precancerous changes) indicating a higher risk of progression to endometrial cancer.

By focusing on the underlying mechanisms of disordered endometrial proliferation, researchers and clinicians can work towards improving diagnostic accuracy, refining treatment approaches, and ultimately, reducing the burden of endometrial hyperplasia and its associated risks.

Epidemiology and Risk Factors: Who is at Risk?

Endometrial hyperplasia, at its core, represents an aberration of the normal endometrial growth process. It is characterized by an abnormal proliferation of the endometrium, the inner lining of the uterus. This seemingly simple definition belies a complex condition with varying degrees of severity and potential for significant health consequences. To effectively manage and mitigate the risks associated with endometrial hyperplasia, it is critical to understand its epidemiology and identify the factors that predispose individuals to this condition.

Prevalence and Incidence

The reported prevalence of endometrial hyperplasia varies, influenced by factors such as diagnostic criteria, population demographics, and the availability of screening programs. Studies indicate that the incidence rises with age, peaking around the time of menopause.

Understanding these baseline statistics is critical for healthcare providers to assess risk within their patient populations and implement appropriate surveillance strategies.

The Role of Hormonal Imbalances

Hormonal imbalances, particularly those involving estrogen and progesterone, play a pivotal role in the development of endometrial hyperplasia.

Estrogen: The Primary Driver

Estrogen is the primary hormone responsible for stimulating the growth and proliferation of the endometrium. In a normal menstrual cycle, estrogen levels rise during the follicular phase, promoting endometrial thickening.

Progesterone: The Counterbalance

Progesterone, released after ovulation, acts as a counterbalance to estrogen, stabilizing the endometrium and preventing excessive growth. It induces secretory changes that prepare the uterine lining for implantation.

Unopposed Estrogen: A High-Risk Scenario

Unopposed estrogen, a condition where estrogen is not adequately counterbalanced by progesterone, is a significant risk factor for endometrial hyperplasia. This situation can arise from various causes, including anovulation, estrogen-only hormone replacement therapy, or conditions that lead to excessive estrogen production.

The imbalance results in continuous endometrial stimulation, increasing the risk of abnormal proliferation and subsequent hyperplasia.

Conditions and Factors Increasing Risk

Several conditions and lifestyle factors can increase the risk of developing endometrial hyperplasia, often by disrupting the delicate hormonal balance.

Polycystic Ovary Syndrome (PCOS)

PCOS is a common endocrine disorder characterized by hormonal imbalances, including elevated levels of androgens and estrogen, as well as infrequent or absent ovulation. The chronic anovulation associated with PCOS leads to prolonged exposure to unopposed estrogen, significantly increasing the risk of endometrial hyperplasia.

Obesity

Obesity is strongly correlated with an increased risk of endometrial hyperplasia. Adipose tissue is an active endocrine organ that converts androgens to estrogen, leading to elevated estrogen levels.

This excess estrogen, coupled with insulin resistance commonly seen in obese individuals, further disrupts hormonal balance and promotes endometrial proliferation.

Diabetes Mellitus

Diabetes mellitus, particularly type 2 diabetes, has been identified as an independent risk factor for endometrial hyperplasia. While the exact mechanisms are still being investigated, insulin resistance and elevated insulin levels may play a role in promoting endometrial cell growth.

Menopause

The menopausal transition is marked by significant hormonal fluctuations. During perimenopause, unpredictable ovulation patterns can lead to periods of unopposed estrogen exposure.

Postmenopausal women receiving estrogen-only hormone replacement therapy are at higher risk, highlighting the importance of combining estrogen with progestin in appropriate cases.

Anovulation

Anovulation, the absence of ovulation, prevents the release of progesterone, leaving the endometrium continuously exposed to estrogen. This is a common feature in conditions like PCOS and can occur during perimenopause. Chronic anovulation significantly increases the risk of endometrial hyperplasia due to the lack of progesterone's protective effects.

Genetic Considerations

While hormonal factors are predominant, genetic predispositions also play a role in endometrial hyperplasia, particularly in cases progressing to endometrial cancer.

PTEN Gene

The PTEN gene is a tumor suppressor gene involved in cell growth and apoptosis. Mutations in PTEN are frequently found in endometrial hyperplasia and endometrial cancer, indicating its importance in regulating endometrial cell proliferation.

MSI (Microsatellite Instability)

MSI is a marker of defective DNA mismatch repair, which is a critical mechanism for maintaining genomic stability. High levels of MSI are associated with an increased risk of endometrial cancer and are often found in atypical endometrial hyperplasia.

PIK3CA Gene

The PIK3CA gene encodes a protein involved in cell growth and proliferation pathways. Mutations in PIK3CA are common in various cancers, including endometrial cancer, and contribute to uncontrolled cell growth and resistance to apoptosis.

Understanding these genetic factors can aid in risk assessment and potentially guide personalized treatment strategies.

Pathophysiology: How Hyperplasia Develops

Endometrial hyperplasia, at its core, represents an aberration of the normal endometrial growth process. It is characterized by an abnormal proliferation of the endometrium, the inner lining of the uterus. This seemingly simple definition belies a complex condition with varying degrees of severity and potentially serious consequences. Understanding the underlying biological mechanisms is crucial for developing effective prevention and treatment strategies.

Normal Endometrial Growth and Shedding

The endometrium undergoes cyclical changes in response to hormonal fluctuations during the menstrual cycle. Estrogen stimulates proliferation, leading to thickening of the endometrial lining in the proliferative phase. After ovulation, progesterone secreted by the corpus luteum induces differentiation of the endometrium in the secretory phase, preparing it for implantation.

If pregnancy does not occur, the corpus luteum regresses, resulting in a decline in both estrogen and progesterone levels. This hormonal withdrawal triggers menstruation, the shedding of the endometrial lining. This tightly regulated process ensures that the endometrium remains healthy and responsive to reproductive signals.

Disruption of Cell Cycle Regulation in Hyperplasia

In endometrial hyperplasia, the normal regulatory mechanisms governing cell growth are disrupted. Unopposed estrogen exposure is a primary driver, leading to excessive proliferation of endometrial cells. This increased proliferation overrides the signals that normally limit growth and differentiation, resulting in an abnormally thickened endometrial lining.

The cell cycle, a series of events that lead to cell division, is tightly controlled by various checkpoints and regulatory proteins. In hyperplasia, these checkpoints may be bypassed or rendered ineffective, allowing cells to divide uncontrollably. Genetic mutations can also contribute to the dysregulation of the cell cycle.

Apoptosis (Programmed Cell Death) and Its Dysregulation

Apoptosis, or programmed cell death, is a crucial mechanism for maintaining tissue homeostasis. It eliminates damaged or unwanted cells, preventing uncontrolled growth. In endometrial hyperplasia, the process of apoptosis is often impaired.

This means that cells that would normally be eliminated persist and contribute to the abnormal proliferation. The resistance to apoptosis can be due to alterations in the expression or function of key apoptotic proteins.

Influence of Hormone Receptors

Hormone receptors play a central role in mediating the effects of estrogen and progesterone on the endometrium.

Estrogen Receptors (ER)

Estrogen exerts its effects by binding to estrogen receptors (ERs) located in the endometrial cells. Activation of ERs triggers a cascade of signaling events that promote cell proliferation and growth. In endometrial hyperplasia, the increased exposure to estrogen leads to overstimulation of ERs, resulting in excessive endometrial growth.

Progesterone Receptors (PR)

Progesterone counteracts the effects of estrogen by binding to progesterone receptors (PRs). PR activation inhibits cell proliferation and promotes differentiation of the endometrium. In some cases of endometrial hyperplasia, the expression or function of PRs is reduced, making the endometrium less responsive to the protective effects of progesterone. This imbalance further contributes to the development of hyperplasia.

The Role of Endometrial Biologists

Researchers specializing in endometrial biology play a crucial role in unraveling the complex mechanisms underlying endometrial hyperplasia. Their work involves studying the molecular pathways involved in endometrial growth, differentiation, and apoptosis. By identifying key targets for intervention, these researchers contribute to the development of more effective treatments and prevention strategies for this condition.

Classification: Understanding the Different Types

Endometrial hyperplasia, at its core, represents an aberration of the normal endometrial growth process. It is characterized by an abnormal proliferation of the endometrium, the inner lining of the uterus. This seemingly simple definition belies a complex condition with varying degrees of severity and potential for malignant transformation. Therefore, a clear classification system is essential for accurate diagnosis, risk stratification, and appropriate clinical management.

Classifying Hyperplasia Based on Cellular Atypia

The presence or absence of cellular atypia is a cornerstone in the classification of endometrial hyperplasia. This distinction fundamentally divides the condition into two broad categories: hyperplasia without atypia and atypical hyperplasia. This classification directs clinical management pathways.

Hyperplasia Without Atypia

Endometrial hyperplasia without atypia indicates an overgrowth of endometrial cells, but these cells retain a relatively normal appearance under microscopic examination. This form of hyperplasia is generally associated with a lower risk of progressing to endometrial cancer compared to its atypical counterpart.

It is often linked to hormonal imbalances, particularly excessive estrogen exposure without sufficient progesterone.

Atypical Hyperplasia

Atypical hyperplasia, on the other hand, signifies the presence of precancerous changes within the endometrial cells. These cells exhibit abnormal features, such as variations in size and shape, altered nuclear characteristics, and disorganized architectural patterns.

Atypical hyperplasia carries a significantly higher risk of progressing to endometrial cancer.

The presence of atypia necessitates more aggressive management strategies.

The World Health Organization (WHO) Classification System

The World Health Organization (WHO) classification system provides a standardized framework for categorizing endometrial hyperplasia. It incorporates the concept of cellular atypia, but further refines the diagnostic criteria based on architectural complexity and cytological features.

The WHO classification distinguishes between two main categories:

• Endometrial Hyperplasia Without Atypia (EHWA)
• Atypical Endometrial Hyperplasia (AEH)

This system is widely adopted by pathologists worldwide. It is used to ensure consistent diagnoses and facilitate communication among healthcare professionals.

Progression to Endometrial Cancer

One of the most significant concerns regarding endometrial hyperplasia is its potential to progress to endometrial cancer. While not all cases of hyperplasia will transform into cancer, understanding the risk factors and timelines associated with this progression is crucial for informed decision-making.

Risk Factors for Progression

Several factors can influence the risk of progression from endometrial hyperplasia to endometrial cancer. Atypical hyperplasia, as mentioned earlier, carries a substantially higher risk.

Other risk factors include:

• Prolonged exposure to unopposed estrogen
• Obesity
• Advanced age
• Genetic predispositions (e.g., Lynch syndrome)

Timelines for Progression

The timeframe for progression from endometrial hyperplasia to endometrial cancer is highly variable and depends on individual factors and the specific type of hyperplasia. In some cases, the transformation may occur over several years, while in others, it can happen more rapidly.

Regular monitoring and appropriate management are essential to mitigate this risk.

It is also important to acknowledge that some lesions diagnosed as atypical hyperplasia may already harbor occult (hidden) areas of early-stage endometrial cancer. This underscores the importance of careful pathological evaluation and comprehensive management strategies.

Diagnosis: Identifying Endometrial Hyperplasia

Endometrial hyperplasia, at its core, represents an aberration of the normal endometrial growth process. It is characterized by an abnormal proliferation of the endometrium, the inner lining of the uterus. This seemingly simple definition belies a complex condition with varying degrees of severity and, most crucially, differing risks of progression to endometrial cancer. Accurate and timely diagnosis is, therefore, paramount for effective management and prevention.

The diagnostic pathway for endometrial hyperplasia involves a multi-pronged approach, integrating initial assessment techniques with more invasive sampling methods and advanced diagnostic tools. These approaches are often critical in order to ascertain the status of the patient. Each stage plays a vital role in building a comprehensive picture of the patient's condition.

Initial Assessment: Non-Invasive Screening

The initial assessment typically begins with a detailed medical history, focusing on menstrual patterns, risk factors, and any reported symptoms such as abnormal uterine bleeding. Following this, non-invasive imaging techniques are employed to visualize the endometrium.

Transvaginal Ultrasound (TVUS) is the primary imaging modality used. This procedure involves inserting a small probe into the vagina to obtain high-resolution images of the uterus and endometrium.

The key measurement obtained via TVUS is endometrial thickness. An abnormally thickened endometrium, particularly in postmenopausal women, raises suspicion for hyperplasia and warrants further investigation. However, it's crucial to acknowledge the limitations of TVUS.

Endometrial thickness alone cannot definitively diagnose hyperplasia, as other conditions like polyps, submucosal fibroids, and even early endometrial cancer can also present with a thickened endometrial stripe. Therefore, TVUS serves as a valuable screening tool, guiding the need for more specific diagnostic procedures.

Endometrial Sampling Techniques: Obtaining Tissue for Analysis

When the initial assessment suggests potential endometrial abnormalities, the next step involves obtaining a tissue sample for histological analysis. Several endometrial sampling techniques are available, each with its own advantages and limitations.

Endometrial Biopsy is a common procedure performed in an outpatient setting. It involves inserting a thin, flexible catheter into the uterus to collect a small sample of the endometrial lining. This sample is then sent to a pathologist for microscopic examination.

Pipelle Biopsy is a specific type of endometrial biopsy that utilizes a narrow, disposable suction device. It is often preferred due to its simplicity, minimal discomfort, and high accuracy in detecting endometrial abnormalities. However, like all blind sampling techniques, it is susceptible to sampling errors, particularly if the hyperplasia is focal or unevenly distributed within the uterus.

Dilation and Curettage (D&C) is a more invasive procedure performed in an operating room. It involves dilating the cervix and then using a curette to scrape the uterine lining. While D&C provides a more thorough sampling of the endometrium compared to biopsy techniques, it is associated with higher risks, including uterine perforation, infection, and Asherman's syndrome (scarring within the uterus). It is generally reserved for cases where biopsy results are inconclusive or when a more comprehensive evaluation is required.

Advanced Diagnostic Tools: Refining the Diagnosis

In certain situations, advanced diagnostic tools may be necessary to further refine the diagnosis and guide treatment decisions.

Hysteroscopy is a procedure that involves inserting a thin, telescope-like instrument called a hysteroscope into the uterus. This allows the physician to directly visualize the uterine cavity, identify any abnormalities such as polyps or suspicious lesions, and obtain targeted biopsies. Hysteroscopy is particularly useful in cases of focal hyperplasia or when imaging suggests the presence of structural abnormalities.

Histopathology is the cornerstone of endometrial hyperplasia diagnosis. This involves the microscopic examination of tissue samples obtained through biopsy, D&C, or hysteroscopy. A pathologist evaluates the cellular architecture, nuclear features, and presence of atypia to determine the type and severity of hyperplasia.

The pathologist's report provides critical information for guiding treatment decisions.

Immunohistochemistry (IHC) is a technique that utilizes antibodies to detect specific proteins within tissue samples. In the context of endometrial hyperplasia, IHC can be used to assess the expression of hormone receptors (estrogen and progesterone receptors) and other markers associated with cell proliferation and differentiation. This information can help predict the response to hormonal therapy and assess the risk of progression to endometrial cancer.

The Crucial Role of Pathologists and Histopathologists

The accurate diagnosis of endometrial hyperplasia hinges on the expertise of pathologists and histopathologists. These specialists are responsible for examining tissue samples under a microscope, interpreting cellular changes, and providing a definitive diagnosis. Their expertise is vital for determining the presence and type of hyperplasia, grading its severity, and assessing the risk of progression to endometrial cancer.

Furthermore, pathologists play a critical role in differentiating endometrial hyperplasia from other conditions that can mimic its appearance, such as endometrial polyps, atrophic endometrium, and early endometrial cancer. Their meticulous evaluation ensures that patients receive the most appropriate and effective treatment.

Treatment Strategies: Managing Endometrial Hyperplasia

Endometrial hyperplasia, at its core, represents an aberration of the normal endometrial growth process. It is characterized by an abnormal proliferation of the endometrium, the inner lining of the uterus. This seemingly simple definition belies a complex condition with varying degrees of severity and, consequently, a spectrum of treatment approaches. These strategies range from medical management with hormonal therapies to more definitive surgical interventions.

This section will explore the various treatment options available, emphasizing the importance of individualized care and the role of healthcare professionals in guiding treatment decisions.

Medical Management of Endometrial Hyperplasia

For many women, especially those with hyperplasia without atypia, medical management serves as the first line of defense. This approach focuses on restoring hormonal balance and controlling endometrial growth.

Progestin Therapy

Progestins, synthetic forms of progesterone, are the cornerstone of medical management.

These medications counteract the effects of estrogen on the endometrium, thereby inhibiting proliferation and promoting shedding. Progestins can be administered in various forms, including oral pills, injections, and intrauterine devices.

The choice of progestin and its route of administration depend on factors such as patient preference, severity of hyperplasia, and presence of other medical conditions.

Levonorgestrel-Releasing Intrauterine Device (LNG-IUD)

The LNG-IUD offers a localized approach to progestin therapy. It delivers a steady dose of levonorgestrel directly to the uterine lining.

This method is particularly effective in reducing endometrial thickness and controlling bleeding. The LNG-IUD also offers the advantage of fewer systemic side effects compared to oral progestins.

Its long-acting nature can also improve patient compliance.

Oral Contraceptives (OCPs)

While not typically the primary treatment for endometrial hyperplasia, OCPs may be considered in certain cases, particularly for younger women or those with concurrent hormonal imbalances.

OCPs contain both estrogen and progestin, providing a more comprehensive approach to hormonal regulation. However, the estrogen component may pose a risk in some patients. Careful consideration and monitoring are essential.

Metformin

Metformin, a medication commonly used to treat type 2 diabetes, has also found a role in managing endometrial hyperplasia, especially in women with polycystic ovary syndrome (PCOS).

PCOS is often associated with insulin resistance and hormonal imbalances that can contribute to endometrial proliferation. Metformin helps improve insulin sensitivity, which, in turn, can regulate hormone levels and reduce the risk of hyperplasia.

Surgical Interventions

In cases where medical management is ineffective, or when atypical hyperplasia is present, surgical intervention may be necessary. Hysterectomy, the surgical removal of the uterus, is the most common surgical option.

Hysterectomy

Hysterectomy offers a definitive solution for endometrial hyperplasia, eliminating the risk of progression to endometrial cancer. It is typically recommended for women who have completed childbearing or who have persistent or severe symptoms despite medical treatment.

The procedure can be performed via various approaches, including abdominal, vaginal, and laparoscopic techniques. The choice of approach depends on factors such as patient anatomy, surgeon experience, and the presence of other gynecological conditions.

While hysterectomy is effective, it is a major surgical procedure with potential risks and complications. Careful consideration of the risks and benefits is essential, along with a thorough discussion with the patient.

The Role of Gynecologists and Gynecologic Oncologists

The management of endometrial hyperplasia requires a collaborative approach involving gynecologists and, in some cases, gynecologic oncologists.

Gynecologists are often the first point of contact for women with abnormal bleeding or other symptoms suggestive of endometrial hyperplasia. They perform initial assessments, order diagnostic tests, and initiate medical management.

Gynecologic oncologists, specialists in cancers of the female reproductive system, become involved when atypical hyperplasia is diagnosed or when there is a concern for underlying or concurrent endometrial cancer. They provide expertise in surgical management and long-term surveillance.

Lifestyle Modifications

Lifestyle modifications, particularly weight management, can play a supportive role in managing endometrial hyperplasia.

Obesity is a known risk factor for endometrial hyperplasia. Excess adipose tissue can lead to increased estrogen production, which, in turn, can stimulate endometrial proliferation.

Weight loss through diet and exercise can help reduce estrogen levels and decrease the risk of hyperplasia. Lifestyle modifications are also important for managing other conditions, such as PCOS and diabetes, that can contribute to endometrial hyperplasia.

Guidelines and Recommendations: Staying Informed

Endometrial hyperplasia management is continually shaped by emerging research and refined clinical understanding. To ensure optimal patient care and informed decision-making, it's crucial to adhere to established guidelines and stay abreast of the latest recommendations from leading medical organizations. This section will explore key guidelines and research findings from ACOG, NCI, SGO, and CDC.

ACOG Guidelines: A Foundation for Clinical Practice

The American College of Obstetricians and Gynecologists (ACOG) offers comprehensive guidelines that serve as a cornerstone for managing endometrial hyperplasia. ACOG provides evidence-based recommendations on diagnosis, treatment, and surveillance, tailored to different patient populations and risk profiles.

These guidelines emphasize the importance of individualized treatment plans based on factors such as:

• Age
• Reproductive desires
• The presence or absence of atypia
• The patient's overall health.

ACOG also provides clear guidance on the use of progestin therapy, surgical management, and long-term monitoring strategies. ACOG guidelines are regularly updated to reflect the latest scientific evidence, ensuring that clinicians have access to the most current and reliable information.

NCI Research: Advancing Our Understanding

The National Cancer Institute (NCI) plays a pivotal role in funding and conducting research aimed at improving our understanding of endometrial hyperplasia and its relationship to endometrial cancer. NCI-supported studies explore a wide range of topics, including:

• The molecular mechanisms underlying hyperplasia development
• The identification of novel biomarkers for early detection
• The evaluation of new therapeutic approaches.

NCI research is instrumental in identifying risk factors, refining diagnostic methods, and developing more effective treatments for endometrial hyperplasia. The findings from NCI-sponsored trials often inform updates to clinical guidelines and influence the direction of future research.

SGO Guidelines: Expert Insights on Complex Cases

The Society of Gynecologic Oncology (SGO) offers specialized expertise in the management of complex gynecologic conditions, including endometrial hyperplasia with atypia and early-stage endometrial cancer. SGO guidelines provide evidence-based recommendations on surgical staging, adjuvant therapy, and surveillance strategies for patients at high risk of recurrence or progression.

SGO emphasizes the importance of a multidisciplinary approach to care, involving:

• Gynecologic oncologists
• Radiation oncologists
• Medical oncologists
• Other specialists as needed.

SGO guidelines are particularly valuable for managing challenging cases of endometrial hyperplasia that require advanced surgical techniques or systemic therapies.

CDC Data: Tracking Prevalence and Trends

The Centers for Disease Control and Prevention (CDC) collects and analyzes data on the prevalence, incidence, and risk factors for endometrial hyperplasia and endometrial cancer. CDC data provide valuable insights into the public health burden of these conditions and help to identify populations at increased risk.

This information is used to develop targeted prevention strategies and to monitor the effectiveness of screening programs. CDC data also contribute to our understanding of the long-term outcomes of endometrial hyperplasia and its impact on women's health. By tracking trends over time, the CDC can help to inform public health policy and to allocate resources effectively.

So, that's the lowdown on endometrial hyperplasia! Remember, if you're experiencing any unusual bleeding or spotting, it's always best to chat with your doctor. Early detection is key, especially when dealing with the disordered proliferation of endometrium. They can help you figure out the best course of action and keep you healthy and happy.