In the United States, endometrial cancer is the fourth most common type of cancer among women. Development of endometrial cancer is the result of multiple genetic mutations. Genes involved in the pathogenesis of endometrial cancer include TP53, KRAS, and PTEN. Approximately 8–30% of patients with atypical endometrial hyperplasia may progress to develop endometrial cancer. The pathophysiology of endometrial cancer depends on the 7 histological subtypes: endometrioid, uterine papillary serous, mucinous, clear cell, squamous cell, mixed and undifferentiated. Common risk factors in the development of endometrial cancer are estrogen exposure, tamoxifen, obesity, diabetes, high blood pressure and genetic disorders. The hallmark of endometrial cancer is abnormal vaginal bleeding. A positive history of bleeding between normal periods in premenopausal women and vaginal bleeding and/or spotting in postmenopausal women is suggestive of endometrial cancer. Pelvic MRI and endometrial biopsy may be diagnostic of endometrial cancer. Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. The optimal therapy for endometrial cancer depends on the stage at diagnosis and comprises total hysterectomy and bilateral salpingo-oophorectomy to most patients if they are surgical candidates.

The earliest descriptions of endometrial cancer were reported in the early 1900s. The association between estrogen and development of endometrial cancer was first reported in the 1970s when the incidence of endometrial cancer significantly increased between 1970 and 1975 following the introduction of estrogen replacement therapy.

Endometrial cancer may be classified according to histology into either type I comprising 80% of endometrial cancers or type II accounting for around 20%.

Development of endometrial cancer is the result of multiple genetic mutations. Genes involved in the pathogenesis of endometrial cancer include TP53, KRAS, and PTEN. The pathophysiology of endometrial cancer depends on the histological subtype.

Causes of endometrial cancer include genetic mutations of the KRAS gene, TP53 gene, TP16 gene, and/or PTEN gene. Other genetic mutations have also been described.

Endometrial cancer in early stage must be differentiated from diseases that cause abnormal uterine bleeding and endometrial thickening on ultrasound, such as endometrial hyperplasia, endometrial polyp, and submucosal uterine leiomyoma. In advanced stages endometrial cancer must be differentiated from uterine sarcoma and uterine lymphoma.

In the United States, endometrial cancer is the fourth most common type of cancer among women. In 2011, the age-adjusted prevalence was approximately 232 per 100,000 and the age-adjusted incidence was approximately 27 per 100,000 in the USA.

Common risk factors in the development of endometrial cancer are estrogen exposure, tamoxifen use, obesity, diabetes, high blood pressure and genetic disorders.

There is insufficient evidence to recommend routine screening for endometrial cancer.

If left untreated, approximately 8–30% of patients with atypical endometrial hyperplasia may progress to develop endometrial cancer. Common complications of endometrial cancer include menorrhagia and metastasis. Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good.

According to the FIGO Staging System, there are 4 stages of endometrial cancer.

The hallmark of endometrial cancer is abnormal vaginal bleeding. A positive history of bleeding between normal periods in premenopausal women and vaginal bleeding and/or spotting in postmenopausal women is suggestive of endometrial cancer.

The MRI is not needed for the diagnosis of endometrial cancer. However, an MRI may be helpful in staging of the disease.

On transvaginal ultrasound, endometrial cancer is characterized by thickening of the endometrium and disruption of a subendometrial halo.

Other diagnostic studies for endometrial cancer include endometrial biopsy

The optimal therapy for endometrial cancer depends on the stage at diagnosis. A combination of chemotherapy and radiation therapy is indicated in stages IIIB- IV.

Surgery is the mainstay of treatment for endometrial cancer stage I-III.

Effective measures for the primary prevention of endometrial cancer include administration of combination oral contraceptives.

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The earliest descriptions of endometrial cancer were reported in the early 1900s. The association between estrogen and development of endometrial cancer was first reported in the 1970s when the incidence of endometrial cancer significantly increased between 1970 and 1975 following the introduction of estrogen replacement therapy.

• The earliest descriptions of endometrial cancer were reported in the early 1900s.
• The association between estrogen and development of endometrial cancer was first reported in the 1970s when the incidence of endometrial cancer significantly increased between 1970 and 1975 following the introduction of estrogen replacement therapy.^[1]
• Surgical staging of endometrial cancer was first suggested in 1988 and was later revised in 2009.^[2]
• The first laparoscopic hysterectomy was reported in 1992.^[3]

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Endometrial cancer may be classified according to histology into either type I comprising 80% of endometrial cancers or type II accounting for around 20%.

Endometrial cancer may be classified according to histology into 2 types:^[1]

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Development of endometrial cancer is the result of multiple genetic mutations. Genes involved in the pathogenesis of endometrial cancer include TP53, KRAS, and PTEN. The pathophysiology of endometrial cancer depends on the histological subtype.

• Endometrial cancer forms when there are errors in normal endometrial cell growth.^[1][2]
• Development of an endometrial hyperplasia (overgrowth of endometrial cells) is a significant risk factor because hyperplasia can and often do develop into adenocarcinoma, though cancer can develop without the presence of a hyperplasia. Within ten years, 8–30% of atypical endometrial hyperplasias develop into cancer, whereas 1–3% of non-atypical hyperplasias do so.^[3]
• Mutations in the KRAS gene can cause endometrial hyperplasia and therefore type I endometrial cancer. Endometrial hyperplasia typically occurs after the age of 40. Endometrial glandular dysplasia occurs with an overexpression of TP53, and develops into a serous carcinoma (type II endometrial cancer).^[4]
• Endometrial cancer frequently metastasizes to the ovaries and fallopian tubes when the cancer is located in the upper part of the uterus and the cervix when the cancer is in the lower part of the uterus.
• The cancer usually first spreads into the myometrium and the serosa, then into other reproductive and pelvic structures. When the lymphatic system is involved, the pelvic lymph nodes and para-aortic lymph nodes are usually first to become involved, but in no specific pattern, unlike cervical cancer.
• More distant metastases are spread by the blood and often occur in the lungs, as well as the liver, brain, and bone.^[5]

Genes involved in pathogenesis of endometrial cancer involve:

• In 10–20% of endometrial cancers, mostly grade 3 (the highest histologic grade), mutations are found in a tumor suppressor gene, commonly TP53 or PTEN.
• In 20% of endometrial hyperplasias and 50% of endometrioid cancers, PTEN suffers a loss-of-function mutation or a null mutation, making it less effective or completely ineffective.^[7] Loss of PTEN function leads to up-regulation of the PI3k/Akt/mTOR pathway, which causes cell growth.^[8]
• The TP53 pathway can either be suppressed or highly activated in endometrial cancer. When a mutant version of TP53 is overexpressed, the cancer tends to be particularly aggressive. TP53 mutations and chromosome instability are associated with serous carcinomas, which tend to resemble ovarian and fallopian carcinomas. Serous carcinomas are thought to develop from endometrial intraepithelial carcinoma.^[8]
• PTEN and p27 loss of function mutations are associated with a good prognosis, particularly in obese women. The Her2/neu oncogene, which indicates a poor prognosis, is expressed in 20% of endometrioid and serous carcinomas. CTNNB1 (beta-catenin; a transcription gene) mutations are found in 14–44% of endometrial cancers and may indicate a good prognosis, but the data is unclear. Beta-catenin mutations are commonly found in endometrial cancers with squamous cells.^[8]
• FGFR2 mutations are found in approximately 10% of endometrial cancers, and their prognostic significance is unclear.^[7]
• SPOP is another tumor suppressor gene found to be mutated in some cases of endometrial cancer: 9% of clear cell endometrial carcinomas and 8% of serous endometrial carcinomas have mutations in this gene.^[9]
• Type I and type II cancers (explained below) tend to have different mutations involved. ARID1A, which often carries a point mutation in type I endometrial cancer, is also mutated in 26% of clear cell carcinomas of the endometrium, and 18% of serous carcinomas. Epigenetic silencing and point mutations of several genes are commonly found in type I endometrial cancer.^[10]
• Mutations in tumor suppressor genes are common in type II endometrial cancer. PIK3CA is commonly mutated in both type I and type II cancers. In women with Lynch syndrome-associated endometrial cancer, microsatellite instability is common.^[8]
• The genetic mutations most commonly associated with endometrioid adenocarcinoma are in the genes PTEN, a tumor suppressor gene, PIK3CA (expresses a kinase), KRAS (expresses GTPase that functions in signal transduction), and CTNNB1 that expresses a protein involved in adhesion and cell signaling. The CTNNB1 (beta-catenin) gene is most commonly mutated in the squamous subtype of endometrioid adenocarcinoma.^[11]
• The genetic mutations seen in serous carcinoma are chromosomal instability and mutations in TP53, an important tumor suppressor gene.^[12]
• The p53 cell signaling system is not active in endometrial clear cell carcinoma.^[13]

On microscopic histopathological analysis, endometrial cancer is characterized by:^[14]

1. Endometrioid (most common; 75%–80%)

• Ciliated adenocarcinoma
• Secretory adenocarcinoma
• Papillary or villoglandular
• Adenocarcinoma with squamous differentiation

• Adenoacanthoma
• Adenosquamous (Adenosquamous tumors contain malignant elements of both glandular and squamous epithelium)

2. Uterine papillary serous (<10%)

3. Mucinous (1%)

4. Clear cell (4%)

5. Squamous cell (<1%)

6. Mixed (10%)

7. Undifferentiated

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Causes of endometrial cancer include genetic mutations of the KRAS gene, TP53 gene, TP16 gene, and/or PTEN gene. Other genetic mutations have also been described.

Endometrial cancer arises following multiple genetic mutations. The following genes are involved in the development of endometrial cancer:

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In early stages endometrial cancer must be differentiated from diseases that cause abnormal uterine bleeding and endometrial thickening on ultrasound, such as endometrial hyperplasia, endometrial polyp, and submucosal uterine leiomyoma. In advanced stages endometrial cancer must be differentiated from uterine sarcoma and uterine lymphoma.

• In early stages endometrial cancer must be differentiated from diseases that cause abnormal uterine bleeding and endometrial thickening on ultrasound, such as endometrial hyperplasia, endometrial polyp, and submucosal uterine leiomyoma. In advanced stages endometrial cancer must be differentiated from uterine sarcoma and uterine lymphoma.^[1]

In the United States, endometrial cancer is the fourth most common type of cancer among women.^[1] In 2011, the age-adjusted prevalence was approximately 232 per 100,000 and the age-adjusted incidence was approximately 27 per 100,000 in the USA.^[2]

• In 2011, the age-adjusted prevalence of endometrial cancer was 232 per 100,000 in the United States.^[2]

• In 2011, the age-adjusted incidence of endometrial cancer was 27 per 100,000 persons in the United States.^[2]

• While the overall age-adjusted incidence of endometrial cancer in the United States between 2007 and 2011 is 24 per 100,000.
• The age-adjusted incidence of endometrial cancer by age category is:^[2]
  • Under 65 years: 16 per 100,000
  • 65 and over: 84 per 100,000

• Endometrial cancer is more prevalent among White patients.
• Shown below is a table depicting the age-adjusted prevalence of endometrial cancer by race in 2011 in the United States.^[2]

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Common risk factors in the development of endometrial cancer are estrogen exposure, tamoxifen use, obesity, diabetes, high blood pressure and genetic disorders.

Some of the risk factors for endometrial cancer are:

1. Estrogen exposure

• Women who have received higher doses or longer periods of estrogen therapy have higher risks of endometrial cancer.^[1]

2. Early menarche

• Women who have menstrual periods at an early age also increases the number of years the body is exposed to estrogen and increases a woman’s risk of endometrial cancer.^[2]

3.Late menopause

• Women who reach menopause at an older age are exposed to estrogen for a longer time and have an increased risk of endometrial cancer.^[2]

4. Nulliparity

• Never being pregnant is also a risk factor for endometrial cancer. Because estrogen levels are lower during pregnancy, women who have never been pregnant are exposed to estrogen for a longer time than women who have been pregnant. This increases the risk of endometrial cancer.^[3]

5. Tamoxifen

• Tamoxifen is one of a group of drugs called selective estrogen receptor modulators, or SERMs. Tamoxifen is used to prevent breast cancer in women who are at high risk for the disease, but it increases the risk of endometrial cancer. This risk is greater in postmenopausal women.^[4]

6. Family history

• Hereditary nonpolyposis colon cancer (HNPCC) syndrome (Lynch syndrome): Women with Lynch syndrome have a 40–60% risk of developing endometrial cancer, higher than their risk of developing colorectal (bowel) or ovarian cancer.^[5] Carcinogenesis in Lynch syndrome comes from a mutation in MLH1 and/or MLH2: genes that participate in the process of mismatch repair, which allows a cell to correct mistakes in the DNA.^[6] Other genes mutated in Lynch syndrome include MSH2, MSH6, and PMS2, which are also mismatch repair genes.
• Cowden syndrome: Women with Cowden syndrome have a 5–10% lifetime risk of developing endometrial cancer, compared to the 2–3% risk for unaffected women.^[7][8] Cowden syndrome is associated with mutations in PTEN, a tumor suppressor gene, that cause the PTEN protein not to work properly leading to hyperactivity of the mTOR pathway.

7. Polycystic ovary syndrome

• Women who have polycystic ovary syndrome have an increased risk of endometrial cancer.

8. Obesity

• Obesity increases the risk of endometrial cancer. This may be because obesity is related to other risk factors such as estrogen levels, polycystic ovary syndrome, lack of physical activity, and a diet that is high in saturated fats.^[9]

11. Diabetes and hypertension

• Women suffering from hypertension or diabetes are at increased risk for developing endometrial cancer.^[10]

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There is insufficient evidence to recommend routine screening for endometrial cancer.^[1]

There is insufficient evidence to recommend routine screening for endometrial cancer.^[1]

Women with Lynch syndrome have a risk of developing endometrial cancer up to 50% higher than the general population.

• Screening for endometrial cancer in women with Lynch syndrome by annual endometrial sampling is recommended starting at age 30 to 35 (or 5 to 10 years prior to the first diagnosed Lynch syndrome-associated cancer in a family member).^[2]

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Complications are usually due to the therapy. They can be classified as –

• Intra-operative-
  • Uterine perforation following D&C or biopsy.
  • Hemorrhage after lymphadenectomy
• Post-operative- typically common as many females have comorbid conditions like obesity, increased age, etc when they develop endometrial cancer. Of note is thromboembolism.

Of all prognostic factors to consider in endometrial cancer, staging is the most important one. Surgical histopathology contributes to it. Clear cell and papillary serous types are associated with a poor prognosis and are included in the histological category of poorly differentiated variety. As far as squamous types are concerned, it is just the adeno component which plays a key role in prognosis. More the adeno component, worse the prognosis.

It is the depth and not the grade of myometrial invasion that is important, as with increasing depth, there are high chances of extra-uterine spread. Lymph node metastasis is equally important and must be correlated with other prognostic factors. A positive peritoneal cytology needs only to be reported but it does not change the stage.

Because endometrial cancer is usually diagnosed in the early stages (70 % to 75 % of cases are in stage 1 at diagnosis; 10 % to 15 % of cases are in stage 2; 10 % to 15 % of cases are in stage 3 or 4), there is a better probable outcome associated with it than with other types of gynecological cancers such as cervical or ovarian cancer. While endometrial cancers are 40% more common in Caucasian women, an African American woman who is diagnosed with uterine cancer is twice as likely to die, possibly due to the higher frequency of aggressive subtypes in that population.

The 5-year survival rate for endometrial cancer following appropriate treatment is:

• 75% to 95% for stage 1
• 50% for stage 2
• 30% for stage 3
• less than 5% for stage 4

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 complications and prognosis

History and Physical

A complete medical and family history and physical examination, engaging cancer genetics counseling and are crucial in narrowing down a diagnosis. Abnormal uterine bleeding is the most common symptom of endometrial cancer. ^[1] Occasionally, cervicovaginal cytology or abnormal vaginal discharge may lead to the diagnosis of endometrial cancer. Pap smears taken within 6 months prior to the diagnosis of endometrial cancers were reported to be abnormal 38% of the time, consistent with adenocarcinoma 21% of the time, and in 13% of cases showed atypical glandular cells. ^[2] The definitive diagnosis of endometrial cancer is accomplished by the use of histology. However, the personal and family history of the patient together with a complete physical examination are instrumental. Intrauterine pregnancy should be considered in women of reproductive age with abnormal uterine bleeding or amenorrhea unless post-menopausal status has been confirmed. If suspicious symptoms, signs, and/or family history are present, basic laboratory evaluation, cervical-vaginal Pap smear, and transvaginal ultrasound generally are considered. Patients with an abnormal Pap smear should undergo further investigation regardless of age. ^[3]

Transvaginal Ultrasound

This is often the next step when suspicious history or physical findings are seen. In some cases, abdominal ultrasound may also be used. In women aged 35 years or younger who are diagnosed with benign gynecologic conditions or non-gynecologic etiologies and are determined to be of low risk for endometrial pathology, transvaginal ultrasound can be skipped. However, if there is a subsequent failure of medical management, transvaginal ultrasound should be performed. ^[4] Transvaginal ultrasound should be performed in younger women with recurrent abnormal uterine bleeding and anovulatory bleeding in women over the age of 35 years together with examination under anesthesia with dilation and curettage or endometrial sampling in an outpatient setting. Any suspicious findings warrants further investigation. Currently, the cut-off for endometrial thickness that requires further investigation in patients with abnormal uterine bleeding is ≥5 mm in post-menopausal women as measured by transvaginal ultrasound. ^[5] However, a recent meta-analysis and systematic review recommended that the cut-off for exclusion of endometrial cancer in women with post-menopausal bleeding be changed to ≤3 mm. ^{[6] [7]}

Endocervical Sampling and Endocervical Curettage

Endocervical sampling[ of endocervical curettage is sometimes done before endometrial sampling so determine if there is involvement of the cervix. Biopsies should be taken of any unusual findings and these may prove useful in planning patient management.

Hysteroscopy

Hysteroscopic examination can be used in detection of endometrial polyps, which can be associated with endometrial cancer particularly among post-menopausal women. ^[8] When used in conjunction with dilation and curettage, hysteroscopy can be used in the removal of these polyps and detection of focal lesions. ^{[9] [10]} Hysteroscopy can also be used to detect submucosal myomas.

Endometrial Biopsy

When there are abnormal findings on transvaginal ultrasound such as endometrial thickness of ≥5 mm or any abnormal uterine or adnexal findings in women with post-menopausal bleeding, .

Other Diagnostic Methods

• If there is recurrent post-menopausal bleeding or the results of an endometrial biopsy is equivocal, evaluation under anesthesia and fractional dilation and curettage should be performed, and the diagnosis may be enhanced by hysteroscopy for the detection of focal lesions. ^{[9] [10]}

• Chest X-ray can be done pre-operatively to evaluate patients for metastasis.

• MRI can be performed in difficult cases when ovarian tumors, adnexal involvement, or parametrial invasion is suspected. ^[11]

• In patients that are Lynch syndrome mutation carriers, it is advisable to perform sonographic imaging, cystourethroscopy, and colonoscopy due to their increased risk of ovarian, urothelial, and colorectal cancer. ^{[12] [13]}

Staging Management of endometrial cancer and its precursor lesions depends upon the histotype and differentiation[[, extent of disease and status of the patient. The extent of endometrial carcinoma is surgically-pathologically classified, or “staged,” according to International Federation of Gynecology and Obstetrics (FIGO) criteria published in 2009 as:

Stage I: Tumor confined to the corpus uteri

• IA: No invasion or invasion into less than half of the myometrium
• IB: Invasion equal into or more than half of the myometrium

Stage II: Tumor invades cervical stroma but does not extend beyond the uterus

Stage III: Local and/or regional spread of tumor

• IIIA: Tumor invades the serosa or corpus and/or adnexa
• IIIB: Vaginal and/or parametrial involvement
• IIIC: Metastases to pelvic and/or para-aortic nodes
  • IIIC1: Positive pelvic nodes
  • IIIC2: Positive para-aortic nodes with or without pelvic nodes

Stage IV: Tumor invades bladder and/or bowel mucosa or distant metastases

• IVA: Tumor invasion of bladder and/or bowel mucosa
• IVB: Distant metastases, including intra-abdominal and/or inguinal nodes

Although positive peritoneal cytology does not change FIGO staging, this finding is associated with other factors that portend a poor prognosis. ^[14]

It is important to understand that staging is a means of coding and reporting the extent of disease and not a formula for managing endometrial cancer. Current FIGO classification by stage depends upon both surgical and pathological findings. Generally, preinvasive neoplastic lesions are diagnosed clinically and pathologically without resort to surgery. Sometimes, it is necessary to clinically and pathologically “stage” cancers when surgery is incomplete or precluded because of co-morbidity or other forbidding reasons.

References

Surgery

About 90% of women with endometrial cancer are treated with some form of surgery. ^[1] It is most often the initial treatment for endometrial cancer. Surgical treatment typically consists of hysterectomy with bilateral salpingo-oophorectomy, which is the surgical removal of the uterus, ovaries, and Fallopian tubes. In the United States,lymphadenectomy is routinely performed for all stages of endometrial cancer, However, in the United Kingdom, the lymph nodes are typically only removed with disease of stage II or greater. ^[2] The benefit of lymphadenectomy in stage I disease is still being contested. ^[3] Women who undergo lymphadenectomy are at risk of morbidity related to surgery or formation of lymphoedema/lymphocyst. ^[4] In stage III and IV cancers, cytoreductive surgery is often the management of choice, ^[5] and omental biopsy may also be performed. ^[6] Surgery can be done as part of palliative therapy in patients with stage IV disease in which there is distant metastasis. ^[3] The prognosis for stage III, stage IV, and recurrent endometrial cancers may be improved with maximum surgical debulking, especially if it is performed till tumor is > 1 cm. ^{[7] [8] [9] [10] [11] [12] [13] [14] [15]} While laparotomy is the traditional surgical procedure, laparoscopic surgery is associated with reduced operative morbidity and similar overall and disease free survival and is the preferred method in patients that are suspected to have early stage primary endometrial cancer. ^[6] Contraindications to surgery occur in about 5–10% of cases and include: ^[3]

• inoperable tumor
• massive obesity
• high-risk operations
• desire to preserve fertility

The side effects of surgical treatment include temporary incontinence, lymphedema and sexual dysfunction.

Adjuvant Therapies

The use of other therapies after surgery is called adjuvant therapy.^[5] These include radiation therapy and chemotherapy. One or both may be used and is often considered in cases of high-risk or high-grade cancers.

Radiotherapy

Adjuvant radiotherapy is often used in stage I and stage II endometrial cancer. It can be delivered via external beam radiotherapy or via vaginal brachytherapy, which is the preferred route due to its lower toxicity. External beam radiotherapy can be used to treat cancer remnants in the pelvis following surgery, while vaginal brachytherapy is used to treat cancer remnants that are located in the vagina. Although external beam radiotherapy significantly reduces the rate of relapse in the pelvis, overall survival and metastasis rates are not improved. ^[16] Overall, vaginal brachytherapy provides a better quality of life than external beam radiotherapy. ^[3] Brachytherapy and/or external beam radiotherapy can also be used when hysterectomy is contraindicated. ^[3]

Chemotherapy

This often involve the use of a combination of paclitaxel (or other taxanes like docetaxel), doxorubicin (and other anthracyclines), and platins (particularly cisplatin and carboplatin). Adjuvant chemotherapy has been found to increase survival in stage III and IV cancer more than added radiotherapy. ^{[5] [3] [1]} Mutations in mismatch repair genes, like those found in Lynch syndrome, can lead to resistance against platins. ^[17] Side effects of chemotherapy include neutropenia, alopecia, and gastrointestinal disturbances. ^[5] Palliative chemotherapy may also be used in patients in which surgical treatment is either not feasible or helpful. Use of chemotherapy at higher doses is associated with longer survival. ^{[5] [1]}

Hormonal therapy

Previously thought to be useful in most cases, hormonal therapy is now considered to helpful in only certain types of endometrial cancer. ^{[16] [5]} About 25% of metastatic endometrioid cancers show a response to progestins. Since endometrial stromal sarcomas typically have estrogen, progestin receptors, or both, they may be treated with with hormonal agents. Progestin receptors function as tumor suppressors in endometrial cancer cells. ^[18] Preliminary research and clinical trials have shown these treatments to have a high rate of response even in metastatic disease. ^[19]

Monitoring

CA-125 is a tumor marker that can be monitored for elevation in endometrial cancer and can be used to determine the response to therapy, especially in serous cell cancer or advanced disease. ^[20] Periodic MRIs or CT scansmay be beneficial in advanced disease. Pelvic examinations are recommended to be conducted every three to four months for the first two years following treatment, and every six months for the next three years. ^[3] PET/CT scanning is recommended if there is a suspicion of recurrence. ^[3]

References