Archive for the Vagina Cancer category.
The histology of cervix cancer is by and large, about 90% at least, squamous lesions. The other 10% are adenocarcinomas arising in the endocervical canal. Really for purposes of treatment and staging, we treat all the same with one little exception so that the pathologist will subdivide for you the biopsy. Saying this is a squamous cell lesion, it’s a large cell non-keratinizing and that really is going to be treated the same, whether it’s keratinizing or non-keratinizing. The one exception that we find on rare occasion is this small cell carcinoma of the cervix, with neuroendocrine elements. An exceedingly rare lesion. Sort of defies the usual spread patterns and prognosis in that it oftentimes hematogenously spreads and spreads widely despite the fact that it appears to be an early lesion, managed by surgery or radiation therapy. The role of chemotherapy in this group of patients is debated. I think most of us would probably add chemotherapy to that patient, even if she had early stage disease. But it’s such a rare lesion we don’t have clear cut clinical evidence of what’s the right thing to do.
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In staging the patients with cervix cancer, the spread patterns are fairly monotonous and routine. Local spread to the vagina, the perimetria, the tissue next to the cervix and invading the cervical stroma are the initial routes of spread. From there into lymphatics and the lymphatics are again in a step-wise fashion, have to metastasize to pelvic lymph nodes before they will go to periaortic or common ileac lymph nodes. It’s a fairly step-wise progression. Hematogenous metastases can be seen in liver and lung and bone. Usually those patients have very advanced local disease, stage III disease, spreading sidewall to sidewall.
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The staging system that we use and have modified over the years is a clinical staging system, rather than a surgical staging system that we use for endometrial cancer or for ovarian cancer. Cervix cancer is a clinically staged disease because most patients won’t undergo surgery as part of their treatment. They’ll be treated with radiation therapy and chemotherapy now, in most cases. We want to determine the extent of the disease on clinical examination, including a good pelvic examination. Cystoscopy and proctoscopy to evaluate whether there is any invasion anteriorly or posteriorly into the bladder and rectum are reasonable. Surgical staging on the other hand, with second look laparotomy in ovarian cancer, is not considered standard of care. It does fit into some of the clinical protocols that are ongoing or is required that the patient have a lymph node dissection prior to entering a randomized trial but certainly would not be considered standard of care. CT scan, on the other hand, is probably the single most effective test for staging, looking at adenopathy, looking at the liver, looking at the potential for obstructive ureters. So a CAT scan is an important part of that patient’s initial work-up. Stage I disease is disease clinically thought to be confined to the cervix. It’s subdivided by depth of invasion. This requires a conization of the cervix to get a big sample of the cervix to evaluate the depth of invasion. And it’s also related to the size of the primary lesion, if it’s a gross lesion less than or greater than 4 cm in diameter. Stage II is just sort of the next concentric ring of spread locally, into the vagina and the perimetria and the tissue beside the cervix. Stage III, lower vagina or out into the pelvic side-wall. Again, sidewall involvement is determined by a gynecologist on pelvic examination or if the patient has an obstructed ureter. Then stage IVa is rectal or bladder involvement, and IVb would be distant metastases such as lung or liver metastases.
Herpes simplex virus infections increase that woman’s risk, women that are HIV positive are at much higher risk, those that are smokers, and those that are immunosuppressed or renal transplant patients for example that have an HPV infection are at much higher risk to go on to develop cervical cancer. There are at least 10-20 million women with HPV infections and probably you can equate that to the same number of men out there. Of those 20 million, only about 1.2 million go on to develop these preinvasive lesions, cervical dysplasia, and only about 13,000 a year develop invasive cancer. Because a patient has HPV show up on a Pap smear with cytologic changes associated with HPV, or has mild dysplasia caused by HPV, doesn’t mean that she is going to go on to develop invasive cancer. Unfortunately we don’t have an antiviral agent or an HPV vaccine yet available. So to identify which patients are at high risk and low risk is somewhat of a clinical challenge to the gynecologist and the GYN-oncologist.
Most patients with invasive cervix cancer we would hope would be picked up with an abnormal Pap smear, appropriately referred to a gynecologist. The patient would undergo colposcopy, which is nothing more than a 15 power dissecting binocular microscope to look at the cervix, identify the lesion, biopsy the invasive lesion and go on to stage and treat. Cold knife conization is a larger biopsy. Yet unfortunately most patients that we see today still have gross lesions that Papanicolaou was trying to prevent or avoid, but have gross lesions that can be directly biopsied by the gynecologist. Identifying that patient is a common problem in the United States yet today.
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The symptoms associated with cervix cancer is vaginal bleeding. It is one of the classic symptoms, although not oftentimes volunteered in my experience, but if you ask the patient, yes she has had bleeding after intercourse; it stops after a day or so and doesn’t reoccur until she has intercourse again. As the cervix cancer progresses you can get pelvic pain, obstruction of the lymphatics and lead to lymphedema or obstruction of ureters and ultimately uremia. But the most common early symptom is abnormal bleeding, and again managing that patient by telephone is inappropriate. She needs to be seen, a Pap smear obtained and examined.
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Invasive squamous cell carcinoma accounts for 90% of all invasive malignancies of the vulva, which are responsible for only 1-4% of all female cancers. Other less-common malignant lesions of the vulva are melanoma, adenocarcinoma, and sarcoma. More than three fourths of all patients diagnosed with cancer of the vulva are age 55 years or older, with at least 30% of these women older than 75 years. Approximately 500 deaths from vulvar cancer occur annually in the United States. Because of recognizable symptoms and ease of examination by biopsy, malignancies of the vulva can be detected in an early stage, when therapy can be curative. Death from vulvar cancer results from failure to control the disease after it has progressed beyond the vulva. Such instances often result from delay by the patient in obtaining care and by the physician in performing diagnostic biopsy. Regular examination of all women and increased efforts in patient education can help minimize treatment delay. Recognition of the clinical characteristics of vulvar malignancies and promotion of ready use of office biopsy could prove highly beneficial. Viagra for woman at cheap online pharmacy.
The cause of vulvar malignancies remains unknown, although the association of squamous cell carcinoma of the vulva with other neoplasms of the anogenital mucosa has long suggested a common etiology. Preliminary data on oncogenesis, however, has not been conclusive. The association of high-risk types of human papillomavirus (HPV) such as 16, 18, 31, 33, 35, and 39 with high-grade epithelial neoplasia and invasive carcinomas of the anogenital tract has been established. Vulvar cancer appears to have a multifactorial etiology, however, and HPV infection alone is probably not sufficient for malignant transformation. Primary among cofactors may be the patient’s own immune competence, including conditions of local immunodeficiency. The role of chronic vulvar dystrophy is unclear, although there is a common association. Whereas the risk of progression of vulvar dystrophy to malignancy is low, vulvar dystrophy is frequently associated with epidermoid carcinoma.
Multicentric and confluent vulvar intraepithelial neoplasia (VIN) lesions predominate among younger women, whereas the unifocal lesions, which are most likely to be associated with invasive carcinoma, are more common in older women. The lesions may appear to be white because of thick surface keratin or red if hyperemia is present within the dermal papillae. Pigmentation is common, especially with bowenoid neoplasia. Often the lesions appear as slightly raised and possibly confluent white areas resembling flat condylomata. Colposcopy with 4-5% acetic acid heightens the whitening and allows for delineation of the margins of the vulvar lesions. Subclinical HPV infections of the vulva can be distinguished with acetic acid at times. Thickened, nodular, ulcerated areas are most suspicious, as are areas of vascular prominence and atypical tissue.
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Benign Anomalies
Adenosis and vaginal epithelial changes, present in as many as 50% of women who were exposed to DES before 18 weeks of gestation, include large transformation zones extending to the vagina, cervical collars, hypoplastic cervices, pseudopolyps, and vaginal septa. As the patient grows older, these changes diminish.
The immature squamous metaplasia noted on colposcopy can lead to overzealous treatment. Among the progeny of women exposed to DES, fewer than 10% with biopsies of these areas will have significant intraepithelial neoplasia. Women with these large transformation zones should be followed with cytologic testing, iodine staining, colposcopy, and careful palpation every 6 months to 1 year. Oral contraceptive use does not increase the risk for genital tract clear-cell adenocarcinoma.
The vaginal changes and anatomic abnormalities of the uterus and fallopian tubes, occurring in some progeny, may increase the risk of early pregnancy loss, ectopic pregnancy, and preterm delivery. Careful monitoring throughout pregnancy is indicated.
Exposure to DES may place women at a small, but statistically significant, risk for developing breast cancer. The possibility of an increased risk of cancer of the uterine corpus has been raised. Because of these increased risks, women who have been exposed to DES should be followed for life with appropriate and cost-effective screening.
The rare primary adenocarcinoma of the vagina usually occurs in postmenopausal women. These lesions may arise from residual glands of müllerian origin. Metastatic lesions (from breast, bowel, cervix, endometrium, and ovary) should be ruled out.
Exposure in utero to DES has been epidemiologically associated with vaginal clear-cell adenocarcinoma since 1971. The registry for this disease now includes more than 600 cases, although millions of women were treated with DES during pregnancy, starting in the 1950s. Thus, the risk that a woman exposed to DES will develop a clear-cell lower genital tract cancer is about 1 per 1,000 women.
Registry-updated reports indicate that the age at diagnosis ranges from 7 to 42 years old. Since 1990, 35 new cases have been reported, raising concern about a second peak of occurrence. Depending on what years the registry is analyzed, 65-80% of women with clear-cell adenocar-cinoma will have a documented history of DES exposure. No history of DES exposure is noted in 20-25% of women with clear-cell adenocarcinoma. When clear-cell adeno-carcinoma is diagnosed, DES-negative patients have a worse prognosis and higher rate of distant metastases than patients who were exposed to DES. Diethylstilbestrol-associated clear-cell adenocarcinomas have a predilection for the exocervix and upper one third of the vagina.
As of 1993, 20 women under observation had developed clear-cell adenocarcinoma. Because most of the clear-cell adenocarcinomas were detected by noting submucosal nodules, careful palpation of the cervix and vagina is recommended when examining these patients. Tall, overweight adolescents may be at a relatively higher risk of developing this neoplasm.
Radical hysterectomy, upper vaginectomy, and bilateral pelvic lymphadenectomy with ovarian preservation are recommended for patients with cervical and upper-vaginal clear-cell adenocarcinoma. For tumors smaller than 2 cm in diameter and with less than 3-mm invasion, wide local excision with node dissection, supplemented by local radiation, has been used with preservation of reproductive potential. For advanced stages, irradiation is recommended.
Although 5-year survival for stage I clear-cell adenocarcinomas is higher than 93%, the 10-year survival rate is 87%. Most recurrences happen within the first 3 years, but late recurrences, 8-20 years later, have been reported. In addition to pelvic examinations during follow-up, careful attention should be directed to the supraclavicular nodes and lungs.
Treatments
Most vaginal carcinomas are best treated with radiation therapy. Patients with occult or smaller than 1-cm, stage I, superficial lesions could be considered for radical surgery. Select patients with a lesion in the upper third of the vagina may be candidates for radical hysterectomy, vaginec-tomy, and bilateral pelvic lymph node dissection. Patients with positive nodes should receive external beam irradiation through appropriately designed ports, particularly if more than three nodes are involved. Patients with mid-vaginal, early-stage cancers are probably best treated with radiation therapy. For nonsurgical candidates, when cancers are superficial, the usual treatment is a combination of interstitial implants and a vaginal cylinder. Doses range from 6,000 to 7,000 cGy to the tumor area. Patients with thick, infiltrating, stage I disease are often treated with additional external beam irradiation.
For other patients with locally advanced squamous cell cancers, individualized radiation therapy is administered. Generally used is 4,000 cGy to the whole pelvis with a 5,000- to 6,000-cGy total parametrial dose, along with a combination of interstitial and intracavitary insertions to deliver a total dose of 7,500-8,000 cGy to the vaginal lesion and 6,500 cGy to parametrial and paravaginal extensions. Use of radiation sensitizers, such as 5-fluorouracil plus cisplatin or mitomycin C, has been reported in recent series with little improvement in survival noted. Vaginal stenosis, vaginal necrosis, and proctitis are common complications. The rarely occurring fistulas to adjacent organs are usually seen in patients in whom a combination of surgery and irradiation has been tried. Ultraradical surgery is usually reserved for patients with local central recurrence.
Survival for patients with stage I vaginal cancer has been reported to range from 72% to 90%, and survival for stage II is around 55%. Approximately 45% of patients with stage III cancer will be 5-year survivors. Patients with stage IVA cancer have a 10-20% survival rate. Relatively improved survival is noted in patients younger than 60 years of age, patients with grade I tumors, and patients with nonbulky disease. Chemotherapy for distant recurrences has been largely ineffective, although cisplatin has been used.