ENDOMETRIAL BIOPSY - 11/09/11
Résumé |
Endometrial biopsy has become an accepted method of evaluating abnormal uterine bleeding (AUB) and of excluding the presence of uterine pathologic conditions such as endometrial cancer and precursors. Because of the documented safety and effectiveness of endometrial sampling devices, the use of endometrial sampling has become an integral part of the workup of premenopausal and postmenopausal women who are suspected of having uterine pathologic conditions. Several office endometrial samplers have a reported diagnostic accuracy similar or better than dilatation and curettage (D & C). This presents a dilemma for clinicians. The endometrial biopsy and the classical D & C procedure are blind sampling techniques. Although each is highly sensitive for detection of endometrial carcinoma, they lack specificity for detecting other intraluminal pathologic conditions such as submucous fibroids and endometrial polyps. In a study53 of resected uteri after curettage was performed, it was shown that in 50% of the cases less than 60% of the uterus was curetted. Since the introduction of this procedure into standard office practice, other techniques such as transvaginal ultrasonography (TVUS) and hysteroscopy have begun to emerge. The office practitioner needs to consider the different modalities and to evaluate each for safety, effectiveness, and patient acceptance. A combination of endometrial diagnostic techniques ultimately may provide the most optimal strategy for evaluation of endometrial pathology.
Carcinoma of the endometrium is the most common invasive gynecologic malignancy, and it is the fourth most common cancer among women, being preceded by cancer of the breast, lung, and colorectum. One of every fifty women in the United States develops this disease during her lifetime, and by American Cancer Society estimates, there were 32,000 new cases of endometrial cancer in 1995. Approximately 19% of these women die of this malignancy. The peak age for cancer of the endometrium is 60 years, and incidence rates exhibit a sharp increase in the early postmenopausal years; then the risk modestly decreases with more advancing age. The majority of women with endometrial cancer fortunately present with stage A in which the cancer is confined to the endometrium and the overall survival rate is greater than 85%.2 There is a familial tendency for some women to exhibit a high incidence of concomitant breast, colon, and endometrial cancer.8 The majority of endometrial tumors are related to chronic unopposed estrogen, endogenous or exogenous.
Prolonged exposure to unopposed endogenous estrogen, which may occur in obese women, women with hyperandrogenic chronic anovulation (formally polycystic ovarian disease), and infertile women, is one of the strongest predisposing risk factors for endometrial cancer. In these women, the endometrium does not develop a secretory phase each month and is in a chronic proliferative stage because of unopposed estrogen stimulation.9 There is a ninefold increased risk of endometrial cancer in women who are more than 50 lb overweight.6 In obese women, the peripheral conversion of androstenedione to estrone takes place in adipose tissue, leading to a chronic hyperestrogenic state. This mechanism may explain why smokers are at decreased risk for endometrial cancer. Smokers experience a shorter perimenopause and an earlier menopause because of reduced estrogenic stimulation and an increased estrogen clearance rate resulting from the induction of hepatic microsomal enzymes.37
Diabetes mellitus and hypertension have been described as independent risk factors for endometrial cancer. These conditions occur most commonly in obese women in whom enhanced peripheral conversion of androstenedione to estrone occurs. Compared with the normal population, the incidence of endometrial cancer in diabetics is 2.8 to 1. These conditions also may be linked to upper body fat distribution. In a study 23 of 597 asymptomatic women with diabetes or hypertension, preinvasive uterine lesions were found in 6.3% of the diabetics compared with 1.3% of the women with hypertension. Among the patients with diabetes, 13.2% had complex or atypical hyperplasia, compared with 11.1% in patients who had diabetes and hypertension. Diabetes but not hypertension is related significantly to risk of endometrial cancer even after weight is adjusted as a continuous variable.9 The presence of noninsulin-dependent diabetes is associated with a slightly higher risk than insulin-dependent diabetes; therefore, hypertension is not associated with any substantial alteration in risk of endometrial cancer and is not considered an independent risk factor for endometrial cancer.
The unopposed administration of exogenous estrogen is associated with the development of endometrial cancer. The risk of developing endometrial cancer among users of unopposed estrogen, compared with women who have never used estrogen, is higher.22 There is a lower risk among users of combination estrogen and progestin therapy. If estrogen is given with a progestin, the risk of developing endometrial cancer is reduced significantly and the protective effect appears to last for at least 15 years after the combination therapy is discontinued.46 A postmenopausal woman with an intact uterus who is taking estrogen alone is more likely to develop simple, complex, or atypical endometrial hyperplasia than one who is not taking estrogen. These same women are significantly more likely to have more unscheduled endometrial biopsies for AUB and curettages than those not taking estrogen.60 A postmenopausal woman with an intact uterus who is taking estrogen plus progestin correctly according to one of the standard regimens has similar rates of hyperplasia as a woman who is not using hormone replacement therapy (HRT) and is at low risk for development of endometrial cancer.
The use of oral contraceptive pills for 12 months or longer also reduces the risk of endometrial cancer by about 50%, and the beneficial effect appears to continue for about 15 years after the oral contraceptive pills are discontinued.11 Postmenopausal women may benefit from this reduced risk if the oral contraceptive pills were used last in the late perimenopausal period.
Women are being offered the option of taking continuous rather than sequential estrogen and progestin for HRT. Patient compliance is improved with the continuous regimen because endometrial stimulation is less than with the sequential method, and eventually amenorrhea is achieved in the majority of women.41 Many women taking HRT present with abnormal bleeding patterns, however. The only way often to determine the cause is to perform an endometrial biopsy. In a randomized, controlled study 15 of 210 postmenopausal women, amenorrhea was achieved in 90% of the continuous HRT group (estradiol, 2 mg, norethisterone acetate, 1 mg/d continuously) after 2 years. In the sequential group, 82% of the women continued to have regular withdrawal bleeding after a 2-year trial. From this study, compliance varied considerably according to the type of HRT used. Compliance was best in the continuous therapy group (93%) after 1 year and 73% after 2 years. The most frequent reasons for discontinuation of the therapy in this group were attributed to continued withdrawal bleeding and irregular bleeding. The compliance rate of the sequential group was 66% after 1 year and 49% after 2 years.
The incidence of endometrial hyperplasia is reduced significantly when estrogen and progestin are used, compared with the use of unopposed estrogen alone.59 Although the possibility of continued regular withdrawal bleeding is higher with the sequential method, unscheduled bleeding with the continuous regimen (especially during the first 6 months of administration) can be even more problematic and can prompt unnecessary endometrial biopsy. In a large randomized, controlled trial of postmenopausal women taking combined or sequential regimens of conjugated equine estrogen with medroxyprogesterone acetate, the women who received continuous HRT had a significantly higher rate of irregular bleeding during the first 6 months of therapy. Amenorrhea was achieved after about 9 months in more than 50% of cases. The women who were taking sequential HRT continued to have withdrawal bleeding in greater than 50% of cases.4
There are conflicting data on whether women receiving tamoxifen for breast cancer are at increased risk for endometrial cancer and precursors.20 Postmenopausal women with breast cancer receiving tamoxifen appear to have a thicker endometrium and a larger volume than controls. Only 28% of the tamoxifen-treated group had an atrophic endometrium compared with 87% of the controls.34 In this particular study, only one case of atypical hyperplasia was found in the tamoxifen group, which represented a failure to show any increased frequency of endometrial precursors in tamoxifen-treated patients.
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| Address reprint requests to Barbara S. Apgar, MD, MS, University of Michigan, Family Practice Center, 14700 East Old US 12, Chelsea, MI 48118, |
Vol 24 - N° 2
P. 303-326 - juin 1997 Retour au numéro
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- ELECTROSURGICAL LOOP EXCISION OF THE CERVIX
- Gary R. Newkirk
- ESOPHAGOGASTRO-DUO DENOSCOPY
- Thomas E. Norris
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