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  • Original Article

    Clinical Treatment and Follow-up of Endometrial Hyperplasia

    Rev Bras Ginecol Obstet. 2000;22(6):325-331

    Summary

    Original Article

    Clinical Treatment and Follow-up of Endometrial Hyperplasia

    Rev Bras Ginecol Obstet. 2000;22(6):325-331

    DOI 10.1590/S0100-72032000000600002

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    Purpose: to evaluate the efficacy of medroxyprogesterone acetate and megestrol acetate in endometrial hyperplasia. Patients and Methods: forty-seven patients with abnormal uterine bleeding were retrospectively evaluated. These patients were submitted to diagnostic uterine curettage and/or endometrial biopsy, with histopathological finding of endometrial hyperplasia. Patients with hyperplasia without atypia received 10 mg/day oral medroxyprogesterone acetate during 10 to 12 days a month. Those with hyperplasia with atypia received 160 mg/day oral megestrol acetate continuously. The length of treatment ranged from 3 to 18 months. Control endometrial biopsy and/or uterine curettage were performed 3 and 6 months from the beginning of treatment, and then periodically to evaluate whether or not regression of hyperplasia occurred. Results: forty-two patients with endometrial hyperplasia without atypia and 5 with hyperplasia with atypia were included. The mean age of the patients was 49.5 ± 10.6 years (22 to 72 years), 70.2% aged over 45 years. Medroxy-progesterone acetate was effective in promoting regression of 83.2% (35/42) of hyperplasia without atypia, and megestrol acetate in 80% (4/5) of hyperplasia with atypia. Despite treatment, lesions persisted in 16.8% (7 cases) of hyperplasia with atypia and in 20% (1 case) of hyperplasia without atypia. No progression to endometrial cancer was seen during the follow-up period of 3 months to 9 years. During follow-up, we found that 18 patients (38.3%) showed amenorrhea, 12 (25.5%) menstrual cycle regulation, and 17 (36.2%) persistent abnormal uterine bleeding and underwent total abdominal hysterectomy. Histological examination of the uterus showed 8 patients with persistence of hyperplastic lesion, 4 with leiomyoma, 3 with adenomyosis, 1 with diffuse uterine myohypertrophy, and 1 with normal uterus, despite regression of the hyperplastic lesions in 9 of the 17 patients. Conclusions: the treatment of endometrial hyperplasia with medroxyprogesterone acetate and megestrol acetate can be a safe alternative for women who refuse to have their uterus removed or those at high risk for surgery. However, a careful monitoring of the endometrium is needed. This can be achieved with periodical endometrial biopsy, transvaginal ultrasonography, and evaluation of the symptoms.

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    Clinical Treatment and Follow-up of Endometrial Hyperplasia
  • Original Article

    Pelvic adhesion prevention: experimental study on rats with different therapeutic agents

    Rev Bras Ginecol Obstet. 2003;25(5):359-364

    Summary

    Original Article

    Pelvic adhesion prevention: experimental study on rats with different therapeutic agents

    Rev Bras Ginecol Obstet. 2003;25(5):359-364

    DOI 10.1590/S0100-72032003000500009

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    PURPOSE: to evaluate the degree of pelvic adhesions in function of time and the different substances used in its prophylaxis. MATERIAL AND METHODS: prospective study with 120 female, albino, virgin Wistar rats, 3 to 4 months of age, weighing approximately 250 g, randomly divided into 10 groups of 12 animals each: control, without lesion; lesions and without treatment; lesions + 0.9% physiologic saline, lesions + Ringer lactate; lesions + 32% dextran 70; lesions + Ringer lactate/heparin; lesions + Ringer lactate/dexamethasone; lesions + Ringer lactate/hydrocortisone/dexamethasone/ampicillin; lesions + Ringer lactate/albumin, and lesions + 1% carboxymethylcellulose. The animals were anesthetized and two types of lesions (scarification and electrocauterization) were performed in the uterine horns, followed by treatment with the solutions, intraperitoneally, to prevent pelvic adhesions. On the 7th, 14th and 28th postoperative days, moments M1, M2 and M3, respectively, the presence of adhesions was evaluated in 4 rats of each group. The methods applied to the quantification of the adhesions were based on Cohen's classification, with scores varying from 0 to 4+ according to the amount, characteristics and location of the adhesions. Statistical analysis was performed by parametric tests for analysis of variance and the Kruskal-Wallis test. RESULTS: the best treatments for prevention of pelvic adhesions in female rats were Ringer lactate/dexamethasone (score 1+ prevalence), 32% dextran 70 to (score 2+ prevalence) and Ringer lactate/hydrocortisone/dexamethasone/ampicillin (score 2+ prevalence). The postoperative period, represented by moment M3, and the surgical technique, predominantly with score 0, influenced adhesiolysis and maintenance of pelvic adhesions in female rats. CONCLUSIONS: the prevention of pelvic adhesions in female rats begins with the surgical process at a smaller extent of tissue damage. The use of prophylactic substances (solutions) had a varied effectiveness, since some were more efficient than others.

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    Pelvic adhesion prevention: experimental study on rats with different therapeutic agents

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