Much evidence has been suggested that cystic, adenomatous, and atypical hyperplasia as well as adenocarcinoma in situ of the endometrium may ultimately progress to invasive cancer. Consequently, these lesions should be considered to be precursors of endometrial cancer. Twelve postmenopausal and three perimenopausal women with vaginal bleeding due to endometrial hyperplasia received 400 mg/d of danazol orally for 3 months. After 15 to 30 days of continuous danazol therapy, the endometrial glands ceased to grow and became smaller and rounder. The lumina of glands were narrow and contained no secretion. The nucleic mitosis of the glands disappeared. All women showed regression of hyperplastic endometrium within 2 to 3 months of initial treatment. In the 15 cases treated, endometrial hyperplasia could be controlled successfully with danazol without further recurrence and/or progression of the disease. In summary, danazol should be an effective and safe alternative therapy to progesterone for the treatment of endometrial hyperplasia. Cancer 66:983-988, 1990.
NDOMETRIAL HYPERPLASIA is generally recognized E as a prodromal or borderline lesion of endometrial carcinoma. In young women, there have been some cases of advanced atypical hyperplasia of the endometrium that have disappeared spontaneously. However, it is unanimously agreed that endometrial hyperplasia in menopausal or postmenopausal women frequently undergoes a malignant change, although the time required for transformation to cancer varies from one report to another.''2
In Japan, endometrial carcinoma once accounted for only approximately 5?h3 of all uterine cancers. In recent years, however, its incidence has shown an apparent i n ~r e a s e ~, ~ and it reached a nationwide mean of 12.3%6 of all uterine cancers in 1985. In the US, endometrial carcinoma has increased most markedly among genital cancers, with 37,000 new cases each year.' The number of cases of endometrial hyperplasia, a potential prodromal