Ingestion of a single tablet containing 2 mg micronized 17beta-estradiol (E-2) produced marked increases in the serum concentrations of E-2 and estrone (E-1) in 9 postmenopausal women. The rise in circulating E-2 became significant within 2 h, reached a maximum (110 pg/ML; 437% increase) at 5 h, and remained significantly elevated at 8 h posttreatment. By 24 h, the serum E-2 concentration was not significantly different than baseline. In contrast, a more rapid (within 1 h) and pronounced (4-fold) increase in the serum concentration of E-1 was observed. This rise continued until a peak (467 pg/ml; 2000%) was reached 6 h posttreatment. Thereafter, the serum E-1 concentration declined progressively but was still significantly elevated (140 pg/ml; P smaller than 0.01) 24 h after treatment. Serum concentrations of FSH AND LH were significantly decreased within 6 and 3 h, respectively and both gonadotropins remained significantly suppressed 24 h following the ingestion of E-2. The ratios of circulating E-1: E-2 reported herein (ca. 3-6) were much higher than those observed by other investigators following iv E-2 (I.E., smaller than 1). Thus the data indicate that micronized E-2 peros is readily absorbed and that during this process a significant portion of the hormone is converted to E-1 by the gstrointestinal tract. In addition, 2 mg oral E-2 exerts significant biologic activity as assessed by serum gonadotropin suppression.

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The San Diego Cytology Registry collected results on cytology examinations on more than 180,000 women; more than 60,000 of these had multiple examinations. The age‐specific prevalence and incidence rates for suspicious and positive cytology and for dysplasia, carcinoma in situ and invasive cancer of the cervix are presented. These are analyzed in terms of the morphogenesis of cervical cancer. Carcinoma in situ reaches its maximum incidence rate among women aged 25 to 29. The rates then decrease and continue at a low level after age 35. This peak of incidence at an early age has implications as to the pathogenesis of cervical cancer. Incidence rates for dysplasia also rise rapidly and at an earlier age than carcinoma in situ. Dysplasia remains at a high incidence over a longer age span than carcinoma in situ but decreases precipitously after age 40. Dysplasia and carcinoma in situ together would exceed the needs for invasive cervical cancer and some would need to terminate by regression. The prevalence rates for dysplasia and carcinoma in situ are several times greater than their respective incidence rates. Estimates of average duration for each are 3.8 years of dysplasia and 8.1 years of carcinoma in situ. Not all new disease developing from a population that has been repeatedly negative cytologically is found in a carcinoma in situ stage. The authors conclude that 10 to 15% of carcinomas of the cervix become invasive early in their development.

No abstract