51세 여자가 갑자기 발생한 심한 복통으로 응급실에 내원하였다. 환자는 1년 전 유방암으로 수술을 시행받았고 6개월 전부터 저용량(하루에 10 mg)의 타목시펜을 복용하기 시작했다. 환자의 복통은 중증의 궤사성 췌장염이 원인으로 밝혀졌다. 환자는 특별한 기저질환이나 약물 복용력은 없었으며 음주도 하지 않았다. 내시경 초음파에서 담석은 보이지 않았다. 환자의 6개월 전 중성지방의 수치는 정상이었으나 응급실 내원 당시의 수치는 2,534 mg/dL로 확인되었다. 고중성지방혈증과 췌장염의 원인으로 타목시펜이 가장 의심되었기에 타목시펜 중단 후 보존적 치료를 시행하였고 회복되어 퇴원하였다. 퇴원시 환자의 중성지방 수치는 정상이었다. 타목시펜은 유방암 치료에 효과적인 약이나 처방 후 지질대사에 대한 추적관찰과 관심이 반드시 필요하다.

This study examined the effects of tamoxifen at different concentrations and treatment periods on proliferation of a human cervical cancer cell line, HeLa. As in the previous studies, Estrogen did not have an effect on the cellular proliferation at low concentrations but significantly reduced proliferation at high concentration (5 ug/ml) based on MTT assay. Treatment with tamoxifen had similar effects. It did not have any significant effect on the HeLa cell proliferation at low concentrations, but significantly reduced proliferation at high concentration (10 uM). In addition, combined treatment with both estrogen and tamoxifen did not alter the inhibitory effects of either estrogen or tamoxifen on cellular proliferation. The inhibitory effects by tamoxifen on HeLa cell proliferation did not differ among different treatment periods. This suggests that tamoxifen may exert anti- proliferative effects at high concentration but does not have synergistic or antagonistic effects against estrogen on HeLa cell proliferation.

The effects of an antiprogesterone (RU 486) and an antiestrogen (tamoxifen) on ovulatory response and oocyte morphology were examined in pregnant mare serum gonadotropin (PMSG)-primed immatare female rats (28 days of age): a comparison has been made on two different regirnens primed with a "control" dose (4 IU) and a "superovulatory" dose (40 IU) of PMSG. Females for control control regimen received three consecutive injections of lmg RU486, lmg tamoxifen, or vehicle at 24, 36 and 48hr, and were killed at 72l'r after PMSG. Animals for superovalatory regimen received lmg RU486, 2.5mg tamoxifen, or vehicle fouowlag the injection schedule comparable to control regimen, and were killed at 60 and 72hr after PMSG. Compared to vehicle group, there was a significant reduction in ovulatory response as judged by the proportion of rats ovulating andi or by the mean number of oocytes per rat for each treatment of RU486 and tamoxifen in both regimens. The activity of tamoxifen in inhibiting the ovulatory response was greater in control, but less in superovulatory regimen than that of RU486 based on the dose employed for each antisteroid. In both regimens, RU 486 did not have any effect 6n the changes in the proportion of degenerate oocytes as well as ovarian weight, well tamoxifen treatment resulted in a marked promotion of oocyte degeneration as well as a great reduction in ovarian weight, compared to each parameter of vehicle group. RU486 treatment in each regimen did not alter the serum levels of any steroid hormones observed. Howerver, tamoxifen treatment was associated with significant increases in serum 17-estradiol and decreases in progesterone in both regimens; also significant increases in androgens in superovulatory regimen. The results illustrate the relative inhibitory activity of RU486 and tamoxifen indicating major steroid hormone involved in PMSG-induced ovulation: 17-estradiol for control and progesterone for superovulatory regimen. It also appears that tamoxifen-associated elevation of circulating 17-estradiol andi or androgens could be in part, a contributing factor to the promotion of oocyte degeneration presumably by producing a hostile oviductal environment after ovulation.ent after ovulation.

These studies were undertaken to examine the interaction of tamoxifen with sex steroid hormones in rat uterine activity. The uterine wet weights of the immature Tat uterus were examined after the administration of estradiol-l7(1g), tamoxifen(50g), progesterone(lmg). The uterotropic activity in immature ovariectomized rats was observed under various treatment conditions following pretreatment with above drugs. The results obtained were as follows:1) Tamoxifen produced significant increase (p <0.01) in uterine wet weight compared with control group, although the increase was not as great as that seen with estradiol-17. Administration of estradiol-17 together with tamoxifen inhibited significantly the increase of uterine wet weight by estradiol-17 (p < 0.01). Coadministration of progresterone with tamoxifen partly blocked the increase of tamoxifen-induced uterine wet weights by progesterone. 2) Estradiol-17after the estradiol-17 pretreatment discontinued the declining uterine wet weights due to the absence of estrogen support, but uteri continued to increase in weight if daily estradiol-17 was maintained. Administration of tamoxifen on the fourth day of estradiol-17 treatment reduced uterine wet weights within 24 hours, and the weights continued to decline with additional tamoxifen. 3) The modest growth of the uterus induced by three daily injections of 5Opg tamoxifen remained stable for five days, with or without additional tamoxifen treatment. Coadministration of tamoxifen with estradiol17 increased slightly the increase of uterine wet weight by tamoxifen. Coadministration of tamoxifen with progesterone inhibited the increase of uterine wet weight by tamoxifen. 4) The modest growth of the uterus induced by three daily injections of lmg progesterone reduced uterine wet weight to the control level for five days. Commencement of tamoxifen or estadiol-17 injections on the fourth day of progesterone treatment rapidly elevated uterine wet weight.