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Sacrococcygeal teratoma is a rare fetal neoplasm with an incidence of 1 in 40,000 births. Antenatal diagnosis is usually made after 22 weeks of gestation. Fetuses with this malformation are at risk of significant perinatal morbidity and mortality. Malignant components, coexisting with life-threatening anomalies, and chromosomal abnormalities are rare. Postulated causes of perinatal death include hydrops, dystocia, tumor rupture, preterm labor secondary to polyhydramnios, and anemia due either to hemorrhage or hemolysis within the tumor. Herein, we present a case of fetal sacrococcygeal teratoma diagnosed as early as 17 weeks of gestation.

A case of endosalpingiosis presented as a multilobular cyst on sonography. The tentative clinical diagnosis was an ovarian tumor; however, laparotomy revealed a degenerative cyst of the uterine myoma with a stalk connecting to the uterus. Histopathologically, it showed characteristics of endosalpingiosis. To our knowledge, such a multilobular cyst of endosalpingiosis originating solely from the uterine serosa has not been reported.

Elevated tumor markers for a post-menopausal woman presenting with a multilocular adnexal mass, ascites, and pleural effusion were interpreted as being highly suspicious of malignancy. This paper describes two cases of ovarian tumors presenting with all signs of malignancy. Following surgical excision of the masses, and histopathological assay, a benign pure struma ovarii and a mucinous cystadenoma were diagnosed by pathologists. The immediate and complete resolution of symptoms were achieved post-operatively, and the previously-evident abnormal tumor markers rapidly declined to the normal range, the two tumors were subsequently classified as pseudo-Meigs' syndromes.

Leiomyoma are very common in the normal uterus; however, they are rather rare in mullerian duct remnant. We report a case of mullerian duct remnant leiomyoma associated with vaginal agenesis. The mass had papillary growth with cystic-solid components by ultrasound. Ovarian cancer was suspected preoperatively. Finally, a fibroid with hyalinization and chondroid metaplasia was diagnosed histopathologically. To the best of our knowledge, this is the first case of mullerian duct remnant leiomyoma with degeneration, mimicking ovarian cancer by ultrasound. We provide the clinical details of this case and discuss a diagnostic pitfall.

Pancreatic cyst mimicking an ovarian cyst ultrasonographically has not yet been reported. We report an elderly woman with such a huge pancreatic cyst whose initial presentation was low abdominal pain. Ultrasound showed a hypoechoic cyst measuring 13.6 x 13.2 x 11.8 cm occupying pelvic cavity. She received laparotomy under the impression of ovarian cyst. Interestingly, the cyst was found to have originated from the pancreas. Total cyst excision was performed and pathologic report was pancreatic microadenoma. The patient's postoperative course was unremarkable.

To evaluate the integrated hypothalamic-pituitary function of euprolactinemic secondary amenorrhea, blood samples of 23 patients were taken every 15 min for 4 hours in examination of pulsatile LH, FSH, PRL secretions and then 2 hours GnRH, TRH tests were performed. Nine normal cycling women (group I) served as the controls. Thirteen amenorrheic women (group II) revealed responsive bleeding to progestin injection and the other 10 women (group III) were nonresponsive. The LH frequency, amplitude, and LH response to GnRH of groups II and I were comparable, whereas delta PRL after TRH in group II (60.8 +/- 18.9 ng/ml) exhibited a significantly (P < 0.05) exaggerated response, as compared with that of group I (43.6 +/- 11.4 ng/ml). The LH frequency (1.3 +/- 0.4/4h) and amplitude (1.7 +/- 0.4 mIU/mL) of group III were significantly lower (P < 0.01) than those in group I (2.4 +/- 0.5 and 2.5 +/- 0.5, respectively), but their delta LH and delta FSH responses to GnRH showed no differences from those of controls. The frequency, amplitude of PRL and delta PRL response to TRH in group III were no significant difference with those of group I. These results suggest that masked PRL hypersecretion and loss of the regulatory pulsatility of gonadotropin release may be responsible in part for the causes resulting to euprolactinemic secondary amenorrhea. The analysis of these hormonal environments is useful for the understanding of clinical perspectives, pathophysiology and management.

To characterize the episodic fluctuations of serum LH, FSH and PRL in women with normally cycling, secondary amenorrhea and polycystic ovary syndrome (PCOS), four groups of women were studied: group I (N = 8) consisted of normal women in the follicular phase of the cycle; group II (N = 10) of women with secondary amenorrhea and positive progesterone withdrawal bleeding; group III (N = 8) of women with secondary amenorrhea and negative progesterone withdrawal bleeding; group IV (N = 9), women with polycystic ovary syndrome (PCOS). Blood samples were obtained at 15 minute intervals for 4 hours during one admission day. Ovarian steroids were measured to evaluate the baseline endocrine environment in each group. Distinct pulsatile fluctuations of serum LH, FSH and PRL were observed in all subjects. These pulses showed a high degree of coincidence in LH with FSH and LH with PRL in each group. However, the mean (+/- SD) frequencies of LH in group III and group IV were significantly lower (P < 0.01) and higher (P < 0.01) than in group I, respectively. The mean frequencies of FSH in groups III and IV were lower (P < 0.05), as compared with those of group I. The mean amplitude of LH in group IV was significantly higher (P < 0.001) than in group I. These results suggest that loss of the regulatory pulsatility of gonadotropin releases may be a contributory cause to anovulation and secondary amenorrhea. The concomitant pulsatile releases of gonadotropin and PRL are essential to reproductive function and their regulatory controls in the follicular phase may be mediated through a common neuroendocrine mechanism in normal and hypogonadal women.

This in vitro study was undertaken to investigate the effects of adenyl purines in human uterine myometrium and uterine arteries. Segments of uterine myometrium and uterine arteries obtained at hysterectomy were isolated and mounted in tissue chambers. The muscle activity was recorded by polygraph. Adenyl purines agonists, such as adenosine, N-[(R)-1-methyl-2 phenylethyl]-adenosine (R-PIA) and 5-N-ethylcarboxamide adenosine (NECA) produced concentration-dependent contraction in human uterine myometrium. The potency order was NECA = R-PIA > adenosine. Adenosine A1 receptor antagonist: 1, 3-dipropyl-8-cyclopentylxanthine (DPCPX) blocked the effect of adenosine in human uterine myometrium. Otherwise, adenyl purines induced dose-dependent relaxation in human uterine artery precontracted by phenylephrine (PE, 10(-5)M). The potency gradient was NECA > R-PIA > adenosine; the results indicate adenyl purine induces uterine myometrium contraction via A1 receptor. However, adenosine causes uterine artery relaxation by A2 receptor.