Susumu Terada

The Possible Effect of Pregnancy on Ménière’s Disease

There are few reports on the course of Ménières disease during pregnancy. We report here the clinical course of Ménières disease before, during and after pregnancy and discuss the possible effect of pregnancy on Ménières disease and the treatment of Ménières disease during pregnancy. In the present case, the vertigo attacks increased up to 10 times per month during early pregnancy, when the serum osmolality was significantly below normal at 268 mosm/kg. As the pregnancy proceeded, the serum osmolality normalized and the vertigo attacks decreased in frequency. The vertigo attacks were treated by oral isosorbide and intramuscular injection of low-dose diazepam. The coincidence of the decline in osmolality with the increase in vertigo attacks points to serum osmolality as a possible factor in the effect of pregnancy on Ménières disease.

Effects of hormone replacement therapy on serum amyloid P component in postmenopausal women

The pentraxin serum amyloid P component (SAP) is a 9.5Sz1-glycoprotein and it has recently been found to be deposited in atherosclerotic lesions or neurofibrillary tangles, which are related to the aging process and Alzheimers disease. The level of SAP was measured by micro single radial-immunodiffusion. Sample sera were obtained from 420 healthy humans, from newborn to 86 years old. The changes in SAP during the menstrual cycle were investigated in 6 women that were 20-21 years. Fifty of the postmenopausal women, suffering from climacteric symptoms, were administered either conjugated estrogen (E), or dehydroepiandrosterone (DHEA). The SAP levels increased with age, being 1.12 +/- 0.82 mg/dl (means +/- S.D.) in neonates, and 6.15 +/- 0.92 mg/dl in persons over 80 years. The SAP level in the females between 15 and 49 years (3.32 +/- 0.95 mg/dl) was significantly (P < 0.001) lower than that in the males in the same age group (5.19 +/- 1.25 mg/dl). The SAP level in the follicular phase was significantly (P < 0.01) lower than that in menstrual phase (menstrual: 4.36 +/- 0.90 mg/dl versus follicular: 2.61 +/- 0.99 mg/dl). In the post-menopausal women that were administered E (1.25 mg/day), the SAP decreased significantly (P < 0.001) from the prelevel of 5.64 +/- 1.40 mg/dl to 4.26 +/- 0.98 mg/dl on the 14th day. In the postmenopausal women that were administered DHEA (60 mg/day), the SAP increased rapidly from the prelevel of 4.97 +/- 0.76 mg/dl to 6.17 +/- 1.20 mg/dl on the 21st day. SAP seems to be a marker that can monitor the effect of hormone replacement therapy.

A follicular cyst during tamoxifen therapy in a premenopausal breast cancer woman.

A large ovarian follicular cyst developed on day 43 of low-dose tamoxifen adjuvant therapy for a premenopausal breast cancer (total drug intake: 860 mg). The serum estradiol level increased to almost ten times the pretreatment level. However, the FSH and LH decreased slightly, and the serum progesterone level remained almost unchanged. It is hypothesized that tamoxifen acted directly on the ovaries to provoke excessive proliferation of the granulosa cells in a follicular cyst, causing it to grow very large, and resulting in elevated E2 levels.

Intracervical fibrin instillation as an adjuvant to treatment for second trimester rupture of membranes

We describe a pregnancy complicated by premature rupture of the membranes at 24 weeks. Delivery with successful outcome was postponed till 31 weeks by cerclage, ritodrine and intracervical instillation of fibrin.

Effect of Testosterone on the Development of Bladder Tumors and Calculi in Female Rats

In order to study the effect of testosterone on bladder calculi and tumor formation in female rats, Wistar rats were administered testosterone for 12, 18 or 24 weeks. Testosterone was found to increase the incidence of both bladder calculi and tumors in intact, but not in oophorectomized rats. It is suggested that testosterone in combination with estrogen may contribute to hyperplasia formation, in turn leading to an increased incidence of bladder calculi and tumors.

A technique of minilaparotomy-assisted vaginal hysterectomy

In minilaparotomy-assisted vaginal hysterectomy, the operation begins vaginally by opening the peritoneal folds and ligating the uterine vessels and uterosacral ligaments. Minilaparotomy is then performed for myomectomy, cutting the fallopian tubes and the utero-ovarian ligaments and detaching any adhesions on the anterior peritoneal angle. In 26 women who underwent this procedure, the feasibility rate was 100% and no intraoperative complications or postoperative morbidity was observed (except in one case of ovarian bleeding), indicating that vaginal hysterectomy assisted by minilaparotomy is a feasible approach for hysterectomy in the setting of large myomas, myomas with adhesions caused by endometriosis or previous pelvic surgery, and adenomyosis.

Effects of dehydroepiandrosterone and other sex steroid hormones on mammary carcinogenesis by direct injection of 7, 12-dimethylbenz(a) anthracene (DMBA) in hyperprolactinemic female rats

The present study was performed to investigate theeffects of dehydroepiandrosterone (DHEA) compared with those ofsex steroid hormones on the mammary tumor inducedby local injection of 7, 12-dimethylbenz(a)anthracene (DMBA) inhyperprolactinemic female rats. Under sustained hyperprolactinemia induced bypimozide (PMZ) from day 21, DMBA was injectedlocally into the mammary glandular tissues on day73. Rats were divided into 5 groups asfollows; steroid free (DP group), 17 β-estradiol (DP+ E2 group), testosterone (DP + T group),progesterone (DP + Prog group), or dehydroepiandrosterone (DP+ DHA group). The growth pattern and histologicalclassification of the tumor in these 5 groupsand rats treated only with DMBA (D group)were examined. All of the tumors grew toa size of 10 mm in diameter andafter retaining the size for a certain duration,increased the size rapidly again (onset of rapidtumor growth). The period from the day ofDMBA administration to that of onset of therapid tumor growth in DP group was shorterthan in D group, and the period inDP + DHA was longer than DP groupand longest in steroid-treated groups. The incidence ofadenocarcinoma was 2 tumors/16 animals in D group,9/11 in DP group, 5/11 in DP +Prog group, 2/7 in DP + E2 group,2/8 in DP + T group, and 0/10in DP + DHA group. The incidence ofadenocarcinoma in each steroid group except in DP+ Prog group was lower than in DPgroup. These results suggest that prolactin (PRL) increasesthe incidence of adenocarcinoma in the DMBA-induced mammarytumor model, and DHEA especially decreases the incidenceof adenocarcinoma.

Effects of Testosterone on the Development of Endometrial Tumors in Female Rats

Long-term treatment of mature virgin female rats with a high dose of testosterone (24 weeks at a total dose of 300 mg) was associated with the development of endometrial adenomatous hyperplasia and resulted in a high incidence of adenocarcinoma when administered in combination with 7,12-dimethyl-benz[a]anthracene (DMBA; 2 mg in 0.1 ml sesame oil) introduced into the uterine cavity. Adenomatous hyperplasia occurred in all testosterone-treated rats, both with and without ovaries. Testosterone may promote the induction of endometrial tumors by DMBA.

Partial Hydatidiform Mole in the Fallopian Tube

An extremely rare case of partial hydatidiform mole located in the right Fallopian tube was diagnosed by ultrasonography and computed tomography. The lesion was excised, and the human chorionic gonadotropin (HCG) level in early morning urine fell below 1,000 IU/ml on postoperative day 11, and the serum HCG-beta level normalized on postoperative day 46.

Induction of ductal carcinomas by intraductal administration of 7,12-dimethylbenz(a)anthracene in Wistar rats

SummaryPostpartum Wistar inbred rats (weaned on the 9th puerperal day) were injected intraductally in one mammary gland with 7,12-dimethylbenze (a) anthracene (DMBA) to selectively induce ductal carcinoma. The incidence of ductal hyperplasia increased with time until it peaked at 7 weeks (12/13 animals) and then decreased. Ductal carcinoma first developed at 9 weeks in 3/12 (2 non-invasive and 1 invasive lesion) and the incidence increased with time until invasive ductal tumors were observed in 9/11 at 20 weeks. Tumors developed only in the DMBA-treated mammary glands and no systemic effects of the carcinogen were observed. Degeneration and detachment of epithelioglandular cells were seen here and there in the ducts and terminal ducts, and epithelioglandular cells proliferated in terminal duct until 2 weeks. Residual trace DMBA powder was detected in terminal ducts and the epithelioglandular layer until 7 weeks. This trace DMBA was considered to be the cause of the development of atypical epithelial cells, inducing ductal carcinomas.