Yoshihiko Yamanaka

Comparison of Magnetic Resonance Imaging and Ultrasonography in the Prenatal Diagnosis of Congenital Thoracic Abnormalities

Objectives: To evaluate prenatal MRI in the diagnosis of fetal thoracic abnormalities and to determine whether MRI provides useful information in addition to that of ultrasonography (US). Methods: Ultrafast MR scanning was performed in 7 pregnant women in whom US was suspicious of fetal congenital anomalies of the thorax [3 cases of congenital diaphragmatic hernia (CDH), 3 cases of chylothorax and 1 case of congenital cystic adenomatoid malformation (CCAM) type III]. The presence, position, size and characteristics of the congenital lesions were determined and compared with postnatal diagnoses. Results: The MRI diagnoses were 3 cases of CDH, 2 of chylothorax and one each of esophageal atresia and CCAM type III. The results of MRI were in agreement with those of US in 6 cases and in disagreement in 1 case of esophageal atresia. Final diagnoses were confirmed at surgery or autopsy in all fetuses. Combined use of MR and US imaging enabled a correct diagnosis in 5 cases and led to an error in the diagnosis of 1 fetus with bronchial stenosis, which had been diagnosed as CCAM type III by US and MRI. MRI led to a correct diagnosis in 1 fetus with esophageal atresia, in whom US had been equivocal in the prenatal diagnosis. Conclusion: MRI helped further characterize the fetal thoracic lesions and confirmed or changed the prenatal diagnosis based on US. MRI seems to be powerful in the prenatal diagnosis of thoracic lesions that are atypical or complicated by multiple abnormalities.

Transient postpartum diabetes insipidus in twin pregnancy associated with HELLP syndrome

Abstract Diabetes insipidus during pregnancy is an uncommon medical problem, and its cause is not entirely clear. We present a woman with twin pregnancy associated with HELLP syndrome, who developed diabetes insipidus during postpartum period. A hypertonic saline infusion study with measurement of plasma arginine vasopressin concentrations confirmed the diagnosis. She had mild response to 1-desamino-8-d-arginine-vasopressin (dDAVP) during the immediate postpartum period. On the 3rd postpartum day two doses of 100μl of dDAVP were administered, and her urinary volume gradually decreased. We could stop dDAVP on the 30th postpartum day. This exacerbation may result from increased vasopressinase activity caused by the excessive production in the placenta due to twin pregnancy, together with the insufficient degradation in the liver due to HELLP syndrome.

Dysfibrinogenemia during pregnancy treated successfully with fibrinogen

There are three types of congenital abnormalities associated with fibrinogen: afibrinogenemia, hypofibrinogenemia and dysfibrinogenemia. Of these, dysfibrinogenemia is usually clinically silent or is associated with mild to moderate bleeding tendency or defective wound healing. The obstetric complications of dysfibrinogenemia include first-trimester abortion, hemorrhage and placental abruption during pregnancy, and thrombophlebitis (1). We report a case of a dysfibrinogenemic patient with a history of recurrent fetal loss due to placental abruption, which was successfully treated with fibrinogen prophylaxis.

Effects of estriol on proliferative activity and expression of insulin-like growth factor-I (IGF-I) and IGF-I receptor mRNA in cultured human osteoblast-like osteosarcoma cells

The present study was undertaken to elucidate whether estriol (E3) affects the proliferative activity and the expression of insulin-like growth factor-I (IGF-I) mRNA and IGF-I receptor (IGF-IR) mRNA in cultured human osteoblast-like osteosarcoma cells (HOS TE85). In this study, the effects of E3 on cultured HOS TE85 cells were compared with those of 17β-estradiol (E2). HOS TE85 cells were subcultured in phenol red-free Dulbeccos modified Eagles medium supplemented with 10% fetal bovine serum for 72 h and then stepped down to serum-free conditions for an additional 72 h in the absence or presence of E3 (3.52 × 10−9, 3.52 × 10−8, 3.52 × 10−7 mol/l) or E2 (3.67 × 10−8 mol/l). Treatment with either E3 (3.52 × 10−8, 3.52 × 10−7 mol/l) or E2 (3.67 × 10−8 mol/l) resulted in an increase in the number of cultured HOS TE85 cells and their uptake of bromodeoxyuridine. Northern blot hybridization with a IGF-I cDNA probe revealed that RNA prepared from cultured HOS TE85 cells contained IGF-I mRNA transcripts of 1.8, 4.4 and 7.5 kb. Treatment with either E3 (3.52 × 10−9, 3.52 × 10−8, 3.52 × 10−7 mol/l) or E2 (3.67 × 10−8 mol/l) resulted in increased expression of the three mRNA transcripts relative tot hose in untreated control cultures. Semi-quantitative, reverse transcription polymerase chain reaction analysis showed that the 440-bp IGF-IR mRNA transcript was present in HOS TE85 cells and that treatment with either E3 or E2 did not affect the IGF-IR mRNA expression in these cells. These results demonstrate that E3 (3.52 × 10−9, 3.52 × 10−8, 3.52 × 10−7 mol/l) exerts profound effects on the proliferative potential of cultured HOS TE85 cells, compatible with that of E2 (3.67 × 10−8 mol/l), through the induction of IGF-I mRNA expression without affecting IGF-IR mRNA expression in these cells.

Effects of Combined Estriol/Pravastatin Therapy on Intima-Media Thickness of Common Carotid Artery in Hyperlipidemic Postmenopausal Women

Background: Several studies show that 17β-estradiol (E2) has protective effects on atherosclerosis in the arterial wall in postmenopausal women. Little information is, however, available regarding the effect of estriol (E3) on atherosclerosis. This study was conducted to investigate the effects of E3 alone and combined E3/pravastatin therapy on intima-media thickness (IMT) of common carotid artery in postmenopausal women. Methods: Thirty-three postmenopausal women were allocated to four groups: daily treatment with E3 (2 mg) alone (E3 group, n = 10), pravastatin (10 mg) alone (pravastatin group, n = 6), combined treatment with E3 (2 mg) and pravastatin (10 mg; E3/pravastatin group, n = 7) and untreated control group (n = 10). All women attended the Kobe University Hospital once a year for routine gynecological and ultrasonographic examinations for the evaluation of atherosclerosis. Results: A significant decrease in IMT was noted in the E3/pravastatin group compared with that in the untreated control group (p < 0.05), whereas there was no significant difference in the reduction rate of IMT in the pravastatin group, E3 group and untreated control group. Conclusions: The combined E3/pravastatin therapy appeared to retard the progression of atherosclerosis in postmenopausal women.

Effects of estriol on cell viability and 1,25-dihydroxyvitamin D3 receptor mRNA expression in cultured human osteoblast-like cells.

It is clinically evident that administration of estriol (E3) increases the bone mass density of the lumbar vertebrae in postmenopausal women, and that combined treatment with estrogen and 1,25-dihydroxyvitamin D3(VD3) increases femoral neck bone mass density compared with treatment with estrogen alone in postmenopausal osteoporotic women. However, the molecular mechanism whereby treatment with E3affects osteoblast cell function is still unknown. This study was conducted first to examine the comparative effects of E3and VD3on the cell viability of cultured human osteoblast-like cells (HOS) and second to determine whether E3affects VD3receptor mRNA expression in HOS. The cell viability and VD3receptor mRNA expression of cultured HOS were assessed by MTT assay and semiquantitative reverse transcriptase—polymerase chain reaction with Southern blot analysis, respectively. The treatment with E3increased the cell viability of cultured HOS compared with untreated control cultures. The increase in cell viability caused by the treatment with E3was further augmented by the combined treatment with VD3. The addition of either E3(3.52 × 10−8 mol/l) or E3(3.52 × 10−7 mol/l) to cultured HOS for 24 h resulted in a fourfold and eightfold increase, respectively, in VD3receptor mRNA expression in HOS, compared with that in untreated control cultures. These results suggest that E3may up-regulate the cell viability of osteoblast cells, and that the concomitant treatment with E3and VD3further augments the cell viability being associated with an E3-induced increase in VD3receptor mRNA expression in those cells.