Prediction of time to delivery by transperineal ultrasound in second stage of labor.

OBJECTIVE: To investigate whether the transperineal sonographic (TPS) parameters angle of progression (AoP) and midline angle (MLA) can predict the time remaining in the second stage of labor. METHODS: We evaluated prospectively women with a singleton pregnancy in cephalic presentation at term between October 2013 and September 2014. TPS volumes were obtained immediately after confirmation by digital vaginal examination of a fully dilated cervix. AoP and MLA were measured offline by analyzing the ultrasound volumes. Progression of labor was evaluated every hour during the second stage. The associations of AoP and MLA with the interval between TPS assessment and delivery were evaluated using multivariable Cox proportional hazards analyses in nulliparous and parous women separately. RESULTS: A total of 557 women were evaluated. An AoP ≥ 160° (adjusted hazard ratio (aHR), 2.52 (95% CI, 1.98-3.19)) and MLA ≤ 10° (aHR, 1.79 (95% CI, 1.35-2.34)) in nulliparous women and an AoP ≥ 150° (aHR, 1.86 (95% CI, 1.34-2.57)) and MLA ≤ 20° (aHR, 1.69 (95% CI, 1.21-2.34)) in parous women were significantly associated with the remaining time in labor. The positive/negative likelihood ratios of AoP, MLA, clinical station (fetal head descent as observed by digital examination) and clinical rotation (fetal head rotation as observed by digital examination) at these cut-off points were 3.6/0.6, 2.0/0.6, 1.6/0.6 and 1.6/0.8, respectively, in nulliparous women, and 2.4/0.6, 1.3/0.7, 7.6/0.5 and 5.2/0.7, respectively, in parous women. CONCLUSION: TPS assessment of AoP and MLA in the second stage of labor was useful for predicting the time remaining in labor and had higher predictive value than did digital vaginal examination in nulliparous women. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.

Clinical characteristics of monochorionic twins with large hemoglobin level discordance at birth.

OBJECTIVES: To evaluate neonatal outcomes and clinical characteristics of monochorionic diamniotic (MCDA) twins with a large intertwin hemoglobin (Hb) difference at birth. METHODS: This was a retrospective cohort study of MCDA twin gestations delivered at Osaka Medical Center and Research Institute for Maternal and Child Health between 2003 and 2012. Cases of pregnancy termination, acardiac twins or intrauterine death were excluded. A large intertwin Hb difference at birth was defined as > 8.0 g/dL according to the postnatal criteria for twin anemia-polycythemia sequence (TAPS). The intertwin reticulocyte count ratio (RCR) was calculated by dividing the reticulocyte count of the anemic twin by that of the polycythemic twin. Cases with Hb differences were divided into two groups according to the RCR, TAPS when the RCR was > 1.7 and acute fetofetal hemorrhage (AFFH) when the RCR was ≤ 1.7. Neonatal outcomes were compared between the TAPS and AFFH groups. RESULTS: During the study period, 432 MCDA twin pregnancies of a total of 532 born at our hospital were analyzed. There were 12 (2.8%) cases of a large intertwin Hb difference. The median gestational age at birth of these cases was 34 (range, 23-38) weeks, and all were delivered by Cesarean section. There were seven (1.6%) cases of TAPS and five (1.2%) of AFFH. The neonatal survival rate was 91.7%; in one pair of twins with TAPS neonatal death occurred. All (100%) cases with TAPS and two (40%) with AFFH required blood transfusion or partial-exchange transfusion for at least one infant. CONCLUSIONS: Although the incidence of TAPS and AFFH may be low in MCDA twins, many affected neonates required treatment for hematological abnormalities. Delivery of MCDA twins via Cesarean section does not appear to prevent AFFH, despite the absence of labor.

ORP150 protects against hypoxia/ischemia-induced neuronal death.

Oxygen-regulated protein 150 kD (ORP150) is a novel endoplasmic-reticulum-associated chaperone induced by hypoxia/ischemia. Although ORP150 was sparingly upregulated in neurons from human brain undergoing ischemic stress, there was robust induction in astrocytes. Cultured neurons overexpressing ORP150 were resistant to hypoxemic stress, whereas astrocytes with inhibited ORP150 expression were more vulnerable. Mice with targeted neuronal overexpression of ORP150 had smaller strokes compared with controls. Neurons with increased ORP150 demonstrated suppressed caspase-3-like activity and enhanced brain-derived neurotrophic factor (BDNF) under hypoxia signaling. These data indicate that ORP150 is an integral participant in ischemic cytoprotective pathways.

Association between maternal active smoking during pregnancy and placental weight: The Japan environment and Children's study.

INTRODUCTION: Maternal smoking during pregnancy is a well-known risk factor for reduced birthweight. However, research investigating the association between maternal smoking and placental weight is scarce and inconsistent. Our study was conducted to evaluate the association between maternal smoking and placental weight and placental weight/birthweight ratio (PW/BW ratio). METHODS: We used data from a birth cohort study, the Japan Environment and Children's Study (JECS). Main outcome measures were placental weight, PW/BW ratio, and the risk of high PW/BW ratio. High PW/BW ratio was defined as PW/BW ratio above the 90th percentile for gestational age and sex of offspring. The association between maternal smoking and placental weight was estimated as crude and as adjusted beta coefficients by applying linear regression analyses. Logistic regression analyses were also performed to estimate the association between maternal smoking and the risk of high PW/BW ratio. RESULTS: Of the 91,951 pregnant women, the mean placental weight and the mean PW/BW ratio were lowest for the group of women who had never smoked. Smokers had higher odds ratio for high PW/BW ratio compared with non-smokers. Furthermore, among smokers, the mean placental weight and mean PW/BW ratio were lowest in women who smoked less than 5 daily cigarettes, and highest in women who smoked 20 or more daily cigarettes during pregnancy. DISCUSSION: Placental weight was greater and PW/BW ratio was higher among smokers compared with non-smokers. Moreover, the number of daily cigarettes was positively associated with heavy placental weight.

Pathogenic role of asialo human chorionic gonadotropin in gestational thyrotoxicosis.

We reported that gestational thyrotoxicosis is induced by thyroid-stimulating activity (TSA) of circulating hCG. However, the serum immunological hCG concentration did not correlate to TSA. To elucidate this, we examined the relation of carbohydrate moieties of hCG to bioactivity in 79 early pregnant women, divided into 4 groups: no emesis, mild emesis, hyperemesis, and gestational thyrotoxicosis with hyperemesis. Serum free T4 (FT4) and free T3 (FT3) levels were significantly higher and TSH was lower in the hyperemesis (FT4, 23.42 +/- 5.02 pmol/L; FT3, 6.26 +/- 1.80 pmol/L; TSH, 0.30 +/- 0.44 mU/L) and in gestational thyrotoxicosis (FT4, 48.65 +/- 14.80 pmol/L; FT3, 14.71 +/- 3.47 pmol/L; TSH, < 0.04 mU/L) groups than in the no emesis group (FT4, 16.99 +/- 2.48 pmol/L; FT3, 5.51 +/- 0.75 pmol/L; TSH, 1.37 +/- 1.23 mU/L; P < 0.0005). TSA was also significantly higher in the hyperemesis (566 +/- 187%) and gestational thyrotoxicosis (832 +/- 168%) groups than in the no emesis group (321 +/- 135%). We found no significant difference among serum hCG concentrations measured by immunoassay in the four groups. To characterize the carbohydrate chains, serum hCG was fractionated by Concanavalin-A and ricin lectin affinity chromatography. The fraction firmly bound to Con-canavalin-A, which contains hCG with high mannose and hybrid-type carbohydrate chains, was significantly higher in the hyperemesis group (91.07 +/- 2.06%; n = 15) than in the no emesis group (89.61 +/- 2.38%; n = 24; P < 0.04). The fraction firmly bound to ricin column, which contains hCG with asialo-carbohydrate chains, was significantly increased in the gestational thyrotoxicosis group (3.44 +/- 1.70%; n = 5) compared with that in the no emesis group (1.77 +/- 0.49%; n = 24; P < 0.03). Serum FT4 positively correlated to the hCG fraction firmly bound to ricin column (r = 0.61; P < 0.001). We conclude that thyrotoxicosis with hyperemesis may be caused by circulating asialo-hCG with higher thyrotropic bioactivity.

Novel type Arabidopsis thaliana H(+)-PPase is localized to the Golgi apparatus.

Vacuolar H(+)-PPase, a membrane bound proton-translocating pyrophosphatase found in various species including plants, some protozoan and prokaryotes, has been demonstrated to be localized to the vacuolar membrane in plants. Using a GUS reporter system and a green fluorescent protein (GFP) fusion protein, we investigated the tissue distribution and the subcellular localization, respectively, of a novel type H(+)-PPase encoded by AVP2/AVPL1 identified in the Arabidopsis thaliana genome. We showed that AVP2/AVPL1 is highly expressed at the trichome and the filament of stamen. Furthermore, the fluorescence of GFP-tagged AVP2/AVPL1 showed small dot-like structures that were observed throughout the cytoplasm of various Arabidopsis cells under a fluorescent microscope. The distribution of this dot-like fluorescent pattern was apparently affected by a treatment with brefeldin A. Moreover, we demonstrated that most dot-like fluorescent structures colocalized with a Golgi resident protein. These findings suggest that this novel type H(+)-PPase resides on the Golgi apparatus rather than the vacuolar membrane.

Molecular and epidemiological studies of Werner syndrome in the Japanese population.

Werner syndrome (WS) is an autosomal recessive genetic disease characterized by many age-related features. The gene responsible for WS (WRN) has been isolated and contains a helicase domain, but its function is unknown. Six different mutations throughout the WRN gene have been reported in the Japanese population. We have studied whether patients with a specific mutation exhibit distinct phenotypes from others. Fourteen patients with different mutations showed almost the same signs and symptoms and, therefore, the C terminal part of the product appears to be crucial for its functions, although other parts may be important as well. Haplotype analyses using 13 microsatellites covering the 2.8-3.0 cM WRN region showed that two out of six different mutations had founder chromosomes. These two founder chromosomes may be evenly distributed throughout the western part of Japan, suggesting that these mutations go back to a time earlier than 1400 years ago.

Protective effect of vitamin E against focal brain ischemia and neuronal death through induction of target genes of hypoxia-inducible factor-1.

Vitamin E has been shown to have protective effects against cerebral ischemia, possibly due to its anti-oxidant effects. However, its non-anti-oxidant, intracellular molecular mechanism remains elusive. For in vivo experiments in rats, orally administered vitamin E significantly reduced not only the brain infarct volume but also space navigation disability after permanent middle cerebral artery (MCA) occlusion. The level of anti-oxidant after MCA occlusion was significantly increased specifically in the ipsilateral brain tissues of vitamin E-treated rats. For in vitro experiments, posttreatment with vitamin E protected primary cultured neurons from nitric oxide-induced insult. Vitamin E induced the expression of the alpha subunit of hypoxia-inducible factor-1 (HIF-1) and its target genes, including vascular endothelial growth factor (VEGF) and heme oxygenase-1. The hypoxia response element on the VEGF promoter was responsible for this vitamin E-induced transcriptional activation of VEGF gene. Taken together, these results suggest that cerebral infarction increased the permeability of vitamin E across the blood-brain barrier, and this increased vitamin E in brain tissue elicited neuroprotective effects not only through scavenging oxidants, as are previously well reported, but also by transactivating HIF-1-dependent genes, which results in protection of brains from ischemic insults.

Changes in concentration of human atrial natriuretic peptide in normal pregnancy and toxaemia.

Changes in concentration of human atrial natriuretic peptide (hANP) in normal and toxaemic pregnancy were examined. The maternal plasma concentration of hANP increased gradually during normal pregnancy to a maximum of 20.0 +/- 2.4 pmol/l (mean +/- S.E.M.) after week 36 of pregnancy. From week 20, the plasma concentrations of hANP were significantly higher than those in non-pregnant women (9.3 +/- 2.0 pmol/l). In toxaemia with hypertension, maternal plasma hANP levels were increased after week 26 of pregnancy (37.7 +/- 6.0 pmol/l) compared with those in normal gravida at the same time (17.1 +/- 1.6 pmol/l). Maternal plasma hANP levels in toxaemia only with oedema were not different from those in normal gravida.

Increase in peripheral natural killer cell activity in patients with autoimmune thyroid disease.

Changes in the activity and number of natural killer (NK) cells in peripheral blood in patients with autoimmune thyroid disease were examined. NK activity was measured in a 4-hr 51Cr-release assay and the number of NK cells was analyzed with FITC-conjugated monoclonal antibodies by use of an automated flow cytometer. NK activity in patients with untreated Graves' disease (n = 25, 39.7 +/- 13.5%, P less than 0.05) and Hashimoto's thyroiditis (n = 18, 41.0 +/- 14.2%, P less than 0.05) was high compared to the activity in non-pregnant controls (n = 61, 32.6 +/- 15.0%). NK activity in patients with postpartum Graves' thyrotoxicosis (n = 11, 48.6 +/- 18.9%) was markedly increased compared to the activity in non-pregnant controls (P less than 0.01) and in postpartum controls (n = 29, 33.8 +/- 15.2%, P less than 0.05), although the mean ages of each group did not differ significantly. Moreover, NK activities in the thyrotoxic state were significantly higher than those in the euthyroid state in the same patients with postpartum Graves' thyrotoxicosis or with postpartum destructive thyrotoxicosis. The number of CD16 positive cells increased in patients with postpartum Graves' thyrotoxicosis. However the number of CD16 and CD57 positive cells were normal in all other groups of patients. These results indicate that an increase of NK activity is associated with exacerbation of autoimmune thyroid disease both in Hashimoto's thyroiditis and in Graves' disease and suggest that NK cells might have an important role for the control of disease activity in autoimmune thyroid disease.

Changes in natural killer cell activity in normal pregnant and postpartum women: increases in the first trimester and postpartum period and decrease in late pregnancy.

Changes in the activity and number of natural killer (NK) cells in peripheral blood in normal pregnant and postpartum women were examined. NK activity was measured in a 4-h 51Cr-release assay and evaluated by conventional relative lytic units and absolute lytic units which represent the total NK activity within a fixed volume of circulating blood. The number of NK cells was analyzed with FITC-conjugated monoclonal antibodies and by use of an automated flow cytometer. Unexpectedly, the relative NK activity increased in the first trimester and also for 1 month postpartum compared to the activity in normal non-pregnant controls. On the other hand, absolute NK activity decreased in the third trimester compared to the activity in normal non-pregnant controls. The percentage of CD57+ cells decreased in the second trimester, but the percentage of CD16+ cells did not change during pregnancy or the postpartum period. The absolute counts of CD57+ cells and CD16+ cells decreased in the second and third trimesters and increased transiently in the postpartum period. These findings indicate that the increased NK activity in the first trimester and at 1 month postpartum is induced by increased cytotoxic activity of individual NK cells, and that the decreased NK activity in late pregnancy is induced by a decrease in the numbers of NK cells. These physiological changes may play an important role in implantation in early pregnancy, protection of the fetal allograft in late pregnancy and in the natural defense against infection during the puerperal period.

Effects of autoantibodies on the course of pregnancy and fetal growth.

OBJECTIVE: To assess the effects of autoantibodies on the course of pregnancy and fetal growth. METHODS: One thousand one hundred seventy-nine healthy women with singleton gestations were screened in early pregnancy for seven kinds of autoantibodies: antithyroid microsomal antibody, antithyroglobulin antibody, two kinds of rheumatoid factor, antinuclear antibody, anti-DNA antibody, and antimitochondrial antibody. RESULTS: In 228 cases (19.3%), at least one autoantibody was found; however, overlap of autoantibodies in the same individual was unexpectedly rare, and only two cases were positive for as many as four autoantibodies. A significantly higher rate of spontaneous abortion was observed in antibody-positive subjects, especially those with antithyroid microsomal (10.4%) or antinuclear antibodies (16.0%), compared with all antibody-negative subjects (5.5%). There were no significant differences in any outcome assessed among subjects positive for antithyroglobulin antibody, anti-DNA antibody, or antimitochondrial antibody compared with all antibody-negative subjects. None of the seven autoantibodies affected the rates of preterm delivery, stillbirth, pregnancy-induced hypertension, malformation, or gender ratio. CONCLUSION: Antithyroid microsomal antibody and antinuclear antibody are the only autoantibodies that increase the abortion rate.

Physiologic thyroid activation in normal early pregnancy is induced by circulating hCG.

In normal early pregnancy, serum free thyroxine (T4) increases and serum TSH decreases, indicating that the thyroid gland is activated physiologically. To identify the factor responsible for this thyroid activation, we measured the serum thyroid-stimulating activity in comparison with the serum level of hCG in 39 normal women in early pregnancy. Serum thyroid-stimulating activity was measured by a sensitive cyclic adenosine 3',5'-monophosphate (cAMP) accumulation assay using a rat thyroid cell line (FRTL-5). Thyroid-stimulating activity was detected in 37 women (95%), and the activities of individuals correlated positively with their serum free T4 levels (r = 0.474; P less than .01) and negatively with their serum TSH levels (r = -0.376; P less than .02). Moreover, serum thyroid-stimulating activity correlated closely with the serum hCG level (r = 0.741; P less than .001), but was completely abolished by pre-treatment of the sera with hCG antibodies. These data indicate that in normal early pregnancy, the thyroid gland is physiologically activated by serum hCG, which has intrinsic thyroid-stimulating activity.

Risk factors for developmental disorders in infants born to women with Graves disease.

OBJECTIVE: To identify risk factors for disorders of fetal growth and thyroid function in the presence of maternal Graves disease. METHODS: Two hundred thirty pregnancies in gravidas with Graves disease were analyzed. Maternal thyroid status was evaluated by serum free thyroxine (T4) or free T4 index, TSH, and TSH-receptor antibody; personal history of thyrotoxicosis and total dose of antithyroid drugs during pregnancy were also noted. Neonatal thyroid function was assessed at birth and on the fifth day after birth. RESULTS: Fifteen neonates (6.5%) were small for gestational age (SGA), and this occurrence was significantly associated with thyrotoxicosis lasting for 30 weeks or more of pregnancy, TSH-receptor antibody level of 30% or more at delivery, history of Graves disease of 10 years or longer, and onset of Graves disease before 20 years of age. However, no significant correlation was found between maternal thyroid hormone level and SGA neonates. Thyroid dysfunction developed in 38 infants (16.5%), of whom only four were SGA; development of this dysfunction was significantly related to the mother's total dose of antithyroid drugs, duration of thyrotoxicosis in pregnancy, and/or TSH-receptor antibody level at delivery. CONCLUSIONS: Duration of maternal Graves disease or thyrotoxicosis, either mild chemical or overt, in pregnancy is significantly associated with SGA neonates. Neonatal thyroid dysfunction is associated with the maternal thyroid condition, especially the serum TSH-receptor antibody level.

Thyroxine requirement during pregnancy for replacement therapy of hypothyroidism.

We examined the dose requirements of thyroxine (T4) and desiccated thyroid during eight pregnancies of six women who had undergone total thyroidectomy for thyroid carcinoma. In five pregnancies from four patients treated with T4, serum free T4, which was measured by a newly developed radioimmunoassay, decreased during pregnancy but increased above the normal range after delivery. Consistent with these changes in free T4, serum TSH (measured by a highly sensitive immunoradiometric assay) increased during pregnancy but returned to an undetectable level after delivery, with one exception. The serum triiodothyronine (T3)-to-T4 ratio, which is related to peripheral conversion of T4 to T3, was lower in patients treated with T4 than in normal controls, regardless of pregnancy. The ratio decreased further during pregnancy, and so relative deficiency of T3 during pregnancy was suspected, especially in T4-treated patients. On the other hand, in two pregnancies from two other patients treated with desiccated thyroid at a dose most equivalent to that of T4, serum free T4 decreased to a low-normal value during gestation but returned to the normal range after delivery, whereas serum TSH scarcely changed during pregnancy. These findings indicate that replacement therapy for pregnant patients with hypothyroidism after total thyroidectomy should include an increased dose of T4; in contrast, the dose of desiccated thyroid need not be changed.

Prenatal detection of ischemic changes in the placenta of the growth-retarded fetus by Doppler flow velocimetry of the maternal uterine artery.

OBJECTIVE: To determine the relationships among the pregnancy outcomes of growth-retarded fetuses, Doppler flow velocimetry of the fetomaternal circulation, and pathologic changes in the placenta. METHODS: Forty-seven fetuses confirmed to be growth-retarded by ultrasonographic biometry were monitored during pregnancy in terms of the resistance indexes of the maternal uterine, fetal umbilical, and fetal middle cerebral arteries. After delivery, the placentas were examined for pathologic changes such as infarction and villous ischemia. RESULTS: Compared with 23 fetuses with nonischemic placentas, 24 growth-retarded fetuses whose placentas showed ischemic lesions were more frequently delivered preterm (P < .001) and by cesarean for fetal distress (P < .01), and they also had lower mean pH, higher carbon dioxide pressure, and lower oxygen pressure values (P < .05). Compared with the fetal umbilical and middle cerebral artery resistance indexes, the uterine artery resistance index showed the highest sensitivity (91.7%), specificity (78.3%), and positive predictive value (81.5%) for detecting placental ischemic changes. Linear discriminative analysis also showed that the uterine artery resistance index had the strongest correlation (P < .00001) with the placental ischemic changes. CONCLUSION: Ischemia of the placenta is associated with an adverse pregnancy outcome in growth-retarded fetuses. The placental ischemic changes can be detected using Doppler flow velocimetry. Measurement of the uterine artery resistance index might be useful for determining the clinical management of growth-retarded fetuses.

Crucial role of serum human chorionic gonadotropin for the aggravation of thyrotoxicosis in early pregnancy in Graves' disease.

Thyrotoxicosis in Graves' disease is often aggravated in early pregnancy and is closely associated with postpartum recurrence of stimulative thyrotoxicosis. To examine whether thyroid-stimulating TSH receptor antibody (TSAb) or human chorionic gonadotropin (hCG), which also has thyroid-stimulating activity (TSA), was responsible for this early aggravation, the respective TSA due to TSAb or hCG was evaluated by a highly sensitive cAMP accumulation assay using FRTL-5 cells. TSA was detectable in all of 11 women in normal early pregnancy, correlated positively with serum hCG concentration, and was abolished completely by the pretreatment of serum sample with the solid-phase hCG antibody coupled with Sepharose 4B. The model serum samples of Graves' disease with pregnancy were made by the mixture of normal pregnant and Graves' sera, and their TSA were reduced by the pretreatment with the solid-phase hCG antibody, just corresponding with the reduction in hCG-induced TSA. TSA of early pregnant sera in 20 patients with Graves' disease decreased significantly but were still positive even after the pretreatment with the hCG antibody. Serial changes in TSAb and hCG-induced TSA were measured in 5 of these 20 pregnant patients. hCG-induced TSA increased associated with the increase in free thyroxine, while TSAb did not show striking change in early pregnancy. These data indicate that (1) respective TSA due to TSAb or hCG can be measured distinctively by using the solid-phase hCG antibody and (2) hCG plays a crucial role in the aggravation of Graves' thyrotoxicosis in early pregnancy.

Differentiation of postpartum thyrotoxicosis by serum thyroglobulin: usefulness of a new multisite immunoradiometric assay.

Destruction-induced thyrotoxicosis and Graves' thyrotoxicosis must be differentiated, since they are treated differently. To find a useful marker, we examined serial changes in serum thyroglobulin (Tg) concentrations in 20 patients with postpartum thyroid disease (9, euthyroid Hashimoto's disease; 11, Graves' disease in remission in early pregnancy). Serum Tg was measured by a new multisite immunoradiometric assay that allows little influence of anti-Tg autoantibodies. Eight women developed destruction-induced thyrotoxicosis 1 to 4 months postpartum, 6 had relapse of Graves' thyrotoxicosis 2 to 4 months postpartum, and 6 remained euthyroid. In destruction-induced thyrotoxicosis, serum Tg 2 months before the onset was 13.3 +/- 11.4 micrograms/L, then clearly increased 1 month before (34.5 +/- 31.9 micrograms/L) and was even higher at the onset of thyrotoxicosis (116.5 +/- 137.1 micrograms/L). In contrast, serum Tg increased only at the onset in Graves' thyrotoxicosis (from 25.9 +/- 25.2 micrograms/L 1 month before to 76.1 +/- 75.3 micrograms/L at the onset, p < 0.05). There was no difference in serum Tg level at the onset between the two disorders. However, when data were expressed as the percent increase from the level one month before, and the cut-off value were taken at 150%, all 7 patients above the cut-off developed destruction-induced thyrotoxicosis, and 6 of 7 below had recurrent Graves' thyrotoxicosis. Thus, serial measurement of serum Tg is useful for the differentiation of destruction-induced thyrotoxicosis from Graves' thyrotoxicosis after delivery.

Leukemia developing after 131I treatment for thyroid cancer in a patient with Werner's syndrome: molecular and cytogenetic studies.

A 40-year-old female patient with Werner's syndrome (WS) suffering from thyroid cancer and myelodysplastic syndrome (MDS) is reported. She had been diagnosed as having WS complicated with thyroid cancer seven years previously. Total thyroidectomy and radioactive iodine (131I, 100 mCi/year) therapy for seven years had slowed the progression of thyroid cancer. She suffered a sudden onset of MDS at the age of 40 years. After six months she died from overt leukemia. We found an additional chromosome aberration of chromosome 10 in the progression of leukemia from MDS.

Hand-assisted laparoscopic splenectomy for idiopathic thrombocytopenic purpura during pregnancy.

A successful case of a hand-assisted laparoscopic splenectomy with low-pressure pneumoperitoneum for autoimmune thrombocytopenic purpura in a patient at 23 weeks' gestation is reported. Preoperative splenic arterial embolization was performed on the same day as the operation using painless contour embolic material and super-absorbent polymer microspheres. The abdominal wall retraction method first was applied to avoid the effects of pneumoperitoneum on systemic hemodynamic alterations. However, a sufficient surgical view could not be obtained, as the intra-abdominal organs were elevated because of the enlarged uterus. A surgical view with 4 to 6-mm Hg pneumoperitoneum was available for the hand-assisted splenectomy. The postoperative course was uneventful, and the patient vaginally delivered a healthy infant. A hand-assisted laparoscopic splenectomy with low-pressure pneumoperitoneum after splenic arterial embolization would be feasible for patients with autoimmune thrombocytopenic purpura during a relatively advanced pregnancy.