Presentation of uterine prolapse is a rare event in a pregnant woman, which can be pre-existent or else manifest in the course of pregnancy. Complications resulting from prolapse of the uterus in pregnancy vary from minor cervical infection to spontaneous abortion, and include preterm labor and maternal and fetal mortality as well as acute urinary retention and urinary tract infection. Moreover, affected women may be at particular risk of dystocia during labor that could necessitate emergency intervention for delivery. Recommendations regarding the management of this infrequent but potentially harmful condition are scarce and outdated. This review will examine the causative factors of uterine prolapse and the antepartum, intrapartum and puerperal complications that may arise from this condition as well as therapeutic options available to the obstetrician. While early recognition and appropriate prenatal management of uterine prolapse during pregnancy is imperative, implementation of conservative treatment modalities throughout pregnancy, these applied in accordance with the severity of the uterus prolapse and the patient's preference, may be sufficient to achieve uneventful pregnancy and normal, spontaneous delivery.
Turner's syndrome is characterized by an ovarian failure which occurs in most cases before puberty and leads to infertility. In less than 10% of women with Turner syndrome, puberty may occur and spontaneous pregnancies is possible but with a high risk of fetal loss, chromosomal and congenital abnormalities. We present the case of a 33-year-old woman with a mosaic Turner's syndrome karyotype 45,X/47,XXX who conceived spontaneously and had two successful pregnancies. Short stature was the only manifestation of Turner's syndrome. In the present report, we reviewed the available literature on the fertility of women with Turner's syndrome and the phenotypic effects of mosaicism for a 47,XXX cell line in Turner's syndrome.
Non-dipping circadian blood pressure (BP) is a common finding in preeclampsia, accompanied by adverse outcomes. Melatonin plays pivotal role in biological circadian rhythms. This study investigated the relationship between melatonin secretion and circadian BP rhythm in preeclampsia. Cases were women with preeclampsia treated between January 2006 and June 2007 in the University Hospital of Larissa. Volunteers with normal pregnancy, matched for chronological and gestational age, served as controls. Twenty-four hour ambulatory BP monitoring was applied. Serum melatonin and urine 6-sulfatoxymelatonin levels were determined in day and night time samples by enzyme-linked immunoassays. Measurements were repeated 2 months after delivery. Thirty-one women with preeclampsia and 20 controls were included. Twenty-one of the 31 women with preeclampsia were non-dippers. Compared to normal pregnancy, in preeclampsia there were significantly lower night time melatonin (48.4 ± 24.7 vs. 85.4 ± 26.9 pg/mL, p50.001) levels. Adjustment for circadian BP rhythm status ascribed this finding exclusively to non-dippers (p50.01). Two months after delivery, in 11 of the 21 non-dippers both circadian BP and melatonin secretion rhythm reappeared. In contrast, in cases with retained non-dipping status (n ¼ 10) melatonin secretion rhythm remained impaired: daytime versus night time melatonin (33.5 ± 13.0 vs. 28.0 ± 13.8 pg/mL, p ¼ 0.386). Urinary 6-sulfatoxymelatonin levels were, overall, similar to serum melatonin. Circadian BP and melatonin secretion rhythm follow parallel course in preeclampsia, both during pregnancy and, at least 2 months after delivery. Our findings may be not sufficient to implicate a putative therapeutic effect of melatonin, however, they clearly emphasize that its involvement in the pathogenesis of a non-dipping BP in preeclampsia needs intensive further investigation.
Arthrogryposis Multiplex Congenital (AMC) is a group of muscular, neurologic and connective tissue disorders, characterized by multiple severe joint contractures and decreased mobility. The incidence of this condition is 1/3000 births while the etiology is variable. Prenatal assessment of arthrogryposis has focused primarily on diminished fetal movement and the presence of joint contractures or skeletal deformities. These findings may not become evident until after 16-18 weeks' gestational age, subsequently, early prenatal diagnosis is difficult. Nowadays, modern ultrasound techniques and special sonographic markers help the clinicians with the prenatal detection of arthrogryposis in every gestational trimester.
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