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At least 199 records · Page 11Linked to original sources
PubMed1984

Maternal Addison's disease and fetal growth retardation. A case report.

Maternal Addison's disease (primary hypoadrenalism) is an infrequent complication of pregnancy that poses a high risk of maternal mortality if not recognized and treated. If adequate steroid replacement therapy is provided, however, there is little risk for the mother during pregnancy. We treated a woman for previously undiagnosed Addison's disease during pregnancy that apparently interfered with normal fetal growth. This case supports Osler's observation that maternal Addison's disease can cause intrauterine fetal growth retardation.

Addison Disease↗
PubMed2002

Feto-maternal microchimerism in connective tissue diseases.

Fetal progenitor cells traffic to the mother during pregnancy and can persist in the maternal circulation for many years. Feto-maternal microchimerism has been reported in women with scleroderma, but its contribution to the disease pathogenesis remains unclear. Furthermore, the involvement of microchimerism in other connective tissue diseases is controversial. We studied 243 females, 122 of whom had previously carried a male fetus (50 healthy controls, 23 patients with scleroderma, and 49 with other connective tissue diseases). The presence of the male-specific SRY sequence was analyzed using a kinetic quantitative ELISA PCR assay that allows detection of one to three male cells in one million female cells. The percentage of SRY-positive samples was not different among women having borne son(s): 16% (95% confidence interval 0.07-0.29) in healthy controls, 21.7% (0.07-0.44) in patients with scleroderma and 25.5% (0.14-0.40) in patients with connective tissue diseases (p=0.25). The mean number of fetal cells was similar in the three groups. Among the 121 females who never carried a male fetus, no healthy woman was SRY positive. However, 33% of patients with scleroderma and 22.9% of women with connective tissue diseases were chimeric, a phenomenon which might be related to early miscarriage(s). Therefore, feto-maternal microchimerism is a common event in both healthy controls and patients with connective tissue diseases, and is unlikely to represent per se a risk factor for these diseases.

Case-Control Studies↗
PubMed2002

How congenital heart disease originates in fetal life.

Knowledge of the early development of the heart has increased rapidly in recent years as microscopic techniques, experimental models using animal, avian and insect species, and various genetic techniques have been brought to bear on the mysteries of human fetal cardiac development. The development of the heart occurs rapidly from embryonic day 18 in humans to the twelfth week of fetal life. The stages include gastrulation and formation of the primitive heart tube with rhythmic contractions appearing at day 21, segmentation of the primitive heart tube, looping, realignment of inflow and outflow segments, septation of the atria, ventricles and outflow segments, formation of atrio-ventricular valves, and development of aortic and pulmonary trunks and aortic arches. The genes and factors currently known to be involved in cardiac development are reviewed, but much is still to be determined as the field is evolving with extraordinary rapidity.

Aorta↗
PubMed1991

In utero intravascular transfusion for treating fetal hemolytic disease.

Technologic advances in ultrasound have led to the ability to access the fetal circulation in utero. Precise evaluation and accurate treatment of fetal hemolytic disease is now possible. This technique of in utero intravascular transfusion has several advantages. It uses a closed system that reduces the risk of infection and air embolus. The proximal extension tubing minimizes manipulation of the hub of the needle, which may lead to dislodgement of the needle, and permits a sampling port with minimal dead space between it and the fetal circulation. The HemoCue hemoglobinometer allows for rapid assessment of the concentration of fetal hemoglobin and, therefore, a shorter interval of time in which the needle is in the umbilical cord. This reduces the risks of trauma to the umbilical cord.

Blood Transfusion, Intrauterine↗
PubMed1993

Prenatal diagnosis of congenital heart disease and fetal karyotyping.

OBJECTIVE: To determine the incidence of aneuploidy among fetuses with congenital heart disease diagnosed in utero. METHODS: From June 1988 through December 1991, 502 fetuses at risk for congenital heart disease underwent fetal echocardiography. Fetal karyotyping was performed whenever a cardiac anomaly was diagnosed. Autopsy reports, postnatal echocardiograms, and angiograms were obtained to confirm the diagnosis. RESULTS: Congenital heart disease was found in 31 of 469 fetuses with complete follow-up. Fifteen of these 31 fetuses (48%) were found to have an abnormal karyotype: five of 17 (29.4%) with isolated cardiac anomalies and ten of 14 (71.4%) with cardiac and extracardiac anomalies. Detected chromosomal abnormalities included six trisomy 21, four trisomy 18, four trisomy 13, and one triploidy 69,XXX. Atrioventricular septal defects and ventricular septal defects were the cardiac malformations most often associated with abnormal karyotypes (77 and 71%, respectively). CONCLUSIONS: The risk of aneuploidy associated with fetal cardiac anomalies is much greater than that associated with elevated maternal age; therefore, fetal karyotyping should be offered whenever a cardiac defect is diagnosed. Advanced gestational age should not represent a deterrent, because the discovery of a lethal trisomy in a fetus with a cardiac malformation can affect dramatically the prognosis and the obstetric and neonatal management. We believe that a screening view such as the four-chamber view should now be included routinely in obstetric ultrasound examinations.

Aneuploidy↗
PubMed1995

Survival of F-reticulocytes in sickle cell disease.

Fetal hemoglobin, Hb F, is known to be an important factor for clinical course of sickle cell disease, as it suppresses polymerization of sickle hemoglobin. To investigate the effect of Hb F on the survival of sickle reticulocytes (young red cells) in circulation, Hb F levels in individual reticulocytes and mature erythrocytes were quantified via fluorescence image cytometry. We first examined unfractionated SS cells from 3 patients with different Hb F levels, and found that Hb F levels in reticulocyte populations were always lower than those in erythrocyte populations. This suggests that subsets of reticulocytes with lower Hb F levels are removed during maturation while those with higher Hb F levels tend to survive to become erythrocytes. The distribution of Hb F in reticulocytes was different among these patients and seems to strongly affect the survival of F-reticulocytes. We also analyzed density-separated fractions, and found that Hb F levels in reticulocytes found in the densest fraction were lower than those in lighter fractions. This suggests that reticulocytes with lower Hb F levels are susceptible to quick dehydration within their maturation period (1-2 days) in circulation.

Anemia, Sickle Cell↗
PubMed1998

Pregnancy, persistent microchimerism, and autoimmune disease.

Fetal cells have been detected in maternal peripheral blood in the majority of normal pregnancies, and the influx of fetal cells into the maternal circulation increases during parturition. Recently, fetal progenitor cells have been found to persist in maternal peripheral blood for decades after childbirth--which has potential implications for some autoimmune diseases in women, such as scleroderma. Scleroderma has a strong female predominance, a steep increase in incidence in women following the childbearing years, and clinical similarity to the chronic graft-versus-host disease that occurs after allogenic bone marrow transplantation. This article explores the hypothesis that microchimerism (nonhost cells) contributes to the pathogenesis of scleroderma and certain other autoimmune disorders.

Autoimmune Diseases↗
PubMed2004

DNA hypo-methylating agents and sickle cell disease.

Fetal haemoglobin (HbF, alpha2) decreases polymerization of sickle haemoglobin (HbS) and high levels correlate with decreased morbidity and mortality in sickle cell disease (SSD). Therefore, a therapeutic goal in SSD is the pharmacologic reactivation of HbF. Silencing of the globin (HbF) gene is associated with DNA methylation. The cytosine analogues 5-azacytidine and 5-aza-2'-deoxycytidine (decitabine) hypomethylate DNA by inhibiting DNA methyl-transferase. In clinical trials, 5-azacytidine and decitabine have demonstrated the greatest efficacy in HbF reactivation. Clinical development of these drugs has been delayed by concerns regarding the carcinogenic potential of 5-azacytidine. Furthermore, controversy regarding DNA hypomethylation versus more generic cytotoxic effects as the mechanism of action suggested that other cytotoxic/cytostatic agents might be as effective. Additional preclinical data and clinical studies of decitabine have tempered many safety concerns and have confirmed that DNA hypomethylation is the mechanism of action. Pharmacologic reactivation of HbF through DNA hypomethylation holds promise as an effective disease modifying intervention for patients with SSD. Larger studies are required to confirm safety and effectiveness with chronic use.

Anemia, Sickle Cell↗
PubMed1994

Clinical application of neuronal grafts in Parkinson's disease.

Fetal neural grafts, rich in dopamine neurons, taken from the ventral mesencephalon and implanted into the dopamine-denervated striatum, can reinnervate the striatum, form synaptic contacts with host neurons, release dopamine and improve motor function. In animal models of Parkinson's disease, the improvement resulting from transplantation is dependent on the number of surviving grafted dopamine neurons and the density and extent of graft-derived reinnervation. The major unresolved scientific question at present is not whether neural grafting is better than established drug treatments but if survival and function of such grafts are at all possible in patients with Parkinson's disease. A more general problem is that if cell transplantation is to become clinically useful for a large number of Parkinsonian patients and also be applied in other neurological disorders, alternative sources of donor tissue must be found; several have been proposed, including adrenal medulla cells and sympathetic ganglia but perhaps the most exciting strategy is to implant cells that have been genetically engineered to synthesize and release L-dopa or dopamine.

Animals↗
PubMed1985

Positive correlation between mature amniotic fluid optical density readings and the absence of neonatal hyaline membrane disease.

Fetal pulmonary maturity is generally determined by analyzing amniotic fluid for surfactants. This task is accomplished by lipid extraction of the fluid and resolution, identification and quantitation of the isolated lipids with thin-layer chromatography. These methods are lengthy, cumbersome and often not available on demand. A quick, simple, reliable and economical test therefore would be highly desirable. We have been able to correlate an optical density (OD) reading of amniotic fluid at 650 nm greater than or equal to 0.15 with the absence of hyaline membrane disease (HMD). For 428 fluids in which an OD reading of greater than or equal to 0.15 was found and delivery occurred within 48 hours, HMD was present in only two infants. The accuracy of the test was 99.53% , with a false-positive rate of 0.47%. With the use of this simple and accurate test one can satisfy the requirement of an on-demand test to determine fetal pulmonary maturity.

Amniotic Fluid↗
PubMed2004

Fetomaternal cell traffic, pregnancy-associated progenitor cells, and autoimmune disease.

Fetal cells in maternal blood are a potential source of fetal genetic material that can be obtained non-invasively. Efforts to isolate these cells from maternal peripheral blood are limited by their low circulating numbers (approximately 1 per ml of maternal blood in euploid pregnancies). Expansion of these cells by culture would provide more cells for diagnosis and give an opportunity to study fetal metaphase chromosomes. Despite extensive optimization of culture conditions, many groups have failed reproducibly to grow fetal cells from pre-procedural maternal samples. An unexpected benefit of this research has been the discovery of a novel population of fetal cells, the pregnancy-associated progenitor cell (PAPC), which remains in maternal blood and tissue for decades following delivery. These cells might play a role in some autoimmune diseases, such as scleroderma. PAPCs appear to have stem cell characteristics, such as the ability to proliferate and differentiate. Recently developed animal models will help to ascertain whether these cells cause disease, respond to disease, or have therapeutic applications.

Adult↗