Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bronchopulmonary dysplasia (BPD) is a common perinatal complication of very low birth weight preterm infants with a significant risk of long-term disability and morbidity. While clinical conditions such as prematurity and mechanical ventilation are its major risk factors, studies suggest that there is an individual susceptibility to BPD. This comprehensive review summarizes data collected about the implication of genetic polymorphisms in BPD and in its risk factors. Some studies have directly related the risk of BPD to genotype. Indeed, carrier states of genetic variants of cytokines (IFNgamma T+874A), adhesion molecules (L-selectin-Pro213Ser), elements of renin-angiotensin system (ACE-I/D), antioxidant enzymes (GST-P1 Val105Ile), and surfactant proteins (SPA1, SPB intron 4) has been identified as risk factors to BPD. Other studies investigated the role of genotype in BPD risk factors. Premature birth has been linked to carrier states of genetic variants with an impact on immune status (such as IL-6 G(-174)C, MBL2 54G/A, VEGF G+405C, HSP72 A+1267G genes) and matrix metalloproteases. Fetal inflammatory response syndrome, a major determinant of BPD is also affected by genotype (including LTalpha A+250G). Disturbed intrauterine lung development and vascularization may also contribute to BPD; these processes may be impaired in the presence of some rare genetic mutations. Furthermore, there is also a genetic component in the susceptibility to other perinatal adaptational disturbances such as respiratory distress syndrome that are associated with an increased need for mechanical ventilation, and, hence, with lung damage. The genetic variants presented in this article may help to identify infants at risk for BPD.
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PMID:Dysplasia: a review. 1772 3

Systemic sclerosis is a systemic, inflammatory, autoimmune disease affecting the skin and viscera, manifesting pathologically with microvascular lesions, perivascular infiltration by mononuclear cells and increased deposition of extracellular collagen. The rarity of the disease as well as its propensity to appear in the early 1940s, explain the low frequency of concurrent scleroderma and pregnancy. However, the marked female excess, as well as the trend for increasing maternal age due to social change and assisted reproductive technologies, renders heightened significance to issues of fertility, pregnancy course and pregnancy outcomes. In the past, scleroderma patients were thought to be at high risk for poor fetal and maternal outcome, but more current retrospective studies show that despite an increased frequency of prematurity and small for gestational age infants, overall maternal and neonatal survival is good. Hence, at present, with close monitoring and appropriate therapy most scleroderma patients can sustain a successful pregnancy. Therapy with hydroxychloroquine and low dose steroids as well as judicious use of intravenous immunoglobulins is permitted. Renal crisis remains the most dreaded complication of a scleroderma pregnancy and necessitates prompt institution of ACE inhibitor therapy despite its potential teratogenicity. In order minimize the risk for renal crisis, pregnancies should be avoided in rapidly progressive diffuse disease as such patients are at a greater risk for developing serious cardiopulmonary and renal problems early in the disease. This review shall focus on the bi-directional effects of scleroderma on fertility and pregnancy as well as on the management of pregnancy and delivery in the scleroderma patient.
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PMID:Pregnancy issues in scleroderma. 2215 99