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

Arterial hypertension is a relatively common complication of pregnancy, affecting about 10% of all normal pregnancies. The American College of Obstetric and Gynecology established in 1972 four different forms of arterial hypertension during pregnancy: a) arterial hypertension related to pregnancy, the so-called pre-eclampsia; b) arterial hypertension unrelated to pregnancy or chronic arterial hypertension; c) Pre-eclampsia superimposed on chronic arterial hypertension, and d) Transient or late arterial hypertension (third trimester). Pre-eclampsia and arterial hypertension are two different illnesses with different approaches and treatments. The mechanisms involved in arterial hypertension and pre-eclampsia of pregnant women are presently very well known, including genetic causes, alterations on the renin-angiotensin system, imbalance between vasoconstrictor and vasodilator agents derived from endothelial activity of the spiral arteries of the placenta, such as; prostacyclins, thromboxane A2, nitric oxide, endothelin-1, etc. The placenta is the key factor in inducing pre-eclampsia, and its expulsion during delivery or cesarean section is the definite cure of the process. All hypertensive forms during pregnancy increase the risks on both the mother and the fetus. Maternal risk is based on renal, metabolic and haematologic disorders, leading in some cases to cerebral haemorrhage or hepatic rupture. In the fetus, pre-eclampsia significantly increases the risk of still-birth, abruptio placentae, hypocalvaria, intrauterine growth retardation, and prematurity. Clinical, biochemical and haematologic manifestations of pre-eclampsia are very typical, facilitating an early and easy diagnosis.
 ...
PMID:[Arterial hypertension and pregnancy: diagnostic criteria and therapeutic approach]. 988 69

The peptide endothelin-1 (ET-1) plays an unknown role in the pathogenesis and progression of two important neonatal pulmonary disorders, chronic lung disease (CLD) of prematurity and persistent pulmonary hypertension of the newborn (PPHN). Inhaled nitric oxide (INO) is a proven vasodilator therapy in PPHN and is an experimental therapy in CLD. We sought to determine the effects, if any, of the interaction of inhaled INO with ET-1 in these two separate disorders. Infants (n=21) with PPHN (mean gestation age, 39.4 weeks; mean birth weight, 3470 g) were treated with INO. All infants were <72 h of age at baseline. Plasma obtained at baseline and after 24 h of INO therapy was assessed for ET-1. The change in ET-1 levels with INO was inversely correlated with change in arterial partial pressure of O(2) (r=-0.71, P=0.0003). A separate group of 33 patients with CLD (mean gestational age, 27 weeks; mean birth weight, 740 g; mean age, 19 days) had tracheal aspirate levels of ET-1 obtained before, during, and after 7 days' administration of INO. Values were normalized by soluble secretory component of IgA. Tracheal aspirate ET-1 levels were detectable before INO therapy. There was no significant change during or after treatment with INO. There was not a significant correlation between baseline fractional inspired O(2) and ET-1 levels. There was a non-significant trend in the correlation between the change in ET-1 and the change in interleukin-8 levels in tracheal aspirate. This report confirms the presence of ET-1 in tracheal aspirate of premature infants who are developing CLD and reaffirms the presence of ET-1 in plasma of infants with PPHN. Short-term INO therapy was associated with a decrease in plasma ET-1 levels in PPHN, but did not affect tracheal aspirate ET-1 in CLD. Given the vasconstrictive, profibrotic, and proinflammatory properties of ET-1, specific ET-1 receptor antagonists could be considered as candidates for trials as adjunct therapy in either or both of these disorders.
 ...
PMID:Interaction of endogenous endothelin-1 and inhaled nitric oxide in term and preterm infants. 1219 7