Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the relationship between the increase in amniotic fluid phosphatidate phosphohydrolase (PAPase) specific activity and the increase in the lecithin/sphingomyelin (L/S) ratio during normal human pregnancy, PAPase specific activity and the L/S ratio were measured in 171 amniotic fluid samples obtained from 164 women who were at 17 to 42 weeks' gestation. The increase in PAPase specific activity in amniotic fluid is parallel to the increase in the L/S ratio. The correlation between PAPase specific activity and the L/S ratio in amniotic fluid from all gestational ages is highly significant. The relationship of PAPase specific activity in amniotic fluid to PAPase specific activity in gastric fluid was investigated in a study of 97 newborn infants. A highly significant correlation was found between these two values. To ascertain if a relationship exists between the specific activity of PAPase in amniotic fluid and the subsequent development of hyaline membrane disease (HMD), 223 neonates who were delivered within 72 hours of amniotic fluid collection were studied. Only one infant developed HMD out of 170 with amniotic fluid PAPase specific activity equal to or greater than 50 nmoles of orthophosphate released X mg.-1 of protein X hr.-1. On the other hand, the finding of an amniotic fluid PAPase specific activity of less than 50 nmoles was of little value in predicting lung immaturity. We believe that these findings are also supportive of the view that PAPase and surfactant are released from the type II pneumocyte as a closely related structural unit, viz., the lamellar body.
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PMID:Fetal lung maturation: human amniotic fluid phosphatidate phosphohydrolase activity through normal gestation and its relation to the lecithin/sphingomyelin ratio. 21 53

A new, rapid technique for determining fetal lung maturity, the FELMA, was tested against the standard lecithin/sphingomyelin (L/S) ratio in predicting hyaline membrane disease (HMD). The FELMA was tested on 236 samples, 154 of which were compared with the L/S ratio; 102 neonates were delivered within 48 hours. There was a significant correlation between methods ( r = 0.47). No neonate with a mature FELMA score developed HMD. Of 5 neonates with HMD, 2 had mature L/S ratio in predicting lung immaturity, providing a rapid result without the necessity of thin-layer chromatography.
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PMID:Evaluation of the FELMA microviscosimeter in predicting fetal lung maturity. 50 94

All 1998 resident infant deaths in the 1969--1977 King County, Washington birth cohort of 139,132 resident live births comprise the data base for epidemiologic comparisons of the sudden infant death syndrome (SIDS) with eight other major infant mortality components: hyaline membrane disease; respiratory distress syndrome; asphyxia of the newborn; immaturity; birth injury; congenital malformation; infection; and "all other." These components were compared with respect to age at death; sex; race; prior fetal loss; prior live-born, now dead; birth plurality; birth weight; maternal age; birth order; marital status; prenatal care; and season of death in an attempt to determine the uniqueness of these purported SIDS risk factors. Only the age at death distribution unequivocally distinguished SIDS from the other components. The combination of low maternal age and multiparity was demonstrated to be putatively synergistic for risk of SIDS, hyaline membrane disease, and respiratory disease syndrome. Only deaths from infection exhibited seasonal variation similar to SIDS. These observations probably reflect secondary associations with as yet unidentified primary risk factors relatable to maternal experience.
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PMID:Epidemiologic comparisons of the sudden infant death syndrome with other major components of infant mortality. 55 88

The clinicopathological associations of 33 singleton infants who died with intraventricular haemorrhage (IVH) without hyaline membrane disease (HMD) ('IVH only') were compared with those of 39 infants who died with IVH+HMD over the same gestation range in order to determine what factors other than those related to HMD may contribute to the pathogenesis of IVH. The incidence of 'IVH only' was inversely related to gestational age in the Hammersmith birth population, whereas the incidence of IVH+HMD rose to a peak at 28-29 weeks' gestation. Infants with 'IVH only' lived longer on average than those with IVH+HMD despite a lower birthweight and shorter gestation. Infants who died in the first 12 hours from 'IVH only' had suffered severe birth asphyxia but in those who died later the main symptom was recurrent apnoea. Fewer infants with asphyxia but in those who died later the main symptom was.recurrent apnoea. Fewer infants with 'IVH only' were given alkali therapy or were connected to the ventilator as compared to those with IVH+HMD, but there were no differences in alkali therapy in those who lived for 12 hours or more. In the 'IVH only' group there was a high incidence of haemorrhage from other sites and of bacterial infections. It is suggested that, in the absence of HMD, extreme immaturity is the main factor determining the occurrence of IVH. Birth asphyxia, apnoeic attacks, haemorrhage, and infections may play subsidiary roles, possibly through development of metabolic acidosis.
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PMID:Intraventricular haemorrhage in the preterm infant without hyaline membrane disease. 87 29

We reviewed 294 pairs of twins born from January, 1966 to December, 1972. In 19 pairs one or both members developed hyaline membrane disease (HMD). Of these, both twins were affected in 12 pairs, twin B alone in six pairs, and twin A alone in one pair. The group affected (19 pairs) had lower gestational age, birth weight, Apgar score, increased incidence of monozygotic (MZ) twins, and higher mortality rate than the group without HMD (275 pairs). MZ twins were more immature than dizygotic (DZ) twins (p less than 0.02). When both twins were affected they had lower gestational age, birth weight, and increased monozygosity than when B alone was affected (p less than 0.05). When twin B alone was affected, he had lower Apgar score than twin A (p less than 0.05). We suggested that (1) HMD occurs in twins because of lung immaturity, as it does in singletons; (2) monozygosity may be a predisposing factor to HMD because of the associated prematurity; and (3) the greater risk of twin B is probably related to birth asphyxia.
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PMID:Hyaline membrane disease in twins. A 7 year review with a study on zygosity. 94 94

To test the hypothesis that intarpartum acidosis has a role in the etiology of hyaline membrane disease (HMD), blood was collected from the umbilical artery (UA) at birth from 110 premature infants and analyzed for hydrogen ion concentration ([H+]), PCO2, standard bicarbonate, and lactic acid. The infants were followed until a definite diagnosis was made of HMD (33 infants), type II respiratory distress syndrome (16 infants) or the absence of respiratory distress (61 infants). In general, infants with HMD were more premature and had lower Apgar scores than nondistressed infants; however, there were no significant differences between the two groups in any acid-base measurement. Only in those patients of 32 to 37 weeks' gestational age was it possible to detect a significant increase in UA [H+] in infants with HMD compared to those without respiratory distress. There was evidence that the reduced Apgar score of infants with HMD may be due to immaturity and abnormal pulmonary function secondary to lung disease. It is concluded that acidosis at birth is not a factor in the development of HMD except possibly in more mature infants.
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PMID:The role of acidosis at birth in the development of hyaline membrane disease. 95 Nov 32

To test whether the presence of airway inflammatory markers differentiated babies with hyaline membrane disease (HMD) who recovered (n = 18) from those in whom bronchopulmonary dysplasia (BPD) developed (n = 18), tracheal aspirate samples from 36 newborn infants with HMD who underwent intubation were collected during days 1 to 28 of life and analyzed for the mucosal antimicrobial proteins lactoferrin and lysozyme. For babies with HMD in whom BPD developed, lactoferrin concentrations were decreased during the first 4 days of life (7 +/- 3, 14 +/- 3, 18 +/- 3, and 18 +/- 3 micrograms/ml, respectively) in comparison with those in babies with HMD who recovered (23 +/- 8, 29 +/- 6, 41 +/- 9, and 81 +/- 19 micrograms/ml); group differences reached statistical significance on days 3 and 4 (p less than 0.05). Lysozyme levels in the secretions of babies with BPD were also lower on day 3 (31 +/- 5 micrograms/ml) than in those of babies who recovered (54 +/- 7.5 micrograms/ml). For babies with BPD whose endotracheal tube remained in place beyond day 4, lysozyme levels on days 5 to 12 were significantly lower for those classified as having severe BPD than for those with mild to moderate BPD. Because lysozyme and lactoferrin are products of serous cells found in submucous glands, it seems possible that the relative immaturity of submucous glands may influence the development of BPD.
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PMID:Lactoferrin and lysozyme deficiency in airway secretions: association with the development of bronchopulmonary dysplasia. 164 Feb 95

Of a total of 755 neonates who died between 1972 and 1988, 331 (43.9%) were subjected to necropsy examination. The ranking of major primary causes of neonatal death was as follows: infections 27.2%, hyaline membrane disease 20.2%, congenital malformations 19.6%, perinatal anoxia 14.5%, immaturity 5.1% and birth trauma 2.7%. Over the years, the prevalence of infections as the cause of death has consistently declined. Compared with that in other contemporary Indian studies, the prevalence of hyaline membrane disease is higher and that of infections and perinatal anoxia relatively lower.
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PMID:Primary causes of neonatal deaths in a tertiary care hospital in Delhi: an autopsy study of 331 cases. 169 78

We studied urine excretion of free and conjugated aldosterone by 12 control infants and 14 infants with hyaline membrane disease (HMD) on the first and seventh days after birth. Both groups had a mean gestational age of 29 weeks. Total urine aldosterone excretion (UAE) and percent excreted as conjugate were similar for both groups on both study days, and did not relate to the severity of respiratory failure in infants with HMD. Sodium intake was higher for infants with HMD on both study days (p less than 0.02), but their urine sodium excretion was only significantly (p less than 0.01) higher on day 7. For total UAE values greater than 3 nmol/kg/d, there was no significant difference between estimated sodium-potassium exchange by control (22 +/- 5%, n = 8) and HMD (31 +/- 5%, n = 10) groups. These data suggest that neither the magnitude of excretion of aldosterone in the urine, the ability to conjugate aldosterone nor the degree of relative distal tubular unresponsiveness to aldosterone are related to the severity of pulmonary immaturity in preterm infants.
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PMID:Hyaline membrane disease and early neonatal aldosterone metabolism in infants of less than 33 weeks gestation. 186 79

The premature baboon delivered by hysterotomy at 140 +/- 2 days (75%) gestation develops hyaline membrane disease (HMD) and left-to-right (L-R) shunting through the patent ductus arteriosus (PDA). To characterize hemodynamic changes that follow premature delivery, we measured systemic and organ blood flow, oxygen transport, and systemic vascular resistance over the first 96 h of life. We compared these measurements with those from more mature animals of the same species. Radiolabeled microspheres were used to measure organ blood flow (in ml.min-1.g-1) at 3 (n = 18), 23 (n = 17), and 96 h (n = 4) in the premature animals, and at 13 +/- 4 mo in the older animals (n = 5). Premature animals demonstrated over the first 96 h of life significant hemodynamic changes that included decreased systemic vascular resistance (P less than 0.001), increased systemic (P less than 0.05), intestinal (P less than 0.05), and hepatic blood flow (P less than 0.05), as well as resolution of L-R PDA shunting. These 96-h values were similar to those of the more mature infant baboons. Blood flow and oxygen transport to the kidneys and cerebrum did not significantly increase over the first 96 h in premature baboons and were significantly less than those of 13-mo-old animals (P less than 0.01, both). We speculate that low renal and cerebral blood flow in the 140-day premature baboon are manifestations of multisystem immaturity and, as such, may represent persistent physiological disturbances that are distinct from the severity of underlying lung disease in HMD.
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PMID:Circulatory changes following premature delivery in a baboon model of hyaline membrane disease. 192 96


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