Properties of alkaline phosphatase isoenzymes in plasma of preterm and term neonates.

1987 ◽  
Vol 33 (10) ◽  
pp. 1778-1782 ◽  
Author(s):  
P M Crofton
Keyword(s):  
Alkaline Phosphatase ◽  
Preterm Neonates ◽  
Plasma Samples ◽  
Intestinal Alkaline Phosphatase ◽  
Adult Type ◽  
Term Infants ◽  
Sialic Acid Content ◽  
Term Neonates ◽  
Single Form ◽  
Alkaline Phosphatase Isoenzymes

Abstract The isoenzymes of alkaline phosphatase (EC 3.1.3.1) in plasma of 37 preterm and 21 term neonates two weeks postpartum have been studied with regard to electrophoretic mobility, sialic acid content, inhibition properties, heat lability, molecular mass, and binding to lectins. Term infants generally had a single form of alkaline phosphatase present in significant amounts, identified by the above criteria as originating in bone. All the preterm neonates had two alkaline phosphatase isoenzymes in plasma, namely, bone- and fetal-type intestinal alkaline phosphatase. Liver-, placental-, and adult-type intestinal alkaline phosphatase were not detected in any of the plasma samples.

Alkaline phosphatase isoenzymes in the plasma of preterm and term infants: serial measurements and clinical correlations.

1987 ◽  
Vol 33 (10) ◽  
pp. 1783-1787 ◽  
Author(s):  
P M Crofton ◽  
R Hume
Keyword(s):  
Alkaline Phosphatase ◽  
Preterm Infants ◽  
Intestinal Alkaline Phosphatase ◽  
Group Status ◽  
Term Infants ◽  
Alkaline Phosphatase Isoenzymes ◽  
Preterm Babies ◽  
Clinical Correlations ◽  
Serial Measurements ◽  
Milk Feeding

Abstract Serial measurements of the bone and fetal intestinal isoenzymes of alkaline phosphatase (EC 3.1.3.1) in the plasma of 43 term and 43 preterm infants, from birth to six weeks later, indicate that the bone isoenzyme gradually increases over this period in both preterm and term infants fed with unsupplemented commercial formulas. Preterm babies given formula supplemented with calcium (with or without additional phosphate) had significantly lower bone isoenzyme activities for most of the study period. The concentrations of fetal intestinal isoenzyme increased, under the stimulation of milk feeding, from generally undetectable at birth to a peak during the first two weeks postpartum, and then declined. This increase was highly significantly negatively correlated with gestational age, the preterm infants having a much higher and more prolonged increase in this isoenzyme than did term infants. Unlike the adult isoenzyme, fetal intestinal alkaline phosphatase in plasma showed no relationship with blood group status.

scholarly journals Reaction Rate Retardation as a Method for Serum Alkaline Phosphatase Isoenzyme Measurement

1980 ◽  
Vol 17 (4) ◽  
pp. 192-198 ◽  
Author(s):  
Pamela B Brown ◽  
K O Lewis
Keyword(s):  
Alkaline Phosphatase ◽  
Reaction Rate ◽  
Serum Alkaline Phosphatase ◽  
Enzyme Reaction ◽  
Intestinal Alkaline Phosphatase ◽  
Wide Range ◽  
Alkaline Phosphatase Isoenzymes ◽  
Sensitivity And Selectivity ◽  
Rate Retardation ◽  
Alkaline Phosphatase Isoenzyme

A method for serum alkaline phosphatase isoenzymes using an enzyme reaction rate analyser is described. The complete urea-induced degradation of enzyme activity is monitored, from which individual isoenzyme activities are obtained by calculating the constituent exponential components of the degradation curve. Activities have been measured with adequate sensitivity and selectivity for up to four isoenzyme components in normal and in pathological sera. The identity of each isoenzyme present is assigned from its characteristic degradation half-life, and by this method bone and liver alkaline phosphatase are clearly distinguished and quantitated, and a composite value for placental-intestinal alkaline phosphatase activity is obtained. The approach promises to be applicable to a wide range of isoenzymes, and in analogy with ‘reaction rate’ the term ‘reaction rate retardation’ is suggested for the procedure.

Macromolecular alkaline phosphatase and an immunoglobulin G that inhibited alkaline phosphatase in a patient's serum.

1983 ◽  
Vol 29 (2) ◽  
pp. 375-378 ◽  
Author(s):  
H Nakagawa ◽  
K Umeki ◽  
K Yamanaka ◽  
N Kida ◽  
S Ohtaki
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Immunoglobulin G ◽  
Significant Loss ◽  
Placental Alkaline Phosphatase ◽  
Type Ii ◽  
Intestinal Alkaline Phosphatase ◽  
Adult Type ◽  
Heat Stable

Abstract Macromolecular alkaline phosphatase (EC 3.1.3.1) was found in the serum of a patient suffering from myasthenia gravis (adult type II) complicated with thymoma, and was shown by immunoelectrophoresis to be bound to immunoglobulins A and G (IgG). Placental alkaline phosphatase, complexed with either the patient's serum or IgG purified from the patient's serum, remained at the origin on electrophoresis, with significant loss of activity. Intestinal alkaline phosphatase, complexed with either the patient's serum or the patient's IgG, migrated to a position similar to that of the macromolecular alkaline phosphatase in the patient's serum on electrophoresis. About 50% of the placental alkaline phosphatase activity was inhibited with 0.1-0.2 g of the patient's IgG per liter, but 6.93 g of the IgG per liter was required for about 20% inhibition of the intestinal alkaline phosphatase activity. The complex of intestinal alkaline phosphatase with the patient's IgG was fairly heat stable. From these results, we concluded that the macromolecular alkaline phosphatase in the patient's serum consisted of intestinal alkaline phosphatase and IgG that was specific for placental alkaline phosphatase.

scholarly journals Production of granulocyte colony-stimulating factor in vitro by monocytes from preterm and term neonates [see comments]

Blood ◽  
1993 ◽  
Vol 82 (8) ◽  
pp. 2478-2484 ◽  
Author(s):  
KR Schibler ◽  
KW Liechty ◽  
WL White ◽  
RD Christensen
Keyword(s):  
Newborn Infants ◽  
Preterm Neonates ◽  
Granulocyte Colony Stimulating Factor ◽  
Serum Concentrations ◽  
Colony Stimulating Factor ◽  
Term Infants ◽  
Term Neonates ◽  
And Function ◽  
Stimulating Factor

Abstract We postulated that defective generation of granulocyte colony- stimulating factor (G-CSF) by cells of newborn infants might underlie their deficiencies in upregulating neutrophil production and function during bacterial infection. To test this, we isolated monocytes from the blood of preterm neonates, term neonates, and adults and, after stimulation with various concentrations of interleukin-1 alpha (IL-1 alpha) or lipopolysaccharide (LPS), quantified G-CSF concentrations in cell supernatants and G-CSF mRNA in cell lysates. When stimulated with plateau concentrations of IL-1 alpha for 24 hours, G-CSF concentrations were higher in supernatants of adult cells (8,699 +/- 5,529 pg/10(6) monocytes) than in those from term infants (2,557 +/- 442 pg, P < .05) or from preterm infants (879 +/- 348 pg, P < .05 v adults). When stimulated with plateau concentrations of LPS, supernatants of monocytes from preterm neonates had less G-CSF than did those from term neonates or adults. G-CSF mRNA content was low in cells from preterm infants, higher in those from term infants, and highest in those from adults. On the basis of the in vitro studies, we speculated that serum G-CSF concentrations might be less elevated in neutropenic neonates than in neutropenic adults. Indeed, serum concentrations were relatively low in all nonneutropenic subjects; 92 +/- 34 pg/mL (mean +/- SEM) in 10 preterm neonates, 114 +/- 21 pg/mL in 16 term neonates, and 45 +/- 13 pg/mL in 11 healthy adults. Serum concentrations were not elevated in 7 neutropenic neonates (39 +/- 17 pg/mL) but were in 8 neutropenic adults (2101 +/- 942 pg/mL, P < .05 v healthy adults). Other studies suggested that the lower G-CSF production in neonates is not counterbalanced by a heightened sensitivity of G-CSF--responsive progenitors to G-CSF. Therefore, we speculate that newborn infants, particularly those delivered prematurely, generate comparatively low quantities of G-CSF after inflammatory stimulation, and that this might constitute part of the explanation for their defective upregulation of neutrophil production and function during infection.

A fetal intestinal-type alkaline phosphatase in hepatocellular carcinoma tissue.

1977 ◽  
Vol 23 (9) ◽  
pp. 1615-1623 ◽  
Author(s):  
K Higashino ◽  
R Otani ◽  
S Kudo ◽  
Y Yamamura
Keyword(s):  
Alkaline Phosphatase ◽  
Electrophoretic Mobility ◽  
Normal Liver ◽  
Heat Stability ◽  
Intestinal Type ◽  
Intestinal Alkaline Phosphatase ◽  
Alkaline Phosphatases ◽  
Adult Type ◽  
Alkaline Phosphatase Isoenzyme ◽  
Hepatocellular Carcinoma Tissue

Abstract We examined 19 hepatoma tissues for alkaline phosphatase isoenzyme and found that six have both the Kasahara isoenzyme and an alkaline phosphatase with a unique electrophoretic mobility, in addition to the liver-type enzyme. From two of six carcinoma tissues, the abnormal enzyme was partly purified and subjected to a detailed analysis, which clarified that the abnormal enzyme resembled a fetal intestinal alkaline phosphatase in most of its enzymic and immunologic properties and also in properties that reflect enzyme structure. This fetal intestinal-type alkaline phosphatase was not found in 24 specimens of normal liver from adults. The relevance of fetal intestinal-type alkaline phosphatase to Kasahara isoenzyme and adult intestinal alkaline phosphatase is discussed. The fetal and adult intestinal alkaline phosphatases differ in electrophoretic mobility, heat stability, and reactivity with concanavalin A. The adult-type enzyme has two components; only the electrophoretically slower, neuraminidase-resistant one is described here.

Production of granulocyte colony-stimulating factor in vitro by monocytes from preterm and term neonates [see comments]

Blood ◽  
1993 ◽  
Vol 82 (8) ◽  
pp. 2478-2484 ◽  
Author(s):  
KR Schibler ◽  
KW Liechty ◽  
WL White ◽  
RD Christensen
Keyword(s):  
Newborn Infants ◽  
Preterm Neonates ◽  
Granulocyte Colony Stimulating Factor ◽  
Serum Concentrations ◽  
Colony Stimulating Factor ◽  
Term Infants ◽  
Term Neonates ◽  
And Function ◽  
Stimulating Factor

We postulated that defective generation of granulocyte colony- stimulating factor (G-CSF) by cells of newborn infants might underlie their deficiencies in upregulating neutrophil production and function during bacterial infection. To test this, we isolated monocytes from the blood of preterm neonates, term neonates, and adults and, after stimulation with various concentrations of interleukin-1 alpha (IL-1 alpha) or lipopolysaccharide (LPS), quantified G-CSF concentrations in cell supernatants and G-CSF mRNA in cell lysates. When stimulated with plateau concentrations of IL-1 alpha for 24 hours, G-CSF concentrations were higher in supernatants of adult cells (8,699 +/- 5,529 pg/10(6) monocytes) than in those from term infants (2,557 +/- 442 pg, P < .05) or from preterm infants (879 +/- 348 pg, P < .05 v adults). When stimulated with plateau concentrations of LPS, supernatants of monocytes from preterm neonates had less G-CSF than did those from term neonates or adults. G-CSF mRNA content was low in cells from preterm infants, higher in those from term infants, and highest in those from adults. On the basis of the in vitro studies, we speculated that serum G-CSF concentrations might be less elevated in neutropenic neonates than in neutropenic adults. Indeed, serum concentrations were relatively low in all nonneutropenic subjects; 92 +/- 34 pg/mL (mean +/- SEM) in 10 preterm neonates, 114 +/- 21 pg/mL in 16 term neonates, and 45 +/- 13 pg/mL in 11 healthy adults. Serum concentrations were not elevated in 7 neutropenic neonates (39 +/- 17 pg/mL) but were in 8 neutropenic adults (2101 +/- 942 pg/mL, P < .05 v healthy adults). Other studies suggested that the lower G-CSF production in neonates is not counterbalanced by a heightened sensitivity of G-CSF--responsive progenitors to G-CSF. Therefore, we speculate that newborn infants, particularly those delivered prematurely, generate comparatively low quantities of G-CSF after inflammatory stimulation, and that this might constitute part of the explanation for their defective upregulation of neutrophil production and function during infection.

scholarly journals Morbidity profile and immediate outcome of late preterm neonates compared to term neonates in a rural tertiary care hospital of Gujarat

2017 ◽  
Vol 4 (4) ◽  
pp. 1329 ◽  
Author(s):  
Manish Rasania ◽  
Prasad Muley
Keyword(s):  
Preterm Infants ◽  
Tertiary Care ◽  
Preterm Births ◽  
Full Term ◽  
Late Preterm ◽  
Preterm Neonates ◽  
Care Hospital ◽  
Term Infants ◽  
Term Neonates ◽  
Late Preterm Infants

Background: Late premature infants are born near term, but are immature. As a consequence, late preterm infants are at higher risk than term infants to develop morbidities. Although late preterm infants are the largest subgroup of preterm infants, there is a very limited data available on problems regarding late preterm infants in rural India.Methods: This is a retrospective cohort study using previously collected data from neonates born at Dhiraj Hospital and neonates who were born outside but admitted at SNCU of Dhiraj Hospital, Piparia, Vadodara district, Gujarat, India between January 2015 to December 2015.Results: 168 late preterm infants and 1025 term infants were included in this study. The need for SNCU admission is significantly higher in late preterm compared to full term (41.07% vs 2.04%). Morbidities were higher in late preterm neonates compared to full term neonates. Sepsis (4.76% vs 1.07%), TTN (10.11% vs 2.04%), hyperbilirubinemia (19.04% vs 9.36%), RDS (1.78% vs 0.09%), hypoglycemia (1.78% vs 0.29%), PDA (1.78% vs 0.58%), risk of major congenital malformation (2.38% vs 0.58%). Need for respiratory support was 5.95% in late preterm vs 2.04% in full term neonates. Immediate neonatal outcome in terms of death and DAMA (non-salvageable) cases was poor in late preterm neonates compared to full term neonates (1.19% vs 0.78%).Conclusions: Late preterm neonates are at higher risk of morbidities and mortalities. They require special care. Judicious obstetric decisions are required to prevent late preterm births. 

Antithrombin III in Full-Term and Pre-Term Newborn Infants : Three Cases of Neonatal Diagnosis of AT III Congenital Defect

1987 ◽  
Vol 57 (03) ◽  
pp. 329-331 ◽  
Author(s):  
V De Stefano ◽  
G Leone ◽  
M P De Carolis ◽  
R Ferrelli ◽  
S De Carolis ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Antithrombin Iii ◽  
Full Term ◽  
Congenital Defect ◽  
Preterm Neonates ◽  
Control Group ◽  
Term Infants ◽  
Term Neonates ◽  
Congenital Deficiency ◽  
At Iii

SummaryAntithrombin III (AT III) plasma levels were investigated in 18 full term neonates and 14 healthy preterm neonates. A control group of 20 healthy adults was also studied. AT III was measured as antigen concentration (Ag) and antithrombin or anti-factor Xa heparin cofactor (H. C.) activities. Crossed immunoelectrophoresis on heparin-agarose (H-CIE) was carried out on plasma samples; moreover the distribution of isoantithrombins was investigated on whole plasma by a technique of crossed immunoelectrofocusing (CIEF). AT III plasma levels in full term infants were significantly lower as compared to the adult values. The preterm newborns group showed a further significant decrease in AT III levels as compared to the full term neonates. In all infants AT III H-CIE runs displayed a single fast moving anodal peak, so that a normal binding to heparin was demonstrated. The CIEF AT III plasma pattern of the adults as well as of all neonates displayed three major peaks at pH range 5.2-4.9, a small amount of AT III at pH 4.9-4.8 and a minor peak at pH 4.8-4.6, so that it was concluded that the isoantithrombins plasma distribution in neonatal age is identical to that of the adult subjects. Four neonates whose mothers were affected by AT III congenital defect were also investigated: diagnosis of congenital deficiency was established in three cases.

Neonatal Apnea: Underlying Disorders

PEDIATRICS ◽  
1979 ◽  
Vol 63 (1) ◽  
pp. 8-12
Author(s):  
Richard L. Naeye
Keyword(s):  
Placenta Previa ◽  
Cord Compression ◽  
Preterm Neonates ◽  
Term Infants ◽  
Abruptio Placentae ◽  
Single Episode ◽  
Term Neonates ◽  
Underlying Disorder ◽  
A Prospective Study ◽  
Neonatal Apnea

Data from a prospective study of 50,826 neonates were used to determine the frequency and significance of disorders related to apnea in newborns. Such apnea proved to be a significant prognosticator for neonatal death. Fifty-eight percent of preterm neonates with multiple apneic episodes and 18% with a single episode died, whereas only 6% of those without recorded apnea died. The rates were 44%, 5%, and 1% for full-term infants. Amniotic fluid infection was the underlying disorder in 35% of the preterm and 25% of the term neonates who had multiple episodes of apnea. A third of the preterm and 25% of the term infants who had such apneic episodes had antecedent hypoxia-related disorders, i.e., abruptio placentae, erythromblastosis fetalis, placenta previa, large placental infarcts, and umbilical cord compression. Among the apneic neonates, those who were infected were twice as apt to die as were those who had hypoxia-related disorders. Hypoplasia of the lungs and easily recognized central nervous system malformations were responsible for most of the apnea-related deaths associated with congenital malformations.

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