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Biomedical subjects

L Sann

Publications and source records attributed to L Sann.

At least 73 records · Page 4Linked to original sources
PubMed1980

Neonatal pattern of adrenergic metabolites in urine of small for gestational age and preterm infants.

Catecholamines (DA, NE, E), methoxyamines (MT, NMN, MN), DOPA and DOPAC were studied in urine of term small for gestational age infants (SGA) and preterm with appropriate birthweights for gestational age (PT) during the first ten days of life. Results were compared to values obtained for full term infants (FT). As a whole no deficit in urine catecholamines was observed in either group of SGA and PT neonates suggesting that capacities to synthesize catecholamines are already developed at birth. Furthermore, in SGA infants, adrenergic function seems to be enhanced during the first four days of life; however, SGA infants with low blood glucose levels excreted amounts of epinephrine similar to those of FT neonates, but much lower than those obtained in normoglycemic SGA neonates. These data suggest that enhanced release of catecholamines is required in SGA infants to maintain the glycemic homeostasis. In premature infants, the adrenergic pattern was highly altered only in younger preterm neonates (31 weeks of gestational age) who excreted more catecholamines than older preterm babies (33 to 36 weeks) or full term neonates; this catecholamine increase in urine of young preterm infants might be related to immaturity of storage vesicles and/or to thermoregulatory or respiratory events. On the other hand, a striking deficit in excretion of DOPAC was observed in small for gestational age infants and in young preterm neonates during the first ten days of life. DOPAC excretion was even lower in SGA than in young preterm neonates. These findings suggest that the maturation of dopaminergic neurons occurs late in gestational age and is greatly dependent on nutritional factors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1980

Effect of early oral calcium supplementation on serum calcium and immunoreactive calcitonin concentration in preterm infants.

Oral calcium supplements (80 mg/kg per 24 h) were given to 23 preterm infants, and the course of serum calcium, magnesium, immunoreactive calcitonin, and gastrin was compared with a control group of 23 matched infants. In the supplemented group, serum calcium concentrations remained at the baseline level (2.31 mmol/l +/- 0.18 SD) while a fall (from 2.27 +/- 0.18 to 1.91 +/- 0.24 mmol/l) was observed at 12-16 hours of age in the control group, with 4 values < 1.75 mmol/l. There was no change in serum magnesium concentration in either group. The postnatal rise of serum immunoreactive calcitonin concentrations in the control group (from 171 +/- 135 to 493 +/- 273 pg/ml at 12-48 hours of age) was not found in the supplemented group. There was a negative correlation between serum calcium and immunoreactive calcitonin levels in the control group, but not in the supplemented group. There was no correlation between serum immunoreactive calcitonin and gastrin concentrations. These data show that oral calcium supplementation can prevent early neonatal hypocalcaemia, and suggest that this effect is achieved at least in part through a reduction of the postnatal rise of serum immunoreactive calcitonin.

Calcitonin↗
PubMed1980

Serum copper and zinc concentration in premature and small-for-date infants.

Serum copper (Cu) and zinc (Zn) concentrations were measured in neonates with an appropriate birth weight for gestational age (AGA) and in small-for-gestational age infants. At 7 days of age, there was a positive correlation between serum Cu concentration and gestational age (GA) (r = 0.63; P < 0.001) and a negative correlation between Zn concentration and GA (r = 0.62; P < 0.01). At 7 days of age, the mean (+/- S.E.) concentrations in AGA full-term infants (Cu, 79 +/- 8 microgram/dl; Zn, 84 +/- 4) were similar to those in small-for-gestational age, full-term infants (Cu, 78 +/- 6 microgram/dl; Zn, 85 +/- 12). In preterm infants, there was also no difference between AGA and small-for-gestational age infants. In 23 AGA infants with a birth weight of less than 1500 g, serum Cu concentration increased from 51 +/- 7 microgram/dl at the age of 7 days to 86 +/- 7 microgram/dl at the age of 60 days (paired t-test: P < 0.05) whereas serum Zn concentration decreased from 149 +/- 9 to 91 +/- 5 microgram/dl (P < 0.01). A positive correlation was found between serum Zn concentration and daily intake of Zn (n = 39; r = 0.3458; P < 0.05), but no correlation was found for serum Cu concentration. The evolution of serum Cu and Zn concentration with total age (GA + postnatal age) in the infants with a low birth weight (i.e., < 1500 g) was similar to the evolution with GA.

Animals↗
PubMed1979

[Necrotizing enterocolitis and milk protein intolerance. Four cases (author's transl)].

We report four cases of necrotizing enterocolitis (NEC) with colonic pneumatosis in two cases and the presence of hemorrhagic colitis, colonic stenosis and adhesive peritonitis. Surgical intervention necessary in two cases confirmed the diagnosis of NEC. Milk protein intolerance was diagnosed clinically in all cases. The evolution was satisfactory in all cases with exclusion of milk protein. The association suggests that milk protein intolerance can play a role in the occurence of necrotizing enterocolitis.

Child↗
PubMed1979

[Antenatal administration of betamethasone. Effects upon neonatal blood glucose in premature infants (author's transl)].

This effect was studied in 23 preterm neonates at the age of 2--8 hours. Betamethasone was administered at a dose of 12 mg intramuscular once or several times before delivery. This glycemia was compared with the glycemia of 52 control preterm infants studied at the same period. In the control preterm neonates, the mean (+/- 1 S.D.) blood glucose level was 0.51 +/- 0.26 g/l versus 0.53 +/- 0.24 g/l in the preterm infants pretreated with betamethasone. The incidence of glycemia less than 0.30 or 0.20 g/l was not significantly different in the two groups. These data show that prenatal betamethasone therapy has no harmful or diserable effect on the neonatal glycemia of preterm infants.

Betamethasone↗
PubMed1979

[Neonatal hyponatremia from maternal origin. Three cases (author's transl)].

The effect of the treatment was controlled by measurements of plasma renin activity and aldosterone concentration. These observations concern maternal toxemia treated by diuretic and dietary sodium restriction two weeks before delivery. In two cases, labor was augmented with oxytocin infusion. These cases illustrate the respective role of sodium depletion and hemodilution in the occurrence of maternal and neonatal hyponatremia. They emphasize the amount of sodium supplementation in these newborn infants.

Adult↗
PubMed1979

Age-related changes in catecholamine metabolites of human urine from birth to adulthood.

Catecholamines (dopamine [DA], norepinephrine [NE], epinephrine [E]), methoxyamines (3-methoxytyramine [MT], normetanephrine [NMN], metanephrine [MN]), DOPA, and acidic metabolites (3,4-dihydroxyphenylacetic acid [DOPAC], vanilmandelic acid [VMA]) were determined in human urines from one day of age to adulthood, in order to investigate sympatho-adrenal development during life. All adrenergic compounds are present in neonate urines on the first day of life, but their postnatal evolution is quite different according to the nature of metabolites. Daily E, MN and VMA amounts remain low until the 10th month of life; daily NE, MT and DOPA levels increase progressively, but, in contrast, NMN amounts are already high in the neonatal period and increase only beyond the fourth year of age. DA is at either age the predominant catecholamine but its elimination is relatively more important in the neonatal period.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Effect of intravenous hydrocortisone administration on glucose homeostasis in small for gestational age infants.

The effects of I.V. hydrocortisone (H) (10 mg/kg) on glucose homeostasis were evaluated at 25 to 85 hours of age in 14 infants who were small for gestational age (SGA) in comparison to 17 control SGA infants. Three hours after H administration, higher levels of plasma glucose than in controls were detected (mean +/- S.E.M.): 4.78 +/- 0.2 vs. 2.88 +/- 0.2 mmol/l (p less than 0.01), while lower levels were found for blood pyruvate (38 +/- 7 vs. 89 +/- 12 mumol/l--p less than 0.01), plasma insulin (6.4 +/- 0.5 vs. 12 +/- 0.8 muIU/ml--p less than 0.05) and plasma glucagon (62.25 +/- 6.6 vs. 81.6 +/- 6.6 pmol/l--p less than 0.05). Three hours after H administration, I.V. injection of L-alanine (150 mg/kg) produced a significant rise over baseline of plasma glucose concentration from 4.78 +/- 0.2 to 5.94 +/- 0.2 mmol/l at 50 min (p less than 0.05), whereas no significant change was observed in controls. There was no significant change in plasma glucagon and insulin concentrations after L-alanine injection in either group. These results show that in SGA infants primed with H, the rise of plasma glucose concentration after L-alanine administration is observed with low plasma insulin levels and without stimulation of glucagon secretion. They suggest that H induced a reduced peripheral utilization of glucose by lowering the plasma levels of insulin and a production of glucose from alanine through gluconeogenesis.

Alanine↗
PubMed1978

Effect of intravenous L-alanine administration on plasma glucose, insulin and glucagon, blood pyruvate, lactate and beta-hydroxybutyrate concentrations in newborn infants. Study in term and preterm newborn infants.

Ten term and eleven preterm newborn infants with appropriate weights for their gestational age were infused for one minute with L-alanine (150 mg/kg) at the age of 29 to 76 hours (mean 48 hours) and circulating levels of glucose, lactate, pyruvate, D-betahydroxybutyrate (D-BOHB), insulin and glucagon were monitored. Plasma glucose concentrations increased from 2.7 +/- 0.16 (mean +/- S.E.M.) to 3.7 +/- 0.2 mmol/l after 50 min (p less than 0.01) in term infants. In preterm infants, after an initial decrease of the glucose level from 3.1 +/- 0.16 to 2.6 +/- 0.16 mmol/l (p less than 0.05), it returned to the baseline level at 50 min: 3.0 +/- 0.2 mmol/l. The blood concentration of D-BOHB decreased in term infants from 192 +/- 37 to 112 + 6 micrometer/l (p less than 0.01) after 40 min. In preterms, its decrease was not significant (p greater than 0.05). Plasma glucagon level rose from 53 +/- 5 to 70 +/- 8 pmol/l after ten minutes (p less than 0.01) in terms infants and from 61 +/- 6 to 75 +/- 9 after 20 min (p less than 0.01) in preterm infants. There were no significant changes in plasma insulin concentrations in either group. Forty minutes after L-alanine infusion, I/G ratios were lower in preterm infants (1.26 +/- 0.14) than in term infants (1.71 +/- 0.25) (p less than 0.01). There was no relationship between the glycemic responses to L-alanine and the basal levels of D-BOHB. The data suggest that the glycemic effect of L-alanine infusion and circulating glucagon depends upon a specific stage in maturation. The antiketogenic effect of L-alanine infusion is observed in term infants as in adults.

Alanine↗
PubMed1978

Copper deficiency and hypocalcemic rickets in a small-for-date infant.

A case of copper deficiency associated with hypocalcemia, radiological features of rickets and hyperparathyroidism is described in a small-for-date infant (gestational age 39 weeks, B.W 1 240 g). Neonatal serum copper (Cu) levels were found between 223 and 138 mumol/l. She was given daily 2 400 U of vitamin D2 and a load dose of 80 000 IU at the age of 55 days. At the age of 79 days, X-rays of the legs and wrist showed spread, cupped and frayed metaphyses. Serum Ca was 1.35 mmol/l, P = 0.99 mmol/l with high alkaline phosphatases (A.P.) 590 IU/ml. But plasma level of 25 hydroxycholecalciferol (25-OH-CC) was normal = 10.8 ng/ml. Serum Cu was low = 3.14 mumol/l and serum immunoreactive parathormone (iPTH) level was elevated: 520 mulEq/ml (N less than or equal to 100). Administration of vitamin D2 (15 mg) induced an immediate normalization of serum Ca, normal serum iPTH (68 mulEq/ml) in one month, normal X-rays in two months and normal A.P. in four months. Serum Cu and ceruloplasmin levels increased slowly without any supplementation to subnormal levels at the age of eight months (14.9 and 1.65 mumol/l. Serum Cu concentrations were found to be normal (16.0--33.7 mumol/l) in five children with hypocalcemic rickets. These results suggest a role of Cu deficiency in the occurrence of this transient vitamin D-resistant rickets.

Calcium↗
PubMed1978

Hypophosphatemia and hyperparathyroidism in a case of Bartter's syndrome.

In an 18-year-old boy with Bartter's syndrome, hypophosphatemia was discovered (2.4 mg/100 ml) with normal serum calcium concentration (9.7 mg/100 ml) and elevated alkaline phosphatase level: 528 mU/ml (normal less than or equal to 150). Skeleton X-rays showed osteomalacia on the pelvic bones and metaphyseal rickets on the wrists. Plasma 25-hydroxycholecalciferol (25-OHCC) concentration was 7.2 ng/ml (normal = 13 +/- 4.4), and serum immunoreactive parathyroid hormone (iPTH) concentration 160 micron1Eq/ml (normal less than or equal to 150). Ca infusion (1500 mg/m2/12 h) induced an increase in serum P level to 3.2 mg/100 ml, in tubular phosphate reabsorption from 72 to 90%, while serum iPTH decreased to 33 micron1Eq/ml. Vitamin D2 administration (45 mg) resulted in increased 25-OHCC concentration to 28 ng/ml and in healing of pelvic osteomalacia. However, there was little change of the radiological aspect of the wrist and of serum phosphorus and iPTH concentrations. In a control 6-year-old hypokalemic girl, administration of parathyroid hormone (8 USP/kg) produced a marked phosphaturic response and an increase in urinary cyclic AMP excretion. These data suggest that hypophosphatemia can be attributed to secondary hyperparathyroidism in the patient with Bartter's syndrome. Hypokalemia does not impair the renal activity of parathyroid hormone.

Adolescent↗
PubMed1977

Congenital rickets. Study of the evolution of secondary hyperparathyroidism.

A case of congenital rickets of nutritional origin is described in a light-for-date premature infant (gestational age 34 weeks, birthweight 1 100 g). X-rays of the long bones showed spread, frayed and cupped metaphyses at birth and at the age of 16 days. Serum calcium was 8.2 mg/100 ml, phosphorus 3.4 mg/100 ml and alkaline phosphatase (A.P):323 IU/ml (N less than or equal to 200) at the age of 3 days. Very high level of serum immunoreactive parathroid hormone (iPTH) was found at the age of 16 days=295 micronlEq/ml (N less than or equal to 50). Evidence of maternal vitamin D deficiency was demostrated by low plasma 25-hydroxycholecalciferol (25-OH-CC):1.0 ng/ml (N:13.2+/-4.2) soon after delivery; it was found to be normal (10.2 ng/ml) six months later. Ca infusion (15 mg/kg/3 h) resulted in a marked fall of serum iPTH (280 to 84 micronlEq/ml). Administration of vitamin D2 (2400 IU/day for 10 days) induced some healing of the metaphyses; A. P. remained elevated (400 IU/ml); plasma 25-OH-CC was normal 10.2 ng/ml and serum iPTH was 115 micronlEq/ml. When 25-OH-CC was given orally for ten days (15 microng/day), plasma 25-OH-CC rose to 64.5 ng/ml with a minor change of serum iPTH (94 micronlEq/ml); X-rays of the bones showed osteoporosis. These results suggest a reduced convertion of 25-OH-CC into 1-25-(OH)2-CC.

Adult↗