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Biomedical subjects

M Koivisto

Publications and source records attributed to M Koivisto.

At least 91 records · Page 5Linked to original sources
PubMed1982

Cholic acid, chenodeoxycholic acid, alpha-1-fetoprotein and alpha-1-antitrypsin serum concentrations in breast-fed infants with prolonged jaundice.

Thirteen breast-fed one-month-old infants with prolonged jaundice not due to known causes were included in this study. All infants were investigated at one and twelve months of age. Serum concentrations of total (TB) and conjugated bilirubin (CB), aspartate (ASAT) and alanine aminotransferase (ALAT), alkaline phosphatase (AP), alpha-1-antitrypsin (alpha-1-AT), alpha-1-fetoprotein (AFP) and the two primary bile acids; cholic (CA) and chenodeoxycholic acid (CDCA) were determined at both ages. The Pi-phenotype of alpha-1-AT was determined at the age of twelve months. The serum concentrations of TB, CB, AP and AFP were elevated at the age of one month but were normal at the age of twelve months. No changes in the serum concentrations of ASAT or ALAT were observed between one and twelve months of age, and the values were within the reference ranges. The serum concentrations of alpha-1-AT were within the reference range at both ages. Two infants were heterozygous for MZ, and they had normal serum alpha-1-AT concentrations. The serum concentrations of CA and CDCA were elevated at the age of one month and were still significantly elevated at the age of twelve months indicating that the infants had slight cholestasis at the age of one month, and that the cholestasis had largely subsided by the end of the first year of life.

Alanine Transaminase↗
PubMed1982

Pituitary-adrenal and testicular function in preterm infants after prenatal dexamethasone treatment.

Pituitary-adrenal and testicular function was monitored by plasma ACTH and testosterone (T) measurements in preterm newborns (gestational age below 36 weeks), exposed in utero to dexamethasone treatment for prevention of respiratory distress syndrome. A group of age-matched premature newborns and full-term infants served as controls. The cord-blood ACTH level was high in each group (logarithmic means 65-75 ng/l), but decreased within the first 2 days of life to mean levels between 20-30 ng/l on days 3 to 10 inclusive. Dexamethasone treatment had no effect on the postnatal ACTH concentrations when compared with preterm or full-term controls. Similarly, no difference in plasma ACTH were found between untreated preterm and full-term infants during the first 10 days of life. T levels in mixed cord blood were on average 2-3 nmol/l in the preterm male infants. An increase to a mean level of 10 nmol/l was seen in 1 h and 1 d samples. Thereafter, the concentration of T decreased to 2-3 nmol/l on days 3-10 postnatally. No effect of dexamethasone treatment was seen on the postnatal pattern of plasma T. When preterm male and full-term male infants were compared, no difference was seen in the T peak in the first day of life. However, the 1-3, and 60-90 days concentrations of T were 2-fold (p less than 0.01-0.05) higher in the preterm group. It is concluded that prenatal dexamethasone treatment of the mother does not influence the postnatal pituitary-adrenal function as monitored by ACTH measurements. Likewise, no effect of this treatment was observed on the postnatal testicular activity of preterm male infants. The immediate postnatal peak in plasma T levels persisted longer in the preterm than in the full-term male infants.

Adrenocorticotropic Hormone↗
PubMed1982

Increased plasma immunoreactive 6-keto-prostaglandin F1 alpha levels in newborns with idiopathic respiratory distress syndrome.

Serial plasma concentrations of immunoreactive 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), the stable hydration product of prostacyclin (PGI2), were measured with radioimmunoassay during the first month of life in 25 preterm infants with idiopathic respiratory distress syndrome (IRDS) and 38 preterm controls with normal heart and lung function. The levels of 6-keto-PGF1 alpha (521 +/- 81 pg/ml, mean +/- S.E.) in the infants with IRDS were higher (P less than 0.05) than those in the controls (335 +/- 42 pg/ml) on the first day of life, but thereafter no difference was seen. The highest first day 6-keto-PGF1 alpha level (1448 pg/ml) was found in the infant who died because of severe IRDS at the age of 19 h. The plasma 6-keto-PGF1 alpha concentrations in the distressed infants correlated positively with the alveolar-arterial oxygen gradient and the need of additional oxygen, but negatively with the arterial pH. In addition, an inverse correlation between the first day concentrations of 6-keto-PGF1 alpha and the lowest arterial oxygen tension in infants needing assisted ventilation was found. The mode of delivery (Cesarean section versus vaginal delivery) the gestational age, birth weight, sex or Apgar scores of the infants were not related to the 6-keto-PGF1 alpha levels on the first day of life. Neither did maternal pre-eclampsia, diabetes mellitus, or antenatal glucocorticoid treatment have any effect on the 6-keto-PGF1 alpha concentrations in the newborns. Our data suggest that a surge of the vasodilatory and antiaggregatory PGI2 is released during the early stage of IRDS, possibly in an attempt to increase the pulmonary perfusion. Our results give further indirect evidence that hypoxia stimulates the PGI2 production. High plasma immunoreactive 6-keto-PGF1 alpha levels during the early phase of IRDS suggest an increased generation of the vasodilatory and antiaggregatory PGI2 in this syndrome. This may be an attempt to overcome the increased pulmonary vasconstriction in IRDS. When the PGI2 formation rapidly declines after the first day of life, a relative PGI2 deficiency may ensue.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

A deletion in chromosome 22 can cause DiGeorge syndrome.

An association between DiGeorge's syndrome and an unbalanced chromosomal rearrangement leading to trisomy 20pter leads to 20q11 and monosomy 22pter leads to 22q11 was found in four individuals belongings to one family. These and other data from the literature are interpreted to suggest that DiGeorge's syndrome can be caused by deletion of a gene located in chromosome 22, probably in band 22q11.

Child, Preschool↗
PubMed1981

Serum cholic acid and chenodeoxycholic acid concentrations in neonatal hyperbilirubinemia.

Primary bile acid concentrations were measured in serum of 332 newborns with neonatal hyperbilirubinemia (serum total bilirubin level greater than 200 mumol/l) and compared with those of 95 nonhyperbilirubinemic neonates (serum total bilirubin level less than 200 mumol/l). The serum concentrations (mumol/l; mean +/- SEM) for cholic acid (8.78 +/- 0.44) and chenodeoxycholic acid (10.5 +/- 0.68) were significantly higher (p less than 0.001) in the hyperbilirubinemic group than in the controls (7.16 +/- 0.48 and 6.67 +/- 0.48, respectively). 80 (24%) of the hyperbilirubinemic newborns had true cholestasis (serum levels of cholic and/or chenodeoxycholic acid higher than mean +/- 2 SD in the reference group). The ratio of cholic to chenodeoxycholic acid was significantly higher (p less than 0.05) in the cholestatic group than in the hyperbilirubinemic newborns without cholestasis. There was no significant differences in the serum concentrations of alkaline phosphatase or lactate dehydrogenase between the cholestatic and noncholestatic groups. In the hyperbilirubinemic newborns, the primary bile acids were indiscriminately raised. Only 8 infants from the 332 newborns had jaundice at the age of 1 month. Of these 8 infants only 2 had neonatal cholestatic hyperbilirubinemia. It thus appears that measurement of serum primary bile acid concentrations has only limited diagnostic value in assessing the severity or prognosis of neonatal hyperbilirubinemia.

Chenodeoxycholic Acid↗
PubMed1981

Enhanced activity of the pituitary-gonadal axis in premature human infants.

The postnatal pituitary-gonadal function of fullterm and premature boys and girls (mean gestational age, 40 and 32 weeks, respectively) was studied by measurements of serum FSH, LH, PRL, and testosterone (T) between 0-25 weeks of postnatal age. During the first 10 postnatal weeks, serum FSH in premature girls reached 10-20 times higher levels than in fullterm girls (mean at 1-5 weeks, 63 and 3.9 mIU/ml, respectively; P < 1.001). During the same time, serum LH levels were 3-4 times higher in premature (12-17 mIU/ml) than in fullterm girls (3.8-4.7 mIU/ml; P < 0.01). In contrast, no difference in serum gonadotropin levels were observed between premature and fullterm boys. Serum T in premature boys (mean, 2.95 ng/ml) reached a significantly higher level (P < 0.01) than in fullterm boys (1.45 ng/ml) from 11-15 weeks of age. The results emphasize the importance of the last weeks of gestation for the functional maturation of the fetal hypothalamic-pituitary-gonadal axis. Interruption of this maturational process by premature birth results in enhanced pituitary gonadotropin production in girls and increased testicular T production in boys.

Female↗
PubMed1981

Aryl hydrocarbon hydroxylase induction in maternal and cord blood mitrogen-treated lymphocytes.

The inducibility of aryl hydrocarbon hydroxylase was measured in mitrogen-activated peripheral lymphocytes from smoking and nonsmoking mothers and their newborn infants (cord blood). The mean inducibility ratio in lymphocytes from smoking women was 4.02 and that for nonsmokers 2.87. Benz(a)anthracene-induced and noninduced AHH activities were 3-6 times higher in the lymphocytes from the cord blood than in those from the mothers. The inducibility ratio in the cord blood lymphocytes from the smoking mothers was 3.65 and did not differ significantly from that for the nonsmokers, 3.54. There was a significant correlation in the induction ratio between maternal and cord blood lymphocytes from the nonsmokers, but not in the smokers. Thymidine incorporation was about twice as high on average in the cord blood lymphocytes as in the maternal lymphocytes. The results demonstrate that the extent and distribution of inducibility were very similar in the maternal and cord blood lymphocytes.

Adolescent↗
PubMed1980

Congenital chloride diarrhea: possibility for prenatal diagnosis.

Two pregnancies, which resulted in the births of infants affected by congenital chloride diarrhea (C.C.D.) are presented. No method is available for prenatal diagnosis of this disorder. In this paper the intrauterine onset of diarrhea is confirmed by amniofoetography and high bilirubin values in amniotic fluid. In the second case the amniotic fluid alpha-fetoprotein (A.F.P.) was detected to be abnormally high at the 29th gestational week.

Adult↗
PubMed1980

Failure of strychnine treatment during the neonatal period in three Finnish children with nonketotic hyperglycinemia.

Three Finnish infants with a severe neonatal-onset-type of nonketotic hyperglycinemia were treated with strychnine nitrate in a daily dosage of 0.2 to 0.9 mg/kg, given orally in four doses. In order to lower the plasma and CSF-glycine concentrations concomitant exchange transfusions (200 to 300 ml/kg of heparinized blood) were carried out in two of these infants. Although the strychnine therapy was started at ages 15, 40, and 62 hours, the strychnine produced no clinical effect, and the exchange transfusion caused only a transient decrease in the plasma glycine level. Despite treatment, the clinical course was the same as in the majority of children with the severe form of the disease--all died within the first ten days of life. Impressive effects of strychnine treatment initiated in two infants at ages 5 and 6 1/2 months, and given in addition to sodium benzoate and anticonvulsants, have been reported. These cases, however, probably represent a less severe type of nonketotic hyperglycinemia. Nevertheless, the therapeutic failure in the present cases probably indicates that strychnine treatment does not solve the therapeutic problems of severe forms of NKH.

Amino Acid Metabolism, Inborn Errors↗
PubMed1980

Unaltered neonatal cell-mediated immunity after prenatal dexamethasone treatment.

To evaluate the effect of prenatal short-term dexamethasone therapy on neonatal cell-mediated immunity, 6 premature infants born after such therapy and 4 controls of the same age were studied by determining blood leukocyte count, relative and absolute amount of acid alphanaphthyl acetate esterase (ANAE)-positive cells, and lymphocyte response to both phytohemagglutinin (PHA) and pokeweed mitogen (PWM) stimulation. All parameters studied were similar in newborns with or without prenatal maternal dexamethasone treatment. The increase in the number of lymphocytes and ANAE-positive cells during the first week of life was similar in both groups. The neonatal peripheral blood lymphocyte function thus does not seem to be disturbed by prenatal short-term dexamethasone treatment.

Dexamethasone↗
PubMed1979

Trisomy 9p with i(9p) and t(9q18p).

The trisomy 9p syndrome in a 2-year-old girl with moderate mental retardation is presented. She has a unique karyotype with a de novo isochromosome 9p and a translocation between 9q and 18p.

Child, Preschool↗