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J Sólyom

Publications and source records attributed to J Sólyom.

72 records · Page 4Linked to original sources
PubMed1980

Oscillations in plasma cortisol levels of newborns during exchange transfusion.

Plasma cortisol concentration was determined in blood samples obtained in six newborns during exchange transfusion at 3--5 minute intervals. A radiotransin-assay using horse serum as a binding protein and toluene-based scintillation fluid for separation of unbound tracer proved to be a relatively specific method for determination of cortisol level in the plasma of newborns. Irregular oscillations were observed in four newborns, whereas a single peak could be demonstrated in two cases during the 40--70 minute period observed. The results suggest that the CRF-ACTH-cortisol secretion may already be episodic in the newborn period.

Autoimmune Diseases↗
PubMed1979

A method for identification and follow-up of patients with a steroid-21-hydroxylase deficiency.

A method is described for the determination of 17 alpha-hydroxyprogesterone from blood samples obtained by heel prick and dried on filter paper. Discs (10 mm diameter) were cut from the filter paper and extracted in the assay tubes with 1 ml of a methanol/diethyl ether/ethyl acetate (50 :45 :5, v/v) solvent mixture. Antibody, tritium-labelled tracer and dextran-coated charcoal were added to assay tubes using a multichannel dispenser. The approach used permits one technician to analyze two series, each of 60 duplicate samples, within one working day. Thus the method is applicable for the centralized screening of suspected cases, while emergency samples may be analyzed at the same time within 4 h. Comparisons with a highly specific but more elaborate technique for the determination of blood 17 alpha-hydroxyprogesterone showed a correlation coefficient of 0.99, and the regression equation for the present method (y) against the established method (x) was y = 1.07x + 2.72. The calculated upper reference limit (mean +/- S.D.) for 17 alpha-hydroxyprogesterone in healthy infants from two days to eight years of age of 7.5 ng/ml of serum.

Adrenal Glands↗
PubMed1979

Plasma renin activity and mineralocorticoid replacement therapy in congenital adrenal hyperplasia.

Plasma renin activity and serum concentrations of sodium and potassium were repeatedly measured in seven children with congenital adrenal hyperplasia due to steroid-21-hydroxylase deficiency, to monitor the sodium balance during treatment. Infants with the salt-losing form had high plasma renin activity levels 5--11 months after subcutaneous implantation of a pellet containing 100 mg deoxycorticosterone acetate. These elevated plasma renin activity levels were suppressed to the normal range by repeated implantation of DOCA pellet. Moderately elevated values of plasma renin activity in older salt-losers normalized after increasing the dietary sodium intake. Plasma renin activity level has superiority over serum electrolyte concentrations as an index of mineralocorticoid deficiency.

Adolescent↗
PubMed1975

Prolonged oral administration of potassium upon aldosterone biosynthesis by rat glomerulosa tissue in vitro.

Steroid production rate of adrenals derived from rats drinking a 0.3 M KC1 + 5% glucose solution for 7 days was compared to that of control rats drinking a 5% glucose solution in order to investigate the effect of potassium loading upon the early and late step of aldosterone biosynthesis. Following potassium loading the quartered adrenals produced more aldosterone but less corticosterone as compared to the control. Potassium loading resulted in an increased aldosterone production rate by capsular adrenals (z. glomerulosa) provided that the corticosterone concentration in the incubation medium was elevated either by incubating it together with the decapsulated adrenal or adding exogenous corticosterone (4--16 mug/ml) to the medium. The corticosterone to aldosterone converting capacity of capsular adrenals is markedly higher in the potassium-loaded rats than in the controls. In the first 15 minutes of incubation the corticosterone production rate of the two groups was equal, aldosterone production rate by capsular adrenals of potassium-loaded rats, being higher than that of control animals. Corticosterone output of capsular adrenals from potassium-loaded rats decreased more rapidly in course of the incubation than it did in control tissue. These results suggest that the increase in aldosterone secretion in vivo following potassium loading is due to the stimulation of conversion of corticosterone to aldosterone in the glomerulosa cells. However, the endogenous corticosterone production during the incubation of glomerulosa cells from pottasium-loaded rats decreases so rapidly that the cells are not capable of producing more aldosterone than the control ones in spite of activated 18-hydroxylase.

Administration, Oral↗
PubMed1975

Steroid production by quartered and capsular rat adrenal gland in response to haemorrhage.

60 min after rapid bleeding (1.5--2.0 per cent of b. w.) both aldosterone and corticosterone production rate by quartered rat adrenals were found to be elevated. However, no difference was observed in the rate of aldosterone and corticosterone production by capsular adrenals of sham operated and hypovolaemic rats. Corticosterone production rate by decapsulated adrenals was much more higher after haemorrhage than in the control group. The same alterations could be observed incubating adrenal tissue with ACTH (0.3 mug per ml). Steroid production rate by quartered adrenals of sodium deficient rats was not affected by high in vitro concentration of angiotensin II (2.5 mug per ml). It is concluded that the effect of acute blood loss on corticosteroid biosynthesis of the rat is mediated by ACTH alone.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Prenatal diagnosis of steroid 21-hydroxylase deficiency by allele-specific amplification.

OBJECTIVE: Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency (21-OHD) is the most common cause of ambiguous genitalia in females at birth. Here, we report the first prenatal diagnosis of 21-OHD by DNA analysis in Hungary. METHODS: Allele-specific amplification (ASA) of the DNA obtained by chorionic villus sampling was performed. RESULTS: The fetus had a homozygous nonsense mutation (Gln318Stop), suggesting a salt-wasting phenotype. Dexamethasone treatment of the mother was started on the 8th gestational week and, as the fetus was an affected female, it was continued until term. The newborn had normal external genitalia at birth, and severe salt-wasting crisis and postnatal virilization was prevented by mineralo- and glucocorticoid replacement therapy. CONCLUSION: 21-OHD was genotyped by ASA, and virilization of the fetus was prevented by antenatal dexamethasone therapy.

Adrenal Hyperplasia, Congenital↗
PubMedDate not supplied

Postnatal changes in blood spot 17-hydroxyprogesterone level in healthy preterm and full-term neonates.

Blood spot 17OH-P concentrations were determined in 14 healthy premature (mean birthweight 1439 g, mean gestational age 30 weeks) and full-term newborn infants (mean birthweight 3532 g, mean gestational age 39.2 weeks) during the first five weeks of life to provide reference data for infants with various gestational and postnatal ages. It was demonstrated that with advancing age there was an abrupt fall in 17OH-P from 296.2 +/- 84.1 nmol/l on the first day to 101.2 +/- 19.5 nmol/l on the 7th day (p less than 0.001) and 75.7 +/- 8.7 nmol/l (p less than 0.05) on the 14th day in premature infants. In full-term neonates its initial value is much lower (90.1 +/- 12.5 nmol/l) and its fall during the first week is much less pronounced (51.5 +/- 6.5 nmol/l, p less than 0.01). Comparing the postnatal changes in 17OH-P in the two groups it proved to be significantly higher in premature than in full-term infants at all ages except for the 4th week. When blood spot 17OH-P values were studied as a function of gestational age at the age of 5 days a significant inverse relationship was found between the two parameters. It is assumed that in addition to placental 17OH-P production and perinatal stress, renal salt wasting may also account for the long lasting elevation of 17OH-P plasma level seen in premature infants.

17-alpha-Hydroxyprogesterone↗