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Gomes LG and Madureira G wrote the paper. Mendonca BB performed the statistical analysis. Bachega TA was the mentor and supervisor of this work. The four co-authors performed follow-ups of the patients in this study.
The protocols for glucocorticoid replacement in children with salt wasting hydroxylase deficiency are well established; however, the current recommendation for mineralocorticoid replacement is general and suggests individualized dose adjustments.
Twenty-three salt wasting hydroxylase deficient patients with good anthropometric and hormonal control were followed in our center since diagnosis. The mineralocorticoid needs of salt wasting hydroxylase deficient patients are greater during early infancy and progressively decrease during the first two years of life, which confirms that a partial aldosterone resistance exists during this time. Our study proposes a safety regiment for mineralocorticoid replacement during this critical developmental period.
ACTH levels rise because of impaired cortisol secretions, thereby stimulating the adrenal cortex and accumulating androgen precursors, which manifest in varying degrees of hyperandrogenism. The severity of clinical symptoms and hormonal abnormalities correlates with the severity of enzymatic impairment manifested through three main phenotypes: Females present with virilized external genitalia at birth, and both sexes present with adrenal crisis in the first months of life.
This adrenal crisis is characterized by hyponatremia, hyperkalemia, hyperreninemia and dehydration and leads to acute circulatory collapse if left untreated 2. SWOHD treatment consists of glucocorticoid and mineralocorticoid replacement in conjunction with sodium chloride supplementation during infancy 3. The guidelines for glucocorticoid replacement in children are well established 3 and include short half-life glucocorticoids to prevent adrenal crises and virilization, along with minimizing the growth suppression associated with longer-acting glucocorticoids 4.
The dose adjustments should be based on clinical and laboratory parameters, such as blood pressure, sodium, potassium and plasmatic renin activity PRA levels 5. Mineralocorticoid replacement doses vary during infancy primarily because of improvements in mineralocorticoid sensitivity, which tends to increase, particularly during the first year of life 6.
The higher mineralocorticoid demand during early infancy is explained by renal function immaturity, the limited sodium content in human breast milk and higher sodium requirements for child development during this period 7 , 8.
Despite the importance of mineralocorticoid treatment during infancy in SWOHD patients, there is a lack of data in the literature concerning the optimal replacement dosage. The study protocol was approved by the Institutional Review Board, and informed consent was obtained from all of the patients or their parents. The inclusion criteria were regular follow-up in our institution from diagnosis or early age maximum 90 days to two years of age and adequate clinical and hormonal control.
Our cohort comprised 23 SWOHD patients who were homogeneously treated and assisted by the same physicians from to The patients were initially treated with cortisone acetate: The patients were evaluated weekly during the first two months of life, monthly from three to six months of life and every three months thereafter. Clinical data, such as height, weight, blood pressure and sodium and potassium levels, were measured at every appointment.
Mineralocorticoid treatment was considered adequate if the sodium and potassium levels were maintained within the normal or near normal range and if the PRA levels were within the upper limit of the normal range. Glucocorticoid treatment did not attempt to normalize the 17OHP levels and was considered adequate if at least three of the four assessments per year of testosterone and androstenedione levels were also normal.
From to , testosterone was measured with radioimmunoassay Diagnostic Systems Laboratories Inc. Androstenedione was measured with radioimmunoassay Diagnostic Systems Laboratories Inc. The genetic analyses of CYP21A2 included Southern blotting, followed by hybridization with a genomic CYP21 probe to investigate large rearrangements 11 and allele-specific PCR to investigate 15 common micro-conversions Direct sequencing was performed when the mutations were not detected in both of the alleles or were not concordant with the phenotype The results are presented as the median, mean and SD.
In the 23 salt wasting 21OHD patients studied, the salt wasting crises occurred at a mean age of 23 days range days. Cortisone acetate doses per square meter were stable during the first two years of treatment.
The boxes at the lower and upper ends represent the lower and upper quartiles, respectively, and the bold horizontal line inside the boxes represents the median dose. The vertical bars reach from the boxes to the non-outlier minimum and maximum values.
In contrast, the cortisone acetate dose adjusted for body surface area was constant during the first two years of life mean dose During the studied period, none of the patients presented with clinical signs of mineralocorticoid overload, such as arterial hypertension, tachycardia or congestive heart failure, or deficiencies e. A Box plots show the serum sodium levels in the basal state, monthly during the first 6 month of life and then every three months during the first two years of treatment.
B Box plots show the serum potassium levels in the basal state, monthly during the first six month of life and then every three months during the first two years of treatment.
Box plots show the PRA levels in the basal state and every three months during the first two years of treatment. In males, the mean height and weight were Appropriate glucocorticoid and mineralocorticoid replacement during infancy in SWOHD children is critical for maintaining a positive sodium balance that enables adequate body growth and brain development.
Studies evaluating the late effect of neonatal sodium deficiency in neurological performance, such as motor function, intelligence IQ , memory, language and behavior, have shown poor neurodevelopment outcomes in the second decade of life Impaired cognitive function has been observed in 21OHD patients, particularly with SWOHD 14 , which reflects the adverse effects of hyponatremia episodes and suboptimal hormone replacement therapy.
However, the acute consequences of mineralocorticoid excess are volume overload and congestive heart failure, and the chronic consequences include growth impairment caused by its glucocorticoid properties Therefore, the goal of therapy in SWOHD patients is to normalize the androgen levels and total-body sodium depletion to allow normal growth and development and avoid volume overload In our study, the required glucocorticoid dose adjusted per square meter was stable during the first two years of life.
In fact, a relative state of aldosterone resistance has been found in the neonatal period 6. Healthy term neonates exhibit extremely high plasma aldosterone levels 6 , 17 , which is most likely an adaptive response to kidney tubular immaturity at birth 6 , 7 , 17 - Additionally, in 21OHD patients, the accumulated androgen precursors, progesterone and 17OH-progesterone 17OHP inhibit mineralocorticoid receptor transactivation by aldosterone Therefore, individual drug adjustments during this period should be assessed weekly rather than monthly.
No potential conflict of interest was reported. National Center for Biotechnology Information , U. Journal List Clinics Sao Paulo v.
Gomes , Guiomar Madureira , Berenice B. Mendonca , and Tania A. Find articles by Larissa G. Find articles by Guiomar Madureira. Find articles by Berenice B. Find articles by Tania A. Open in a separate window. Statistics The results are presented as the median, mean and SD.
Footnotes No potential conflict of interest was reported. Congenital adrenal hyperplasia due to hydroxylase deficiency. The molecular biology, biochemistry, and physiology of human steroidogenesis and its disorders. Congenital adrenal hyperplasia due to steroid hydroxylase deficiency: The Journal of clinical endocrinology and metabolism. Reduced final height outcome in congenital adrenal hyperplasia under prednisone treatment: Management of the child with congenital adrenal hyperplasia.
Physiological partial aldosterone resistance in human newborns. Holtback U, Aperia AC. Molecular determinants of sodium and water balance during early human development. Sodium homeostasis in term and preterm neonates.
Archives of disease in childhood. Management of congenital adrenal hyperplasia: Molecular genotyping in Brazilian patients with the classical and nonclassical forms of hydroxylase deficiency. Low frequency of CYP2B deletions in Brazilian patients with congenital adrenal hyperplasia due to hydroxylas deficiency.
Estudo multicentrico de pacientes brasileiros com deficiencia da hidroxilase: Effect of salt supplementation of newborn premature infants on neurodevelopmental outcome at years of age. Archives of disease in childhood Fetal and neonatal edition. Impaired cognitive function in women with congenital adrenal hyperplasia.
Monitoring of therapy in congenital adrenal hyperplasia. Normalization of height and excess body fat in children with salt-wasting hydroxylase deficiency. Low renal mineralocorticoid receptor expression at birth contributes to partial aldosterone resistance in neonates. Plasma aldosterone levels in the 1st week of life in infants of less than 30 weeks gestation. European journal of pediatrics. Padidela R, Hindmarsh PC.
Mineralocorticoid deficiency and treatment in congenital adrenal hyperplasia. Agonistic and antagonistic properties of progesterone metabolites at the human mineralocorticoid receptor. Studies in human lactation: Breast milk sodium concentration, sodium intake and weight loss in breast-feeding newborn infants.
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