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Congenital Adrenal Hyperplasia: Experience in Iranian Patients Journal of www.ComprPed.com Congenital Adrenal Hyperplasia: Experience in Iranian Patients 1, 2* 2 3 Maryam Razzaghy Azar , Mona Nourbakhsh , Mitra Nourbakhsh 1 Inborn Error of Metabolism, Endocrinology and Metabolism Research Center, Tehran University of Medical Sciences, Tehran, IR Iran 2 Department of Pediatrics, H. Aliasghar Hospital, Tehran University of Medical Sciences, Tehran, IR Iran 3 Department of Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, IR Iran Corresponding author: * Maryam Razzaghy Azar, Inborn Error of Metabolism, Endocrinology and Metabolism Research Center, Tehran University of Medi- cal Sciences, Tehran, IR Iran.Tel: +98-21 66942903, Fax: +98-21 66421054, E-mail: [email protected] ABSTRACT Background: Congenital adrenal hyperplasia (CAH) is an autosomal recessive disorder stemming from one of the enzymatic defects in the biosynthesis of cortisol from cholesterol. In the majority of instances the disorder comprises deficiency of 21-hydroxylase (21-OHD). This defect causes excessive androgen production from adrenal source, which leads to virilization with varying degrees of severity (Prader grade 1-5) in female fetuses. Objectives: To determine the frequency of different types of congenital adrenal hyperplasia, rate of consanguinity, family occurrence, birth weight, and final height and weight. Patients and Methods: Medical records of patients with CAH between 1968 and 2011 were reviewed. Results: Out of 617 patients, 79.6% had 21-hydroxylase deficiency (21-OHD). In 21-OHD group 94.5% had classical type and 5.5% were non-classic. Among the classic type 78% had salt-wasting form (SW) and 22% simple virilizing (SV). Both 21-OHD-SV and SW were diagnosed more frequently in females. Frequency of other types were as follow: 11-hydroxylase deficiency (11-OHD), 13.3%; 3ß-hydroxysteroid dehydrogenase deficiency (3ß –OHD), 4.1%; lipoid adrenal hyperplasia, 1.1%; 17-hydroxylase deficiency, 1%; hypoaldostronism, 0.6% and Antley-Bixler, 0.3%. Parental consanguinity was present in 62.6% and familial occurrence was reported in 42.6% of the patients. Sixteen girls had grade 5 virilization of Prader staging (SW, 10; SV, 2; 11-OHD, 4). The most prevalent Prader stage was 4 in 21-OHD-SW and 11-OHD. In 21-OHD-SV, 9 patients had Prader grade 4 and 5 virilization. The difference between mid-parental height and final height was highest in 21-OHD-SV; its SDS was (-1.2 ± 1.1). Birth weight of all patients was normal except for 5 patients. The frequency of low and very low birth weight was not significantly different from the general population. All patients were assigned as their genetic gender except for 5 patients with delayed diagnosis or parental opposition. Conclusions: The prevalence of different types of CAH, grade of virilization, final weight, height and birth weight, were recorded from the referral patients. Keywords: Congenital Adrenal Hyperplasia, Height, Weight, Grade of Virilism, Birth Weight Safnek Published by , 2013. cc 3.0 DOI: 10.17795/compreped- Article type: Research Article; Received: 19 Apr 2012, Revised: 24 May 2012, Accepted: 29 May 2012; 5244 Implication for health policy/practice/research/medical education: Clinical experience on a large series of CAH patients in a tertiary care hospital. Please cite this paper as: Razzaghy-Azar M, Nourbakhsh M, Nourbakhsh M. Congenital Adrenal Hyperplasia: Experience in Iranian Patients. J Compr Ped. 2013:4(1):54-61. Copyright © 2013, Iranian Society of Pediatrics. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which per- mits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Congenital Adrenal Hyperplasia: Experience in Iranian Patients Razzaghy Azar M et al. 1. Background high levels of 24 hour urinary 17-OHCS and pregnanetriol or high serum levels of 17-OHP and hypertension, were Congenital adrenal hyperplasia (CAH) is an autosomal diagnosed as having 11-OHD. A 3ß-hydroxysteroid dehy- recessive disorder that is due to one of the enzymatic de- drogenase deficiency (3ß-OHD) was the diagnosis when fects which occur in cortisol biosynthesis from cholester- the 17-OHP level was high (due to peripheral conversion ol. The most prevalent type is 21-hydroxylase deficiency of 17-hydroxypregnenolone to 17-OHP), in boys who pre- (21-OHD). This defect causes excessive androgen produc- sented with salt-wasting and ambiguous genitalia and tion from adrenal source, which leads to virilization of in girls who had salt-wasting with no or low grade am- varying severity (Prader grade 1- 5) in female fetuses (1). biguity, high DHEA-S and low androstenedione. Patients Moreover, in some types of this disorder there is under- who had 17-hydroxylase deficiencies (17-OHD) presented virilization of males. Management of this condition con- due to the absence of secondary sexual characteristics at sists of medical treatment with glucocorticoids, miner- the age of puberty. They had hypertension, high proges- alocorticoids (in salt-wasters) and surgical repair of the terone, low estradiol, high follicle stimulating hormone external genitalia. There is general agreement about the (FSH) and luteinizing hormone (LH), low cortisol, high need for primary surgical intervention before 2 years of ACTH, low PRA and normal aldosterone. Patients with age (2, 3). hypoaldostronism (Hypoaldo) had salt-wasting crisis, 2. Objectives low sodium, high potassium with high PRA, but frequent measurements of 17-OHP, cortisol and ACTH were normal The aim of this study is to present the clinical experi- initially and during the follow-up period. Boys were di- ence accumulated over 43 years on a large series of CAH agnosed as having lipoid adrenal hyperplasia (Lipoid) if patients in a tertiary care hospital. Frequency of differ- they presented with; a female phenotype, salt-wasting ent types, degree of virilization, final height and weight, manifestations, low cortisol, low 17-OHP and high ACTH birth weight and unusual cases are reported. levels, and girls who had the same manifestations, were relatives of these boys and documented by genetic study. 3. Patients and Methods Height and weight of the patients were considered final Medical records of 617 patients with CAH from 1968 to when growth had stopped for more than 6 months with 2011 were reviewed. Diagnoses were based on clinical bone age > 16 years in girls and > 17 years in boys. Mid- manifestations and measurement of 24 hour urinary parental height (target height) was calculated as mean of 17-ketosteroids (17-KS), pregnanetriol and 17-hydroxycor- parental heights plus 6.5 cm for males and minus 6.5 cm ticosteroids (17-OHCS) (using the Porter-Silber method) for females. The difference of the patient’s height with until 1985 and the assessment of serum 17-hydroxypro- mid-parental height (MPH) was determined. Standard gesterone (17-OHP) and serum cortisol at 8 AM, ACTH, deviation scores (SDS) of height were calculated for the fi- aldosterone, plasma renin activity (PRA), dehydroepian- nal height and MPH of the patients using these formulas drosterone (DHEA) and androstenedione by radio im- according to CDC2000: munoassay thereafter. Clinical manifestations in salt- Height SDS =(patient height-height 50% for age)/(SD for wasting types were; dehydration, poor feeding, failure age) to thrive, vomiting, lethargy, sometimes cyanosis and and shock, and diagnostic laboratory tests included; low se- MPH SDS =(MPH-height 50% for 20 yr)/(SD for 20 yr) rum sodium, high serum potassium and high PRA. Pa- The difference between the patient’s height SDS and tients with 21-OHD were detected by the presence of high mid-parental height SDS (final H- MPH SDS) was also de- termined. Final body mass index (BMI) was calculated by 24 hour urinary 17-KS and pregnanetriol (before 1985) and 2 high serum 17-OHP (after 1985). Simple virilizing type of the formula, weight (kg)/height (m ). Weight status was 21-hydroxylase deficiency (21-OHD-SV) was diagnosed in considered; underweight when BMI was < 18.5, normal girls who had ambiguous genitalia, without salt-wasting weight 18.5–24.9, overweight 25.0–29.9, and obese 30 or manifestations. This condition was also diagnosed in boys higher. Bone age was determined according to the atlas who presented with pseudoprecocious puberty, without of Greulich and Pyle. The gender of the patients was de- hypertension. The patients with non-classical form of tected by karyotyping with a banding method. 21-hydroxylase deficiency (NC21-OHD) had normal geni- 4. Results talia. They had normal blood pressure, and manifested with premature adrenarche in childhood or adrenarche Among 617 patients with congenital adrenal hyperpla- that precedes testicular enlargement during puberty in sia, 260 patients (42%) were male and 356 cases (58%) were males, or was manifested by hirsutism during or after female and one patient with Antley-Bixler syndrome had adolescence in females. They had high levels of 17-OHP a karyotype of 45, XO. The most prevalent type of CAH was at 8 AM and in suspicious cases a provocative test with 21-OHD (79.6%). The prevalence of different types of CAH short-acting ACTH was conducted. The patients, who had according to gender is shown in (Table 1 , 2) and (Figure 1). 4 55 J Compr Ped. 2013: (1) Razzaghy Azar M et al. Congenital Adrenal Hyperplasia: Experience in Iranian Patients Table 1. Frequency of Different Types of CAH In our study of the 491 cases with 21-OHD, 94.5% had clas- Gender No. (%)a Total No. (%) b Type sic and 5.5% had a non-classic type of this disorder; 78% Female Male of all classic types had salt-wasting and 22% had a simple 21-OHD 300 (61) 191 (39) 491 (79.6) virilizing form. Salt-wasting and simple virilizing forms 11-OHD were more common in girls, and NC21-OHD was diag 39 (48) 43 (52) 82 (13.3) 3-βOHD nosed in 24 girls and 3 boys.
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