Authors' reply
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《美国医学杂志》
Hirabai Cowasji Jehangir Medical Research Institute,Jehangir Hospital,Pune 411 001, India
We have not mentioned the frequency of monitoring 17-hydroxyprogesterone (17 OHP) in the article, but it was done three monthly. Our study spans the period from late 1999 to 2002. Those were the times when the 18 OHP assays were freely available in Pune where the study was conducted, hence the availability of 17 OHP testing was not an issue and did not affect the monitoring schedule.
We would like to point out that the increment in our paper is in the height velocity standard deviation score (SDS) and not in the height SDS as has been mentioned in the comment. As suggested by our monitoring, no patient was uncontrolled leading to rapid growth acceleration, and no new central precocious puberty was noted. There was one patient with central precocious puberty who was excluded from the analysis.
Many of our patients were diagnosed very soon after birth and hence did not have advancement in the skeletal age in the first place. A large number of our patients i.e. 3 from group one and 5 from group two were less than 2-yrs-old at the time of the study. The Tanner Whitehouse 3 Atlas More Details does not allow the calculation of bone age under two years of age.[1] Another problem is that no Indian bone-age standards are available for comparisons.
One of the primary requirements to calculate predicted height is bone age. As has already been mentioned above, many of our patients were less than two years, and as a reliable bone age was not available, we decided not to calculate predicted heights.
One of the key messages of our paper was to point out to medical personnel dealing with children with CAH alll over India, that hydrocortisone (HC) is now freely available for use in these children. If we had waited till our children reached final height the whole purpose of our paper would have been defeated.
Although one paper by Rivkees et al[2] suggests that dexamethasone should be used in children, there are several reports recommending the use of hydrocortisone in infants and children.[3],[4] In fact, the Consensus Statement on 21-Hydroxylase Deficiency from The Lawson Wilkins Pediatric Endocrine Society and The European Society for Pediatric Endocrinology published in 2002 states that HC is considered the drug of first choice during infancy, and childhod and long-acting glucocorticoids may be an option at or near the completion of linear growth.[5] To make a further point on the paper by Rivkees et al, it is based on final height predictions rather than the actual achieved final height, and the height predictions do not always correlate with the final height achieved in these children.[6]
References
1. Tanner JM, Healy MJ, Goldstein H, Cameron N. In Assessment of skeletal maturity and prediction of adult height ( TW3 method). 3rd edn. London; WB Saunders, 2001.
2. Rivkees SA, Crawford JD. Dexamethasone treatment of virilizing congenital adrenal hyperplasia: The ability to achieve normal growth. Pediatrics 2000; 106 : 767-773.
3. Silva IN, Kater CE, Cunha CF, Viana MB. Randomized controlled trial of gowth effect of hydrocortisone in congenital adrenal hyperplasia. Arch Dis Child 1997; 77 : 214-218.
4. Styne DM, Richards GE, Bell JJ et al. Growth patterns in congenital adrenal hyperplasia. Correlation of glucocorticoid therapy with stature. In Lee PA, Plotnik LP, Kowarski AA et al. eds. Congenital adrenal hyperplasia . Baltimore; University Park Press, 1977: 247-263.
5. Joint LWPES/ESPE CAH Working Group. Consensus Statement on 21-Hydroxylase Deficiency from The Lawson Wilkins Pediatric Endocrine Society and The European Society for Paediatric Endocrinology. Journal of Clinical Endocrinology and Metabolism 2002; 87 : 4048-4053.
6. Frisch H, Waldhauser F, Lebl J, Solyom J, Hargitai G, Kovacs J et al. Growth in disorders of adrenal hyper function. Horm Res 2002; 57 : 95-101.(Khadilkar Vaman, Khadilka)
We have not mentioned the frequency of monitoring 17-hydroxyprogesterone (17 OHP) in the article, but it was done three monthly. Our study spans the period from late 1999 to 2002. Those were the times when the 18 OHP assays were freely available in Pune where the study was conducted, hence the availability of 17 OHP testing was not an issue and did not affect the monitoring schedule.
We would like to point out that the increment in our paper is in the height velocity standard deviation score (SDS) and not in the height SDS as has been mentioned in the comment. As suggested by our monitoring, no patient was uncontrolled leading to rapid growth acceleration, and no new central precocious puberty was noted. There was one patient with central precocious puberty who was excluded from the analysis.
Many of our patients were diagnosed very soon after birth and hence did not have advancement in the skeletal age in the first place. A large number of our patients i.e. 3 from group one and 5 from group two were less than 2-yrs-old at the time of the study. The Tanner Whitehouse 3 Atlas More Details does not allow the calculation of bone age under two years of age.[1] Another problem is that no Indian bone-age standards are available for comparisons.
One of the primary requirements to calculate predicted height is bone age. As has already been mentioned above, many of our patients were less than two years, and as a reliable bone age was not available, we decided not to calculate predicted heights.
One of the key messages of our paper was to point out to medical personnel dealing with children with CAH alll over India, that hydrocortisone (HC) is now freely available for use in these children. If we had waited till our children reached final height the whole purpose of our paper would have been defeated.
Although one paper by Rivkees et al[2] suggests that dexamethasone should be used in children, there are several reports recommending the use of hydrocortisone in infants and children.[3],[4] In fact, the Consensus Statement on 21-Hydroxylase Deficiency from The Lawson Wilkins Pediatric Endocrine Society and The European Society for Pediatric Endocrinology published in 2002 states that HC is considered the drug of first choice during infancy, and childhod and long-acting glucocorticoids may be an option at or near the completion of linear growth.[5] To make a further point on the paper by Rivkees et al, it is based on final height predictions rather than the actual achieved final height, and the height predictions do not always correlate with the final height achieved in these children.[6]
References
1. Tanner JM, Healy MJ, Goldstein H, Cameron N. In Assessment of skeletal maturity and prediction of adult height ( TW3 method). 3rd edn. London; WB Saunders, 2001.
2. Rivkees SA, Crawford JD. Dexamethasone treatment of virilizing congenital adrenal hyperplasia: The ability to achieve normal growth. Pediatrics 2000; 106 : 767-773.
3. Silva IN, Kater CE, Cunha CF, Viana MB. Randomized controlled trial of gowth effect of hydrocortisone in congenital adrenal hyperplasia. Arch Dis Child 1997; 77 : 214-218.
4. Styne DM, Richards GE, Bell JJ et al. Growth patterns in congenital adrenal hyperplasia. Correlation of glucocorticoid therapy with stature. In Lee PA, Plotnik LP, Kowarski AA et al. eds. Congenital adrenal hyperplasia . Baltimore; University Park Press, 1977: 247-263.
5. Joint LWPES/ESPE CAH Working Group. Consensus Statement on 21-Hydroxylase Deficiency from The Lawson Wilkins Pediatric Endocrine Society and The European Society for Paediatric Endocrinology. Journal of Clinical Endocrinology and Metabolism 2002; 87 : 4048-4053.
6. Frisch H, Waldhauser F, Lebl J, Solyom J, Hargitai G, Kovacs J et al. Growth in disorders of adrenal hyper function. Horm Res 2002; 57 : 95-101.(Khadilkar Vaman, Khadilka)