Study of growth in prepubertal asthmatics
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《美国医学杂志》
1 University of Alexandria, Alexandria, Egypt,2 Royal Hospital for Sick Children, Edinburgh, Scotland,
Abstract
Objective. The aim of this pilot study was to assess whether long standing asthma affects growth in prepubertal Egyptian children before initiation of long-term corticosteroid therapy. Methods. Children with asthma were divided into two groups according to asthma severity, moderate (n=24) and severe (n=14) and were compared for their physical and skeletal growth with a control group (n=15) using standard deviation score (SDS) and oneway ANOVA (analysis of variance) test. Results. No statistically significant differences were found between various growth parameters (weight, height, BMI, upper segment lower segment ratio, and skin fold thickness in asthmatic and normal children, although a positive correlation was found between the age at which the asthma presented and the height in all asthmatic children, r= 0.288, p= 0.036. The bone age standard deviation scores (SDS) were 0.97 mean, -0.165 and -0.572 for controls, moderate and severe asthmatics respectively (P<0.05), and significant inter group difference between the 2 asthmatic groups (moderate and severe) and the controls was found. Conclusion. The authors conclude that there was no significant major effect of asthma per se on growth parameters in children, but that skeletal maturation was influenced by long standing asthma.
Keywords: Asthma; Growth; Prepubertal children; Midparental height
Asthma is one of the few chronic diseases that are increasing in prevalence despite better understanding of its pathogenesis and improved treatment It is defined as "a chronic inflammatory disorder of the airways in which many cells. including mast cells and eosinophils play a role. which in genetically susceptible individuals. can cause symptoms associated with widespread variable airflow obstruction due to mucosal oedema. secretion of mucus. epithelial damage and bronchoconstriction that is often reversible either spontaneously or with treatment. and cause an associated increase in airway responsiveness to a variety of stimuli.[1]
Being one of the most common and most important illnesses during both the pediatric and adulthood periods it can retard growth in the former and disturb social well being and normal life style in both.[2]
Depending on history, physical examination, laboratory data, pulmonary function tests and the need for medication, patients can be classified as having mild, moderate or severe asthma.[3]
The growth process is complex. Linear growth occurs primarily as a result of chondrogenesis. Normally, there also occurs the synchronous process of osteogenesis; the formation of bone in cartilage. In some endocrine disorders, these two processes do not occur synchrono~ and a comparison of linear growth and bone development can give important clues.[4]
The aim of this study was to determine the effect of asthma on growth before puberty. The effect of asthma on linear growth is controversial as shown previously.[5] The process of studying growth is a complex one which becomes even more so in children suffering from a chronic illness, and receiving a variety of diets and medications due to the multiplicity of factors involved.[5] In case of severe bronchial asthma, the multiplicity of factors to be considered is immense. The degree of incapacitation the illness imposes on the child may logically be a factor influencing growth. In addition, the chronic asthmatic child will be subjected to dietary trials, which often eliminate important nutrients from his or her diet. There is also a question of heredity and atopy, and lastly, the problems of drug therapy especially glucocorticoids.[5]
Materials and Methods
The Asthma Group
Inclusion Criteria
Forty consecutive patients who were diagnosed with either moderate or severe asthma were were referred by their General Practitioners to the Pediatric department of El-Shatby Pediatric Hospital (SPH) which is a tertiary referral hospital and the governmental students' hospital (OSH) which is another city hospital in Alexandri, either in acute exacerbation or for follow up. The age range was between 4 and 13 years with a mean age of 7.71 years complaining from uncontrolled asthma for at least 2 years
Out of the 40 asthmatic children 38 were followed till the end of the study (25 males and 13 females) and two were lost because of failure to maintain the follow up visits till the end of the study i.e. for 9 months.
Exclusion criteria
Children who were on any form of long term steroid therapy at any point of time, those who had asthma for less than 2 years period or those who were suffering from any other illness which might influence growth.
The control group. Fifteen age and sex-matched healthy children with a mean age of 7.1 years (10 males and 5 females) served as a control group. Other factors taken into consideration in matching the control group with asthmatics were the residence, which was comparable in all the studied children, and the mid-parental height both are indicators of the economic' and the genetic background respectively. The control group was recruited from the children attending the outpatient clinic after being treated from minor ailments e.g. upper respiratory tract infection. The study protocol was subject to Ethics committee approval at the study centre before commencement.
All the studied children were subjected to detailed history taking for asthma in asthmatics together with clinical examination including anthropometrical measurements; weight, height using a standard physician's weight scale and height scale with stadiometer, triceps, subscapular and abdominal skin fold thickness (SFT) using Harpenden skin fold calliper, ,upper segment lower segment ratio (US/LS) and body mass index (BMI)[6] at the initial visit and after 3 months and at the end of follow up after 9 months, as well as assessment of asthma severity using a score sheet and a prepared questionnaire.[7],[8]
In terms of asthma severity, fourteen patients out of the 38 were described as severe asthmatics, while 24 as moderate asthmatics. Categorisation of asthma was based on the frequency, severity and chronicity of symptoms and consequently the medications received, and lastly the requirement for hospitalisation in the previous episodes as well as the presenting one.[7],[8]
All children were assessed for eligibility at admission to the emergency/outpatient unit. Patients were eligible if they were between the ages, of 4 and 13 vears and had a known history of asthma (defined as at least 1 previous episode of wheezing or a history of chronic cough that required treatment with bronchodilators or anti-inflammatory agents). Only children with moderate to severe asthma. (defined as requiring inhaled Ih-agonists a minimum of every 2 hours having a forced expiratory volume in 1 second [FEV1] of 25%-80% of the predicted volume, or having a clinical asthma score of 3-9[9] on admission, or uncontrolled asthma based on past history and a score sheet[7],[8] were recruited.
Analysing the difference between the studied groups regarding the anthropometries was through comparing the % change in each parameter at the end of the follow up period using t-test and one-way ANOV A between groups followed by pair-wise comparison using unpaired t-test.[10] The chi-square test was used to compare between height SDS of all children.[10]
Bone age assessment was also done through a plain x-ray of the left hand and wrist using the Tanner-White house technique.[11],[12],[13] In addition, plain x-ray chest postero-anterior view to exclude other pathological conditions that can simulate asthma clinically,[3] tuberculin test (Manteaux test) to exclude active T.B.[3] d peak expiratory flow rate (PEFR) was measured in each patient every 3 weeks due to lack of facilities to provide every child with an individual peak flow meter. Patients were followed up for the asthma nearly every 3 weeks and were managed according to their response to the treatment received.
Results
Clinical response regarding control of asthma improved in most patients during the first few months of treatment and follow up.
Anthropometric measurements
[Table - 1] demonstrates some demographic and clinical characteristics of the 3 studied groups; controls, moderate and severe asthmatics, where the groups were matched in all the variables.
When comparing the percent changes in all growth parameters from basal to final recordings among the 3 studied groups, it was found that the differences were not statistically significant [Table - 2].
[Figure - 1] compares the mean weights of the three studied groups at the beginning (basal) and at the end of the study (final), where the differences were not statistically significant, P > 0.05.
Using the height standard deviation score (HT SDS) in studying linear growth delineated that the mean basal and final Ht SDS were not significantly different among the 3 studied groups, P> 0.05 [Figure - 2].
There was a positive correlation between the age at which the disease presented and basal height of both moderate and severe asthmatics, r=0.288 and P=0.036 [Figure - 3].
[Figure - 4] shows a positive correlation between the MPH and the mean basal height of all the studied children (patients and controls), with a correlation coefficient r= 0.232.
Bone age. The mean (SDS) bone age was significantly different in the three groups.
Mean values were 0.971, -0.165 and -0.573 for controls, moderate and severe asthmatics respectively, P< 0.001
Significant differences were found between each of the two asthmatic groups (moderate and severe) and the normal childran, where P value was < 0.001 and 0.001 for both whereas the moderate and severe asthmatics did not differ significantly in terms of their skeletal maturation P>0.05 [Table - 3].
[Figure - 5]. shows the difference between the mean bone age SDS in the three groups, where the severe asthmatics had the lowest mean value. The mean bone age SDS for controls, moderate and severe asthmatics was 0.970, -0.165 and -0.572 respectively. P< 0.05.
Lastly, mean bone age was not significantly different in those with a positive family history of allergy (-0.325) compared to those without family history (-0.302). P>0.05.
Discussion
0In this study, the asthma state did not influence the children's growth. These results coincide with those of previous studies[14],[15] about bronchial asthma as a cause for concern about growth.
Height in normal individuals is a strongly genetically determined characteristic.[16] In addition to taking it into consideration in matching the control group with asthmatics, the MPH, gives an indicators of the economic and the genetic background respectively.
This means that the measured parental height can give good indication of the target height to which a child is aiming, and whether the asthmatic children followed their genetic potential for growth or not.
As regards the, BMI among asthmatics and control children, the differences were not statistically significant. The same findings were reported in a previous study done by Kaplan et al[17], which showed no difference between the general population and the cohort with asthma.
In one study carried out in the UK to investigate the height, weight and BMI of children with asthma in the community found no difference from the general population apart from children who were receiving high dose inhaled corticosteroids (ICS), where they appeared to be shorter than their contemporaries and deserved long-term follow-up.[15]
In a long-term prospective study from Australia,[18] children with severe asthma were found to attain normal height. This observation was confirmed in several subsequent studies.[19],[20] Indeed one report suggested that children with mild asthma grew to a marginally greater final height than non-asthmatics,[20] and even with more severe disease, children who were treated with 300-600 mg BDP/day for more than one year attained normal final height.
In the present study, a strong positive correlation was found between the age of onset of the disease and the basal Ht SDS of all children with asthma, which indicate that the earlier the disease onset, the more likely the child will be shorter.
These results are in keeping with those of another study done to assess the growth of a group of asthmatics in relation to the age of onset of asthma, in which the weight and height were predominantly in the 50th percentile or below in 68.4% of children in which the disease started before 2 years of age.[21]
Nevertheless, as suggested by other researchers,[22] if growth impairment occurs in childhood, it is likely to be temporary and reversible.
The skeletal maturation of the studied children in this work showed significant delay in both moderate and severe asthmatics when compared to the normal group, a finding that might be expected in the context of the chronic inflammatory state present in asthmatics. These fmdings are in keeping with other studies where delay in skeletal maturation was observed in severe asthmatics before and after treatment with steroids. Before treatment, skeletal maturity was below the reference mean in the majority of children.[23],[24] However, after control of disease activity and with effective treatment regimens, the effect on skeletal maturation was not found to be pronounced and did not affect the ultimate growth outcome.
In the context of the previously reported association of short stature and skeletal retardation in children with bronchial asthma or atopic dermatitis,[25] in the present study, the relation between family history of allergy and bone age was studied, however, the difference between skeletal maturation of atopic and non-atopic children was not significant. A study done by Baum et al[25] showed that 11.6% of atopic asthmatic children had a skeletal retardation of more than 2 years. It was concluded that skeletal delay could be regarded as a direct consequence of the atopic state of the individual.
In conclusion, this study showed no significant major effect of asthma on physical growth, apart from skeletal maturation, which was found to be significantly retarded in asthmatics compared to normal children.
References
1.Global Initiative for Asthma, National Heart, Lung and Blood Institute. Global Strategy for Asthma Management and Prevention. Bethesda, Md: Global Initiative for Asthma, National Heart, Lung and Blood Institute; 2004.
2.Davies RJ, Abdelziz MM. New insights into the understanding of asthma. Chest 1997; 2 : 1-11
3.Sly RM. In Nelson WE, Behrman RE, Kleigman RM et al., eds. Nelson Text book of Paedietrics. 16th edn. Philadelphia,. Pennsylvania WB Saunders, Company. 2000.
4.Aynsly-Green A. Growth. In S. Godfrey and JD Baum, eds. Clinical Pediatric Physiology. Oxford; Blackwell Scientific Publication 1979; 434-468.
5.Falliers CJ, Szentivanyi, Mc Bride M et al. Growth rate of children with intractable asthma. J Allergy 1961; 32(5) 421-435.
6.Gennuso J, Epstein LH, Paluch RA et al. The relationship between asthma and obesity in urban minority children and adolescents. Arch Paediatr ado lese Med 1998; 152: 1197-1200.
7.Tal A, Bavilski C, Yohai D. Dexamethasone and salbutamol in the treatment of acut~ wheezing in infants. Plediatr 1983; 71: 13-18.
8.Ferguson AC, Murray AB, Wah-Jun T. Short stature and delayed skeletal maturation iJ1 children with allergic diseases. J Allergy Clin lmmunol 1982; 69 : 461-466.
9.Parkin PC, Macarthur C, Saunders NR et al. Development of a clinical asthma score for use in hospitalized children between 1 and 5 years of age. J Clin EPidemii 1996; 49 : 821-825.
10.Saunders BD, Trapp RG. Basic and clinical statistics. USA; Prentice, Hall, International Incorporation; 1990.
11.Roche AF, Davila GH, Leyman SL. A comparison between Greulich-Pyle and Tanner Whitehouse assessment of skeletal maturity. Radiology 1971; 98 : 273-280.
12.Tanner JM, Whitehouse RH. Atlas of children's growth: normal variation and growth disorders. Londonj Academic Press (1982).
13.Handmarsh PC and Brook CGD. Normal Growth and its Endocrine Control. In CGD Brook, ed. Clinical Paediatric Endocrinology 3rd edition. London: Blackwell Science. 1995; 85-106.
14.Neville RG, Mc Cowan, Thomas G et al. Asthma and growth- cause for concern Asthma and growth in Tayside children. Ann Hum Biol 1996; 23(4) : 323-33l.
15.Klein GL, Dunghy CI, Golant SP. Growth and the nutritional status of non-steroid dependent asthmatic children. Ann Allergy 1991; 67(1): 80-84.
16.Hawk W, Brook CGD. Family resemblance of height, weight and body fatness. Arch Dis Child 1979; 54 : 877-879.
17.Kaplan BA, Brush G, Mascie-Taylor CGN. The relationship of childhood asthma and wheezy bronchitis with weight,. height and body mass index. Human Biology 1987; 59(6): 921-931.
18.Martin AJ, mc Lenan LA, Landan LI et al. The natural history of childhood asthma to adult life. BMJ 1980; 280: 1397-1400.
19.Shobat M, Shobat T, Kedem R et al. Childhood asthma and growth outcome. Arch Dis Child 1987; 62 : 63-65.
20.Grumach AC, Carneiro-Sampaio MM, Lima JL et al. The growth curve in asthmatic children. Allerg Immunopathol(Madr) 1985; 13(3): 221-228.
21.Patel L, Clayton PE, Jenney ME et al. Adult height in patients with childhood onset atopic dermatitis. Arch Dis Child 1997 Joo; 76(6): 505-508.
22.Wales JKH, Milner RDG. Variation in lower leg growth with alternate day steroid treatment. Arch Dis Child 1988; 63 : 981-983.
23.Oberger E, Taranger J, Bruning B et al. Long-term treatment with corticosteroidsl ACTH in asthmatic children. IV. Skeletal maturation. Acta Paediatr Scand 1986; 75(5): 744-749.
24.Baum WF, Schneyer U, Lantzsch AM et al. Delay of growth and development in children with bronchial asthma, atopic dermatitis and allergic rhinitis. Exp Clin Endocrinol Diabetes 2002; Apr; 110(2) : 53-59.
25.Baum WF, Kloditz E, Theimarm HH. Atopic skeletal maturation as a possible cause for short stature and thoracic deformity in children with asthma. Kinderarzt Prax 1993 (Oct); 61(7-8): 285-290.(Ismail NF, Aly SM, Abdu MO, Kafash DN, K)
Abstract
Objective. The aim of this pilot study was to assess whether long standing asthma affects growth in prepubertal Egyptian children before initiation of long-term corticosteroid therapy. Methods. Children with asthma were divided into two groups according to asthma severity, moderate (n=24) and severe (n=14) and were compared for their physical and skeletal growth with a control group (n=15) using standard deviation score (SDS) and oneway ANOVA (analysis of variance) test. Results. No statistically significant differences were found between various growth parameters (weight, height, BMI, upper segment lower segment ratio, and skin fold thickness in asthmatic and normal children, although a positive correlation was found between the age at which the asthma presented and the height in all asthmatic children, r= 0.288, p= 0.036. The bone age standard deviation scores (SDS) were 0.97 mean, -0.165 and -0.572 for controls, moderate and severe asthmatics respectively (P<0.05), and significant inter group difference between the 2 asthmatic groups (moderate and severe) and the controls was found. Conclusion. The authors conclude that there was no significant major effect of asthma per se on growth parameters in children, but that skeletal maturation was influenced by long standing asthma.
Keywords: Asthma; Growth; Prepubertal children; Midparental height
Asthma is one of the few chronic diseases that are increasing in prevalence despite better understanding of its pathogenesis and improved treatment It is defined as "a chronic inflammatory disorder of the airways in which many cells. including mast cells and eosinophils play a role. which in genetically susceptible individuals. can cause symptoms associated with widespread variable airflow obstruction due to mucosal oedema. secretion of mucus. epithelial damage and bronchoconstriction that is often reversible either spontaneously or with treatment. and cause an associated increase in airway responsiveness to a variety of stimuli.[1]
Being one of the most common and most important illnesses during both the pediatric and adulthood periods it can retard growth in the former and disturb social well being and normal life style in both.[2]
Depending on history, physical examination, laboratory data, pulmonary function tests and the need for medication, patients can be classified as having mild, moderate or severe asthma.[3]
The growth process is complex. Linear growth occurs primarily as a result of chondrogenesis. Normally, there also occurs the synchronous process of osteogenesis; the formation of bone in cartilage. In some endocrine disorders, these two processes do not occur synchrono~ and a comparison of linear growth and bone development can give important clues.[4]
The aim of this study was to determine the effect of asthma on growth before puberty. The effect of asthma on linear growth is controversial as shown previously.[5] The process of studying growth is a complex one which becomes even more so in children suffering from a chronic illness, and receiving a variety of diets and medications due to the multiplicity of factors involved.[5] In case of severe bronchial asthma, the multiplicity of factors to be considered is immense. The degree of incapacitation the illness imposes on the child may logically be a factor influencing growth. In addition, the chronic asthmatic child will be subjected to dietary trials, which often eliminate important nutrients from his or her diet. There is also a question of heredity and atopy, and lastly, the problems of drug therapy especially glucocorticoids.[5]
Materials and Methods
The Asthma Group
Inclusion Criteria
Forty consecutive patients who were diagnosed with either moderate or severe asthma were were referred by their General Practitioners to the Pediatric department of El-Shatby Pediatric Hospital (SPH) which is a tertiary referral hospital and the governmental students' hospital (OSH) which is another city hospital in Alexandri, either in acute exacerbation or for follow up. The age range was between 4 and 13 years with a mean age of 7.71 years complaining from uncontrolled asthma for at least 2 years
Out of the 40 asthmatic children 38 were followed till the end of the study (25 males and 13 females) and two were lost because of failure to maintain the follow up visits till the end of the study i.e. for 9 months.
Exclusion criteria
Children who were on any form of long term steroid therapy at any point of time, those who had asthma for less than 2 years period or those who were suffering from any other illness which might influence growth.
The control group. Fifteen age and sex-matched healthy children with a mean age of 7.1 years (10 males and 5 females) served as a control group. Other factors taken into consideration in matching the control group with asthmatics were the residence, which was comparable in all the studied children, and the mid-parental height both are indicators of the economic' and the genetic background respectively. The control group was recruited from the children attending the outpatient clinic after being treated from minor ailments e.g. upper respiratory tract infection. The study protocol was subject to Ethics committee approval at the study centre before commencement.
All the studied children were subjected to detailed history taking for asthma in asthmatics together with clinical examination including anthropometrical measurements; weight, height using a standard physician's weight scale and height scale with stadiometer, triceps, subscapular and abdominal skin fold thickness (SFT) using Harpenden skin fold calliper, ,upper segment lower segment ratio (US/LS) and body mass index (BMI)[6] at the initial visit and after 3 months and at the end of follow up after 9 months, as well as assessment of asthma severity using a score sheet and a prepared questionnaire.[7],[8]
In terms of asthma severity, fourteen patients out of the 38 were described as severe asthmatics, while 24 as moderate asthmatics. Categorisation of asthma was based on the frequency, severity and chronicity of symptoms and consequently the medications received, and lastly the requirement for hospitalisation in the previous episodes as well as the presenting one.[7],[8]
All children were assessed for eligibility at admission to the emergency/outpatient unit. Patients were eligible if they were between the ages, of 4 and 13 vears and had a known history of asthma (defined as at least 1 previous episode of wheezing or a history of chronic cough that required treatment with bronchodilators or anti-inflammatory agents). Only children with moderate to severe asthma. (defined as requiring inhaled Ih-agonists a minimum of every 2 hours having a forced expiratory volume in 1 second [FEV1] of 25%-80% of the predicted volume, or having a clinical asthma score of 3-9[9] on admission, or uncontrolled asthma based on past history and a score sheet[7],[8] were recruited.
Analysing the difference between the studied groups regarding the anthropometries was through comparing the % change in each parameter at the end of the follow up period using t-test and one-way ANOV A between groups followed by pair-wise comparison using unpaired t-test.[10] The chi-square test was used to compare between height SDS of all children.[10]
Bone age assessment was also done through a plain x-ray of the left hand and wrist using the Tanner-White house technique.[11],[12],[13] In addition, plain x-ray chest postero-anterior view to exclude other pathological conditions that can simulate asthma clinically,[3] tuberculin test (Manteaux test) to exclude active T.B.[3] d peak expiratory flow rate (PEFR) was measured in each patient every 3 weeks due to lack of facilities to provide every child with an individual peak flow meter. Patients were followed up for the asthma nearly every 3 weeks and were managed according to their response to the treatment received.
Results
Clinical response regarding control of asthma improved in most patients during the first few months of treatment and follow up.
Anthropometric measurements
[Table - 1] demonstrates some demographic and clinical characteristics of the 3 studied groups; controls, moderate and severe asthmatics, where the groups were matched in all the variables.
When comparing the percent changes in all growth parameters from basal to final recordings among the 3 studied groups, it was found that the differences were not statistically significant [Table - 2].
[Figure - 1] compares the mean weights of the three studied groups at the beginning (basal) and at the end of the study (final), where the differences were not statistically significant, P > 0.05.
Using the height standard deviation score (HT SDS) in studying linear growth delineated that the mean basal and final Ht SDS were not significantly different among the 3 studied groups, P> 0.05 [Figure - 2].
There was a positive correlation between the age at which the disease presented and basal height of both moderate and severe asthmatics, r=0.288 and P=0.036 [Figure - 3].
[Figure - 4] shows a positive correlation between the MPH and the mean basal height of all the studied children (patients and controls), with a correlation coefficient r= 0.232.
Bone age. The mean (SDS) bone age was significantly different in the three groups.
Mean values were 0.971, -0.165 and -0.573 for controls, moderate and severe asthmatics respectively, P< 0.001
Significant differences were found between each of the two asthmatic groups (moderate and severe) and the normal childran, where P value was < 0.001 and 0.001 for both whereas the moderate and severe asthmatics did not differ significantly in terms of their skeletal maturation P>0.05 [Table - 3].
[Figure - 5]. shows the difference between the mean bone age SDS in the three groups, where the severe asthmatics had the lowest mean value. The mean bone age SDS for controls, moderate and severe asthmatics was 0.970, -0.165 and -0.572 respectively. P< 0.05.
Lastly, mean bone age was not significantly different in those with a positive family history of allergy (-0.325) compared to those without family history (-0.302). P>0.05.
Discussion
0In this study, the asthma state did not influence the children's growth. These results coincide with those of previous studies[14],[15] about bronchial asthma as a cause for concern about growth.
Height in normal individuals is a strongly genetically determined characteristic.[16] In addition to taking it into consideration in matching the control group with asthmatics, the MPH, gives an indicators of the economic and the genetic background respectively.
This means that the measured parental height can give good indication of the target height to which a child is aiming, and whether the asthmatic children followed their genetic potential for growth or not.
As regards the, BMI among asthmatics and control children, the differences were not statistically significant. The same findings were reported in a previous study done by Kaplan et al[17], which showed no difference between the general population and the cohort with asthma.
In one study carried out in the UK to investigate the height, weight and BMI of children with asthma in the community found no difference from the general population apart from children who were receiving high dose inhaled corticosteroids (ICS), where they appeared to be shorter than their contemporaries and deserved long-term follow-up.[15]
In a long-term prospective study from Australia,[18] children with severe asthma were found to attain normal height. This observation was confirmed in several subsequent studies.[19],[20] Indeed one report suggested that children with mild asthma grew to a marginally greater final height than non-asthmatics,[20] and even with more severe disease, children who were treated with 300-600 mg BDP/day for more than one year attained normal final height.
In the present study, a strong positive correlation was found between the age of onset of the disease and the basal Ht SDS of all children with asthma, which indicate that the earlier the disease onset, the more likely the child will be shorter.
These results are in keeping with those of another study done to assess the growth of a group of asthmatics in relation to the age of onset of asthma, in which the weight and height were predominantly in the 50th percentile or below in 68.4% of children in which the disease started before 2 years of age.[21]
Nevertheless, as suggested by other researchers,[22] if growth impairment occurs in childhood, it is likely to be temporary and reversible.
The skeletal maturation of the studied children in this work showed significant delay in both moderate and severe asthmatics when compared to the normal group, a finding that might be expected in the context of the chronic inflammatory state present in asthmatics. These fmdings are in keeping with other studies where delay in skeletal maturation was observed in severe asthmatics before and after treatment with steroids. Before treatment, skeletal maturity was below the reference mean in the majority of children.[23],[24] However, after control of disease activity and with effective treatment regimens, the effect on skeletal maturation was not found to be pronounced and did not affect the ultimate growth outcome.
In the context of the previously reported association of short stature and skeletal retardation in children with bronchial asthma or atopic dermatitis,[25] in the present study, the relation between family history of allergy and bone age was studied, however, the difference between skeletal maturation of atopic and non-atopic children was not significant. A study done by Baum et al[25] showed that 11.6% of atopic asthmatic children had a skeletal retardation of more than 2 years. It was concluded that skeletal delay could be regarded as a direct consequence of the atopic state of the individual.
In conclusion, this study showed no significant major effect of asthma on physical growth, apart from skeletal maturation, which was found to be significantly retarded in asthmatics compared to normal children.
References
1.Global Initiative for Asthma, National Heart, Lung and Blood Institute. Global Strategy for Asthma Management and Prevention. Bethesda, Md: Global Initiative for Asthma, National Heart, Lung and Blood Institute; 2004.
2.Davies RJ, Abdelziz MM. New insights into the understanding of asthma. Chest 1997; 2 : 1-11
3.Sly RM. In Nelson WE, Behrman RE, Kleigman RM et al., eds. Nelson Text book of Paedietrics. 16th edn. Philadelphia,. Pennsylvania WB Saunders, Company. 2000.
4.Aynsly-Green A. Growth. In S. Godfrey and JD Baum, eds. Clinical Pediatric Physiology. Oxford; Blackwell Scientific Publication 1979; 434-468.
5.Falliers CJ, Szentivanyi, Mc Bride M et al. Growth rate of children with intractable asthma. J Allergy 1961; 32(5) 421-435.
6.Gennuso J, Epstein LH, Paluch RA et al. The relationship between asthma and obesity in urban minority children and adolescents. Arch Paediatr ado lese Med 1998; 152: 1197-1200.
7.Tal A, Bavilski C, Yohai D. Dexamethasone and salbutamol in the treatment of acut~ wheezing in infants. Plediatr 1983; 71: 13-18.
8.Ferguson AC, Murray AB, Wah-Jun T. Short stature and delayed skeletal maturation iJ1 children with allergic diseases. J Allergy Clin lmmunol 1982; 69 : 461-466.
9.Parkin PC, Macarthur C, Saunders NR et al. Development of a clinical asthma score for use in hospitalized children between 1 and 5 years of age. J Clin EPidemii 1996; 49 : 821-825.
10.Saunders BD, Trapp RG. Basic and clinical statistics. USA; Prentice, Hall, International Incorporation; 1990.
11.Roche AF, Davila GH, Leyman SL. A comparison between Greulich-Pyle and Tanner Whitehouse assessment of skeletal maturity. Radiology 1971; 98 : 273-280.
12.Tanner JM, Whitehouse RH. Atlas of children's growth: normal variation and growth disorders. Londonj Academic Press (1982).
13.Handmarsh PC and Brook CGD. Normal Growth and its Endocrine Control. In CGD Brook, ed. Clinical Paediatric Endocrinology 3rd edition. London: Blackwell Science. 1995; 85-106.
14.Neville RG, Mc Cowan, Thomas G et al. Asthma and growth- cause for concern Asthma and growth in Tayside children. Ann Hum Biol 1996; 23(4) : 323-33l.
15.Klein GL, Dunghy CI, Golant SP. Growth and the nutritional status of non-steroid dependent asthmatic children. Ann Allergy 1991; 67(1): 80-84.
16.Hawk W, Brook CGD. Family resemblance of height, weight and body fatness. Arch Dis Child 1979; 54 : 877-879.
17.Kaplan BA, Brush G, Mascie-Taylor CGN. The relationship of childhood asthma and wheezy bronchitis with weight,. height and body mass index. Human Biology 1987; 59(6): 921-931.
18.Martin AJ, mc Lenan LA, Landan LI et al. The natural history of childhood asthma to adult life. BMJ 1980; 280: 1397-1400.
19.Shobat M, Shobat T, Kedem R et al. Childhood asthma and growth outcome. Arch Dis Child 1987; 62 : 63-65.
20.Grumach AC, Carneiro-Sampaio MM, Lima JL et al. The growth curve in asthmatic children. Allerg Immunopathol(Madr) 1985; 13(3): 221-228.
21.Patel L, Clayton PE, Jenney ME et al. Adult height in patients with childhood onset atopic dermatitis. Arch Dis Child 1997 Joo; 76(6): 505-508.
22.Wales JKH, Milner RDG. Variation in lower leg growth with alternate day steroid treatment. Arch Dis Child 1988; 63 : 981-983.
23.Oberger E, Taranger J, Bruning B et al. Long-term treatment with corticosteroidsl ACTH in asthmatic children. IV. Skeletal maturation. Acta Paediatr Scand 1986; 75(5): 744-749.
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