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Hgh steroid for height

Therefore, simply utilizing HGH to help adults grow taller after the age of 18 is not going to work in most cases. The only candidates for HGH past the age of 18 are adults that have growth plates that are not yet closed. There are some people that will fit this scenario and a simple x-ray can be taken that will display whether or not growth plates are open allowing for the use of HGH.

Per medical restrictions, in order to receive a HGH prescription the patient needs to be formally diagnosed with both GHD and height deficiency beforehand. This health care practitioner performs one or more stem cell therapies that have not yet been approved by the United States Food and Drug Administration. You are encouraged to consult with your primary care physician prior to undergoing a stem cell therapy. Toggle navigation. The benefit obtained seems dose dependent and benefits of 7.

The topic has remained controversial. The objective was to conduct a retrospective analysis of our experience with children with ISS treated with 0. Eighty eight of our children 68 males and 20 females attained an adult height or near adult height of In the analysis of the subgroups, the adult height and adult height gain of children with non-familial short stature were significantly higher than of familial short stature.

No difference was found in the cohorts with normal or delayed puberty in any of the subgroups, except between the non-familial short stature and familial short stature puberty cohorts. This has implications for the interpretation of the benefit of treatment in studies where the number of children with familial short stature in the controls or treated subjects is not known.

The treatment was safe. There were no significant adverse events. The IGF-1 values were essentially within the levels expected for the stages of puberty. Our experience was quite positive with normalization of the heights and growth of the children during childhood and the attainment of normal adult heights, the main two aims of treatment. Children with idiopathic short stature ISS do not attain a normal adult height.

In the three randomized controlled studies Cochran Central Register Control Trials , the adult height of the controls was In an additional 6 non-randomized controlled studies the adult height of the controls ranged between Growth hormone treatment significantly improves the growth velocity and the adult height of children with ISS [ 10 - 13 ] and is considered safe [ 14 - 16 ]. Nevertheless, the use of growth hormone has remained controversial [ 17 - 19 ], mainly because of the modest benefit [ 20 , 21 ] and high cost [ 22 , 23 ].

The impression is that despite the significant gain in height, growth hormone treated children remain short as adults, in the lower level of the normal range; an improvement in adult height after years of treatment in the order of 4 cm and a benefit that is less than in other conditions for which GH has been licensed [ 20 , 21 ]. Many of the studies, however, used GH doses of 0. Furthermore, some of the studies included children with intrauterine growth retardation or with familial short stature, which may have affected the results.

The benefit obtained seems dose dependent and mean benefits of 7. There have been also ethical issues raised [ 25 ] and considerations expressed as to whether ISS should be considered a disease, whether the degree of psychosocial morbidity warrants treatment [ 26 - 28 ], whether it is enhancement or endo-cosmetology rather than treatment [ 29 ], and whether treatment has any effect in health related quality of life [ 30 - 32 ]. As the name idiopathic indicates, the cause is unknown.

A variety of genes affecting growth, of genes along the growth hormone IGF-I axis [ 33 - 38 ], polygenic traits determined by polymorphisms [ 39 ], heterozygous GHR mutations, a dominant negative mutation of the GHR causing familial short stature [ 40 ] and mutations in other genes have now been demonstrated in children previously classified as ISS [ 41 - 43 ].

So the label of normal short children may not be appropriate. All these concerns have been extensively discussed in a number of publications [ 44 ] and taken in consideration in the Consensus of the International Pediatric Endocrine Societies [ 45 ]. The interest of the child is the primary concern. The main goal of the treatment is the normalization of the height during childhood and improvement of the adult height.

Children with a height of less than -2 SDS [ 45 ] or a height of more than 2 SDS below their midparental target height, warrant consideration for treatment. Idiopathic short stature describes a heterogeneous group of children of unknown etiology with variable response to growth hormone [ 46 ].

It is defined as short children with a height below -2 SD 2. Ritalin [ 45 , 47 ]. Specifically, the children with ISS have normal birth weight, and no growth hormone deficiency [ 45 ]. The criteria do not include midparental height MPH. Thus, studies of idiopathic short stature have included two groups of children: those affected with nonfamilial short stature NFSS and those with familial short stature FSS , who may be different in their response to treatment, adult heights, and attainment of MPH.

Children with FSS, without treatment, may attain an adult height near or equal to midparental height, but shorter than the normal population [ 48 , 49 ]. It is possible, also, that the modest or small benefit obtained by growth hormone treatment in a number of studies was because many of the children were affected with familial short stature.

After the Consensus on the definition of idiopathic short stature in [ 50 ], ISS also includes what previously was known as constitutional delay of growth and puberty CDGP. A number of studies have indicated that the adult height attained in children with CDGP, with heights below -2 SDS, is less than the MPH and that they remain somewhat shorter than normal [ 51 , 52 ], some with average heights in the 10 th percentile [ 53 ] or 5 th percentile [ 54 , 55 ].

As the result of the aforementioned, there is consideration of the need to subcategorize the children into different groups: NFSS and FSS and in both, normal puberty and delayed puberty [ 45 , 56 ]. We conducted a retrospective analysis of our experience with children with ISS treated with rhGH, with the aim of comparing the different subgroups and assessing the benefit by comparison with historical controls.

The study was approved by the Institutional Review Board of the Hospital and consent and assent approvals were obtained. Of the children with idiopathic short stature treated with rhGH 0. The groups were further divided into those with normal puberty and delayed puberty. The duration of treatment was 5. All the children met the criteria for ISS with the height below The age at start of treatment ranged between 4. The children were seen every 3 months and the rhGH dose was adjusted at each visit.

With the normal weight gain the dose would decrease to 0. The dose ranged from 0. The dose was not increased for puberty. An MRI of the brain was obtained at the time of the growth hormone stimulation testing on many of them in the past. This is no longer felt needed. Karyotypes were obtained in many.

Bone age was determined by Greulich and Pyle standards and adult height predicted by Bayley-Pinneau tables. Heights were measured by a wall-mounted stadiometer. The heights at the onset of treatment were expressed as SDS for chronologic age. The height SDS was calculated in the usual manner: height of the subject in cm minus the mean height for age or adults divided by the SD in cm from the mean.

The last bone age available in our records was To obtain final adult heights, the potential remaining growth of some children whose heights were obtained before closure of the epiphyses near adult height was calculated. These numbers for calculated final adult heights were not included in the numbers reported and it will be addressed later Additional file 1 : Table S1.

Pubertal development was assessed by the method of Tanner. Males with testicular volume of less than 4. Children whose heights were below the midparental height SDS target range of Children whose fathers or mothers were below The classification of delayed onset of puberty includes the previously used definition of constitutional delay of growth and puberty CDGP in accordance with the international consensus [ 45 ].

No addition for secular trend was needed, since there was no or minimal increase in secular trend in the United States National Health Statistics between and All had a good response to rhGH treatment. An analysis of intent to treat to adult height was conducted. Growth hormone secretion was evaluated by hours overnight frequent sampling on a number of the children in the s; we no longer do that. This method was not available early in the study and a number of the determinations were made as Somadomedin C.

Paired and unpaired, two-tailed Student T test was used to compare the means of the different groups. A p value of 0. Correlations to assess the factors influencing AHs young age, delayed bone age, distance to MPH, etc. A few growth charts in Figure 1 illustrate what we observed in many children: a catch up growth for the first 3 or more years of treatment to a level expected for the midparental height, a subsequent normal growth, the growth spurt with puberty and the attainment of a normal adult height.

Growth charts of 3 individual males showing the response to GH treatment. Growth charts: A. Height SDSs of all subjects, males and females, before and after treatment. All ISS males and females, B. All ISS males, and C. All ISS females. All of them attained a height within 2 SD except two children with familial short stature, The average height of the 88 children was The adult height gain was 1.

The 20 females attained an adult height of The adult height gain was 2. The only difference between the males and the females was in the MPH of The mean adult height of Also for the females the mean adult height of The results obtained are shown in Table 2 , applicable statistics in Table 3 and illustrations or graphs in Figure 2. The mean adult height attained by the 47 males was The latter statistically different, but it would appear to be of no clinical significance 2.

The adult height of the 20 children with normal puberty, In the 27 children with delayed puberty the adult height of In the 16 female children with NFSS, the adult height was The adult height gain for the 47 males with NFSS was 2. The results obtained in the 21 males and 4 females with FSS are shown in Table 2 , applicable statistics in Table 3 and illustrations in Figure 2. The adult height attained by the 21 males was The number of females with FSS was only 4 and the values may not accurately represent the values of a larger group.

The adult height was The values are in Table 2 , statistics in Table 4 and illustrations in Figure 2. The adult height of The adult height gain for the 47 NFSS was 2. Similar results were obtained when the males and females were grouped, Table 4. There was no difference in the baseline heights, The adult height gain indicates the response to treatment and ranged from 0.

Of interest, however, was that the response to treatment was less in FSS 0. For the females the number with FSS is small, 4, the result are probably not an accurate reflection of the group and statistics could be doubtful false results. Nevertheless, comparisons with the 16 females with NFSS were made.

We definitely observed the variability in response. AH was For the 68 males non-familial and familial short stature , the AH gain was 1. The AH was The comparison of the values for different measures obtained for all the children with normal puberty and delayed puberty, males 68 and 20 females, in all the subgroups, NFSS and FSS, males and females are shown in Table 2.

In the study of Rekers-Mombarg, et al. The gain in SDS from childhood height to adult height adult height gain varied from 0. It became of interest to know if the changes that we observed in adult height and adult height gain of our treated subjects were somewhat related to age and not to treatment, even though we did not see differences in our children with normal puberty usually younger and those with delayed puberty usually older. There was a significant difference in the age of children with NFSS with normal puberty 8.

Similarly, there was a significant difference in the age of children with FSS with normal puberty The gain in height is very variable for individuals and averages are not accurate or useful to predict the benefit that an individual will obtain. The gain in height depends on the pubertal growth, benefit of growth hormone, and bone age.

In the aforementioned case, Table 5 , depending on the age, bone age, progress of bone age, pubertal growth, and growth hormone response, the gain in height could range from 1. The only way that we could inform the subjects of the benefit that he or she could obtain, is the way that we do it now.

Based on the height and the bone age, the predicted adult height is obtained. The subject can be informed that based on our experience, growth hormone should be of benefit to him or her, to improve the adult height. The benefit could be 5 cm, 7.

Then the provider and the subject decide whether treatment is continued to attain the maximum height or ended when he or she is satisfied with the height. Children were observed for a period of time prior to treatment, so that their growth rates could be assessed. In a retrospective review we could know the children who were lost to follow up and, consequently, analyze their growth rates prior to and during treatment.

Growth rates determined for less than 6 months were not included. Thus, there was no bias on the reported effect of GH on children treated to adult height. Complaints of myalgia or arthralgia of the legs early in the treatment, which promptly subsided without adjustment of the GH dose, were very rare. Two of the children had a low serum TSH and free T 4 subclinical hypothyroidism and were treated with levothyroxine, which was discontinued after cessation of treatment.

Concerns have been raised on the possibility of side effects in the future from high levels of IGF-1 because of its mitogenic effect [ 16 , 59 ]. Therefore, it became of interest to know the levels of IGF-1 with treatment. The levels of IGF-1 prior to treatment, during treatment for different stages of puberty, and after treatment are illustrated in Figure 4 and Table 7. Except for a few, all the values were within the range expected for the pubertal stage.

Only 8. These values are less than those reported in patients with growth hormone deficiency treated with 0. Seventeen percent of the values were higher than 2 SD after 2 years of treatment [ 60 ]. Delbert A. Fisher; One of the limitations of our study is the lack of controls. Fortunately, there are, presently, a number of randomized and nonrandomized controlled studies that would permit assessment of the benefit, by comparisons of the adult height attained and AH gain in our treated children with those of historical untreated controls.

The adult height and adult height gain AH minus Baseline height are measurements that the investigators obtain and should be more accurate than comparisons based on attainments of PAH or MPH see later. MPH was not used to calculate benefit of treatment. The adult height gain corrects for baseline differences in the different studies in treated subjects and controls, provides information on the benefit of treatment, and permits comparison of groups not matched for baseline heights.

The comparison of adult heights provides also information on the benefit, and when the baselines heights are not different or the AHs are corrected for baseline heights differences, yields the same results as the adult height gain. The reports on SDS permit comparisons of different populations and calculation of the benefit in centimeters based on the centimeters for SD of adults in a particular population.

In this presentation we used 6. The benefit in centimeters would be different in different populations depending on the centimeters for SD of adults. Adult height and adult height gain of treated children in our study versus published untreated controls. Adult height of controls of published studies versus adult height of treated children in our study.

The numbers for the different studies for the baseline, adult height and adult height gain of controls and our treated subjects are in Table 8. Adult height gain of controls of published studies versus adult height gain of treated children in our study. The benefit from treatment for the adult height for our children The analysis of the adult height gain, Table 8 , showed somewhat similar results. The average baseline height of the 9 published studies, Table 8 , was In the study of Rekers-Mombarg et al.

The adult height of our 47 treated NFSS boys of Actually, the adult height of our 47 NFSS boys of This benefit of 8. Comparisons of our results with published Adult Heights of controls and treated children. Table 9 shows the benefit of different doses of growth hormone on the adult height.

In published studies the benefit obtained in adult height was usually less than 4 cm over controls with doses of less than 0. And it was more than 5 cm 6. In our study, the benefit with a dose of 0. The benefit in adult height gain that corrects for differences in baseline heights of our treated children were higher than the adult height gain of the controls in the published studies by 1.

Of interest is that the results in the only two studies that have been published are similar, Table This was also the conclusion of Dahlgren J [ 12 ] in his analysis of these 2 studies. This observation seems to be consistent in the three different studies and has implications for interpretation of results with treatment, in studies where the number of children with FSS in the controls and treated subjects is not known, and in the selection of controls for non-randomized or randomized studies.

The reported impression, by review of published studies, is that the benefit of treatment of children with ISS is less than in other conditions for which GH has been licensed [ 20 , 21 , 61 ]. Our results compare well with those obtained in GH treated children in other conditions for which GH has been approved, growth hormone deficiency GHD , small for gestational age SGA , or Turner syndrome. The adult height of our 88 children with ISS of In a review of four randomized controlled trials RCTs comprising children with SGA treated with growth hormone range of 0.

There was no difference between the 2 dose regimens. The adult height gain in our study exceeded controls by 1. Our results of an increase of 7. In 61 patients with Turner syndrome [ 64 ], treated with 0.

Despite this increase, the adult height of treated patient with Turner syndrome was still outside the normal range. Our experience with the growth hormone treatment of children with ISS was a positive one, with the normalization of the height and growth during childhood and adolescence after 2 or 3 years of treatment and the attainment of a normal adult height of There were no significant adverse effects.

All the parents of the children and the children in our study who attained adult heights were pleased with the results, happy for their children to be normal and grateful for the treatment. The most consistent perception of the parents of the benefit was the improvement of self-esteem in their children, and of the children to be happy to be normal and not different. Other benefits perceived were cessation of teasing, bullying and psychological stress.

The reason for the children lost to follow-up, all growing well and benefiting from treatment, is not known. One can speculate that some were content to be within normal range in height, some may have had difficulty with copays, may have moved, did not care to have more injections, even though all reported that the injections were not painful, and so on.

The benefit obtained in our study seems to be better than that reported in a number of previous studies and there must be some reason. Care was taken in the selection of children to be certain they met qualifications, in the measurements, in the analysis of data and compilation of results. By our observations, there may be two possible reasons, among others; namely the dose of growth hormone used dose dependent effect , and the effect of including an unknown number of children with FSS in the group in previous studies.

Our observations in 88 children clearly show a significant benefit of GH treatment 0. The benefit in the adult height of our treated subjects over the adult height of published historical controls was 9. This benefit is higher by 5 or 6 cm than the benefit obtained in subjects treated with 0. The benefit was only 1. This dose dependent effect has been reported previously in studies using 0. A dose effect for children with ISS was shown by Wit et al.

Also in a randomized controlled study by McCaughey et al. In view of the aforementioned, it is possible that the stated modest benefit of 4 cm with the treatment of ISS is related to the low dose of GH used and to averaging the results without taking in consideration the difference in the benefit from different doses. In the meta-analysis conducted by Finkelstein et al. The reported benefit of treatment over controls, on the average was 5.

Two of the studies used dosages of GH of 0. In the review of Guyda H et al. Seven of the studies used doses of GH ranging from 0. The difference of the adult height range from In three of the studies using 0. So the difference of adult height from As a consequence of the averaging, the improved benefit obtained, in SDS or cm, with the higher doses of GH is not reflected in the reports, as is illustrated in Table 9 , averaging results of published studies with no benefit By our results, the adult height and adult height gain were significantly higher by 0.

This seems to be a consistent finding in different studies and has implications for the interpretation of the results observed in published studies. The inclusion of a high number of children with FSS in the treated cohort will yield lower results. And also, it has implications for the selection of controls in randomized or non-randomized controlled studies, since the number of children with FSS in the treated or control groups may affect the results.

It is difficult to assess how this has affected the results of previous studies, since most or practically all of the published studies included all the children as ISS and did not mention whether they were NFSS or FSS. The assessment of the benefit from treatment with GH is sometimes difficult, even in controlled studies, because the proportion of children with FSS and NFSS, normal and delayed puberty, and at times IUGR, may not be the same in the treated and control groups.

As previously mentioned, to assess the benefit of treatment, comparison of the AH gain adult height minus the baseline height and the AH attained of the treated and control groups would seem to be the best method, because they are based on measurements by the investigator. Also useful would be the comparison between the groups on the attainment of target height. Target heights, however, are often based on self-reported parental heights.

In addition, children with FSS may attain heights near or equal to the MPH without treatment, so the inclusion of a different number of children with FSS in the group may influence the attainment of MPH and render the interpretation as benefit of treatment inaccurate.

Furthermore, there are a number of reported methods to calculate MPH [ 47 ], which may give different results for the benefit when comparing AHs and MPHs. It would also be difficult to compare the benefit of different studies using different methods for calculating MPH. Commonly used methods tend to over-predict AH, especially in young males and in children with delayed bone age, and under-predict if the bone age is not delayed [ 69 ].

Also, the individual variability of the tempo of progression of the bone age, either faster or slower than usually expected, as illustrated in Figure 1 , affects the accuracy of the PAH.

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The results obtained are shown in Table 2 , applicable statistics in Table 3 and illustrations or graphs in Figure 2. The mean adult height attained by the 47 males was The latter statistically different, but it would appear to be of no clinical significance 2. The adult height of the 20 children with normal puberty, In the 27 children with delayed puberty the adult height of In the 16 female children with NFSS, the adult height was The adult height gain for the 47 males with NFSS was 2.

The results obtained in the 21 males and 4 females with FSS are shown in Table 2 , applicable statistics in Table 3 and illustrations in Figure 2. The adult height attained by the 21 males was The number of females with FSS was only 4 and the values may not accurately represent the values of a larger group.

The adult height was The values are in Table 2 , statistics in Table 4 and illustrations in Figure 2. The adult height of The adult height gain for the 47 NFSS was 2. Similar results were obtained when the males and females were grouped, Table 4. There was no difference in the baseline heights, The adult height gain indicates the response to treatment and ranged from 0.

Of interest, however, was that the response to treatment was less in FSS 0. For the females the number with FSS is small, 4, the result are probably not an accurate reflection of the group and statistics could be doubtful false results. Nevertheless, comparisons with the 16 females with NFSS were made. We definitely observed the variability in response. AH was For the 68 males non-familial and familial short stature , the AH gain was 1.

The AH was The comparison of the values for different measures obtained for all the children with normal puberty and delayed puberty, males 68 and 20 females, in all the subgroups, NFSS and FSS, males and females are shown in Table 2. In the study of Rekers-Mombarg, et al. The gain in SDS from childhood height to adult height adult height gain varied from 0. It became of interest to know if the changes that we observed in adult height and adult height gain of our treated subjects were somewhat related to age and not to treatment, even though we did not see differences in our children with normal puberty usually younger and those with delayed puberty usually older.

There was a significant difference in the age of children with NFSS with normal puberty 8. Similarly, there was a significant difference in the age of children with FSS with normal puberty The gain in height is very variable for individuals and averages are not accurate or useful to predict the benefit that an individual will obtain.

The gain in height depends on the pubertal growth, benefit of growth hormone, and bone age. In the aforementioned case, Table 5 , depending on the age, bone age, progress of bone age, pubertal growth, and growth hormone response, the gain in height could range from 1.

The only way that we could inform the subjects of the benefit that he or she could obtain, is the way that we do it now. Based on the height and the bone age, the predicted adult height is obtained. The subject can be informed that based on our experience, growth hormone should be of benefit to him or her, to improve the adult height. The benefit could be 5 cm, 7. Then the provider and the subject decide whether treatment is continued to attain the maximum height or ended when he or she is satisfied with the height.

Children were observed for a period of time prior to treatment, so that their growth rates could be assessed. In a retrospective review we could know the children who were lost to follow up and, consequently, analyze their growth rates prior to and during treatment. Growth rates determined for less than 6 months were not included. Thus, there was no bias on the reported effect of GH on children treated to adult height. Complaints of myalgia or arthralgia of the legs early in the treatment, which promptly subsided without adjustment of the GH dose, were very rare.

Two of the children had a low serum TSH and free T 4 subclinical hypothyroidism and were treated with levothyroxine, which was discontinued after cessation of treatment. Concerns have been raised on the possibility of side effects in the future from high levels of IGF-1 because of its mitogenic effect [ 16 , 59 ].

Therefore, it became of interest to know the levels of IGF-1 with treatment. The levels of IGF-1 prior to treatment, during treatment for different stages of puberty, and after treatment are illustrated in Figure 4 and Table 7. Except for a few, all the values were within the range expected for the pubertal stage.

Only 8. These values are less than those reported in patients with growth hormone deficiency treated with 0. Seventeen percent of the values were higher than 2 SD after 2 years of treatment [ 60 ]. Delbert A. Fisher; One of the limitations of our study is the lack of controls. Fortunately, there are, presently, a number of randomized and nonrandomized controlled studies that would permit assessment of the benefit, by comparisons of the adult height attained and AH gain in our treated children with those of historical untreated controls.

The adult height and adult height gain AH minus Baseline height are measurements that the investigators obtain and should be more accurate than comparisons based on attainments of PAH or MPH see later. MPH was not used to calculate benefit of treatment.

The adult height gain corrects for baseline differences in the different studies in treated subjects and controls, provides information on the benefit of treatment, and permits comparison of groups not matched for baseline heights. The comparison of adult heights provides also information on the benefit, and when the baselines heights are not different or the AHs are corrected for baseline heights differences, yields the same results as the adult height gain. The reports on SDS permit comparisons of different populations and calculation of the benefit in centimeters based on the centimeters for SD of adults in a particular population.

In this presentation we used 6. The benefit in centimeters would be different in different populations depending on the centimeters for SD of adults. Adult height and adult height gain of treated children in our study versus published untreated controls.

Adult height of controls of published studies versus adult height of treated children in our study. The numbers for the different studies for the baseline, adult height and adult height gain of controls and our treated subjects are in Table 8. Adult height gain of controls of published studies versus adult height gain of treated children in our study. The benefit from treatment for the adult height for our children The analysis of the adult height gain, Table 8 , showed somewhat similar results.

The average baseline height of the 9 published studies, Table 8 , was In the study of Rekers-Mombarg et al. The adult height of our 47 treated NFSS boys of Actually, the adult height of our 47 NFSS boys of This benefit of 8. Comparisons of our results with published Adult Heights of controls and treated children. Table 9 shows the benefit of different doses of growth hormone on the adult height. In published studies the benefit obtained in adult height was usually less than 4 cm over controls with doses of less than 0.

And it was more than 5 cm 6. In our study, the benefit with a dose of 0. The benefit in adult height gain that corrects for differences in baseline heights of our treated children were higher than the adult height gain of the controls in the published studies by 1. Of interest is that the results in the only two studies that have been published are similar, Table This was also the conclusion of Dahlgren J [ 12 ] in his analysis of these 2 studies.

This observation seems to be consistent in the three different studies and has implications for interpretation of results with treatment, in studies where the number of children with FSS in the controls and treated subjects is not known, and in the selection of controls for non-randomized or randomized studies. The reported impression, by review of published studies, is that the benefit of treatment of children with ISS is less than in other conditions for which GH has been licensed [ 20 , 21 , 61 ].

Our results compare well with those obtained in GH treated children in other conditions for which GH has been approved, growth hormone deficiency GHD , small for gestational age SGA , or Turner syndrome. The adult height of our 88 children with ISS of In a review of four randomized controlled trials RCTs comprising children with SGA treated with growth hormone range of 0. There was no difference between the 2 dose regimens.

The adult height gain in our study exceeded controls by 1. Our results of an increase of 7. In 61 patients with Turner syndrome [ 64 ], treated with 0. Despite this increase, the adult height of treated patient with Turner syndrome was still outside the normal range. Our experience with the growth hormone treatment of children with ISS was a positive one, with the normalization of the height and growth during childhood and adolescence after 2 or 3 years of treatment and the attainment of a normal adult height of There were no significant adverse effects.

All the parents of the children and the children in our study who attained adult heights were pleased with the results, happy for their children to be normal and grateful for the treatment. The most consistent perception of the parents of the benefit was the improvement of self-esteem in their children, and of the children to be happy to be normal and not different.

Other benefits perceived were cessation of teasing, bullying and psychological stress. The reason for the children lost to follow-up, all growing well and benefiting from treatment, is not known. One can speculate that some were content to be within normal range in height, some may have had difficulty with copays, may have moved, did not care to have more injections, even though all reported that the injections were not painful, and so on.

The benefit obtained in our study seems to be better than that reported in a number of previous studies and there must be some reason. Care was taken in the selection of children to be certain they met qualifications, in the measurements, in the analysis of data and compilation of results.

By our observations, there may be two possible reasons, among others; namely the dose of growth hormone used dose dependent effect , and the effect of including an unknown number of children with FSS in the group in previous studies. Our observations in 88 children clearly show a significant benefit of GH treatment 0.

The benefit in the adult height of our treated subjects over the adult height of published historical controls was 9. This benefit is higher by 5 or 6 cm than the benefit obtained in subjects treated with 0.

The benefit was only 1. This dose dependent effect has been reported previously in studies using 0. A dose effect for children with ISS was shown by Wit et al. Also in a randomized controlled study by McCaughey et al. In view of the aforementioned, it is possible that the stated modest benefit of 4 cm with the treatment of ISS is related to the low dose of GH used and to averaging the results without taking in consideration the difference in the benefit from different doses.

In the meta-analysis conducted by Finkelstein et al. The reported benefit of treatment over controls, on the average was 5. Two of the studies used dosages of GH of 0. In the review of Guyda H et al. Seven of the studies used doses of GH ranging from 0. The difference of the adult height range from In three of the studies using 0. So the difference of adult height from As a consequence of the averaging, the improved benefit obtained, in SDS or cm, with the higher doses of GH is not reflected in the reports, as is illustrated in Table 9 , averaging results of published studies with no benefit By our results, the adult height and adult height gain were significantly higher by 0.

This seems to be a consistent finding in different studies and has implications for the interpretation of the results observed in published studies. The inclusion of a high number of children with FSS in the treated cohort will yield lower results. And also, it has implications for the selection of controls in randomized or non-randomized controlled studies, since the number of children with FSS in the treated or control groups may affect the results.

It is difficult to assess how this has affected the results of previous studies, since most or practically all of the published studies included all the children as ISS and did not mention whether they were NFSS or FSS. The assessment of the benefit from treatment with GH is sometimes difficult, even in controlled studies, because the proportion of children with FSS and NFSS, normal and delayed puberty, and at times IUGR, may not be the same in the treated and control groups.

As previously mentioned, to assess the benefit of treatment, comparison of the AH gain adult height minus the baseline height and the AH attained of the treated and control groups would seem to be the best method, because they are based on measurements by the investigator.

Also useful would be the comparison between the groups on the attainment of target height. Target heights, however, are often based on self-reported parental heights. In addition, children with FSS may attain heights near or equal to the MPH without treatment, so the inclusion of a different number of children with FSS in the group may influence the attainment of MPH and render the interpretation as benefit of treatment inaccurate.

Furthermore, there are a number of reported methods to calculate MPH [ 47 ], which may give different results for the benefit when comparing AHs and MPHs. It would also be difficult to compare the benefit of different studies using different methods for calculating MPH. Commonly used methods tend to over-predict AH, especially in young males and in children with delayed bone age, and under-predict if the bone age is not delayed [ 69 ].

Also, the individual variability of the tempo of progression of the bone age, either faster or slower than usually expected, as illustrated in Figure 1 , affects the accuracy of the PAH. Recent critical reviews [ 20 , 21 , 61 ] concluded that to date no study has fulfilled the criteria for high quality and strong recommendations, in part owing to the small number of children in the studies, and felt that additional high quality trials up to the achievement of adult height would be necessary to determine the efficacy, ideal dosage, long term safety of growth hormone therapy and to address health related quality of life and cost issues.

There is agreement with their recommendations. Even though rhGH has proven to be a remarkably safe medication for 27 years at the doses recommended, long surveillance studies have been suggested by many, because of the mitogenic effect of IGF Regarding the dose, there has been many and probably enough trials with a dose of less than 0. Doses higher than 0. Additional genetic studies may give useful information to explain the variability of response.

In the past 27 years, since rhGH became available in , there have been 3 or 4 randomized studies, up to the achievement of adult height, and, apparently, they did not provide the answers. It may take 8 or more years to get results from more randomized trials.

It is hoped that we do not wait for the answer; many children could benefit while we wait. One of the main problems that has been often addressed in the past is the significant cost, which limits the availability to children who may need it, raises questions about the use of health resources, and a number of ethical considerations [ 25 ].

One may question whether studies would seem applicable to solve the problem of cost; participation from the pharmaceutical industry would be required. The high cost of biopharmaceuticals is a problem concerning public health services around the world, is in the public domain a , and to reduce cost and increase affordable access to treatment may not be as simple as one may think [ 70 - 72 ].

This is based on the pharmacy bills given to the family for the purchase of GH b. This cost is applicable to any child treated with GH, whether it be growth hormone deficiency, Turner syndrome, intrauterine growth retardation or ISS. If the price was reasonable, many of the objections to treatment, concerns for use of heath resources, and ethical considerations would subside.

Cost influences pediatric endocrinologists in their decision to treat [ 75 ], and third party payers private insurances or health agencies, state or national in their decision to support treatment [ 74 ]. Also, if the price was reasonable, it, probably, would be the right thing to do to help the children to attain an adult height within the range judged to be normal by National Health Standards and by society.

It would not harm anybody. Children with ISS do not attain a normal adult height: adult heights of Growth hormone treatment significantly increases the adult height, but the benefit obtained with doses of less than 0. The benefit obtained seems dose dependent and a benefit of 7, 7. The treatment was quite helpful with normalization of the height and growth during childhood and attainment of normal adult heights.

Eighty eight 68 males, 20 females attained an adult height of Similar results were obtained in the only 2 studies previously reported. No difference was found in the cohorts with normal or delayed puberty in any of the subgroups, except between the NFSS and FSS subgroups.

This has implications for the interpretation of the benefit of treatment in studies where the number of children with FSS in the controls or treated subjects is not known. There have been, probably, enough trials with a dose of less than 0. Studies with doses from 0. Additional high quality studies have been suggested to determine the efficacy, ideal dosage, health related quality of life, long term safety of GH therapy, and cost.

There is agreement among investigators for these recommendations. In the past 27 years, since rhGH became available in , there have been 3 or 4 randomized studies to adult height, but, apparently, did not provide the answers. It is the hope that we do not wait for the answer; many children could benefit while we wait.

See The Economist Economist. JFS contributed to conception and design, treatment of subjects, acquisition, analysis and interpretation of data, drafting and final approval of the manuscript and agrees to be accountable for all aspects of the work. NJT contributed to testing, acquisition, analysis, and interpretation of data, drafting of the manuscript and final approval of the version to be published. The adult heights reported were adult or near adult heights.

There was a potential growth remaining of children whose heights were obtained before closure of the epiphyses near adult height and before growth ended. Based on the last bone age available on the record, the predicted adult height was calculated i.

The effect on the average adult height of the group is shown. This potential growth remaining was not included in the figures reported for adult heights, but could be taken into consideration to determine final adult height and the benefit of growth hormone treatment. Genentech was kind enough to provide us with the correlation they obtained in their laboratory of GH samples assayed by both methods. All ISS males, B.

NFSS males, C. FSS males, D. The results of the individual heights prior to treatment and AHs are plotted at the respective ages after treatment and the MPHs are plotted to the right: A. ISS males, B. ISS females. National Center for Biotechnology Information , U. Int J Pediatr Endocrinol. Published online Jul Author information Article notes Copyright and License information Disclaimer. Corresponding author. Juan F Sotos: gro. Received Jan 30; Accepted Jun This article has been cited by other articles in PMC.

Objective The objective was to conduct a retrospective analysis of our experience with children with ISS treated with 0. Results Eighty eight of our children 68 males and 20 females attained an adult height or near adult height of Conclusion Our experience was quite positive with normalization of the heights and growth of the children during childhood and the attainment of normal adult heights, the main two aims of treatment.

Keywords: Idiopathic short stature, Growth hormone, Short children, Short stature. Introduction Children with idiopathic short stature ISS do not attain a normal adult height. Subjects Of the children with idiopathic short stature treated with rhGH 0. Open in a separate window.

Statistics Paired and unpaired, two-tailed Student T test was used to compare the means of the different groups. Results A few growth charts in Figure 1 illustrate what we observed in many children: a catch up growth for the first 3 or more years of treatment to a level expected for the midparental height, a subsequent normal growth, the growth spurt with puberty and the attainment of a normal adult height.

Figure 1. Figure 2. Variability of the Response to Treatment with Growth Hormone We definitely observed the variability in response. The effect of puberty The comparison of the values for different measures obtained for all the children with normal puberty and delayed puberty, males 68 and 20 females, in all the subgroups, NFSS and FSS, males and females are shown in Table 2.

The effect of age at start of treatment and duration of treatment In the study of Rekers-Mombarg, et al. Abbreviations : min minimum, max maximum. Analysis of intent to treat to adult height Children were observed for a period of time prior to treatment, so that their growth rates could be assessed.

Figure 3. Safety and IGF-1 levels Complaints of myalgia or arthralgia of the legs early in the treatment, which promptly subsided without adjustment of the GH dose, were very rare. There were no other side effects. Figure 4. Table 7 IGF Benefit obtained by treatment One of the limitations of our study is the lack of controls. Figure 5. Figure 6. Baseline Adult height Adult height gain Published study [Ref. Discussion Our experience with the growth hormone treatment of children with ISS was a positive one, with the normalization of the height and growth during childhood and adolescence after 2 or 3 years of treatment and the attainment of a normal adult height of The effect of the inclusion of children with FSS By our results, the adult height and adult height gain were significantly higher by 0.

Assessment of Benefit The assessment of the benefit from treatment with GH is sometimes difficult, even in controlled studies, because the proportion of children with FSS and NFSS, normal and delayed puberty, and at times IUGR, may not be the same in the treated and control groups. Other considerations Recent critical reviews [ 20 , 21 , 61 ] concluded that to date no study has fulfilled the criteria for high quality and strong recommendations, in part owing to the small number of children in the studies, and felt that additional high quality trials up to the achievement of adult height would be necessary to determine the efficacy, ideal dosage, long term safety of growth hormone therapy and to address health related quality of life and cost issues.

Conclusion Children with ISS do not attain a normal adult height: adult heights of Endnotes a The high price of pharmaceuticals is in the public domain. Competing interests The authors declare that they have no competing interests. Supplementary Material Additional file 1: Table S1: The adult heights reported were adult or near adult heights. Share on email Email.

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Human Growth Hormone- Does It Slow Aging? Increase Height? 10 Ways to Boost Naturally

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