Prevalence Of Growth Hormone Deficiency Research Articles

WS04.2 Growth hormone deficiency (GHD) in adult patients (pts) with cystic fibrosis (CF)

Introduction CF adult pts complain signs and symptoms that overlap with the GHD: loss of muscle mass, physical function, occurrence of bone fragility, cardiovascular complications and lower stress tolerance. Aim To assess the prevalence of GHD in a cohort of CF adults. Methods 41 pts (30M) with a mean age of 36.9±10.7 yrs were enrolled. Exclusion criteria: liver or lung transplantation, age Results Enrolled subjects had the following characteristics: BMI:21.7±2.8 kg/m 2 FEV1: 61.9±18.3%, FEF25–75 39±23.7%, CVF 78.7±19.5%. All pts with GHD have a severe genotype: have both alleles with mutations of the first 3 classes. Evaluation of the GH-IGF1 axis revealed 34.2% with a GHD: severe in 12.2% and partial in 22%. In severe GHD, mean GH peak was 9.2±1.3 ng/ml and mean IGF1 185.4±51.5 ng/ml, in partial GHD mean GH peak 13.2±1.5, mean IGF1 208±39.7, and in pts with normal GH response, mean GH peak was 51±38.6, mean IGF1 210.6±77.5. All pts with severe GHD showed a ΔF508 mutation (60% in homozygous). We found a significant difference in GHD pts than no GHD: in BMI (23.4±2.4 vs 20.9±2.7) and fasting glucose (115.9±29.1 vs 87.7±13.7) and that these variables are inversely correlated with the GH peak (BMI: R=−0.33, p = 0.04; fasting glucose: R=−0.31, p = 0.05). Discussion To our knowledge there are no studies on the GHD in adults pts CF. You have to follow these pts over time to assess the impact of GHD on general health; should be increased cases in the study to see if this data is confirmed.

Abstract #244: Prevalence of Growth Hormone Deficiency in Type1 DM Patients at a Tertiary Care Centre in India

Abstract #244: Prevalence of Growth Hormone Deficiency in Type1 DM Patients at a Tertiary Care Centre in India

GH deficiency after traumatic brain injury: improvement in quality of life with GH therapy: analysis of the KIMS database.

Prevalence of GH deficiency (GHD) caused by traumatic brain injury (TBI) is highly variable. Short-term studies show improvement in quality of life (QoL) during GH replacement (GHR), but long-term data are lacking. The aim of this study was to analyse the clinical characteristics of post-traumatic hypopituitarism and the QoL effects of long-term GHR. Pfizer International Metabolic Database patients with GHD caused by TBI and by non-functioning pituitary adenoma (NFPA) were compared regarding: clinical characteristics at baseline and 1-year of GHR, and QoL response up to 8-years of GHR (QoL-AGHDA total scores and dimensions) in relationship with country-specific norms. TBI patients compared with NFPA patients were younger, diagnosed with GHD 2.4 years later after primary disease onset (P<0.0001), had a higher incidence of isolated GHD, higher GH peak, a more favourable metabolic profile and worse QoL, were shorter by 0.9 cm (1.8 cm when corrected for age and gender; P=0.004) and received higher GH dose (mean difference: 0.04 mg/day P=0.006). In TBI patients, 1-year improvement in QoL was greater than in NFPA (change in QoL-AGHDA score 5.0 vs 3.5, respectively, P=0.04) and was sustained over 8 years. In TBI patients, socialisation normalised after 1 year of GHR, self-confidence and tenseness after 6 years and no normalisation of tiredness and memory was observed. Compared with NFPA, TBI patients presented biochemically with less severe hypopituitarism and worse QoL scores. GHR achieved clinically relevant, long-term benefit in QoL.

Low prevalence of growth hormone deficiency in Turkish patients with Hashimoto’s thyroiditis

Hashimoto's Thyroiditis (HT) is frequently isolated, but may also be associated with other autoimmune disorders. Autoimmune hypophysitis can result in growth hormone deficiency (GHD). Various prevalences of GHD have been reported in HT in several different ethnic populations. The aim of this study was assessing the prevalence of GHD in Turkish population with HT. Two hundred twenty-seven (208 females and 19 males, mean age 40.1±10.8years, range 18-64 years) patients with euthyroid HT were included. All patients were euthyroid with or without T4 treatment (median TSH 2.2mIU/L, range 0.2-4.2mIU/L; median FT4 15.6pmol/L, range 12-22pmol/L; and median FT3 4.5pmol/L, range 3.0-6.2pmol/L), and median TPO-Ab was 817IU/mL (range 63 to>3,000). One hundred and thirty-six of them were using medications including L-thyroxine (59.9%). Insulin-like growth factor-I (IGF-I) levels of 210 patients (92.5%) were normal. Glucagon stimulation testing in 17 subjects revealed GHD (peak<3 mcg/L) in two subjects. We then performed insulin tolerance test (ITT) to both of them as the gold standard confirmatory test. One patient had no GH response to ITT, either. Our data reveal the prevalence of GHD (based on low IGF-I and ITT result) in this particular group of Turkish HT patients as 0.4%. We conclude that the isolated GHD is rarely observed in HT in our population. The prevalence of GHD is 0.4% in this particular group of Turkish HT patients suggesting that routine investigation of GHD is not mandatory.

Research in brief

Research in brief

Etiology of growth hormone deficiency in children and adolescents

Growth hormone deficiency (GHD) can be isolated or associated with deficiency of other pituitary gland hormones. According to age at diagnosis, causes of GHD are divided into congenital or acquired, and according to etiology into recognized and unknown. We analyzed etiology and prevalence of GHD, demographic data at birth, age, body height (BH) and bone age at diagnosis as well as the frequency of other pituitary hormone deficiencies. The study involved 164 patients (109 male).The main criterion for the diagnosis of GHD was inadequate response of GH after two stimulation tests.The patients were classified into three groups: idiopathic, congenital and acquired GHD. Idiopathic GHD was confirmed in 57.9% of patients, congenital in 11.6% and acquired in 30.5%. The mean age at diagnosis of GHD was 10.1 +/- 4.5 years.The patients with congenital GHD had most severe growth retardation (-3.4 +/- 1.4 SDS), while the patients with idiopathic GHD showed most prominent bone delay (-3.6 +/- 2.3 SDS).The prevalence of multiple pituitary hormone deficiency was 56.1%, in the group with congenital GHD 73.7%, acquired GHD 54.0% and idiopathic GHD 53.7%.The frequency of thyrotropin deficiency ranged from 88.2-100%, of adrenocorticotrophin 57.1-68.8% and of gonadotrophins deficiency 57.1-63.0%, while deficiency of antidiuretic hormone was 2.0-25.0%. Although regular BH measurements enable early recognition of growth retardation, patients' mean age and degree of growth retardation indicate that GHD is still diagnosed relatively late. A high incidence of other pituitary hormone deficiencies requires a detailed investigation of the etiology of disorders and evaluation of all pituitary functions in each child with confirmed GHD.

Novel neuronal and endocrine autoantibody targets in autoimmune polyendocrine syndrome type 1

Context. Although pituitary autoantibodies have frequently been reported in Autoimmune Polyendocrine Syndrome type 1 (APS1), the autoimmune involvement of the hypothalamic-pituitary axis remains to be elucidated. Objective. Our aim was to identify in APS1 patients novel autoantibodies, especially against hypothalamic-pituitary targets, and to correlate their presence with clinical features. Patients. We analyzed 14 APS1 patients from Sardinia, compared to other diseases and healthy donors. Measure(s). We used immunohistochemistry, on tissues substrates from various neuroendocrine organs, to detect autoantibody targets. Immunoenzymatic assays, as well as absorption with specific antigens were used to reveal autoantibodies against growth hormone (GH), luteinizing hormone (LH) and somatocrinin (GHRH). Clinical evaluations included GH secretory and cardiovascular autonomic neuropathy tests. Results. Sera from 12/14 APS1 patients revealed autoantibodies reacting with the hypothalamic-pituitary axis, cerebellum, substantia nigra, and/or adrenal medulla, as well as with GH, LH and/or GHRH. Of APS1 patients, 5 showed GH deficiency, in association (4/5 cases) with autoantibodies to hypothalamic and/or pituitary targets. Hypogonadotrophic hypogonadism was revealed in one APS1 patient, together with autoantibodies against gonadotropes. Autonomic neuropathy was detected in 5 of 10 patients, associated with autoantibodies to adrenal medulla in 2 cases. Of 5 patients with autoantibodies to cerebellar neurons, 2 reported emotional or memory alterations. Conclusions. The majority of Sardinian APS1 patients developed autoantibodies to an assortment of neuroendocrine cells. Novel targets of clinical relevance may include pituitary hormones, uncharacterized pituitary targets, and adrenal medullary cells. An high prevalence of GH deficiency, and possibly of autonomic neuropathy, were also revealed.

Pituitary Dysfunction in Adult Patients after Cranial Radiotherapy: Systematic Review and Meta-Analysis

Cranial radiotherapy is an important cause of hypopituitarism. The prevalence of hypopituitarism varies considerably between studies. We conducted a systematic review and meta-analysis of reported prevalences of hypopituitarism in adults radiated for nonpituitary tumors. We searched PubMed, EMBASE, Web of Science, and the Cochrane Library to identify potentially relevant studies. Studies were eligible for inclusion with the following criteria: 1) cranial radiotherapy for nonpituitary tumors and/or total body irradiation for hematological malignancies; 2) adult population (>18 yr old); and 3) report on endocrine evaluation. Data review was done by two independent reviewers. Besides extraction of baseline and treatment characteristics, also endocrine tests, definitions, and cutoff values used to define pituitary insufficiency were extracted. Eighteen studies with a total of 813 patients were included. These included 608 patients treated for nasopharyngeal cancer (75%) and 205 for intracerebral tumors. The total radiation dose ranged from 14 to 83 and 40 to 97 Gy for nasopharyngeal and intracerebral tumors, respectively. The point prevalence of any degree of hypopituitarism was 0.66 [95% confidence interval (CI), 0.55-0.76]. The prevalence of GH deficiency was 0.45 (95% CI, 0.33-0.57); of LH and FSH, 0.3 (95% CI, 0.23-0.37); of TSH, 0.25 (95% CI, 0.16-0.37); and of ACTH, 0.22 (95% CI, 0.15-0.3), respectively. The prevalence of hyperprolactinemia was 0.34 (95% CI, 0.15-0.6). There were no differences between the effects of radiotherapy for nasopharyngeal vs. for intracerebral tumors. Hypopituitarism is prevalent in adult patients after cranial radiotherapy for nonpituitary tumors. Therefore, all patients treated by cranial radiotherapy should have structured periodical assessment of pituitary functions.

The GH/IGF-I Axis and Pituitary Function and Size in Adults with Prader-Willi Syndrome

Background: In adults with Prader-Willi syndrome (PWS), limited information is available about pituitary function, more specifically the prevalence of growth hormone deficiency (GHD). The aim of this study was to gain more insight into endocrine function in PWS adults, with emphasis on GH secretion. Methods: 15 randomly selected adult PWS individuals were included and 14 healthy brothers and sisters served as a control group. Main outcome measures were IGF-I, IGFBP-3 and peak GH level after a combined GHRH-arginine test. Other pituitary hormone deficits are diagnosed based on serum levels of the concerning hormones. The size of the pituitary gland was measured on MRI images. Results: In PWS adults, IGF-I levels were low and IGFBP-3 levels normal when compared to healthy controls. GHD was diagnosed in 8–38% of the PWS patients, depending on the criteria used. Hypogonadism was present in 87% of the patients. Hypothyroidism and adrenal insufficiency could also be demonstrated. Anterior pituitary size was lower in PWS individuals when compared to healthy controls. Conclusion: In this study, pituitary hormone deficiencies are demonstrated in a considerable number of adults with PWS, hypogonadism and GHD being most prominent. Furthermore, the anterior pituitary is smaller in comparison with healthy controls.

Prevalence of growth hormone deficiency in adult polytransfused β-thalassemia patients and correlation with transfusional and chelation parameters

Dysfunction of GH-IGF-I axis has been described in many patients affected by β-thalassemia major (TM), especially in children and in adolescents. Recent studies have demonstrated the necessity to evaluate adult patients affected by TM to establish the presence of this alteration which could be relevant in the pathogenesis of cardiac and bone disease, frequently present in this hematological condition. The pathogenesis of this alteration, correlated in the past with iron overload, is not yet completely understood. The aim of this paper is to evaluate GH-IGF-I axis in a group of adult polytransfused β-thalassemic patients (TM) and to correlate the results with transfusional and chelation parameters. We performed an arginine plus GHRH stimulation test in 28 adult TM patients. Ferritin, IGF-I, liver enzymes, and liver iron concentration, assessed by a superconducting quantum interference device (SQUID) susceptometer were also determined. Moreover, in each patient we evaluated the bone status by a dual-energy X-ray absorptiometry study. We found the presence of GH deficit in 9 patients (32.1%). There were no significant differences between the two groups regarding the value of ferritin, liver enzymes, and liver iron concentration, assessed by SQUID. The group affected by GH deficit showed a worse bone profile. This study confirms the necessity to screen the status of GH/IGF-I axis in this group of patients, even in adult age. The presence of GH deficiency does not seem to be correlated with the efficacy parameters of transfusional and chelation therapy. Other mechanisms, additional to iron overload, could therefore play a role in the pathogenesis of this clinical condition. The presence of GH deficit seems to be very important on clinical aspects, like bone disease, that are crucial for quality of life in these patients.

Prevalence of GH deficiency in cured acromegalic patients: impact of different previous treatments

Radiotherapy (RT) for pituitary adenomas, including GH-secreting ones, frequently leads to GH deficiency (GHD). Data on the effects of surgery alone (S) on dynamic GH secretion are limited. The aim of the study was to investigate the occurrence of GHD in acromegalic patients treated with different therapeutic options. Fifty-six patients in remission from acromegaly, (33 F & 23 M, age: 54+/-13 years, body mass index (BMI): 28.4+/-4.1 kg/m(2), 21 with adequately substituted pituitary deficiencies) treated by S alone (n=33, group 1) or followed by RT (n=23, group 2), were investigated for GHD by GHRH plus arginine testing, using BMI-adjusted cut-offs. Several metabolic and cardiovascular parameters (waist circumference, body fat percentage, blood pressure, fasting and post-oral glucose tolerance test glucose, HbA1c, insulin resistance and lipid profile) were evaluated in all the patients and 28 control subjects with known diagnosis of GHD. Serum GH peak after challenge was 8.0+/-9.7 microg/l, without any correlation with post-glucose GH nadir and IGF-1 levels. The GH response indicated severe GHD in 34 patients (61%) and partial GHD in 15 patients (27%). IGF-1 were below the normal range in 14 patients (25%). The frequency of GHD was similar in the two treatment groups (54% in group 1 and 70% in group 2). No significant differences in metabolic parameters were observed between acromegalic patients and controls with GHD. Severe GHD may occur in about 60% of patients treated for acromegaly, even when cured after S alone. Thus, a stimulation test (i.e. GHRH plus arginine) is recommended in all cured acromegalic patients, independently from previous treatment.

Prevalence of GH and other anterior pituitary hormone deficiencies in adults with nonsecreting pituitary microadenomas and normal serum IGF‐1 levels

GH is usually the first pituitary hormone to be affected following a pathological insult to the pituitary; however, data on the prevalence of GH deficiency in patients with nonsecreting pituitary microadenomas and normal serum IGF-1 levels are scarce. This study aims to evaluate the prevalence of GH and other anterior pituitary hormone deficiencies, and to determine whether microadenomas per se could be associated with reduced GH response rates to GHRH-arginine stimulation. Analytical, retrospective, two-site case-control study. Thirty-eight patients with nonsecreting pituitary microadenomas (mean size 4.2 mm) and normal serum IGF-1 levels were studied. Anterior pituitary function testing, including the GHRH-arginine test to examine GH reserve, was performed in all patients. Serum IGF-1 levels and peak GH levels in the patients that passed the GHRH-arginine test were compared with 22 age- and BMI-matched healthy controls. Nineteen patients (50%) failed the GHRH-arginine test and had higher body mass index (BMI) than those that passed the GHRH-arginine test and healthy controls. Peak GH levels in patients that passed the GHRH-arginine test were lower compared to healthy controls and 19 patients (50%) had at least one other pituitary hormone deficit. A negative correlation (r = -0.42, P < 0.01) between peak GH levels and BMI was identified, but no correlations were found between peak GH and serum IGF-1 levels. Our data demonstrated that a substantial number of patients with nonsecreting pituitary microadenomas failed the GHRH-arginine test despite normal serum IGF-1 levels, and had at least one other pituitary hormone deficiency, suggesting that nonsecreting microadenomas may not be clinically harmless. We therefore recommend long-term follow-up with periodic basal pituitary function testing, and to consider dynamic pituitary testing should clinical symptoms arise in these patients.

The Neuroendocrine Effects of Traumatic Brain Injury

The Neuroendocrine Effects of Traumatic Brain Injury

The Neuroendocrine Effects of Traumatic Brain Injury

Neuroendocrine dysfunction after traumatic brain injury (TBI) is under-diagnosed, under-treated, and may adversely affect the rate of recovery. Single or multiple pituitary-target hormone disruption occurs in up to two-thirds of persons with TBI, most commonly affecting the gonadal and growth hormone axes. The time course of decline in and recovery of pituitary function in relation to cognitive dysfunction and rehabilitation progress are not well described. This article reviews the clinical spectrum of neuroendocrine deficits after TBI and their underlying mechanisms. Future studies of the effects of hormonal replacement on recovery are recommended.

Growth hormone deficiency (GHD) in adult thalassaemic patients

Short stature and growth hormone deficiency (GHD) are frequent occurrences in thalassaemic children, while data on the prevalence of GHD in adult patients are lacking. Therefore, we elected to study the growth hormone and insulin-like growth factor-I (GH-IGF-I) axis in a large group of adult thalassaemic subjects. Cross-sectional study on the prevalence of GHD in 94 adult thalassaemic patients (69 with thalassaemia major and 25 with thalassaemia intermedia, 39 men and 55 women, aged 31.5 +/- 6.8 years, on sex steroid replacement when necessary). All patients underwent GHRH (1 microg/kg as an i.v. bolus) plus arginine (0.5 g/kg as a 30 min i.v. infusion) testing. Severe GHD was defined by GH peaks lower than 9 microg/l, whereas partial GHD was defined by GH peaks ranging from 9-16.5 microg/l. Blood samples for IGF-I, ferritin and pseudocholinesterase measurements were collected. Urinary free cortisol (UFC) levels were also assayed. Severe GHD was demonstrated in 21 of the 94 patients (22.3%), while 18 additional patients (19.1%) displayed partial GHD. GH peaks were positively correlated with IGF-I standard deviation score (SDS) (r = 0.22, P < 0.05), although 1 of the 21 patients with severe GHD showed normal IGF-I SDS values, and 44 of the 55 patients with normal GH reserve displayed low IGF-I SDS. A strong positive correlation (r = 0.48, P < 0.0001) between IGF-I SDS and pseudocholinesterase was identified. No correlations were found between ferritin and UFC levels on the one hand and GH peaks and IGF-I SDS on the other. Findings from this study demonstrate that GHD, either partial or severe, is not a rare occurrence in adult thalassaemic patients. GHD is associated with a higher prevalence of low serum IGF-I levels, recorded also in patients with normal GH secretion. The lack of correlation between ferritin and both GH peaks and IGF-I SDS suggests that mechanisms additional to iron overload, whose relevance cannot however be definitely ruled out, play a role in the pathophysiology of somatotrophin-somatomedin deficiency in this clinical condition. The positive correlation between IGF-I SDS on the one hand and GH peaks and pseudocholinesterase values on the other hand indicates that reduced liver protidosynthetic activity, in addition to somatotrophin secretory status, is a major determinant of the impaired IGF-I production in thalassaemia. Therefore biosynthetic GH replacement therapy in GH-deficient thalassaemic adults is worth considering.

The Prevalence of Growth Hormone Deficiency and Celiac Disease in Short Children

To assess the occurrence of growth hormone deficiency (GHD) in patients with celiac disease (CD) referred for short stature. A retrospective, multi-center study. A total of 7066 children with short stature were referred to a number of centers for second-line evaluation over a 5-year period. All patients were screened for CD by antiendomysial antibodies (EMA) and antitissue transglutaminase IgA. Those with positive sera underwent intestinal biopsy. The EMA-negative patients and the EMA-positive ones who did not grow after 1 year of gluten-free diet underwent endocrinological investigation. Among the 7066 short children (age 2-14 years) evaluated, 650 (9.2%) had GHD and 44 (0.63%) had CD. An association of both CD and GHD was found in 16 short children (0.23%); these children did not grow after 1 year of gluten-free diet and therefore GH treatment was started. GH secretion should be evaluated in celiac patients showing no catch-up growth after an appropriate period on a gluten-free diet in spite of reversion to seronegativity for EMA.

Prevalence and demographic features of childhood growth hormone deficiency in Belgium during the period 1986-2001.

Since the availability of recombinant human growth hormone (rhGH) all children with growth hormone deficiency (GHD) living in Belgium are offered rhGH treatment after approval by a peer-review board. In this study, we evaluated the prevalence and demographic features of childhood GHD in Belgium during the period 1986-2001 and we compared them with the data from other countries. Diagnostic, demographic and baseline auxological data of 714 children diagnosed as having GHD between 1986 and 2001 were retrieved from the database of the Belgian Study Group for Paediatric Endocrinology. The prevalence of GHD in Belgium was estimated to be 1/5600. The origin of GHD was idiopathic (idGHD) in 41% of the patients, congenital (congGHD) in 20% and acquired (acqGHD) in 35%. During the first 4 years (1986-1989) more patients were classified as idGHD; thereafter the distribution between the three aetiology groups did not change. In all groups, boys outnumbered girls but this preponderance was especially pronounced in congGHD patients (male:female=4:1) with a central malformation that associates an anterior pituitary hypoplasia, a missing, fine or normal pituitary stalk and an ectopic posterior pituitary. Thirteen percent of the patients with idGHD, 50% with congGHD and 52% with acqGHD had multiple pituitary deficiencies. Patients with congGHD were the youngest (mean+/-s.d. age: 6.5+/-4.7 years) and were the shortest (-3.0+/-1.3 standard deviation score (SDS)) at the start of rhGH treatment. There was no time trend over the studied period for age and height at onset of GH therapy. In Belgium, the prevalence of childhood GHD can be estimated as 1/5600 which is comparable to other recent surveys. The yearly number of new patients for the different aetiologies and the auxological parameters have remained relatively constant over the last 16 years.

Increased prevalence of growth hormone deficiency in patients with vernal keratoconjuntivitis; an interesting new association.

Vernal keratoconjunctivitis (VKC) is a chronic conjunctivitis that mainly affects children living in temperate areas. The notable difference between genders and VKC's resolution with puberty have persistently suggested a role of hormonal factors in VKC development. To describe six cases of males with VKC and growth hormone deficiency (GHD) reported as a long-term follow-up during rhGH treatment. Six consecutive male patients (median age at GHD diagnosis 9.7, range 7.9 to 13.1 years) with VKC, were recruited from July 2005 to July 2013 at the Paediatric Endocrinology Unit of Anna Meyer Children's Hospital in Florence, Italy. In these patients, anthropometric data were collected periodically. In three of these patients, data were collected to near-adult or adult height. Familial history was uneventful for all patients. The target height was normal, ranging from 0.65 standard deviation scores (SDS) to 2.01 SDS. The patients showed a normal birth-weight (from -1.21 to 1.35 SDS) and birth-length (from -0.93 to 1.21 SDS). At GHD diagnosis, all of the patients exhibited demonstrated important growth retardation (from -2.05 to -2.78 SDS). Plasmatic concentrations of IGF-1 and IGFBP-3 were low (from -1.85 to -3 SDS and from -1.81 to -2.76 SDS, respectively). GH stimulation tests showed classic GHD symptoms in all of the patients. Pubertal onset was normal. All of the patients treated with rhGH responded well to rhGH treatment. Adult height, evaluated in three patients, was in accordance with their target height. To our current knowledge, we have described for the first time six patients affected by VKC with GH deficiency, in some of whom we performed a long-term follow-up to adult height. Further studies will be needed to establish whether GHD may be a common feature of VKC patients. Nevertheless, it appears to be useful to carefully follow statural growth of VKC patients, while the possibility of a GH deficiency must to be taken into account in the presence of growth failure.

Acid-base homeostasis in children with growth hormone deficiency.

Although the primary use of growth hormone (GH) is to promote linear growth, it is also known to affect many metabolic processes and to influence renal function. In laboratory animals, growth hormone deficiency (GHD) causes a mild metabolic acidosis that is corrected by GH treatment. We observed a patient with GHD who initially presented with acidosis of unclear etiology and corrected the acidosis with GH treatment. To determine: 1) whether children with GHD have lower mean serum bicarbonate concentrations than do children with short stature because of other causes; and 2) whether the presence of a low serum bicarbonate concentration increases the probability of GHD among children with short stature. We collected data from the medical records of 143 children with short stature who had serum electrolyte concentrations measured as part of their initial evaluations, 66 with GHD and 77 with short stature as a result of other causes. We compared mean serum bicarbonate concentrations and bicarbonate standard deviation scores (SDS) between these two groups and determined the probability of GHD for patients according to bicarbonate SDS. The mean serum bicarbonate concentration was significantly lower in patients with GHD (mean standard deviation [SD]; 23.9 [0.4] mEq/L vs 25.2 [0.3] mEq/L) as was the bicarbonate SDS (-0.12 [0.14] SD vs 0.38 [0.10] SD). Twelve (75%) of 16 patients with bicarbonate SDS </=-1 SD had GHD compared with 7 (28%) of 25 patients with bicarbonate SDS >1 SD. Patients with bicarbonate SDS between -1 SD and 1 SD had an intermediate probability of GHD, 46/102 (45%), similar to the overall prevalence of GHD in the study population (46%). Mean bicarbonate concentrations and bicarbonate SDS increased significantly in 9 patients who had repeat electrolyte measurements during treatment with GH (mean bicarbonate; 21.7 [1.1] mEq/L vs 26.9 [0.59] mEq/L, mean bicarbonate SDS; -1.24 [0.43] SD vs 0.55 [0.27] SD). Serum bicarbonate concentrations are lower in patients with GHD than in patients with short stature as a result of other causes. In addition, serum bicarbonate concentrations rise with GH treatment in patients with GHD. The probability of GHD is increased for patients with bicarbonate SDS </=-1 SD and decreased for patients with bicarbonate SDS >1 SD. These findings indicate a role for GH in maintaining normal acid-base homeostasis and suggest that GHD should be considered in children whose growth failure is attributed to other causes of acidosis.

Utah Growth Study: Growth standards and the prevalence of growth hormone deficiency

Serial measurements of elementary-school children were conducted for 2 consecutive years to assess height and growth velocity and to determine the prevalence of growth hormone deficiency (GHD) in American children. Trained volunteers measured 114,881 children the first year; 79,495 growth rates were calculated after the second measurements. The height and growth velocity curves generated were very similar to the currently used charts. We examined 555 children with short stature (<3rd percentile) and poor growth rates (<5 cm/yr). Five percent had an endocrine disorder. The presence of GHD (peak level, <10 ng/dl with two provocative tests) was found in 16 previously unrecognized children; 17 children from this school population were already known to have GHD. Boys outnumbered girls 2.7:1 ( p = 0.006). Six girls with Turner syndrome also were identified. We conclude that (1) the growth curves generated in the 1960s and 1970s are valid for children of the 1990s; (2) most children growing <5 cm/yr (a commonly used threshold rate) will not have an endocrine disorder; (3) many children (48% in this study) with GHD and others with Turner syndrome may currently be unrecognized and untreated; (4) GHD appears to be more common in boys; and (5) the prevalence of GHD in the United States is at least 1:3480. (J P EDIATR 1994;125:29-35)