A recent study identified 198 proteins whose levels in the plasma change across the menstrual cycle in women of reproductive age; one of which is GH1 (Growth Hormone 1). Both plasma GH1 and estradiol levels first peak during the same phases of the menstrual cycle (late follicular phase). Previous reports also showed that GH1 expression (both mRNA and protein) is upregulated by estradiol. Based on these observations, we here hypothesize that circulating estradiol levels might be responsible, at least to a certain extent, from the changes in GH1 protein levels in the plasma during the menstrual cycle in women of reproductive age. Considering the importance of GH1 in the female reproductive system, this potential estradiol-regulated changes in GH1 protein levels in the circulation during the menstrual cycle need to be better understood.
The growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis is the principal endocrine system regulating postnatal growth, skeletal development, metabolism, and tissue homeostasis. Although growth hormone has long been recognized as the primary hormonal regulator of somatic growth, recent advances have demonstrated that the growth hormone receptor (GHR) is the critical molecular determinant in signal transduction and diverse biological effects of GH. This review summarizes current knowledge of GHR structure and activation, emphasizing the conformational mechanisms that initiate intracellular signaling through the JAK2-STAT5, MAPK/ERK, and PI3K-AKT-mTOR pathways. We further discuss how these signaling cascades coordinate growth, cellular differentiation, protein synthesis, and metabolic regulation. Attention is given to growth hormone receptor deficiency, Laron syndrome, which has emerged as one of the most informative human models for understanding the physiological consequences of impaired GH signaling. Studies of the Ecuadorian cohort have demonstrated that lifelong GHR deficiency not only results in severe short stature and characteristic body proportionality but also promotes enhanced insulin sensitivity, preserves glucose homeostasis despite increased adiposity, and induces a remarkably low incidence of malignancy. These findings have substantially expanded current understanding of the GH-IGF axis beyond linear growth, revealing its central role in metabolic homeostasis, aging, and cancer biology. Collectively, the evidence supports the concept that modulation of GHR signaling influences multiple interconnected physiological systems and provides valuable insights into potential therapeutic strategies targeting growth, metabolic disorders, and cancer.
PURPOSE:Given the lack of established dosing strategies for polyethylene glycol recombinant long-acting human growth hormone (PEG-rhGH) in pubertal patients with idiopathic short stature (ISS), it is necessary to develop optimal dosing regimens. This study aims to explore relevant clinical and prognostic factors influencing the efficacy of PEG-rhGH in pubertal ISS patients, and to evaluate the efficacy and safety of higher-dose PEG-rhGH. METHODS:A retrospective real-world group study analyzed efficacy and safety data from 118 children with ISS treated with PEG-rhGH. RESULTS:Following 12 months of PEG-rhGH treatment in children with ISS:① Pre-pubertal demonstrated significantly greater gain in height standard deviation score (HtSDS) and higher height velocity(HV) than the pubertal group (ΔHtSDS: 0.98 ± 0.47 vs. 0.52 ± 0.33, p < 0.001; HV: 10.65 ± 1.55 cm/year vs. 9.98 ± 1.76 cm/year, p = 0.035).②The high-dose group showed significantly greater gain in HtSDS and higher HV compared to the low-dose group (ΔHtSDS: 0.98 ± 0.45 vs. 0.62 ± 0.42, p < 0.001; HV: 11.99 ± 1.25 cm/year vs. 9.69 ± 1.43 cm/year,p < 0.001).③HtSDS gain exhibited a dose-dependent effect with PEG-rhGH treatment. ④The high-dose group did not exhibit additional treatment-emergent adverse events (TRAEs) compared to the low-dose group. CONCLUSION:Pubertal constitutes a negative predictive factor for PEG-rhGH efficacy in children with ISS, and the efficacy of PEG-rhGH is dose-dependent. Therefore, higher dose (≥0.23 mg/kg/week) of PEG-rhGH treatment is beneficial to enhance the efficacy of pubertal ISS patients. No serious adverse events were observed. WHAT IS KNOWN:WHAT IS NEW.
The Growth Hormone - Insulin-like Growh Factor - axis promotes linear growth in children and adolescents and accounts for approximately 1/3 of adult height. In Primary IGF-I deficiency (PIGFD) insensitivity to the actions of GH results in short stature. The most severe phenotype in children with genetic defects in the GH receptor gene is known as Laron Syndrome with height SDS of -6 to -12 in childhood and an adult height of 120-130 cm. Treatment with recombinant human (rh) IGF-1 is approved to promote linear growth in children with severe PIGFD and the EMA approval required that data on children on therapy and up to 5 years post-treatment is collected in the Global Increlex Growth Forum Database (IGFD) registry. In this review, the findings in five publications on rhIGF-1 therapy in children with SPIGFD based on data from the Global IGFD registry are discussed and compared with previous publications on cohorts of patients with severe PIGFD including children with Laron Syndrome. The registry started inclusion of patients in 2008 from 10 European countries (EU IGFD Registry) and have continued collecting data from eight European countries and the US since 2021 (Global IGFD registry). At data cut-off (03 April 2025), there were 346 patients in the registry database including patients with a large variation of phenotypes from Laron Syndrome to a less severe phenotype. The findings include real-world data on effectiveness assessing short- and long-term height gain as well as near adult height, pubertal development and growth dynamics and safety assessing hypoglycemic events, which is the most frequent targeted adverse event. Real-world data from the Global IGFD registry confirms previous data on rhIGF-1 therapy and demonstrates that short and long-term height improves in a majority of children with SPIGFD with similar height improvements compared to children with Laron Syndrome. The registry data points to baseline characteristics including age at treatment initiation that predicts response to therapy. Hypoglycemia is the most common adverse event and hypoglycemia prior to start of therapy or a diagnosis of Laron Syndrome increases the risk. However, very few events over a course of therapy are reported on an individual basis.
PURPOSE:This study aimed to identify clinical and biochemical predictors of short- and long-term surgical outcomes in patients with acromegaly, with a particular focus on postoperative risk stratification using a consensus-based IGF-1 normalization framework. METHODS:This retrospective, single-center cohort study collected data of consecutive patients with acromegaly who underwent transsphenoidal surgery between 2000 and 2022. In accordance with the latest consensus, short-term (3-6 months) and long-term (>6 months) outcomes were primarily stratified by IGF-1 status and the presence of residual tumor. Multivariable regression and Cox proportional hazards models were used to identify predictors of outcomes and disease-free survival (DFS). RESULTS:Poor short-term outcomes were associated with higher Knosp grade (OR = 9.52, 95%CI: 2.02-44.92), larger tumor size (OR = 5.20, 95%CI: 2.36-11.48), and elevated baseline IGF-1 (OR = 1.003, 95%CI: 1.001-1.005). Long-term recurrence was independently predicted by higher baseline IGF-1 (OR = 1.01, 95%CI: 1.002-1.008), elevated postoperative GH (OR = 1.49, 95%CI: 1.01-2.21), and elevated postoperative IGF-1 (OR = 1.02, 95%CI: 1.01-1.04). Patients with early biochemical persistence without residual tumor (Group B) had a significantly increased risk of long-term persistence compared to those with early remission (adjusted OR = 5.85, 95%CI: 1.77-19.31). Higher baseline and postoperative IGF-1 levels were also associated with shorter DFS. CONCLUSIONS:Pre- and postoperative IGF-1 levels showed consistent prognostic value for long-term outcomes, supporting the clinical utility of an IGF-1-centric stratification strategy. Notably, while preoperative GH levels show limited prognostic value, postoperative GH elevation remained associated with long-term recurrence. This framework facilitates individualized follow-up and long-term management of acromegaly.
Adult growth hormone deficiency (AGHD) is associated with altered body composition, reduced quality of life, and increased cardiovascular risk, which can be mitigated by growth hormone (GH) replacement. Recently, once-weekly somapacitan has been introduced as an alternative to daily somatropin, but its effects on thyroid hormones remain unclear. We retrospectively studied 22 AGHD patients switched from somatropin to somapacitan at a university hospital (2017-2023). IGF-1 and TSH showed no changes; however, FT3 and FT4 levels significantly decreased, particularly in patients receiving levothyroxine. Multiple regression identified baseline FT4, rather than levothyroxine use, as independently associated with ΔFT4. These findings suggest the need for careful monitoring of FT4 and potential adjustment of thyroid hormone replacement during somapacitan therapy.
BACKGROUND:The rate of growth hormone (GH) deficiency (GHD) after traumatic brain injury (TBI) among children and adolescents remains uncertain, partly because of limited follow-up. OBJECTIVE:To evaluate a novel diagnostic approach for post-TBI GHD based on height velocity (HV), IGF-1 levels, and response to recombinant human growth hormone (rhGH), and to estimate its incidence. METHODS:In this prospective, longitudinal study, 31 patients (aged 2.4-18.6 years) hospitalized for TBI underwent complete clinical and hormonal evaluations every 3 months for ≥1 year. Eleven were excluded because they had reached their final or near-final height. The criteria for GHD diagnosis included (a) HV below -1 SDS, (b) at least one IGF-1 level below -1 SDS during the first 2 years after TBI, and (c) increase in HV (>2 SDS) and IGF-1 (>1 SDS) during rhGH therapy. RESULTS:Four patients met criteria for GHD. During the second year after TBI, HV-SDS ranged from -1.42 to -3.41, and height-SDS declined. All patients had at least one IGF-1 value below -1 SDS, while GH stimulation tests were often discordant with HV and IGF-1 levels. Therapy with rhGH led to marked increases in HV-SDS (≥2.73) and IGF-1-SDS (≥1.34) in all 4 patients. Fourteen children maintained normal HV, despite abnormal stimulation tests in some cases. CONCLUSION:Extended HV monitoring combined with IGF-1 assessment and therapeutic rhGH response was more effective than GH stimulation tests alone for diagnosing post-TBI GHD. The GHD incidence was 13%, underscoring the importance of extended auxological follow-up in pediatric patients after TBI.
BACKGROUND:Growth hormone deficiency (GHD) is a common cause of short stature in children, associated with impaired growth and psychosocial challenges. Long-acting growth hormone (LAGH) formulations may reduce treatment burden compared with daily recombinant human GH (rhGH), but real-world evidence in treatment-naïve children with LAGH is still limited. METHODS:We conducted a retrospective observational study including 30 treatment-naïve children with isolated GHD at a tertiary hospital in Greece. Fifteen children initiated somatrogon and 15 received daily rhGH. Patients were evaluated at baseline and at 6, 12 and 18 months for anthropometric parameters and serum IGF-1 values. RESULTS:Height z-score improved over time in both groups, with no significant differences between weekly and daily therapy at any time point. BMI z-score increased significantly during the first 6 months in the weekly GH group and remained higher at 12 months, whereas no sustained differences were observed in the daily GH group. Serum IGF-1 Z-score increased over time in both groups, though the difference was not statistically significant. No patients discontinued therapy due to adverse events. CONCLUSION:Somatrogon was effective and well tolerated in treatment-naïve children with GHD, providing sustained growth improvement and a potential advantage for adherence due to reduced injection frequency. However, increased body weight gain shown in the weekly GH group raises concerns and needs further confirmation and justification.
Growth hormone (GH) and insulin-like growth factor-I (IGF-I) production decline in conjunction with the catabolic changes seen in normal aging, a developmental stage that has been termed the somatopause. While GH-replacement therapy for the somatopause would seem to be a reasonable therapeutic option, studies conducted over the past decades have shown that this treatment leads to only minor changes in body composition but no clinically significant improvements in health or well-being. Numerous adverse side effects have been well-documented. Despite the paucity of data supporting this therapy, many clinicians and wellness influencers still advocate its use, and anti-aging clinics frequently prescribe GH or GH-stimulating peptides. Most endocrinologists, however, agree that GH therapy for the somatopause cannot be recommended unless new carefully performed longitudinal studies demonstrate that this therapy can safely lead to important physiologic improvements in the lives of elderly patients.
Alexander von Humboldt's early nineteenth-century explorations of the Andes established foundational methods in biogeography and environmental science, emphasizing measurement, spatial integration, and the interdependence of natural systems. Nearly two centuries later, southern Ecuador became the site of a landmark discovery in endocrine genetics: a population with growth hormone receptor deficiency (Laron syndrome) characterized by severe insulin-like growth factor-1 (IGF-1) deficiency. This article examines the historical and scientific continuity of observation in the Ecuadorian Andes, linking Humboldt's integrative natural philosophy with modern approaches to human molecular physiology. While no direct historical connection exists between Humboldt's writings and the later identification of this endocrine condition, the shared geographic setting underscores the enduring scientific value of place-based investigation.
Traumatic brain injury (TBI) is a significant public health concern globally, contributing to substantial morbidity and mortality across all age groups. Clinical manifestations range from no symptoms to mild alterations of consciousness to a comatose state and death. Endocrine abnormalities should no longer be considered rare after TBI, with growth hormone deficiency (GHD) being the most common pituitary hormone abnormality followed by hypogonadism, hypocortisolism, and hypothyroidism. Yet the clinical entity of GHD is often under-recognized, as the presenting symptoms can be mistaken as part of the TBI itself. In addition, the severity of other post-TBI comorbidities, lack of guidelines of when to perform hormonal testing and the practical difficulties of conducting GH stimulation testing are important factors that contribute to the delay or missing the diagnosis altogether. Furthermore, there are no validated GH cut-points of currently available GH stimulation tests in TBI patients per se. Following the confirmation of diagnosis of GHD, previous studies have shown that the poor outcomes of post-TBI GHD could be improved and possibly even reversed by GH replacement; however, to date, data on the beneficial effects of such long-term therapy in TBI patients remains scarce. The present review reports evidence on post-TBI GHD, including clinical consequences if untreated, challenges in screening and diagnostic work-up, and principles of therapeutic management. It is essential for healthcare providers to be aware and to screen for this enigmatic clinical entity. There remains an unmet need for developing stronger evidence, and for guidelines establishing recommendations for screening and diagnosis so that they can be incorporated as optimal standard of care in the management of TBI patients.
OBJECTIVE:Long-acting growth hormone (GH) formulations have been developed to reduce treatment burden and improve adherence in children with growth hormone deficiency (GHD). Somatrogon is a long-acting recombinant GH analog designed for once-weekly administration and has demonstrated comparable efficacy to daily somatropin in clinical trials. However, real-world data evaluating growth outcomes after transitioning from daily GH therapy to somatrogon remain limited. This study aimed to evaluate growth outcomes, biochemical responses, and predictors of treatment response during the first six months following the transition from daily somatropin to once-weekly somatrogon. METHODS:This retrospective cohort study included 121 children with confirmed GHD who had received daily somatropin therapy (35 μg/kg/day) for at least one year before switching to once-weekly somatrogon (0.66 mg/kg/week). Auxological measurements and IGF-1 levels were evaluated at baseline and at 3 and 6 months after treatment transition. Height standard deviation score (SDS) and growth velocity were compared between treatment periods. Correlation analysis was used to evaluate the relationship between IGF-1 SDS and growth response. Multivariable linear regression analysis was performed to identify predictors of growth response. RESULTS:The mean height gain during the final six months of somatropin therapy was 4.11 ± 2.01 cm, compared with 4.96 ± 1.56 cm during the first six months of somatrogon therapy. Height SDS increased significantly during the first three months following the transition to somatrogon compared with the final three months of somatropin therapy (0.17 ± 0.24 vs 0.08 ± 0.23; p = 0.02). However, the overall six-month change in height SDS did not differ significantly between treatment periods (p = 0.11). Mean IGF-1 SDS increased significantly from 0.12 ± 1.54 at baseline to 0.96 ± 1.96 at six months (p < 0.001). No statistically significant linear association was detected between IGF-1 SDS and height SDS improvement (r = 0.05, p = 0.62). Multivariable regression analysis identified baseline height SDS as the strongest predictor of growth response (β = -0.14, p = 0.003). Prepubertal patients showed greater height SDS improvement compared with pubertal patients (p = 0.04). CONCLUSION:Switching from daily somatropin therapy to once-weekly somatrogon showed similar short-term growth patterns over a six-month follow-up period within the limitations of a within-patient observational design in children with GHD. Growth response appeared to be influenced primarily by baseline height status and pubertal stage rather than circulating IGF-1 levels alone did not show a detectable linear association with growth response in this cohort. These findings support the use of somatrogon as an effective and practical alternative to daily GH therapy in routine clinical practice. These findings suggest that growth outcomes were maintained following treatment transition; however, results should be interpreted cautiously given the observational design.
Traumatic brain injury (TBI) is a common injury that can lead to significant and prolonged morbidity. Growing evidence suggests hypopituitarism is prevalent after TBI and if left untreated, contributes to high symptom burden, limited rehabilitation participation, and poor functional recovery. The neurorehabilitation specialist is uniquely situated to identify patients at risk of hypopituitarism during all phases of recovery. There is significant overlap in symptom presentation between hypopituitarism and primary symptoms of TBI. Fatigue, disrupted sleep, altered cognition, weakness, exercise intolerance, and declining mental health can occur due to the brain injury or hypopituitarism, making clinical diagnosis challenging. Collaboration with endocrinologists can aid in organizing timely and appropriate workup, diagnosis, and initiation of hormone replacement therapy. Understanding the clinical features, timing, and trajectory of hypopituitarism after TBI allows neurorehabilitation specialists to facilitate diagnosis and treatment of hypopituitarism which may enhance rehabilitation engagement, improve symptom burden, and ultimately optimize recovery.
Under normal circumstances, the GH/IGF-I axis is the main hormonal influence for longitudinal growth and adult height in males and females. Opposite to that, epiphyseal fusion, skeletal characteristics and fat distribution are mediated by estrogen in a sex-specific manner.While we have previously demonstrated that longitudinal growth and body proportionality are affected by serum IGF-I concentration (Guevara-Aguirre et al., 2025 (1)), now we present evidence demonstrating that body proportions in Laron syndrome (LS) are affected but independently of sex. Considering that the percent difference between males and females is comparable not only in Laron syndrome subjects but also in its relatives as well as in normal populations, it is suggested that the GH/IGF-I signaling and serum IGF-I influence body proportions in a similar fashion in both sexes.We conclude that the status of GH/IGF-I signaling and serum IGF-I influence body segment proportionality in a comparable manner in both sexes and that this notion might apply to all normal humans.
Cancer remains as the most feared human disease and embodies deep psychological and physical suffering (1). It is one of the unsolved medical problems nowadays and constitutes a heavy burden not only for the individual and his family but also for health systems worldwide (2). In this context, cancer prevention and early diagnosis and treatment is of cardinal importance; hence, identification of cancer risk factors in the genesis of human cancer is an urgent necessity. Among these deleterious influences, obesity and aberrantly increased growth hormone receptor (GHR) signaling have been identified as two of the most relevant factors in the etiology of malignancy (3, 4).Considering the above premises, attempts at effectively and safely treating patients with cancer are within the noblest aims in medicine and science. At present, radical surgery, radio and chemotherapy, targeted therapy, and immunotherapy are the basis for dealing with this widespread issue (5). Nevertheless, and especially in several types of cancer, all efforts are ineffective (6). In consequence, strategies to discover new medicines aimed at safely and effectively treating individuals affected by cancer are needed. Similarly, adjuvant methods aimed at making more effective use of standard therapies are required.Contextually, a new experimental approach to dealing with melanoma, liver cancer, pancreatic cancer, and cholangiocarcinoma, some of the most lethal malignancies in humans, has been developed based on the previous discovery of a GHR antagonist used for acromegaly and its mode of action (7, 8). Development of new drugs for cancer treatment is partially based on observations in humans who have a distinct phenotype that combines obesity -the most epidemiologic risk factor in cancer etiology- along with absent growth hormone receptor (GHR) signaling (4, 9).
Children born small for gestational age (SGA) represent a heterogeneous population with an increased risk of persistent short stature and adverse metabolic outcomes later in life. Although most SGA infants exhibit spontaneous catch-up growth during early childhood, approximately 10-15% fail to do so and remain short as adults. Growth hormone (GH) therapy has been used for several decades in this subgroup and is currently approved in many countries worldwide. This review summarizes the biological rationale for GH treatment in SGA children, current indications for therapy, and differences among international guidelines regarding age at initiation and dosing strategies. Available evidence on growth response, predictors of treatment efficacy, and expected gains in near-adult height is discussed, together with data on safety and metabolic monitoring. Particular attention is given to the importance of early treatment initiation, individualized dose adjustment, and sustained therapy through the prepubertal years. The response to GH in syndromic forms of SGA, including Silver-Russell syndrome, is also reviewed. Finally, emerging data on long-acting GH formulations are briefly addressed, highlighting current knowledge gaps and the need for long-term outcome studies.
BACKGROUND:Growth hormone deficiency (GHD) in children is a complex endocrine disorder that requires dynamic testing for accurate diagnosis due to the pulsatile nature of growth hormone (GH) secretion. The clonidine test is widely used as a standard diagnostic tool due to its favorable safety profile and effectiveness. Insulin-like growth factor-1 (IGF-1) has emerged as a potential adjunct marker; however, its diagnostic accuracy is limited when used alone. This study aims to evaluate the diagnostic effectiveness of combining low IGF-1 with a single clonidine stimulation test for diagnosing pediatric GHD. METHODS:A retrospective cohort study was conducted at King Chulalongkorn Memorial Hospital, including 214 children with short stature (aged 2-16 years) evaluated between August 2019 and January 2025. GHD was confirmed in 63 patients using two GH stimulation tests (peak GH <7 ng/mL). Serum IGF-1 levels were expressed as standard deviation scores (SDS) and analyzed at cutoff points of ≤ -1, -1.5, -2, -2.5, and - 3 in combination with clonidine test results. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated. RESULTS:The combination of IGF-1 SDS ≤ -2.5 and a single clonidine test (peak GH < 7 ng/mL) demonstrated a sensitivity of 31.6% and a specificity of 98.6%. The positive predictive value (PPV) was 92.3%, and the negative predictive value (NPV) was 73.7%. Additionally, a cutoff of IGF-1 SDS ≤ -1.5 yielded a sensitivity of 60.5% and specificity of 95.9%. CONCLUSION:An IGF-1 SDS cutoff of ≤ -2.5 combined with a single failed clonidine test demonstrated high specificity for GHD and may provide additional diagnostic confidence in selected patients, potentially reducing the reliance on a second stimulation test.
Post traumatic hypopituitarism (PTHP) occurs in 30-50% of individuals with chronic moderate-severe TBI as well as individuals with mild TBIs who remain symptomatic after a year. Growth hormone deficiency (GHD) occurs in approximately 15-20%, Gonadotropin deficiencies in 10%, as well as Thyroid and Adrenocorticotropin deficiencies in 4-12%. Individuals frequently have more than one deficiency. These numbers cover a wide range and vary based on time of testing, cut-points and methods used. Recent studies have shown hypoaminoacidemia and altered gut microbiome in a subset of individuals with mTBIs with subjective complaints of fatigue and altered cognition: Brain Injury Associated Fatigue and Altered Cognition (BIAFAC). These individuals may become symptomatic months to years after the injury and frequently have a diminished response to growth hormone stimulation testing, although not always below the established cut points for Growth Hormone Deficiency (GHD). Recognition of BIAFAC for its similarities and differences from PTHP by physicians dealing with TBI will lead to more thorough evaluations and may eventually lead to better treatment options for these individuals. This paper will begin with a discussion of the relevance of anatomy to post -TBI changes, and how hypoaminoacidemia may play a role in the symptoms after TBI.
CONTEXT:Comprehensive assessments of the prevalence of prediabetes and glucose intolerance are scarce for acromegaly. OBJECTIVE:To estimate the prevalence of pre-operative glucose homeostasis in patients with acromegaly, including diabetes mellitus (DM), impaired fasting glucose, impaired glucose tolerance, and prediabetes. DESIGN:The study encompassed patients diagnosed with acromegaly at Taipei Veterans General Hospital from 1977 to 2020. Known DM was defined as the use of anti-diabetic medication. Newly diagnosed DM was defined as any of the following conditions: a fasting PG concentration ≥ 126 mg/dL, 2-h glucose concentration ≥ 200 mg/dL during the OGTT, or HbA1c level ≥ 6.5%. Normal glucose tolerance (NGT) was defined as a fasting PG concentration < 100 mg/dL, 2-h glucose concentration < 140 mg/dL during the OGTT, HbA1c level < 5.7%, and not using anti-diabetic medication. Patients who did not meet the criteria for either DM or NGT were classified as having prediabetes. RESULTS:Of 177 patients, 83 (46.9%) had diabetes-39 pre-existing and 44 newly diagnosed. Normal glucose tolerance (NGT) occurred in 32 patients (18.1%), while 62 (35.0%) had prediabetes. Among those with prediabetes, impaired fasting glucose was noted in 59 (39.3% of those with fasting data), impaired glucose tolerance in 47 (34.3% of those with OGTT data), and HbA1c levels of 5.7-6.4% in 19 (28.0% of those with HbA1c data). CONCLUSION:Our findings on diagnosis and prevalence of various blood-glucose statuses in patients with acromegaly at the pre-operative stage may suggest novel mechanisms worthy of further investigation.
