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Copeptin in Growth Hormone-Treated Patients.

ABSTRACT: Growth hormone (GH) changes body composition, including increasing body water. GH is known to have an anti-natriuretic effect in the kidney, but little is known of its effect on arginine-vasopressin (AVP) release. We studied the effect of GH on AVP release by measurement of copeptin, a fragment from the same precursor protein, in GH-treated patients with GH deficiency. The study was designed as a retrospective cohort study of biobank samples from 34 patients substituted with GH between 1999 and 2004. Copeptin and insulin-like growth factor 1 (IGF-1) results were compared with previously obtained data. An increase in IGF-1 and copeptin was seen at 3 and 6 months' treatment compared to baseline. Between the 3 and 6 months follow up, copeptin levels were stable. There was a difference in HbA1c between 3 and 6 months (p < 0.01) and between baseline and 6 months (p = 0.042), with higher levels at 6 months. In addition, LDL levels were lower at the 6 months follow up (p = 0.046). The waist circumference at 3 months was lower (p = 0.02). To conclude, three months of GH treatment increased the levels of copeptin and the increase remained at 6 months. This could be a compensatory mechanism balancing the anti-natriuretic effect of GH treatment seen in previous studies.

SUBMITTER: Sjostrom A

PROVIDER: S-EPMC9570667 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

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Copeptin in Growth Hormone-Treated Patients.

Sjöström Anna A Chisalita Simona I SI Höybye Charlotte C

Journal of clinical medicine 20220920 19

Growth hormone (GH) changes body composition, including increasing body water. GH is known to have an anti-natriuretic effect in the kidney, but little is known of its effect on arginine-vasopressin (AVP) release. We studied the effect of GH on AVP release by measurement of copeptin, a fragment from the same precursor protein, in GH-treated patients with GH deficiency. The study was designed as a retrospective cohort study of biobank samples from 34 patients substituted with GH between 1999 and ...[more]

PMID: 36233377

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Project description:BackgroundRecombinant human growth hormone treatment can optimize growth potential; however, optimal outcomes are not always achieved for several reasons, including poor adherence. The overall objective of this project was to design a patient support program to maximize the chances of treatment success for people being treated with somatropin injection. An approach known as the behavior change wheel was used to enhance the development of the patient support program. The behavior change wheel provided a comprehensive framework to support the design of interventions.ObjectiveThe aim of this paper was to describe how the steps of the behavior change wheel were applied to the development of a patient support program for individuals with growth hormone deficiency undergoing treatment with somatropin.MethodsWe followed a series of steps that align to tenets of the behavior change wheel, namely, a narrative literature review to identify which behaviors needed to change and the potential drivers of and barriers to the behaviors, the selection of an intervention strategy and discrete behavior change techniques, and, finally, intervention specification.ResultsA recent systematic review identified a range of potentially modifiable factors found to have an influence on patient adherence to growth hormone treatment. Insights from the systematic review were used to guide the development of a patient support program. The final design of the patient support program consisted of four elements: (1) a personalization questionnaire to tailor support for each individual, (2) tailored reminder and support SMS text messages, (3) nurse-led phone calls, and (4) Easypod connect, an automated electronic autoinjector drug-delivery device with a transmitter and connection platform for Saizen (somatropin) that allows automatic recording, storage, and transmission of drug-usage data, thus providing insight into suboptimal adherence.ConclusionsThe patient support program that was designed is currently being piloted with patients to assess engagement with the program and determine its impact on patient outcomes. Results from the pilot will be used to further refine the program to ensure it meets user needs.

Project description:BackgroundX-linked hypophosphatemia (XLH) is characterized by increased serum concentrations of fibroblast growth factor 23 (FGF23), hypophosphatemia and insufficient endogenous synthesis of calcitriol. Beside rickets, odonto- and osteomalacia, disproportionate short stature is seen in most affected individuals. Vitamin D analogs and phosphate supplements, i.e., conventional therapy, can improve growth especially when started early in life. Recombinant human growth hormone (rhGH) therapy in XLH children with short stature has positive effects, although few reports are available. Newly available treatment (burosumab) targeting increased FGF23 signaling leads to minimal improvement of growth in XLH children. So far, we lack data on the growth of XLH children treated with concomitant rhGH and burosumab therapies.ResultsThirty-six patients received burosumab for at least 1 year after switching from conventional therapy. Of these, 23 received burosumab alone, while the others continued rhGH therapy after switching to burosumab. Children treated with burosumab alone showed a minimal change in height SDS after 1 year (mean ± SD 0.0 ± 0.3 prepubertal vs. 0.1 ± 0.3 pubertal participants). In contrast, rhGH clearly improved height during the first year of treatment before initiating burosumab (mean ± SD of height gain 1.0 ± 0.4); patients continued to gain height during the year of combined burosumab and rhGH therapies (mean ± SD height gain 0.2 ± 0.1). As expected, phosphate serum levels normalized upon burosumab therapy. No change in serum calcium levels, urinary calcium excretion, or 25-OHD levels was seen, though 1,25-(OH)2D increased dramatically under burosumab therapy.ConclusionTo our knowledge, this is the first study on growth under concomitant rhGH and burosumab treatments. We did not observe any safety issue in this cohort of patients which is one of the largest in Europe. Our data suggest that continuing treatment with rhGH after switching from conventional therapy to burosumab, if the height prognosis is compromised, might be beneficial for the final height.

Project description:ObjectiveCopeptin, a marker for stress mirroring vasopressin concentrations, has been shown to increase upon insulin-induced hypoglycaemia in patients after transsphenoidal surgery of pituitary adenomas. Patients with type 1 diabetes mellitus are prone to hypoglycaemia, but no data about copeptin levels upon hypoglycaemia are available. Furthermore, the perception of hypoglycaemia can vary from total unawareness to disabling episodes. The aim of this study was to investigate whether copeptin increases upon hypoglycaemia in patients with type 1 diabetes mellitus and is associated with the degree of hypoglycaemia awareness.Materials and methodsIn this prospective observational study, 17 patients with type 1 diabetes underwent a standardized insulin infusion test. Blood sampling for glucose and copeptin was performed at baseline and after 60 minutes (min). To assess hypoglycaemia associated symptoms the Mood and Symptom Questionnaire (MSQ) was conducted at baseline and after 60 min.ResultsDuring insulin infusion, blood glucose decreased from 5.1 (SD±0.2) to 3.0 (±0.5) mmol/L at 60 min (p<0.001). Copeptin concentrations increased from 3.2 (±1.7) to 3.8 (±1.9) pmol/L (p = 0.03). Mood and Symptoms Questionnaire scores increased from 14 (±3.0) to 18 (±5.8), (p = 0.006). Patients with good hypoglycaemia awareness had an increase in copeptin from 3.0 (±1.8) to 4.2 (±2.4) pmol/L (p = 0.03) in contrast to patients more unaware of hypoglycaemia who only showed an increase in copeptin from 3.3 (±1.6) to 3.6 (±1.4) pmol/L (p = 0.4). There was a trend to a larger copeptin increase in patients aware of hypoglycemia compared to patients unaware of hypoglycemia (p = 0.074).ConclusionCopeptin increases in patients with type 1 diabetes upon insulin induced hypoglycaemia. Interestingly, the copeptin increase seems associated with the degree of hypoglycaemia awareness. This hypothesis warrants further verification.Trial registrationClinicalTrials.gov NCT00515801.

Project description:IntroductionGrowth hormone (GH) secretion and release is a complex and highly regulated process. Any alteration disturbing synthesis, secretion or biological action of GH, results into growth hormone deficiency (GHD). GHD is of two types-isolated growth hormone deficiency (IGHD) and combined pituitary hormone deficiency (CPHD), of which IGHDis more common. The genes implicated in its etiology are growth hormone 1(GH1) and receptor of growth hormone-releasing hormone (GHRHR). Mutations within the coding region and/or either entire or partial deletions of the GH1gene lead to IGHD. In addition, GH1 possesses upstream regulatory elements and a promoter with binding sites for various transcription factors, which control its expression.AimThe study was planned with an aim to identify entire GH1 locus deletion, mutations in the GH1 coding region and sequence variations (polymorphisms) in the promoter region of the gene in patients with IGHD.Materials and methodsThirty patients clinically diagnosed with IGHD and 30 healthy individuals who formed the controls were enrolled for the study. Genomic DNA was isolated from peripheral blood sample and processed for amplification of the desired regions followed by direct sequencing and/or restriction endonuclease digestion.ResultsOut of the 30 IGHD patients screened, 20% of the cases showed consanguinity and 16% had a positive family history. Seven percentage of the patients showed homozygous deletion of the GH1gene while rest of them had heterozygous deletion. Screening of the coding region of GH1 showed sequence variations in exon 1 in 20% of the patients whereas the promoter region showed the presence of polymorphisms-rs2005171 in 20%, rs2005172 in 15% and rs11568828 in 18% of the cases. The haplotype comprising rs2005171 and rs2005172 was observed in four patients.ConclusionThe present study is an attempt to characterize the GH1 locus in IGHD patients. To the best of our knowledge this is the first study of its kind where entire GH1locus, upstream regulatory elements and promoter region have been studied. Such an analysis would provide valuable information on the etiology of IGHD.

Project description:The prevalence of idiopathic oligozoospermia has been esteemed as high as 75%. An Italian survey has reported bilateral testicular hypotrophy in 14% of final-year high school students. The search for determinants of testicular growth in childhood is important for the primary prevention of spermatogenic failure. Therefore, this retrospective study aimed to evaluate the testicular growth and pubertal onset in deficient children treated recombinant human growth hormone (rhGH). To accomplish this, the clinical charts of 93 patients with GH deficiency (GHD) were carefully reviewed. Their mean age at the time of diagnosis was 11.2 ± 2.4 years. rhGH was administered for 44.0 ± 22.4 months, and the onset of puberty was recorded after a mean of 25.8 ± 22.4 months from the first rhGH administration. As expected, serum insulin-like growth factor 1 (IGF1) levels increased significantly after treatment. Before rhGH therapy, the Tanner stage was I in 59 out of 70 boys (84.3%), II in 8/70 (11.4%), III in 3/70 (4.3%). No one was on stage IV or V. The mean Tanner stage was 1.19 ± 0.51. At the last visit, the Tanner stage was I in 8/72 boys (11.1%), II in 6/72 (8.3%), III in 6/72 (8.3%), IV in 16/72 (22.2%), and V in 36/72 (50.0%). After a mean of 44.0 ± 22.4 months of rhGH treatment, the mean Tanner stage was 4.05 ± 1.30. Patients treated with rhGH showed a significant testicular volume (TV) growth over time, whereas no growth was observed in age-matched but not yet treated patients, even when the age was compatible with a spontaneous start of puberty. The multivariate regression analysis showed that the duration of treatment and the mean rhGH dose significantly predicted the percentage of TV increase. In contrast, age, serum FSH, and IGF1 levels, and final rhGH dose did not impact TV growth over time. In conclusion, these findings suggest that GH may play a role in testicular growth and pubertal onset, despite the descriptive nature of this study. Further properly designed studies are needed to confirm these findings. This knowledge may be useful to implement the diagnostic-therapeutic algorithm in case of a lack of testicular growth in childhood.

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Copeptin in Growth Hormone-Treated Patients.

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Copeptin in Growth Hormone-Treated Patients.

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