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Glycemic profile in patients with acromegaly treated with somatostatin analogue

Hypothesis. The growth hormone (GH) excess displayed in acromegaly induces insulin resistance up to diabetes mellitus (DM). The somatostatin analogues (as octreotide LAR) are useful in controlling the GH levels but disturbances of glucose metabolism might be seen. Objective. This study evaluates the...

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Autores principales: Valea, A, Carsote, M, Ghervan, C, Georgescu, C
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Carol Davila University Press 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4564028/
https://www.ncbi.nlm.nih.gov/pubmed/26361517
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author Valea, A
Carsote, M
Ghervan, C
Georgescu, C
author_facet Valea, A
Carsote, M
Ghervan, C
Georgescu, C
author_sort Valea, A
collection PubMed
description Hypothesis. The growth hormone (GH) excess displayed in acromegaly induces insulin resistance up to diabetes mellitus (DM). The somatostatin analogues (as octreotide LAR) are useful in controlling the GH levels but disturbances of glucose metabolism might be seen. Objective. This study evaluates the acromegalic glycemic profile under octreotide. Methods & Results. Out of the total number of patients (N=34) diagnosed with active acromegaly, only some were followed (N=25; male/ female ratio: 6/ 19; mean age: 51.8 years) by testing GH, IGF1 (Insulin Growth Factor 1), basal glucose and oral glucose tolerance test (OCGTT) at baseline, 6 and 12 months under Octreotide (first 6 months with 20 mg/ 28 days + 6 months with 30 mg/ 28 days). Pre-treatment values were 17.6% of patients had DM, 14.7% - impaired glucose tolerance, 26.5% - impaired fasting glucose, and 41.2% - normal assays. From the statistical point of view, the DM patients were significantly older and had higher GH levels than the acromegalic without glycaemia disturbances. They did not achieve significant changes in basal blood glucose and glycated hemoglobin after 6 months, neither after 12 months. After 6 months, there were no significant changes in basal glycaemia in patients with normal baseline glycaemia but 2-hours OGTT glucose values were significantly lower than initially (82.35 mg/ dl vs. 93 mg/ dl, p=0.005) consistent with reduced levels of GH and IGF1. After 12 months, both basal and 2-hours glucose levels in OGTT were similar to baseline despite the significant lower GH (3.3 vs. 6.61 ng/ mL, p=0.003) and IGF1 (332 vs. 713 ng/ mL, p=0.001). Conclusions. Octreotide therapy induces an improvement in glycemic profile in patients with active acromegaly without diabetes mellitus consistent with decreased levels of GH and IGF1. In patients with diabetes, partial control of glucose metabolism is due to inadequate suppression of GH and IGF1 after one year of treatment.
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spelling pubmed-45640282015-09-10 Glycemic profile in patients with acromegaly treated with somatostatin analogue Valea, A Carsote, M Ghervan, C Georgescu, C J Med Life Case Presentations Hypothesis. The growth hormone (GH) excess displayed in acromegaly induces insulin resistance up to diabetes mellitus (DM). The somatostatin analogues (as octreotide LAR) are useful in controlling the GH levels but disturbances of glucose metabolism might be seen. Objective. This study evaluates the acromegalic glycemic profile under octreotide. Methods & Results. Out of the total number of patients (N=34) diagnosed with active acromegaly, only some were followed (N=25; male/ female ratio: 6/ 19; mean age: 51.8 years) by testing GH, IGF1 (Insulin Growth Factor 1), basal glucose and oral glucose tolerance test (OCGTT) at baseline, 6 and 12 months under Octreotide (first 6 months with 20 mg/ 28 days + 6 months with 30 mg/ 28 days). Pre-treatment values were 17.6% of patients had DM, 14.7% - impaired glucose tolerance, 26.5% - impaired fasting glucose, and 41.2% - normal assays. From the statistical point of view, the DM patients were significantly older and had higher GH levels than the acromegalic without glycaemia disturbances. They did not achieve significant changes in basal blood glucose and glycated hemoglobin after 6 months, neither after 12 months. After 6 months, there were no significant changes in basal glycaemia in patients with normal baseline glycaemia but 2-hours OGTT glucose values were significantly lower than initially (82.35 mg/ dl vs. 93 mg/ dl, p=0.005) consistent with reduced levels of GH and IGF1. After 12 months, both basal and 2-hours glucose levels in OGTT were similar to baseline despite the significant lower GH (3.3 vs. 6.61 ng/ mL, p=0.003) and IGF1 (332 vs. 713 ng/ mL, p=0.001). Conclusions. Octreotide therapy induces an improvement in glycemic profile in patients with active acromegaly without diabetes mellitus consistent with decreased levels of GH and IGF1. In patients with diabetes, partial control of glucose metabolism is due to inadequate suppression of GH and IGF1 after one year of treatment. Carol Davila University Press 2015 /pmc/articles/PMC4564028/ /pubmed/26361517 Text en ©Carol Davila University Press http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Case Presentations
Valea, A
Carsote, M
Ghervan, C
Georgescu, C
Glycemic profile in patients with acromegaly treated with somatostatin analogue
title Glycemic profile in patients with acromegaly treated with somatostatin analogue
title_full Glycemic profile in patients with acromegaly treated with somatostatin analogue
title_fullStr Glycemic profile in patients with acromegaly treated with somatostatin analogue
title_full_unstemmed Glycemic profile in patients with acromegaly treated with somatostatin analogue
title_short Glycemic profile in patients with acromegaly treated with somatostatin analogue
title_sort glycemic profile in patients with acromegaly treated with somatostatin analogue
topic Case Presentations
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4564028/
https://www.ncbi.nlm.nih.gov/pubmed/26361517
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