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Lung-Yi Loey Mak
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The global prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has increased over the past three decades and is estimated to be 30% as of 2022.1 As an indication of disease burden, MASLD-related liver transplantation has already surpassed many other aetiologies as a leading indication of transplant waitlisting in the West.2 Metabolic dysfunction underlies the pathogenesis of […]
touchREVIEWS in Endocrinology. 2026;22(1): Online ahead of journal publication
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Pituitary Disorders
Roula Zahr, Maria Fleseriu
9 mins
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Published Online: Aug 6th 2018 European Endocrinology, 2018;14(2):57–61 DOI: https://www.frankenthalerfoundation.org
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Acromegaly is a rare disease, caused largely by a growth hormone (GH) pituitary adenoma. Incidence is higher than previously thought. Due to increased morbidity and mortality, if not appropriately treated, early diagnosis efforts are essential. Screening is recommended for all patients with clinical features of GH excess. There is increased knowledge that classical diagnostic criteria no longer apply to all, and some patients can have GH excess with normal GH response to glucose. Treatment is multifactorial and personalised therapy is advised.
Acromegaly, growth hormone, pituitary adenoma, somatostatin receptor ligand
Acromegaly is a chronic disorder characterised by growth hormone (GH) hypersecretion, predominantly caused by a pituitary adenoma.1 Disease prevalence ranges from 2.8–13.7 cases and annual incidence is between 0.2–1.1 cases/100,000 people; however, real incidence is likely much higher.2,3 Average age at diagnosis ranges from 40–50 years 4–6 and mean delay in diagnosis is approximately 10–11 years. More than 95% of acromegalic cases are secondary to a pituitary adenoma: somatotrophs or GH-producing cells. In <5% of cases, acromegaly is related to a hypothalamic or neuroendocrine tumours, which secrete GH-releasing hormone, leading to excess GH. Peripheral GH-secreting tumours are exceedingly rare.1
GH stimulates synthesis of insulin-like growth factor 1 (IGF-1) from the liver and systemic tissues. Hypersecretion of GH leads to excess production of IGF-1. IGF-1 mediates most of the phenotypic features and metabolic effects of GH, but GH excess also has direct detrimental effects.1,7 Acromegaly is associated with increased morbidity and mortality, but mortality returns to that of the normal population after appropriate treatment and biochemical normalisation.8,9 This review focusses on several recent updates related to acromegaly diagnosis and treatment.
Screening is recommended for all patients presenting with clinical features of acromegaly (such as mass tumour effects, systemic effects of GH/IGF-1 excess, cardiovascular and metabolic features, respiratory and bone/joint manifestations and/or other endocrine consequences). However, screening may also be considered in patients with several medical conditions known to be associated with acromegaly such as type 2 diabetes mellitus, carpal tunnel syndrome, debilitating arthritis, hypertension and sleep apnoea.10–12 Awareness of these comorbidities is critical for early detection of acromegaly.
Biochemical screening is the first step for an acromegaly diagnosis. Endocrine Society guidelines and experts’ consensus recommend using age- and sex-adjusted IGF-1 levels in combination with GH nadir during an oral glucose tolerance test (OGTT) to diagnose and rule out acromegaly.13,14 Measuring serum IGF-1 is usually the initial screening test. Considerable variation in laboratory results for IGF-1 obtained from different assays,15 pose a hindrance to diagnosis. For example, these discrepancies may lead to inaccurate exclusion of a diagnosis. This has been reported in up to 30% of patients in different laboratories.16 Given the methodological differences between assays and to establish accurate laboratory results, interpretation reference intervals must be method-specific, adjusted for age and sex, and stratified according to Tanner stages.17 Equivocal or elevated IGF-1 levels require further diagnosis confirmation in most patients. An OGTT with 75 g glucose is considered the gold standard for diagnosing acromegaly. However, similar to IGF-1 assays, the GH assay method can impact the absolute GH concentration reported by a laboratory.18 As a consequence, the assay method may also impact the cut-off for GH suppression following oral glucose load.19 Current widely used cut-offs for GH after OGTT are 1.0 and 0.4 ng/dL. However, these may not be accurate for all commercial assays, and method-specific values for GH cut-offs must be reported when available.13,20
Severe obesity, prolonged fasting and malnutrition reduce IGF-1 levels in patients without acromegal
