Endocrinol Metab.  2020 Jun;35(2):206-216. 10.3803/EnM.2020.35.2.206.

Precision Therapy in Acromegaly Caused by Pituitary Tumors: How Close Is It to Reality?

Affiliations
  • 1Division of Endocrinology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea
  • 2Department of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China

Abstract

Acromegaly presents with an enigmatic range of symptoms and comorbidities caused by chronic and progressive growth hormone elevations, commonly due to endocrinologic hypersecretion from a pituitary gland tumor. Comprehensive national acromegaly databases have been appearing over the years, allowing for international comparisons of data, although still presenting varying prevalence and incidence rates. Lack of large-scale analysis in geographical and ethnic differences in clinical presentation and management requires further research. Assessment of current and novel predictors of responsiveness to distinct therapy can lead to multilevel categorization of patients, allowing integration into new clinical guidelines and reduction of increased morbidity and mortality associated with acromegaly. This review compares current data from epidemiological studies and assesses the present-day application of prognostic factors in medical practice, the reality of precision therapy, as well as its future prospects in acromegaly, with a special focus on its relevance to the South Korean population.

Keyword

Acromegaly; Precision medicine; Growth hormone; Pituitary neoplasms

Figure

  • Fig. 1 Flowchart representing current clinical, imaging, histological and molecular predictors, as well as future predictors whose role can be finalized with developments in translational research [2,9,23–26,28–38,55,61,63–66]. GH, growth hormone; IGF-1, insulin-like growth factor-1; MRI, magnetic resonance imaging; SSTR2, somatostatin receptor subtype 2; D2R, dopamine d2 receptor; AIP, aryl hydrocarbon receptor interacting protein; ZAC1, pleomorphic adenoma gene 1 like zinc finger 1; RKIP, Raf kinase inhibitor protein; GNAS1, guanine nucleotide binding protein, alpha stimulating 1; SST5TMD4, somatostatin receptor subtype 5 splicing variant; SNP, single nucleotide polymorphism.


Cited by  1 articles

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Kyungwon Kim, Cheol Ryong Ku, Eun Jig Lee
Endocrinol Metab. 2023;38(5):463-471.    doi: 10.3803/EnM.2023.1820.


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