Modern possibilities of tumor-oriented diagnostics and treatment of acromegaly

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Abstract

Background. Acromegaly is a heterogeneous disease combining many histological subtypes of somatotrophic tumors which differ in clinical and pathological manifestations, final size, development scenario, immunological profile, and sensitivity to treatment.

Objective. Comprehensive clinical, morphological and radiological stratification of somatotrophic tumors in order to clarify the tumor morphotype and predict the success of the proposed treatment.

Methods. We examined 82 patients with acromegaly who underwent non-radical adenomectomy and received 1st generation somatostatin analogues (SA1) for a long time. The results of treatment were compared with the clinical, immunophenotypic and radiological features of somatotrophic tumors.

Results. It was found that densely granulated somatotrophic tumors (DGST) were characterized by a pronounced expression of the 2nd subtype somatostatin receptors (SR) and good sensitivity to SA1, while sparsely granulated somatotrophic tumors (SGST) were larger, with low expression of the 2nd subtype SR and resistance to SA1. During radiological examination, DGST and SGST showed comparative hypo- or hyperintensity of the tumor signal on T2-weighted MRI. Based on the results of SA1 treatment, biochemical remission was achieved in patients with DGST, while disease activity remained in patients with SGST.

Conclusion. The results of the work confirm the existence of fundamental clinical, morphological and radiological differences between DGST and SGST, as well as the need for a differentiated approach to the pharmacotherapy of acromegaly. The magnitude of the decrease in insulin-like growth factor-1 after 3–6 months of treatment of more than 55% of the initial level was an additional predictor of the long-term effectiveness of SA1. The introduction of the indicator of the relative intensity of the tumor signal on T2-weigthed MRI into clinical practice will improve the diagnosis of acromegaly and optimize the treatment strategy.

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About the authors

Mikhail B. Antsiferov

Endocrinological Dispensary of the Moscow Healthcare Department

Email: r-wp@mail.ru
ORCID iD: 0000-0002-9944-2997
Russian Federation, Moscow

Alexey V. Petryaikin

Scientific and Practical Clinical Center for Diagnostics and Telemedicine Technologies

Email: r-wp@mail.ru
ORCID iD: 0000-0003-1694-4682
Russian Federation, Moscow

Tatiana M. Алексеева

Endocrinological Dispensary of the Moscow Healthcare Department

Email: r-wp@mail.ru
ORCID iD: 0000-0003-0066-845X
Russian Federation, Moscow

Evgeniy V. Pronin

Endocrinological Dispensary of the Moscow Healthcare Department

Author for correspondence.
Email: r-wp@mail.ru
ORCID iD: 0000-0001-6094-3623

Endocrinologist, Endocrinological Dispensary of the Moscow Healthcare Department, Moscow, Russia

Russian Federation, Moscow

Anna N. Khoruzhaya

Scientific and Practical Clinical Center for Diagnostics and Telemedicine Technologies

Email: r-wp@mail.ru
ORCID iD: 0000-0003-4857-5404
Russian Federation, Moscow

Safi M. Tamaeva

I.M. Sechenov First Moscow State Medical University (Sechenov University)

Email: r-wp@mail.ru
ORCID iD: 0009-0006-4140-0942
Russian Federation, Moscow

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Supplementary files

Supplementary Files
Action
1. JATS XML
2. Fig. 1. Expression of the 2nd p/t SR in PSO and RSO (IRS scores)

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3. Fig. 2. Dynamics of the level of IGF-d [ng/ml (Me)] against the background of AC1 treatment in patients with PSO and RSO

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4. Fig. 3. Prognostic significance of the values of the decrease in the level of IGF-1 after 3 and 6 months for assessing the effectiveness of long-term treatment of AC1

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5. Fig. 4. The final values of IS with a decrease in IGF-1 after 3-6 months less or more than 55% of the initial level during the treatment of AC1 (Me)

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6. Fig. 5. Examples of T2-weighted MRI images of patients from the created database before treatment initiation

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7. Fig. 6. Relative intensity of the PSO and RSO signal on T2 VI [Me (25/75%)Min/Max]

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8. Fig. 7. The final value of IS in patients with relative hypo- and hyperintense signals on T2 VI

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