Surgical treatment of pituitary adenomas
https://doi.org/10.52888/0514-2515-2026-368-1-135-145
Abstract
The diagnosis of “pituitary adenoma” within the WHO Classification of Endocrine System Tumors is established based on a combination of clinical manifestations, neuroimaging findings (primarily MRI), and histopathological examination with immunohistochemistry. Since 2004, pituitary tumors have been officially classified as endocrine neoplasms, with a distinction introduced between adenomas and carcinomas. The latter designation applies to cases in which the primary pituitary neoplasm is accompanied by distant metastases in cranial, spinal, or other sites. Previously, adenomas were subdivided into typical and atypical forms: an atypical adenoma was diagnosed in the presence of invasive growth, marked cellular atypia, and a Ki-67 proliferation index exceeding 3%, in the absence of metastasis. However, since the 2017 revision, the international classification of pituitary tumors no longer includes the concept of atypical adenoma, thereby simplifying the terminology and shifting the focus toward morphological and clinico-radiological characteristics for diagnostic purposes.
About the Authors
U. Kh. RakhmonovTajikistan
Rakhmonov Umed Khurshedovich – applicant of the Department of Neurosurgery and Combined Trauma
Dushanbe
tel.: +992500000024
R. N. Berdiev
Tajikistan
Berdiev Rustam Namozovich – Doctor of Medical Sciences, Professor, Head of the Department of Neurosurgery and Combined Trauma
Dushanbe
References
1. Astafieva L.I. Clinical and morphological features and results of drug and surgical methods of treatment of prolactin-secreting pituitary macroadenomas Astafieva L.I. 2012. (In Russ.)
2. Hernandez-Ramirez, L.C. Familiar pituitary adenomas. Pituitary disorders: Diagnosis and Management L.C. Hernandez-Ramirez. John Wiley Son. 2013.
3. Dalantaeva, N.S., Dedov I.I. Genetic and metabolic characteristics of familial isolated pituitary adenomas. Obesity and Metabolism. 2013;2:10. DOI 10.14341/2071-8713-4817. (In Russ.)
4. Trivellin G. Gigantism and acromegaly due to Xq26 microduplications and GPR101.The New England journal of medicine. 2014;371:2363–2374.
5. Daly A.F. Gigantism, acromegaly, and GPR101. The New England journal of medicine.2015.
6. Xekouki P. Succinate dehydrogenase (SDHx) mutations in pituitary tumors: could this be a new role for mitochondrial complex II and/or Krebs cycle defects? .Endocr. Relat. Cancer. 2012;19(6):3340.
7. Kuznetsov S. L. Clinical studies. The importance of the early response gene c-fos and its expression products in neurons during various actions. State budgetary educational institution of higher education I. M. Sechenov First Moscow State Medical University, Ministry of Health and Social Development of the Russian Federation. Moscow: Biomeditsina. 2013. (In Russ.)
8. Beckers A. X-LAG: How did they grow so tall?. Ann. Endocrinol. 2017;78(2):131–136.
9. Daly A.F. GHRH excess and blockade in X-LAG syndrome. Endocr. Relat. Cancer. 2016;23(3):161–170.
10. Naves L.A. Aggressive tumor growth and clinical evolution in a patient with X-linked acro-gigantism syndrome. 2016;51(2):236–244.
11. Apellaniz-Ruiz M. Mesenchymal Hamartoma of the Liver and DICER1 Syn-75 drome. N. Engl. J. Med. 2019;380(19):1834–1842.
12. Poma A.M. DICER1 somatic mutations strongly impair miRNA processing even in benign thyroid lesions.2019;10 (19):1785–1797.DOI 10.18632.
13. Pigarova E. A. Registry of patients with tumors of the hypothalamic-pituitary region. National survey of the diagnostic and treatment capabilities of acromegaly in various regions of the Russian Federation. Working Group of the OGGO registry. Borodich: 2017. (In Russ.)
14. Zhou Y. MEG3 noncoding RNA: a tumor suppressor. J. Mol. Endocrinol. – 2012;48: R45–R53.
15. Mamedova E.O. Pituitary adenomas in the context of hereditary syndromes Problems of Endocrinology. 2014;4:53. (In Russ.)
16. Orlova E.M. Carney complex – a syndrome of multiple endocrine neoplasias. Problems of Endocrinology. 2012:3. (In Russ.)
17. Makazan N. V. The role of molecular genetic research methods in the diagnosis of McCune-Albright syndrome. Problems of Endocrinology. 2017;63(6):360–368. (In Russ.)
18. Dwight T. Familial SDHA Mutation Associated With Pituitary Adenoma an- dPheochromocytoma. Paraganglioma JCEM. 2013;98:1103–1108.
19. Korbonits M. AIP-related familial isolated pituitary adenomas. Gene Reviews. 2012 June 21.
20. Robertson J.C. DICER1 syndrome: DICER1 mutations in rare cancers. Cancers. 2018;10(5):143.
21. Brenneman M. Temporal order of RNase IIIb and lossof-function muta-tions during development determines phenotype in DICER1 syndrome: A unique vari-ant of the two-hit tumor suppression model. F1000 Research. 2015;214.
22. Липатенкова А.К. Иммуногистохимические и рентгенологические особенности гормонально-неактивных аденом гипофиза. Проблемы эндокринологии. 2015;61(6):4–9.
23. Thakker R.V. Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4). Molecular and Cellular Endocrinolog. 2014;386(1-2):2–15.
24. Forlino A. PRKACB and Carney complex. N. Engl. J. Med. 2014;370(11):1065–1067.
25. Foulkes W. D. DICER1: mutations, microRNAs and mechanisms. Nat. Rev. Cancer.2014;14(10):662–672.
26. Beckers A. Familial isolated pituitary adenomas (FIPA) and the Pituitary adenoma predisposition due to mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene. Endocrine Reviews. 2013;34 (2):239–277.
27. Trivellin G. Gigantism and acromegaly due to Xq26 microduplications and GPR101 mutation. N. Engl. J. Med. 2014;371(25):2363–2374.
28. Pronin V.S. Modern strategy for diagnosis and treatment with somatotropin. Vasilieva. 2013. (In Russ.)
29. Novikova E.I. Next-generation sequencing (NGS): application for molecular genetic research in oncology. Moscow: Russian Scientific Center of Roentgenology and Radiology. 2016. (In Russ.)
30. Cavaco B.M. Identifi cation of de novo germline pathogenic variants in the HRPT2 gene in two apparently sporadic cases with challenging parathyroid tumor diagnoses. Endocr. Pathol. 2011;22:44–52. (In Russ.)
31. Mamedova E.O. Hereditary forms of primary hyperparathyroidism Osteoporosis and osteopathy. 2018;21(2):23–29. (In Russ.)
32. Menara M. SDHD Immunohistochemistry: A New Tool to Validate SDHx Mutations in Pheochrom cytoma/Paraganglioma. Endocrinol. Metab.2015;100(2):287–291. DOI 10.1210/ jc.2014-1870. 80
33. Denes J. Heterogeneous genetic background of the association of pheo-chromocytoma/paraganglioma and pituitary adenoma – results from a large patient co-hort .J. Clin. En-docrinol. Metab. 2015;100(3):531–541.
34. Wang C. microRNA expression profile and differentially-expressed genes in prolactinomas following bromocriptine treatment. Oncology Reports. 2012;27:1312–1320.
35. Reincke M. Mutations in the deubiquitinase gene USP8 cause Cushing’s disease. Nature Reviews Genetics. 2015;31–38.
36. Perez-Rivas L.G. The gene of the ubiquitin-specific protease 8 is frequently mutated in adenomas causing Cushing’s disease. The Journal of Clinical Endocrinology & Metabolism. 2015.
37. Ma Z.Y. Recurrent gain-of-function USP8 mutations in Cushing’s disease. Cell Research. 2015;25:306–316.
38. Newey P.J. Whole-exome sequencing studies of nonfunctioning pituitary adenomas. The Journal of Clinical Endocrinology & Metabolism. 2013;98:796– 800.
39. Thakker R.V. Clinical Practice Guidelines for MEN1. The Journal of Clinical Endocrinology & Metabolism. 2012;97(9):2990–3011.
40. Thakker R.V. Clinical Practice Guidelines for MEN1. The Journal of Clinical Endocrinology & Metabolism. 2012;97(9):2990–3011.
41. Vargas-Poussou. R. Familial hypocalciuric hypercalcemia types 1 and 3 and primary hyperparathyroidism: similarities and differences.The Journal of Clinical Endocrinology & Metabolism. 2016;101(5):2185–2195.
42. Iacobone M. Hereditary hyperparathyroidism – a consensus report of the European Society of Endocrine Surgeons (ESES). Langenbecks. Arch. Surg. 2015;400(8):867–886.
43. Dogadin S.A. Treatment of acromegaly with longacting octreotide: effective control of disease activity and tumor volume reduction. Clinical Endocrinology. 2012: 4. (In Russ.)
44. Zhou Y. Genetic and epigenetic mutations of tumor suppressive genes in sporadic pituitary adenoma. Mol. Cell Endocrinol. 2014;386(1-2):16–33.
45. Rostomyan L. Clinical and genetic characterization of pituitary gigantism: an international collaborative study in 208 patients. Endocr. Relat. Cancer. 2015;22:745– 757.
46. Iacovazzo D. Germline or somatic GPR101 duplication leads to X-linked acrogigantism: a clinico-pathological and genetic study. Acta Neuropathol. Commun. 2016;4:56.
47. Beckers A. X-linked acrogigantism syndrome: clinical profile and thera-peutic responses. Endocr. Relat. Cancer. 2015;22(353):67.
48. Caimari F. Risk category system to identify pituitary adenoma patients with AIP mutations. J. Med. Genet. 2018;55(254):60.
Review
For citations:
Rakhmonov U.Kh., Berdiev R.N. Surgical treatment of pituitary adenomas. Health care of Tajikistan. 2026;(1):135-145. (In Russ.) https://doi.org/10.52888/0514-2515-2026-368-1-135-145
JATS XML























