Thirty years ago, a hypothesis stating that preoperative shrinkage of growth hormone (GH) producing macroadenomas with somatostatin receptor ligands (SRLs) may improve surgical outcome was put forward. Since then, multiple retrospective, non-randomized studies as well as four contemporary prospective, randomized studies have been performed to evaluate the validity of that hypothesis and are critically reviewed in this manuscript.

With the exception of an occasional retrospective study the great preponderance of evidence could not confirm this hypothesis. Similarly, while all prospective studies suggested better surgical outcome for SRL-pretreated tumors 3 months post surgery, the differences in outcomes between pretreated and untreated control patients disappeared after 6–12 months.

Thus, preoperative treatment of macrosomatotropinomas with SRLs should not be relied upon as a means to achieve complete tumor removal and cannot be recommended.

Pheochromocytomas and paragangliomas (PPGLs) are rare catecholamine-secreting neuroendocrine tumours, up to 40% of which occur in the setting of a hereditary syndrome. The incidence is 2 to 8 per million persons per year. The peak incidence occurs in the third to fifth decades of life. According to the most recent classification, chromaffin tumours refer to malignant neoplasms. The incidence of metastasis in pheochromocytomas is 10%; in paragangliomas it is 25%. Clinical manifestations of PPGLs are caused by the excess of catecholamines. More than 20 hereditary gene mutations are known to result in PPGLs development. According to the molecular and cellular pathophysiology, all currently known mutations can be divided into 2 groups: the first group – SDHх, SDHAF2 (the assembly factor of SDH, FH, MDH2) – disrupts the Krebs cycle and mitochondrial energy transport chain; the second group – RET, NF1, TMEM127, MAX – leads to mutations in receptor protein kinases (tyrosine kinase), activating intracellular signal pathways (PI3K-AKT-mTOR and MYC), which are responsible for cell growth, growth regulation and cell differentiation. As a result, HIF transcription factors are stabilized (oxidative stress), and DNA methylation is changed, which leads to severe disturbances in gene expression and to malignant transformations of cells. There are three main biochemical phenotypes of PPGLs: noradrenergic, adrenergic and dopaminergic. According to the tumor type, the patient’s age and family history, complementary genetic testing and molecular visualization are recommended. In clinical practice, the biochemical tumor phenotype, its stage, family history and especially the genetic tumor “passport” allow to choose the best molecular visualization method (SPECT-CT/PET-CT) to personalize treatment and prognosis.

Hypoparathyroidism is the most common complication after surgery on the thyroid gland. All authors confirm the fact that the main cause of hypoparathyroidism is a violation of the blood supply of parathyroid glands, as well as their damage or even accidental removal during surgery. Having analyzed the real cases, and based on our own experience, we came to the conclusion that in order to prevent complications, we will need to study the types of blood supply of the parathyroid glands in details. To this end, we have performed 46 unilateral microdissections and X-ray angiography studies of the arterial supply at 23 organocomplexes of the neck. 42 upper and 43 lower parathyroid glands were detected. It has been established that the main feeding vessel of parathyroid glands is the inferior thyroid artery (type I). The association of glands with the inferior thyroid artery was revealed in 71.8% of cases. A mixed variant of blood supply (simultaneously from the superior and inferior thyroid arteries) was revealed in 14.1% cases (type II). Only 10.6% of the gland were fed isolated from the superior thyroid artery (type III). In addition, in 8.7% cases in the preparations there was no inferior thyroid artery. In 3.5% cases, the connections of the lower parathyroid glands with the thyroid arteries were not reliably detected. Most probably, their feeding was provided at the expense of small collaterals from surrounding organs (type VI).

Primary hyperparathyroidism is common clinical endocrine disorder with a prevalence between 1–2%. Solitary parathyroid adenomas account from 80 to 85% of cases of PHPT, hyperplasia and multiple adenomas is up to 15%, parathyroid carcinoma is a very rare cause of PHPT, accounting for about a 1% of cases. Clinically aggressive and atypical adenomas should be separately noted because of severe clinical course and life-threatening hypercalcemia, high morbidity and mortality, unknown malignant potential. No definite criteria are considered to be present to distinguish preoperatively atypical adenoma from parathyroid typical adenoma or carcinoma. The clinical course of the disease remains the only tool that allows to suspect an aggressive tumor on the preoperative stage. We present the clinical case of a 61-year-old female patient with a clinically “aggressive” course of PHPT and severe metabolic disturbances of bone tissue due to the atypical adenoma of the parathyroid gland.