We do not recommend population screening for diabetes insipidus (DI) (B3). We recommend to perform diagnostic testing for central diabetes insipidus (CDI) in patients who underwent neurosurgery, after skull and brain trauma, subarchnoid hemorrhage (B3). We recommend excluding thirst impairment during all stages of diagnostic assessment (С3). We recommend excluding DI in cases of persistent hypotonic polyuria: excretion of more than 3 L. or more than 40 mL/kg of urine daily; urine osmolality less than 300 mOsm/kg or urinary specific gravity less than 1004 g/L in all urine samples or during Zimnitsky test (В3). After hypotonic polyuria is confirmed, we recommend excluding of the main causes of nephrogenic diabetes insipidus (NDI) (B3). We recommend simultaneous measurement of urine osmolality and blood osmolality/sodium level in order to confirm DI. Blood hyperosmolality (more than 300 mOsm/kg) and/or hypernatremia with low urine osmolality (less than 300 mOsm/kg) confirms DI (B2). If testing does not reveal these findings, we recommend performing a fluid deprivation test to exclude primary polydipsia (PP) (B2). Desmopressin test is recommended to distinguish CDI and NDI (B2). In cases of CDI we recommend to perform head MRI with contrast (B3). In cases of NDI we recommend assessing renal structure and function and possible electrolyte disturbances (C3). In cases of PP we recommend to refer a patient to psychiatrist (B3). We recommend treating CDI with synthetic vasopressin analogue desmopressin (B1). We recommend an individual approach in choosing desmopressin dosage form (B2). As the initial dose is difficult to predict when starting desmopressin treatment, we recommend titrating the dosage using two approaches: the average dose and as required (C4). We recommend educating the patients to ensure knowledge of the features of various desmopressin dosage forms (C4). To decrease the risk of water intoxication, we recommend educating the patients to the water intake regimen adherence (С4). When CDI is accompanied by thirst impairment, we recommend titrating the dose in a clinical setting, with assessment of blood sodium, bodyweight and/or urine volume (C4).

We recommend acromegaly to be ruled in all patients with characteristic changes in appearance (A3). In all patients without characteristic changes in appearance, we recommend to rule out acromegaly, if several clinical signs suspicious for acromegaly are present (B3). We recommend acromegaly to be ruled out in all patients with pituitary adenoma (B3). We recommend to rule out acromegaly in all patients with prolactin-secreting adenomas (C4). For laboratory confirmation of acromegaly, we recommend to measure serum insulin-like growth factor-1 (IGF-1, somatomedin C) level (A3). In patients without obvious clinical signs of acromegaly and/or with a moderate increase in IGF-1 levels (IGF-1 index less than 1.3), we recommend to assess the response of somatotropic hormone (GH) to hyperglycemia (GH during an oral glucose tolerance test) (B3). In all patients with biochemically confirmed acromegaly, magnetic resonance imaging of the pituitary gland with intravenous contrast is recommended to assess pituitary adenoma size, location and growth pattern (A3). We recommend to measure blood glucose and glycated hemoglobin in all patients with confirmed acromegaly (B3). We recommend to measure serum prolactin levels in all patients with acromegaly (B3).In all patients with acromegaly and pituitary adenoma, transnasal transsphenoidal adenomectomy is recommended as first-line treatment if the patient’s consent is given and there are no contraindications (A1). For all patients with acromegaly for whom neurosurgical treatment is indicated, surgical intervention is recommended in medical centers, specializing in pituitary diseases, by neurosurgeons who perform at least 50 such operations per year (A3). We recommend that morphological and immunohistochemical examination of the removed pituitary adenoma is performed in all patients with acromegaly (A3). We do not recommend routine medical therapy for acromegaly before surgery as a mean to reduce tumor size (B2).For patients with acromegaly in whom neurosurgical treatment is not indicated or ineffective or while patient awaiting for the effect of radiation therapy, we recommend medical therapy (A1). Long-acting first-generation somatostatin analogues are recommended as first-line drug therapy for acromegaly. In case of partial/complete resistance to or intolerance to somatostatin analogs, pegvisomant is recommended as a second-line medical therapy for acromegaly (A1). We recommend starting pegvisomant from a single dose of 40–80 mg per day subcutaneously, then continue injections at a starting dose of 10 or 15 mg per day with IGF-1 monitoring after 4–6 weeks and dose adjustment if necessary (B2). In patients with acromegaly and a moderate increase in IGF-1 levels, we recommend to initiate cabergoline as medical monotherapy or, if somatostatin analogs are ineffective, in combination with them (B2).In patients with acromegaly, if the disease remains active after surgical treatment, if drug treatment is unavailable, intolerable or ineffective, and repeated neurosurgical intervention is inappropriate, it is we recommend radiation therapy (A1). A multidisciplinary approach is recommended in the management of acromegaly complications (C3).

The relevance of cachexia syndrome is determined by its high prevalence in clinical practice. It accompanies the course of not only oncological diseases, but also the majority of chronic somatic pathologies, such as chronic heart failure, renal failure, diabetes mellitus, chronic obstructive pulmonary disease, acquired immunodeficiency syndrome, rheumatoid arthritis, Alzheimers disease and others. It is known that even a slight weight loss in patients can determine an unfavorable prognosis of the underlying disease and reduce the effectiveness of therapy, and sometimes it becomes the direct cause of death of the patient. Cachexia is a complex metabolic syndrome, which is based on a violation of the central regulation of metabolism. The dangerous combination of decreased appetite (anorexia) and increased metabolism is the result of an imbalance in energy exchange. Treatment of cachexia syndrome is ineffective and limited in means. Given the progressive and irreversible nature of this syndrome, early diagnosis and prevention of its development are the primary task of the doctor. The article describes the main pathogenetic aspects of the development of cachexia syndrome. They can be common in different diseases. The article discusses the difficulties of diagnosing cachexia syndrome, the possibilities and prospects of treatment.

Medical article медицинская статья

В статье представлен клинический случай развития постоянной формы центрального несахарного диабета (ЦНД) у пациента после тяжелой черепно-мозговой травмы (ТЧМТ) в результате дорожно-транспортного происшествия. Подросток 16 лет поступил в лечебное учреждение в состоянии комы (6 баллов по шкале комы Глазго) с диагнозом: сочетанная травма; острая ТЧМТ; ушиб головного мозга тяжелой степени; субарахноидальное кровоизлияние; вдавленный многооскольчатый перелом свода черепа справа; протяженный перелом основания черепа; ушиб внутренних органов. На 3-и сутки развились полиурия и гипернатриемия (155 ммоль/л); диагностирован ЦНД и начата терапия десмопрессином в таблетированной форме через зонд. При выходе из комы (21-е сутки) отмечено появление жажды на фоне продолжения терапии. В связи с сохраняющейся жаждой и полиурией произведен перевод на терапию десмопрессином в виде спрея, на этом фоне отмечено уменьшение выделения мочи до 3—3,5 л в сутки. Симптоматика ЦНД наблюдалась и через 2 года после ТЧМТ, при этом функция аденогипофиза оставалась сохранной. Представленный случай является примером развития постоянного несахарного диабета у подростка с ТЧМТ, находившегося под длительным наблюдением. Клиническая картина ЦНД в состоянии комы проявлялась только полиурией и гипернатриемией, а по мере повышения уровня сознания присоединилась жажда. Вероятными причинами развития ЦНД явились повреждение нейрогипофиза и частичное повреждение стебля гипофиза в результате протяженного перелома основания черепа и/или необратимого вторичного повреждения гипоталамуса вследствие диффузного аксонального повреждения головного мозга после ТЧМТ.

Introduction: Currently, cabergoline therapy is the main treatment for prolactinomas. The use of the drug in most cases leads to regression of the tumor, normalization of prolactin (PRL) levels, and restoration of gonadotropic function. The mechanism of its action in tumor cells “in vivo” tracked in dynamics in the same human tumor is of considerable interest. Materials and Methods: A 30-year-old male was admitted to N.N. Burdenko National Medical Research Center of Neurosurgery. An magnetic resonance imaging (MRI) revealed a giant pituitary adenoma. The level of PRL was more than 5000 mU/l (30-360) (serum dilution was not used to determine PRL). Transcranial microsurgical removal of the tumor was performed. He was treated by cabergoline after surgery. Endoscopic transsphenoidal approach was repeated with subtotal removal of the rest of the tumor. Morphological and immunohistochemical studies of the tumor were done. Results: A morphological study revealed PRL-positive tumor with a Ki-67 LI of 8% with a distinctive expression of D2R, CD31, and CD34 markers. Control MRI in 3 months after surgery revealed remnants of a tumor of endoinfrasellar localization, the tumor remainders were found in endoinfrasellar localization. The tumor retained pronounced immunopositivity to PRL and D2R and a decrease in the Ki-67 to 2% and in the expression of CD31 and CD34. Subsequent therapy with cabergoline resulted in persistent normoprolactinemia, restoration of androgenic function, and absence of tumor recurrence during the 10-year follow-up period. Conclusions: Cabergoline is an effective treatment for prolactinoma, which leads to tumor regression. One of its mechanisms is the reduction of the proliferative index and tumor angiogenesis.