Vol 10, No 1 (2016)

National clinical recomendations
Russian Association of Endocrinologists Clinic Guidelines for Thyroid Nodules Diagnostic and Treatment
Bel'tsevich D.G., Vanushko V.E., Mel'nichenko G.A., Rumyantsev P.O., Fadeyev V.V.

Abstract

Russian guidelines for diagnostic of thyroid nodules gained some actual questions: necessity of ultrasound (US)-screening of the thyroid cancer, indications for fine needle aspiration and exam of calcitonin, necessity of unification of US andcytopathology classification for signs of thyroid nodules.

Endocrine Surgery. 2016;10(1):5-12
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Review of literature
Relevance and perspective concept of investigation of subclinical Cushing syndrome.
Kuznetsov N.S., Latkina N.V., Kaminarskaya Y.A.

Abstract

Subclinical Cushing’s syndrome is the most widespread variant of hormonal activity among adrenal incidentalomas. The clinical significance of this condition has been confirmed by numerous studies showing “metabolic consequences” of chronic autonomous cortisol hypersecretion. Some clinical symptomatology of metabolic syndrome, such as obesity, impaired carbohydrate metabolism and hypertension, are peculiar to subclinical hypercorticism more than to population. This requires a thorough examination of patients with adrenal incidentalomas for hormonal activity, as well as determining the indications for surgical intervention. In the current era of evidence-based medicine, the overall management of these tumors remains empirical. The pathogenesis of subclinical Cushing’s syndrome remains unclear. Understanding of the mechanisms of chronic autonomous cortisol hypersecretion would enable to identify clinical and genetic heterogeneity of this condition, to determine prognosis and indications for surgery and to develop pharmacological methods of treatment. The purpose of this article is to review the current views on the diagnosis, pathogenesis and treatment of subclinical Cushing’s syndrome, identifying perspective directions of work.

Endocrine Surgery. 2016;10(1):13-22
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Clinical practice
Comments to the project of Russian clinical practice guidelines for diagnosis and treatment of differentiated thyroid cancer.
Bubnov A.N., Chernikov R.A., Slepcov I.V., Semenov A.A., Konstantinovich C.I., Makar'in V.A., Uspenskaja A.A., Timofeeva N.I., Novokshonov K.J., Karelina J.V., Fedorov E.A., Maljugov J.N., Fedotov J.N.

Abstract

The article is dedicated to the discussion about the project of Russian clinical practice guidelines for diagnosis and treatment of differentiated thyroid cancer.
Endocrine Surgery. 2016;10(1):23-27
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Clinical Case
Secondary hyperaldosteronism, caused by abnormalities of the renal vessels, in clinical endocrinologist
Markova T.N., Parshin V.V., Mishchenko N.K.

Abstract

Aldosterone levels increase in clinical practice may be due to primary or secondary hyperaldosteronism. Secondary hyperaldosteronism (CAA) is a clinical syndrome caused by increased synthesis of renin juxtaglomerular apparatus of the kidneys in response to lower perfusion pressure in the afferent glomerular arteriole. This mechanism leads to activation of the renin-angiotensin-aldosterone system with a consequent increase in systemic blood pressure. Clinically manifested CAA secondary (systemic) arterial hypertension, the most common form of parenchymal renal disease and renal vascular lesions. Renovascular diseases are a heterogeneous group of pathologies, which includes atherosclerosis of renal arteries, the most common cause; fibromuscular dysplasia (FMD); other more rare diseases, accompanied by a narrowing of the lumen of the renal vessels. Some authors consider the possibility of including a group of renovascular disease presence of multiple renal arteries. Тhe article presents the clinical cases of secondary hyperaldosteronism, caused by FMD and abnormal amounts of the renal arteries, manifested hypertension and increased levels of aldosterone in the blood. Carrying out a detailed search of the diagnostic determination of the ratio of aldosterone to plasma renin helped eliminate endocrine genesis of the disease and to identify the true cause of aldosteronism.

Endocrine Surgery. 2016;10(1):28-34
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