Ghrelin is a peptide consisting of 28 amino acid residues that is secreted in the stomach and to a lesser extent in other organs. It is a stimulant of growth hormone secretion (GHS), promoting the release of GH by activating the so-called GHS-receptors. These receptors are predominantly concentrated in the hypothalamic-pituitary region, but are also found in other tissues, which explains the wide range of effects of GHR, including stimulation of the secretion of GH, prolactin and adrenocorticotropic hormone (ACTH); effects on sleep and behavior, increased appetite and a positive energy balance; diabetic effect on carbohydrate metabolism, control of gastric secretion and peristalsis. In addition, the experiments have repeatedly shown the positive inotropic effect of ghrelin on the heart, vasodilation, and cell proliferation.

The wide biological spectrum of action of ghrelin makes it promising to study and apply new knowledge in various fields of medicine: endocrinology, gastroenterology, immunology, oncology and cardiology.

Menopause, being the end of the reproductive period of a woman’s life, is characterized by changes in the endocrine balance in the body, significantly affecting health, quality of life and general life prognosis. These changes can be more significant and even take on a fatal character with "forced", artificial (surgical) menopause.

The first report on increased production of 17-ketosteroids in healthy children before puberty was published by N. Talbot et al. in 1943. F. Albrigth et al. introduced the concept of "adrenarch", which everyone has used for the past 50 years. Later, with the advent of more advanced methods, it was shown that increased excretion of 17-ketosteroids during this development period is due to increased secretion of the adrenal cortex of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS). It must be emphasized that the content of other adrenal androgens - androstenedione and lip-hydroxyandrostenedione - does not increase during the adrenarche period. An increase in their secretion is recorded at the age of 6–8 years, that is, it is somewhat behind the activation of DHEA secretion.

It must be remembered that androstenedione is also a product of DHEA metabolism in peripheral tissues. In contrast, lip-hydroxyandrostenedione can form only in the cortical layer of the adrenal gland, which is due to the presence of the corresponding enzyme system, which is localized in the adrenal tissue.

Medullary thyroid cancer (MTC) is a fairly rare disease, accounting for 5–7% of all cases of thyroid cancer. The sporadic form of thyroid cancer is observed in 70–80% of cases, family (inherited - autosomal dominant type of inheritance) - in 20-30%. Familial forms of MTCG are caused by point mutations in the RET proto-oncogen (Rearranged during Transfection). To date, about 25 germinal (inherited) mutations are described in the world literature in 19 codons of the RET gene, which are found in 97% of patients with MEN 2A, in 95% with MEN 2B and in 86% of patients with SMR.

In 2005, 50 years passed since Jerome Conn described arterial hypertension caused by hyperproduction of aldosterone by a tumor of the adrenal cortex.

Subacute thyroiditis (de Kerven's thyroiditis, giant cell thyroiditis, granulomatous thyroiditis) - a self-limiting inflammatory disease of the thyroid gland (thyroid gland), presumably of viral etiology, is the most common cause of pain in the thyroid gland. The disease (probably without an autoimmune component) is characterized by a 4-phase course (thyrotoxicosis, euthyroidism, hypothyroidism and restoration of normal functioning of the thyroid gland), its duration is from several weeks to several months. The subacute thyroiditis was first described by de Kerven in 1904. In most cases, if the disease has a characteristic clinical picture, the diagnosis of subacute thyroiditis is not difficult and, with adequate treatment, the patient will recover completely.

There are 3 alternative methods of treating benign thyroid diseases that occur with thyrotoxicosis syndrome: medication, surgery, and radioiodine therapy. However, there are some features in the approaches to the treatment of autoimmune and non-immune hyperthyroidism.

The relationship between thyroid pathology and bone tissue was first noticed as early as 1891, when Recklinghausen described multiple fractures in a patient with untreated thyrotoxicosis. Despite the fact that in the modern etiological and pathogenetic classification of osteoporosis, thyrotoxicosis is included in the group of secondary osteoporosis, various aspects of the action of thyroid hormones on bone tissue continue to be studied to this day.

The purpose of this review is to discuss the mechanisms of the influence of thyroid hormones on bone and, to a greater extent, to analyze new information on the biological and clinical significance of TSH for bone tissue. The review also provides information on the physiology of bone remodeling and the mechanisms of activation of receptors for thyroid hormones and TSH, which is necessary for a more complete understanding of hypotheses that explain the possible ways TSH affects bone cells.

80 years have passed since the birth of the famous scientist-endocrinologist, consultant of the Endocrinological Research Center of the Russian Academy of Medical Sciences, corresponding member of the Russian Academy of Medical Sciences, laureate of the Lenin Prize, Honored Scientist of the Republic of Uzbekistan, Doctor of Medical Sciences, Professor Rajab K. Islamambekov.