In pulmonary granulomatoses, immunoendocrine interactions lead to hormonal disturbances. Some of them (for example, hypervitaminosis D and hyperprolactinemia in lung sarcoidosis) have been known for a long time, but calcitonin regulation in this disease has not been studied at all. 95 male and female patients from 22 to 69 years old were comprehensively investigated. Among them 53 people were with a diagnosis of lung tuberculosis (1st group) and 42 patients — with lung sarcoidosis (2nd group). The control group consisted of 30 apparently healthy donors. In addition to the general clinical examination (anamnesis, physical examination, clinical blood analysis with additional determination of leukocytic and nuclear indices of intoxication), all persons enrolled in the study underwent serum concentration measurements of: procalcitonin, cortisol, triiodothyronine (T3), thyroxine (T4), thyrotropin (TSH) and prolactin by ELISA. In terms of the frequency of concomitant endocrinopathies (diabetes mellitus, diseases of the reproductive system and thyroid gland), the groups of patients with lung tuberculosis either sarcoidosis were comparable (p>0.05). The patients were in a stable compensated status, but the nature of complaints and changes in the blood tests of patients (tendencies towards anemia, an increase in the number of leukocytes, elevated indices of intoxication) indicated the presence of a syndrome of excessive systemic action of proinflammatory autacoids, which was more pronounced in tuberculosis than in sarcoidosis. Simultaneously both in lung tuberculosis and sarcoidosis (to a lesser extent), a unidirectional endocrine response of the body was noted: the development of subclinical hypothyroidism with an increase in TSH, prolactin and cortisol levels. Procalcitonin levels averaged 2.3±0.3 ng/ml in lung tuberculosis and 1.1±0.1 ng/ml — in lung sarcoidosis patients (between groups p <0.05). In healthy individuals this prohormone was absent in the blood in all cases (p<0.05 with groups 1 and 2). In both lung granulomatoses, there is a syndrome of excessive systemic action of proinflammatory autacoids. Hyperprocalcitoninemia in lung sarcoidosis is documented in this study for the first time in the world literature. It can be interpreted either as an evidence in favor of the bacterial aetiology of sarcoidosis, or as an argument against the notion of a marker role of hyperprocalcitoninemia for bacterial inflammation. In our opinion, the latter reflects the syndrome of excessive systemic action of proinflammatory autacoids, regardless of its aetiologies.