Aging is a multi-factor biological process that inevitably affects everyone. Degenerative processes, starting at the cellular and molecular levels, gradually influence the change in the functional capabilities of all organs and systems. Progeroid syndromes (from Greek. progērōs prematurely old), or premature aging syndromes, represent clinically and genetically heterogeneous group of rare hereditary diseases characterized by accelerated aging of the body. Progeria and segmental progeroid syndromes include more than a dozen diseases, but the most clear signs of premature aging are evident in Hutchinson-Guilford Progeria Syndrome and Werner Syndrome. This review summarizes the latest scientific data reflecting the etiology and clinical picture of progeria and segmental progeroid syndromes in humans. Molecular mechanisms of aging are considered, using the example of progeroid syndromes. Modern possibilities and potential ways of influencing the mechanisms of the development of age-related changes are discussed. Further study of genetic causes, as well as the development of treatment for progeria and segmental progeroid syndromes, may be a promising direction for correcting age-related changes and increasing life expectancy.

Primary hyperparathyroidism (PHPT) is the third most common endocrine disease after diabetes mellitus and thyroid pathology. Recent epidemiological and experimental data have shown that long-term maintenance of low vitamin D levels in the blood can lead to the development of hyperplastic processes in the cells of the parathyroid glands, followed by autonomous production of parathyroid hormone. In PHPT vitamin D insufficiency or deficiency according to various sources occurs with a frequency of 5377% of cases. The literature review indicates more severe disease in patients with concomitant vitamin D deficiency. The expediency of preoperative assessment of vitamin D levels in all patients with PHPT in order to minimize the risk of hypocalcemia after parathyroidectomy is discussed. This article presents the relationship between vitamin D deficiency and PHPT, as well as possible methods for correcting vitamin D deficiency in PHPT. Molecular and cellular mechanisms of the occurrence of pathological processes in the parathyroid glands under conditions of low vitamin D levels are presented.