Muminov Azim Sharifovich (1)
In recent years, more and more attention has been paid to modifiable factors affecting recovery from severe fractures. One of these factors is vitamin D, a hormone that regulates mineral metabolism and immunity. Vitamin D deficiency is extremely common: about 50-70% of trauma patients have a level of 25(OH)D is below the norm [1]. Studies have linked vitamin D deficiency to an increased risk of infectious complications (pneumonia, urinary tract infections) and even thromboembolism in patients with severe injuries [2]. In addition, vitamin D deficiency can slow down osteogenesis, leading to a longer period of bone fusion [3, 2]. Against the background of deficiency, there is often a concomitant imbalance of immunoglobulins and cytokines. Correction of vitamin D deficiency and targeted immunocorrection (for example, the introduction of immunoglobulins) in the acute period of injury will reduce the incidence of purulent complications and improve outcomes.
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