Vitamin D deficiency is a common, underdiagnosed condition that has received increased attention around the world.1 The Endocrine Society guidelines and the Institute of Medicine (IOM) recommend screening in populations at risk, as no evidence currently exists to support screening at a population level.2 Candidates for vitamin D screening include those who are at a specific risk of vitamin D deficiency and patients who are experiencing, or are at risk of, specific medical conditions associated with hypovitaminosis D.1,2 Decreased vitamin D levels strongly interact with different pathogenic mechanisms in chronic obstructive pulmonary disease (COPD).
From September 2015 to August 2016, serum vitamin D was analysed and COPD Assessment Tests (CAT) were completed in a total of 55 patients. COPD patients can be categorised in different stages of severity, into mild, moderate, severe, and very severe disease, according to their forced expiratory volume in the first second (FEV1) score.3,4 Nowadays, COPD classification includes CAT, dyspnoea scale, and number of exacerbations the patient experiences per year.3
With the progressive loss of pulmonary function, patients become more prone to acute exacerbation5 of their disease, which frequently requires hospitalisation, and may lead to respiratory failure and death,6 as well as a faster decline in FEV1.7 The systemic consequences of Vitamin D deficiency appear when serum levels do not reach 30 ng/mL. Furthermore, vitamin D boosts the innate immune response upon infection. Vitamin D may control many pathways within pathogenic mechanisms.6 It appears to act on innate immune cells and it can reduce the expression of toll-like receptors (TLR), which are critical in the induction of the early immune response and the priming of the adaptive immune system.5,7 High levels of vitamin D are potent inhibitors of dendritic cell maturation, with lower expression levels of major histocompatibility complex (MHC) Class II molecules, downregulation of costimulatory molecules, and lower production of proinflammatory cytokines.3
The mean age was 66.44 (±11.86 years), with a total of 39 males and 16 females. The prevalence of vitamin D deficiency (<30 ng/mL) was 98.4%. Vitamin D average was 14.33 ng/mL in males and 14.4 ng/mL in females. There was an association between CAT D, the most severe score, and vitamin D (p=0.016).
There is a high prevalence of vitamin D deficiency in patients with COPD (98.4%). There was an association between CAT D and vitamin D (p=0.016). The question remains as to whether deficit or preventing adequate vitamin D supplementation can reverse the course of the disease. Vitamin D strongly interacts with different pathogenic mechanisms in COPD.7 Prevalence of vitamin D deficiency is particularly high in COPD patients and increases with the severity of COPD. This finding may potentially be a way of preventing further deterioration of pulmonary function. Reduced vitamin D levels may thus enhance proinflammatory pathways, reduce the downregulation of T cells, and impair the innate defence against bacteria and viruses, possibly leading to clinical disease onset and/or further pulmonary deterioration.3 Randomised controlled trials are needed to explore the systemic consequences in the pathogenesis of COPD exacerbation/infections/deterioration.