Abstract
Research on vitamin D in patients with nontuberculous mycobacterial (NTM) pulmonary disease (PD) is limited. We aimed to compare the vitamin D parameters of patients with NTM-PD to those of a healthy control group, and to assess the possible predictive markers for a clinical response. We prospectively enrolled 53 patients with NTM-PD between January 2014 and December 2016. The clinical data and vitamin D indices, including total, free, bioavailable 25-(OH)D, and vitamin D binding protein (VDBP) genotyping, were measured at baseline and six months after enrollment. An external dataset of 226 healthy controls was compared with the NTM-PD group. The mean age of subjects was 53 years; 54.5% were male. The NTM-PD group was older, predominantly female, and had a lower body mass index (BMI) than the controls. The proportion of patients with vitamin D concentration <50 nmol/L was 52.8% in the NTM-PD group and 54.9% in the control group (p = 0.789). The bioavailable 25-(OH)D concentrations of the NTM-PD group and the controls were similar (6.9 nmol/L vs. 7.6 nmol/L, p = 0.280). In the multivariable analysis, bioavailable 25-(OH)D concentrations were associated with NTM-PD, adjusting for age, sex, BMI, and VDBP levels. Bioavailable 25-(OH)D concentrations were significantly associated with susceptibility to NTM-PD, but not with treatment outcomes. Lower bioavailable 25-(OH)D might be a risk factor for NTM-PD.
Highlights
Nontuberculous mycobacteria (NTM) are ubiquitous organisms that cause chronic pulmonary disease (PD) [1]
The most important point of our study was that serum bioavailable and free vitamin D levels were measured for the first time in patients with NTM-PD
We found that the free and bioavailable 25-(OH)D levels of patients with NTM-PD were similar to those of healthy controls, bioavailable vitamin D
Summary
Nontuberculous mycobacteria (NTM) are ubiquitous organisms that cause chronic pulmonary disease (PD) [1]. Malnutrition, which is frequently seen in patients with NTM-PD [5,6,7,8], has been shown to be a poor prognostic factor by previous studies [9,10]. The active form of vitamin D, 1,25-(OH) D3 , which is mainly hydroxylated in the kidney from an inactive form of 25-(OH)D, is converted by a macrophage [15]. This activated vitamin D augments innate immunity by the fusion of phagolysosomes [11] and activates the intracellular signaling pathway by binding vitamin D binding protein (VDBP). Along with vitamin D, VDBP exerts immunological effects directly via neutrophil chemotaxis and a macrophage-activating factor (MAF), and indirectly by binding to activated vitamin D [12,16]
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