Kinder and his colleagues assessed the prevalence of vitamin D deficiency in a cohort of patients with interstitial lung disease, who are often treated with corticosteroids. The detrimental effect of chronic use of corticosteroids on bone health has been well established, according to the researchers. Of the patients included in the study, 51 had interstitial lung disease and 67 had other forms of interstitial lung disease related to autoimmune connective tissue diseases.
A vitamin D insufficiency was defined as a serum level of less than 30 ng/mL. A level of less than 20 ng/mL was considered deficient. Both insufficient and deficient levels were prevalent in the study. In the overall sample, lower vitamin D levels were associated with reduced forced vital capacity (P=0.01). When the analysis was restricted to patients with connective tissue disease, both forced vital capacity and diffusing capacity of lung for carbon monoxide — a measure of the lung’s ability to transfer gases from the air to the blood — were significantly reduced (P<0.05 for both). After adjustment for several potential confounders — including age, corticosteroid use, race, and season, the presence of connective lung disease was a strong predictor of vitamin D insufficiency (OR 11.8, 95% CI 3.5 to 40.6).
According to the researchers, a pathogenic role of low vitamin D in the development of autoimmune diseases such as interstitial lung disease is plausible because of the immunoregulatory role of the biologically active form of vitamin D, 1,25-(OH)2D. “All cells of the adaptive immune system express vitamin D receptors and are sensitive to the action of 1,25-(OH)2D,” they wrote. “High levels of 1,25-(OH)2D are potent inhibitors of dendritic cell maturation with lower expression of major histocompatibility complex class II molecules, down-regulation of costimulatory molecules, and lower production of proinflammatory cytokines.” “A common theme in the immunomodulatory functions of vitamin D is that higher levels are immunosuppressive,” they continued, “which is consistent with a potential role for hypovitaminosis D in the pathogenesis of autoimmune disorders.”
In a statement, Len Horovitz, MD, a pulmonary specialist at Lenox Hill Hospital in New York City, commented that “vitamin D is known to promote wound healing, and to benefit the immune system. So it is not surprising to find that patients with immune lung disorders are vitamin D deficient.” He said that all of his patients are screened and treated for vitamin D deficiency with supplements. The study authors noted that further research is needed to determine whether supplementation is associated with improved outcomes. The study was limited, Kinder and his colleagues wrote, by its use of patients from a single center in Cincinnati.
In addition, the cross-sectional design of the study did not evaluate whether vitamin D supplementation is associated with any improved clinical outcomes. To examine that issue, the team called for prospective controlled interventional studies to determine whether vitamin D7 supplements can ameliorate symptoms and improve outcomes in connective tissue disease-related interstitial lung disease.
Source reference: Hagaman J, et al “Vitamin D deficiency and reduced lung function in connective tissue-associated interstitial lung diseases” Chest 2011; DOI: 10.1378/chest.10-0968.
A popular pastime for many older people is to try and figure out their chances of getting one ailment or another. Mayo Clinic researchers have simplified it – they have figured out the lifetime risk of developing rheumatoid arthritis and six other autoimmune rheumatic diseases for both men and women. “We estimated the lifetime risk for rheumatic disease for both sexes, something that had not been done before — separately or collectively,” says Cynthia Crowson Mayo Clinic biostatistician and first author. “Prevalence and incidence rates existed, but prevalence figures underestimate individual risk and incidence rates express only a yearly estimate.”
The researchers were looking for an accurate basis to offer an easy-to-understand average risk over a person’s lifetime, knowing that risk changes at almost every age. They used data from the Rochester Epidemiology Project, a long-term epidemiology resource based on patients in Olmsted County, Minn. The cohort of 1179, consisted of patients diagnosed between 1955 and 2007, allowed the team to extrapolate the nationwide estimates.
The adult lifetime risk in the United States of having some kind of inflammatory autoimmune disease is 8.4 percent for women and 5.1 percent for men. Based on year 2000 population figures, that means one woman in 12 and one man in 20 will develop one of the conditions in their lifetime. The authors consider that a substantial risk and say their findings should encourage more research on the value of early diagnosis and intervention for people with increased genetic risk of arthritis. They hope the new figures will help in counseling patients and in fundraising efforts to find improved treatments.
The research was supported by the National Institutes of Health.
Working in the laboratory, the scientists isolated fragments of DNA in cells to study the effects of exposure to calcitriol, the “active” form of vitamin D. Their findings are published in the journal Genome Research.
Vitamin D influences DNA through a “go-between” protein called the vitamin D receptor (VDR). The protein is activated by the vitamin and attaches itself to DNA at the binding sites the researchers identified. VDR binding was enriched in disease-associated regions of the genetic code and also areas linked to traits such as tanning, height and hair colour.
Study leader Dr Sreeram Ramagopalan, from the Wellcome Trust Centre for Human Genetics, at Oxford University, said: “There is now evidence supporting a role for vitamin D in susceptibility to a host of diseases. Vitamin D supplements during pregnancy and the early years could have a beneficial effect on a child's health in later life. “Some countries, such as France, have instituted this as a routine public health measure.”
Vitamin D is chiefly made in the body as a result of the skin's exposure to sunlight. A small number of foods also contain the vitamin, including oily fish and eggs, but 90% comes from being in the sun. In many northern countries, a lack of sun can lead to vitamin D deficiency. Over-zealous use of sunscreen can also prevent vitamin D production. It is estimated that more than half the UK population do not get enough vitamin D, and worldwide a billion people may be deficient in the vitamin. Lack of vitamin D affects bone growth and development, leading to rickets in children and bone fractures in adults.
The study supports the theory that lighter, more sun-sensitive skins evolved as people migrated north out of Africa to maximise vitamin D production in the body. A significant number of the VDR binding sites were in DNA regions where genetic changes are commonly found in people of European and Asian descent.
“Vitamin D status is potentially one of the most powerful selective pressures on the genome in relatively recent times,” said co-author Professor George Ebers, also from the Wellcome Trust Centre for Human Genetics. “Our study appears to support this interpretation and it may be we have not had enough time to make all the adaptations we have needed to cope with our northern circumstances.”