Vitamin D Deficiency Linked to Disease Severity, Mortality Risk in IPF Patients, Study Shows

Vitamin D Deficiency Linked to Disease Severity, Mortality Risk in IPF Patients, Study Shows

Vitamin D deficiency in patients with idiopathic pulmonary fibrosis (IPF) is associated with functional and clinical predictors of disease severity and a higher risk of mortality, according to a new study.

The findings also revealed that vitamin D is able to partially prevent lung fibrosis in a mouse model.

The research, “Vitamin D prevents experimental lung fibrosis and predicts survival in patients with idiopathic pulmonary fibrosis,” was published in the journal Pulmonary Pharmacology & Therapeutics.

Besides the regulation of calcium and phosphate, vitamin D has shown anti-inflammatory, anti-bacterial, and cell protective activities. In addition, vitamin D deficiency has been associated with a risk of developing respiratory diseases, including chronic obstructive pulmonary disease. It has also been linked with indicators of disease severity in various types of organ fibrosis, or scarring, which suggest a potential prognostic value.

Based on these observations, researchers in Greece decided to investigate the role of vitamin D in experimental and human lung fibrosis.

They used a mouse model of pulmonary fibrosis, in which fibrosis was induced by a compound called bleomycin. From day 3 to day 13 after bleomycin treatment, the animals received vitamin D orally (at 2 ug/kg of body weight).

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Results showed that vitamin D partially reversed lung fibrosis in these animals, as assessed by lower levels of hydroxyproline (an amino acid that is a major component of collagen). It also reduced levels of RNA (a molecule produced from DNA for protein production) of col1a1 and col3a1 (the genes coding for type I and III collagen, respectively), as well as a-SMA (a gene also associated with fibrosis).

The team also tested the effects of vitamin D administration in mouse lung fibroblasts — cells that produce collagen and are key players in fibrosis. Fibroblasts were pre-treated with vitamin D for 24 hours, and then stimulated with TGF-beta1, which is a protein known to promote fibrosis.

Results indicated that pre-treatment with vitamin D lessened the responsiveness of lung fibroblasts to TGF-beta1, as reflected in significant RNA reductions of col1a1col3a1, and a-SMA. Smad3 phosphorylation, or activation (a pro-fibrotic protein mediator), also was prevented.

Researchers collected serum samples from 93 patients with IPF (mean age 71.7 years) and 40 patients with other forms of interstitial lung disease (ILD, mean age 69.4 years) to measure vitamin D levels.

These patients showed lower-than-normal mean vitamin D serum concentrations (18.76 in IPF and 18.54 ng/ml in ILD, both under the reference value of 20 ng/ml), which correlated with measures of lung function, namely percent predicted forced vital capacity, diffusing capacity of the lungs for carbon monoxide (the lungs’ capacity to transfer oxygen from the air sacs into the blood), and GAP score (a clinical prognostic tool)

Importantly, vitamin D levels below a threshold of 17.9 ng/ml identified a group of IPF patients with greater likelihood of mortality.

Overall, “our study suggests that [vitamin D] may display protective effects on experimental lung fibrosis and reliably predict clinical outcomes in patients with IPF,” the researchers wrote. According to them, a median vitamin D serum threshold of 17.9 ng/ml is a “strong predictor of all-cause mortality.”

The findings also suggest that IPF patients are at high risk of developing vitamin D deficiency, “and thus should be screened accordingly, for early supplementation treatment and prediction of clinical outcomes,” the team wrote.

A clinical trial exploring the therapeutic potential of vitamin D as add-on therapy to standard of care in patients with IPF “is sorely needed,” the team concluded.

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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3 comments

    • Gary D. Chace says:

      I was diagnosed with IPF in May 2014. I started on OFEV in Oct. of 2014. After one year on the OFEV the disease had progressed slightly. After two, three, and four years there has been no progression. I have noticed that in the last two months I have needed to adjust my oxygen up and I am beginning to be more winded and fatigued than usual. I’m scheduled for a function test and to see my doctor in April. I believe the OFEV has been working for me but no two patients are the same. I have a friend who was diagnosed in June of 2016 and started on OFEV shortly after but the IPF has continued to progress. He is no longer on OFEV and has been placed on the transplant list. I hope this answers some of your questions. I’ll pray that you will be one that the OFEV helps.

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