Vitamin D and health: perspectives from mice and man. J Bone Miner Res ; — Holick MF. Vitamin D deficiency. Lips P. Vitamin D physiology. Prog Biophys Mol Biol ; 4 —8. DeLuca HF.
Chronic obstructive pulmonary disease: molecular and cellularmechanisms
Overview of general physiologic features and functions of vitamin D. Estimation of optimal serum concentrations of hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr ; 18 — Need for additional calcium to reduce the risk of hip fracture with vitamin D supplementation: evidence from a comparative metaanalysis of randomized controlled trials. J Clin Endocrinol Metab ; — J Steroid Biochem Mol Biol ; — Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications.
Endocr Rev ; — Identification and immune regulation of hydroxyvitamin Dalpha-hydroxylase in murine macrophages. Clin Exp Immunol ; — Immunoregulation by 1,dihydroxyvitamin D3: basic concepts. J Steroid Biochem Mol Biol ; 93 — Vitamin D signaling in immune-mediated disorders: Evolving insights and therapeutic opportunities. Mol Aspects Med ; — Effect of Vitamin D on falls: a meta-analysis. JAMA ; — Prospective study of predictors of vitamin D status and cancer incidence and mortality in men.
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Vitamin D and the Lung - Mechanisms and Disease Associations | Augusto A. Litonjua | Springer
Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Plasma hydroxyvitamin D levels and risk of incident hypertension. Hypertension ; — Vitamin D deficiency and risk of cardiovascular disease.
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Mathieu C, Adorini L. The coming of age of 1,dihydroxyvitamin D 3 analogs as immunomodulatory agents. Trends Mol Med ;8: — The nature of small-airway obstruction in chronic obstructive pulmonary disease. Chest ; S —S. Elastin fragments drive disease progression in a murine model of emphysema. J Clin Invest ; — Antielastin autoimmunity in tobacco smoking-induced emphysema. Linden A, Adachi M. Neutrophilic airway inflammation and IL Allergy ; — The immunopathogenesis of chronic obstructive pulmonary disease: insights from recent research.
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Proc Am Thorac Soc ;4: — Barnes PJ. Immunology of asthma and chronic obstructive pulmonary disease. Nat Rev Immunol ;8: — What's in season for rheumatoid arthritis patients? Seasonal fluctuations in disease activity. Rheumatology Oxford ; — Koli K, Keski-Oja J. Vitamin D3 regulation of transforming growth factor-beta system in epithelial and fibroblastic cells—relationships to plasminogen activation. J Investig Dermatol Symp Proc ;1: 33 — Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process.
Peripheral muscle weakness contributes to exercise limitation in COPD. Systemic effects of COPD. Respir Med ;99 Suppl B: S3 — COPD as a lung disease with systemic consequences—clinical impact, mechanisms, and potential for early intervention. COPD ;5: — Exercise training in COPD: how to distinguish responders from nonresponders. The lumen of small airways is reduced by mucosal thickening containing an inflammatory exudate, which increases with the severity of disease.
The mechanism for lymphoid follicle formation in more severe disease is unknown, but may reflect a response to chronic bacterial colonisation and acute exacerbations of inflammation. The mechanisms of fibrosis around the airway are not yet understood, but are likely to represent an attempt to repair chronic inflammation. Amajor barrier to understanding the contribution of small airway obstruction is the difficulty in quantifying small airway obstruction in patients using measurements of airflow due to the high variability and poor reproducibility of measurements Both panacinar and centrilobular emphysema may occur in smokers The role of emphysema in causing airflow obstruction in COPD have been examined by measuring macroscopic emphysema in resected lung or on computerised tomography CT scans in relation to tests of lung function, or by measuring static transpulmonary pressure P L as a measurement of alveolar disease.
Many studies have shown significant, albeit weak, correlations between the grading of macroscopic emphysema and various tests of lung function 25 , However, the assessment of macroscopic emphysema is dominated by destroyed or poorly functioning lung, whereas lung function tests reflect predominantly the function of the best surviving lung.
In the extreme case of nonventilated emphysematous bullae surrounded by normal lung, the two assessments are virtually independent, with lung function tests measuring only the reduced volume of surviving lung. In more common types of emphysema, a simple two compartment model does not apply, but usually there will be greater heterogeneity of disease with more and more units becoming poorly functional as disease progresses, resulting in a rise in residual volume and a fall in vital capacity.
P L measured using an oesophageal catheter is plotted against airflow conductance or maximal expiratory flow at different lung volumes to indicate the contribution of alveolar disease and by implication emphysema to airflow limitation, with the assumption that the rest is due to intrinsic airway disease 27 — However, it is not certain that the magnitude of decline in P L accurately reflects the severity of emphysema and its effects on the airways.
Reduction in P L is likely to be largest with relatively uniform emphysema, as occurs in panacinar emphysema e.
In practice a reduction in conductance or maximum flow that is completely explained by a reduction in P L is unusual, except in mild disease. Retrograde catheter studies in excised lungs from patients with severe airflow obstruction due to COPD have all found large increases in peripheral resistance at standard P L 30 — But there are many other possible changes in airway function due to emphysema which would result in an increased resistance at a given P L , including abnormal angulation or compression of normal airways by surrounding overdistended lung, loss of parallel airways due to emphysematous destruction, or to functional loss of patent airways supplying poorly ventilated areas of lung.
The effects of emphysema may not always reduce P L , e. Present analyses of airway morphology are not sufficient to reveal the anatomical basis of the consistent physiological finding of an increase in peripheral airflow resistance. Emphysema may play a more prominent role in severe disease as the decline in lung function accelerates. The contribution of mucus hypersecretion to airflow limitation in COPD is still uncertain. Although early studies supported the view that mucus hypersecretion was not associated with any physiological defect 33 , 34 , more recent studies have demonstrated that mucus hypersecretion may be a potential risk factor for accelerated decline in lung function 35 , The early studies examined the early stages of COPD and also included an occupational cohort.