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Volume 104, Issue 4, Pages 564-570 (April 2010)


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Elevated 1, 25-dihydroxyvitamin D levels are associated with protracted treatment in sarcoidosis

Dashant Kavathiaa, John D. Buckleyb, Dhanwada Raoc, Benjamin Rybickid, Robert BurkeeCorresponding Author Informationemail address

Received 23 July 2009; accepted 7 December 2009. published online 13 January 2010.

Summary 

Background

Active vitamin D metabolite, 1, 25-dihydroxyvitamin D, has pleomorphic effects on both innate and acquired immunity. Sarcoid granuloma derived 1, 25-dihydroxyvitamin D leads to hypercalcemia, but the association of 1, 25-dihydroxyvitamin D with the clinical phenotype of the disease is currently unknown.

Objective

To determine the relationship between serum 1, 25-dihydroxyvitamin D levels and the degree of sarcoidosis disease chronicity.

Design

Serum 1, 25-dihydroxyvitamin D levels were measured and associated with sarcoidosis activity and phenotypes as assessed by Sarcoidosis Severity Score and Sarcoidosis Clinical Activity Classification respectively.

Results

Fifty nine patients were recruited with 44% having a sub-acute onset, and the chronic disease phenotype. There was no significant difference in serum 1, 25-dihydroxyvitamin D levels by chest radiograph stage (p = 0.092) nor did the levels correlate with the Sarcoidosis Severity Score (r = −0.16; p = 0.216). Serum 1, 25-dihydroxyvitamin D levels were associated with patients requiring repeated regimens of systemic immunosuppressive therapy or >1 year of therapy (SCAC Class 6). Increasing quartiles of serum 1, 25-dihydroxyvitamin D level was associated increased odds of the chronic phenotype (OR 1.82, 95% CI, 1.11, 2.99, p = 0.019). The majority (71%) of the patients with levels >51 pg/mL required chronic immunosuppressive therapy as defined by SCAC class 6.

Conclusions

In patients with sarcoidosis, elevated 1, 25-dihydroxyvitamin D levels are associated with chronic treatment needs.

a Henry Ford Hospital, Division of Pulmonary and Critical Care Medicine, K 17, 2799 W Grand Blvd, Detroit, MI 48202, USA

b Division of Pulmonary and Critical Care Medicine, Indiana University, Indianapolis, IN, USA

c Division of Endocrinology, Henry Ford Health System, Detroit, MI, USA

d Department of Biostatistics and Research Epidemiology, Henry Ford Health System, Detroit, MI, USA

e Division of Pulmonary and Critical Care Medicine, Henry Ford Health System, Detroit, MI, USA

Corresponding Author InformationCorresponding author. Tel.: +1 (313) 916 2436; fax: +1 (313) 916 9102.

PII: S0954-6111(09)00407-7

doi:10.1016/j.rmed.2009.12.004


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