Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


Unsuppressed Parathyroid Hormone in Patients with Autoimmune Rheumatic Diseases: Implications for Vitamin D Supplementation.

Sainaghi1,  Pier Paolo, Bellan2,  Mattia, Antonini3,  Giuseppina, Bellomo3,  Giorgio, Pirisi1,  Mario

Immuno-Rheumatology Outpatient Unit, DMCS, "A. Avogadro" University and IRCAD (Interdisciplinary Reseach Center of Autoimmune Diseases), Novara, Novara, Italy
Immuno-Rheumatology Outpatient Unit, DMCS, "A. Avogadro" University, Novara, Italy
Laboratory of Chemistry and Clinical Research, DSM, "A. Avogadro" University and "Maggiore della Carità" Hospital, Novara, Italy

Background:

Conflicting data have been reported concerning the relationship between vitamin D deficit and autoimmune rheumatic diseases (ARD), but desirable vitamin D concentrations in ARD patients have not been defined taking into consideration calcium homeostasis. In fact, a plasma 25(OH)vitamin D (VITD) concentration should be considered optimal when able to suppress parathyroid hormone (PTH). Therefore, our aim was to verify the hypothesis that ARD patients may be more refractory to PTH suppression by VITD.

Methods:

Data from 105 consecutive ARD patients (including rheumatoid arthritis, polymyalgia rheumatica, spondyloarthritis and other connective tissue diseases) attending a tertiary level immuno-rheumatology clinic, and 1542 consecutive adult patients tested at our central laboratory from 2008 to 2010 (controls) were collected. After exclusion of patients with renal failure, known primary hyperparathyroidism, and hypercalcemia (N.=522), plasma VITD, PTH, calcium and phosphorus concentrations were compared between these two groups.

Results:

Plasma VITD concentrations were <25 nmol/L in 257 patients (severe deficit, 22.8%), >=25 but <75 in 661 (mild deficit, 58.8%) and >=75 in 207 (normal, 18.4%). Despite similar mean age, plasma VITD, calcium and phosphate values (p=n.s.), PTH was higher in ARD (74.8±25.5 pg/ml) than in controls (65.1±24.2, p<0.001). Moreover, mean PTH was always higher in ARD vs controls in all above defined VITD categories.

Figure 1.

As expected, the proportion of patients with increased PTH (>=73 pg/ml) was inversely related to VITD; suppressed PTH was observed in 96.9 %[95.8–98.0; 95%CI] of controls with VITD >=75 nmol/L. However, PTH was increased more frequently in ARD vs controls.

Figure 2.

At multivariate analysis, low VITD values (F: 59.3, p<0.001) and the presence of an ARD (14.4, p<0.0003) were independent predictors for an increased PTH.

Conclusions:

Patients with ARD have an impaired vitamin D metabolism evidenced by an increased PTH concentration for any plasma VITD range. Therefore, vitamin D supplementation to ARD patients should be targeted to reach full PTH suppression and not simply to obtain VITD concentrations considered optimal in other categories of patients.

To cite this abstract, please use the following information:
Sainaghi, Pier Paolo, Bellan, Mattia, Antonini, Giuseppina, Bellomo, Giorgio, Pirisi, Mario; Unsuppressed Parathyroid Hormone in Patients with Autoimmune Rheumatic Diseases: Implications for Vitamin D Supplementation. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :2160
DOI: 10.1002/art.29924

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