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Volume 46, Issue 2, Pages 551-555 (February 2010)


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Bone involvement in clusters of autoimmune diseases: Just a complication?

Francesca Lombardia, Adriana Franzeseb, Dario Iafuscoc, Antonio del Puented, Antonella Espositod, Francesco Priscoc, Riccardo Tronconeb, Giuliana ValerioeCorresponding Author Informationemail address

Received 9 July 2009; received in revised form 14 September 2009; accepted 27 September 2009. published online 23 October 2009.

Abstract 

Bone loss, described in individual groups of patients with Type 1 diabetes (T1D), autoimmune thyroid disease (ATD) or celiac disease (CD) is usually viewed as a complication of these diseases. There is increasing evidence that alterations in the immune system may directly affect bone mass. Clustering of autoimmune diseases in the same individual might predispose to higher risk of osteopenia due to imbalance in immune regulation. The aim of this study was to evaluate bone involvement in clusters of the most common autoimmune diseases (T1D, ATD and CD) in children.

The study was performed at a tertiary care center for the care of pediatric diabetes. One-hundred-two patients with T1D alone or associated with ATD and/or CD were studied; 13 patients had cluster of three autoimmune diseases. Amplitude-dependent speed of sound (AD-SoS) was measured by phalangeal quantitative ultrasound and expressed as standard deviation score (SDS). AD-SoS SDS < −2 was considered indicative of osteopenia.

Osteopenia was equally distributed among children with T1D alone (8.1%), T1D associated with ATD (7.7%) or CD (10.3%), while it was 53.8% in patients presenting with three autoimmune diseases. Poor compliance to gluten-free diet increased osteopenia to 18.8% in patients with T1D and CD and 80% in patients with three autoimmune disorders. No difference among groups was found with regard to gluco-metabolic control, calcium metabolism, thyroid function.

In conclusion bone impairment in multiple autoimmune diseases might be considered not only a complication due to endocrine or nutritional mechanisms, but also a consequence of an immunoregulatory imbalance. Alterations of homeostatic mechanisms might explain an imbalance of osteoclast activity leading to osteopenia.

Edited by: D. Burr

a Department of Pediatrics, Carlo Poma Hospital, Mantova, Italy

b Department of Pediatrics, Federico II University, Naples, Italy

c Department of Pediatrics, Second University, Naples, Italy

d Department of Clinical and Experimental Medicine, Rheumatology Research Unit, Federico II University, Naples, Italy

e School of Movement Sciences (DiSiST), Parthenope University, Naples, Italy

Corresponding Author InformationCorresponding author. Dipartimento di Studi delle Istituzioni e dei Sistemi Territoriali, Università di Napoli Parthenope, via Medina 40, 80133 Napoli, Italy. Fax: +39 81 7464234.

PII: S8756-3282(09)01959-0

doi:10.1016/j.bone.2009.09.034


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