Chronic fatigue syndrome: a risk factor for osteopenia?

Nijs, Jo; De Meirleir, Kenny; Englebienne, Patrick; McGregor, Neil

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Volume 60, Issue 1 , Pages 65-68, January 2003

Chronic fatigue syndrome: a risk factor for osteopenia?

Jo Nijs
- Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel, Brussel, Belgium
- Correspondence to: Jo Nijs, PT, MSc MT, Vakgroep MFYS/Sportgeneeskunde, AZ-VUB KRO gebouw-1, Laarbeeklaan 101, 1090 Brussel, Belgium. Phone: +32-2-477-4604; Fax: +32-2-477-4607
Kenny De Meirleir
- Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel, Brussel, Belgium
- Fatigue Clinic, Vrije Universiteit Brussel, Brussel, Belgium
Patrick Englebienne
- Department of Nuclear Medicine, Brugmann Hospital/Academic Hospital, Vrije Universiteit Brussel and Université Libre Bruxelles (V.U.B.–U.L.B.), Brussels, Belgium
Neil McGregor
- Collaborative Pain Research Unit, Department of Biological Sciences, Faculty of Science, University of Newcastle, Callaghan, NSW, Australia

Received 7 January 2002; accepted 8 May 2002.

Abstract

No data documenting a possible depletion of bone mineral density in patients with chronic fatigue syndrome (CFS) are currently available. However, recent pathophysiological observations in CFS patients may have deleterious consequences on bone density. Firstly, the deregulation of the 2,5A synthetase RNase L antiviral pathway and its associated channelopathy, implicates increased demands for calcium and consequent increased calcium-re-absorption from the skeletal system. Secondly, Mycoplasma fermentans which has been frequently associated with CFS, produces a lipopeptide, named 2-kDa macrophage-activating lipopeptide (MALP-2), which stimulates macrophages. MALP-2 has been shown to enhance bone resorption in a dose-dependent manner, at least in part by stimulating the formation of prostaglandins. Thirdly, decreased levels of insulin-like growth factor I (IGF-I) have been reported in CFS-patients. IGF-I is critical to the proliferation of osteoblasts. Consequently, depleted levels of IGF-I may shift the balance between osteoclastic and osteoblastic activity towards bone resorption.