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Celiac disease: A missed cause of metabolic bone disease ( must read )

Discussion in 'Endocrinology' started by neo_star, Jan 23, 2013.

  1. neo_star

    neo_star Moderator

    Nov 4, 2012
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    Celiac disease: A missed cause of metabolic bone disease

    Ashu Rastogi[SUP]1[/SUP], Sanjay K Bhadada[SUP]1[/SUP], Anil Bhansali[SUP]1[/SUP], Rakesh Kochhar[SUP]2[/SUP], Ramakrishnan Santosh[SUP]3[/SUP]
    [SUP]1[/SUP] Department of Endocrinology, PGIMER, Chandigarh, India
    [SUP]2[/SUP] Department of Gastroenterology, PGIMER, Chandigarh, India
    [SUP]3[/SUP] Apollo Hospital, Hyderabad, India

    [TABLE="class: leftNav"]
    [TD="class: pageSub"]Abstract[/TD]
    [TD="class: inthis, align: right"][/TD]

    Celiac disease (CD) is a highly prevalent autoimmune disease. The symptoms of CD are varied and atypical, with many patients having no gastrointestinal symptoms. Metabolic bone disease (MBD) is a less recognized manifestation of CD associated with spectrum of musculoskeletal signs and symptoms, viz. bone pains, proximal muscle weakness, osteopenia, osteoporosis, and fracture. We here report five patients who presented with severe MBD as the only manifestation of CD.

    Materials and Methods:
    Records of 825 patients of CD diagnosed during 2002-2010 were retrospectively analyzed for clinical features, risk factors, signs, biochemical, and radiological parameters.

    We were able to identify five patients (0.6%) of CD who had monosymptomatic presentation with musculoskeletal symptoms and signs in the form of bone pains, proximal myopathy, and fragility fractures without any gastrointestinal manifestation. All the five patients had severe MBD in the form of osteopenia, osteoporosis, and fragility fractures. Four of the five patients had additional risk factors such as antiepileptic drugs, chronic alcohol consumption, malnutrition, and associated vitamin D deficiency which might have contributed to the severity of MBD.

    Severe metabolic disease as the only presentation of CD is rare. Patients show significant improvement in clinical, biochemical, and radiological parameters with gluten-free diet, calcium, and vitamin D supplementation. CD should be looked for routinely in patients presenting with unexplained MBD.

    Selected Excerpts

    CD affects bone mineral metabolism by multiple mechanisms. Etiopathogenesis of osteoporosis may differ according to whether the presentation is classic or atypical. The mild, asymptomatic forms may reduce bone mass by a different mechanism related to the secretion of inflammatory cytokines with increase in interferon-, IL- 6, TNFα, and IL-18 and reduced levels of IL-12. The inflammatory cytokines (IL-1, IL-6, and TNFα) increase bone resorption, by acting directly on the osteoclasts or increasing the RANKL/OPG ratio. However, the classic severe forms of CD with evident malabsorption cause reduction in plasma calcium, vitamin D levels, and vitaminD transporting protein (calbindin). These deficits lead to secondary hyperparathyroidism, which in turn leads to increased bone remodeling resulting in reduced bone mass, alteration of bone quality, with the consequent reduction in bone strength, and risk of fractures. Other endocrine factors that may contribute to this process are a reduction in IGF-1 related to the malabsorption of zinc and reduced levels of leptin.


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