Osteoporosis
Who is at risk of osteoporosis?How common is osteoporosis in coeliac disease?
Management of osteoporosis in people with coeliac disease
Osteoporosis is defined as 'a systemic skeletal disease characterised by low bone mass and micro architectural deterioration with consequent increase in bone fragility and susceptibility to fracture'. Osteoporosis is a major cause of hip fractures, broken wrists and spinal problems in those aged 50 plus.
There have been a number of reports showing evidence of reduced bone mineral density, osteopenia or osteoporosis in 20-50% of patients newly diagnosed with coeliac disease (CD)(1). The presence of overt malabsorption leads to greater bone loss, but even in asymptomatic patients, bone mineral density is significantly lower than in healthy volunteers (2). 'Thin' bones are, therefore, the commonest complication of CD.
Since relatively few people are diagnosed with osteoporosis in time for effective therapy to be administered, the diagnosis of CD gives an opportunity for preventative action to be taken. All patients with CD should receive general advice to protect and maintain bone health.
Although people with CD have a low bone mass they do not appear to have an increased fracture risk.
Who is at risk of osteoporosis?
There are many risk factors for osteoporosis including endocrine, metabolic and nutritional disorders, and drugs. Below are factors associated with an increased risk:
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Gender - Women have much lower bone density than men
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Race - Caucasian and people of Asian origin are at greater risk than people of African-American origin
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Genetics - A family history of fracture is an important risk factor
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Increasing age
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Oestrogen levels - After menopause, there is a period of rapid bone loss due to oestrogen deficiency. Some women may also lose bone before menopause if they have infrequent periods or lack of normal amounts of oestrogen
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Drugs - Many drugs may affect bone density, such as glucocorticoids, thyroid hormone, heparin, and certain diuretics
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Diet - A low calcium diet for many years or chronic malabsorption of calcium is associated with lower bone density
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Exercise - Lack of bone building exercise, such as walking or running
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Smoking - Smoking prevents the deposition of bone, and is associated with lower bone density in men and women
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Alcohol - Two or more alcoholic drinks a day have been shown to have the same effect on bone as smoking
Some factors - specifically related to CD - may increase the risk of bone loss and require careful assessment. These include:
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Late or delayed diagnosis of CD in adult life
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Lapses from the gluten-free diet
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Persistent villous atrophy
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Lactose intolerance
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Low BMI
Many of the above problems may result in chronic malabsorption of foods with calcium.
How common is osteoporosis in coeliac disease?
CD is considered to be one of the most frequent predisposing conditions to metabolic osteopathy. Studies have shown that more than 75% of untreated adults with CD suffer from osteopenia or osteoporosis.
Patients on a gluten-free diet show a lower prevalence of bone loss, suggesting that dietary therapy may improve bone mineral density (BMD), however BMD may not return to that seen in a matched population (3,4,5). The prevalence of reduced bone density after one year of a gluten-free diet is similar to that after three years, suggesting that the extent of bone mass gain in the first year of dietary treatment is indicative of overall BMD improvement (6). Reduced BMD is also seen in DH, although to a lesser extent then in CD, except where the BMI is less than 20kg/m (3,7)
There is evidence that early treatment of CD in childhood prevents bone loss and most patients reach normal peak densitometric values (8) .
The diagnosis of low BMD
To diagnose metabolic osteopathy in CD, a test which directly measures bone density (i.e. DEXA scan) should be performed.
Bone mass measurements can be expressed in two ways:
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Z score: This index represents the number of standard deviations by which the patient value differs from the mean value of an age- and sex-matched reference population.
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T score: This index represents the number of standard deviations by which the patient value differs from the mean of a young adult reference population.
Densitometric criteria for diagnosis of WHO criteria use T Score only -
Osteopenia: - 2 < Z score < -1 and - 2.5 < T score < -1
Osteoporosis: Z score < -2 and T score < -2.5
Pathophysiological aspects
The pathogenesis of bone damage in CD is multifactorial; both systemic and local mechanisms may play a role.
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Intestinal malabsorption secondary to mucosal lesions leads to calcium malabsorption and subnormal levels of serum calcium, leading to secondary hyperparathyroidism and increased bone turnover. Intestinal malabsorption can also lead to general malabsorption and a reduced BMI.
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Several other mechanisms may contribute to render calcium unavailable for intestinal absorption, such as a decreased dietary calcium intake secondary to lactase deficiency, precipitation of endogenous calcium in the intestinal lumen as calcium soaps, increased intestinal secretion or decreased reabsorption.
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The production of pro-inflammatory cytokines, responsible for osteoclast activation, is the key point for a local-acting mechanism. Cytokines are involved in the mechanisms of cell-to-cell communication and some of them are implicated in both normal and abnormal bone remodelling.
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The presence of bone specific antibodies in sera of coeliacs has also been suggested to be a co-factor in the pathophysiology of CD-associated bone damage (9).
Bone derangement in coeliacs should be considered as a high turnover osteoporosis, as increased resorption is not compensated by enhanced neoformation. These changes in bone are similar to those seen in Crohn's disease, but what is surprising about the finding in CD is the occurrence of osteopenia or osteoporosis even in patients with very minor presenting symptoms.
In females with CD the role of associated gynaecological disorders should be considered. Amenorrhoea is a more common finding in coeliac disease than the general population and sex hormone imbalance represents an important risk factor for the development of osteoporosis.
Management of osteoporosis in people with coeliac disease
Bone mass measurement in patients with coeliac disease
There are doubts about the need to measure BMD in coeliacs, in addition, there are no clear guidelines on which patients should undergo bone mass measurement and when the first and subsequent measurements should be performed. In 1998 the British Society for Gastroenterology published its guidelines for osteoporosis in patients with CD, which recommended BMD measurement at diagnosis. A more recent paper by the same authors concluded that due to doubt about the increased fracture rates in coeliac patients, the current guidelines should be changed (10).
A report by Corazza et al has suggested the following:
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Children: There is evidence that very early treatment of CD in childhood prevents bone loss and most patients reach normal peak densitometric values. Consequently, there is no need to perform bone mass measurement in children if fully compliant with the gluten-free diet.
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Adults: A report has suggested that in coeliacs diagnosed in adulthood, an approach based on clinical presentation should be followed.
- Coeliac patients with overt malabsorption are potentially at a higher risk for osteoporosis and bone fractures, than asymptomatic coeliacs. Consequently, it has been suggested that in symptomatic patients BMD should be measured at diagnosis and after 2 years on a strict GFD. Only patients whose baseline BMD is below normal require a follow-up scan.
- Asymptomatic patients may not require bone measurement at diagnosis, but instead BMD should be measured after the first year of strict adherence to a GFD. The decision to begin therapy with mineral-active drugs would thus be taken on the basis of dietary regimen efficacy. -
In women, if the diagnosis is made earlier the BMD should be measured at the menopause. A single measurement at menopause may not be adequate because there is considerable variation in the rate and duration of rapid perimenopausal bone loss. Therefore, it is suggested to repeat the BMD after two years in those whose BMD does not suggest osteoporosis (11).
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In men BMD should be measured at about 55 years of age if they presented at an earlier age.
How to minimise the risk
Bone loss starts to exceed bone replacement after the age of 35. For patients with CD the most important factor in minimising the risk of osteoporosis is adhering to a GFD. Patients should be given general advice about exercise (particularly weight bearing), smoking, alcohol excess, and adequate dietary calcium.
For adults with coeliac disease, it is recommended to aim for 1000mg of calcium per day. For post menopausal women and men over the age of 55 years, an increased requirement of 1200mg is recommended (12).
The use of supplements should be decided on an individual basis.
There are no guidelines that recommend a higher requirement for calcium in children with coeliac disease. Following a calcium rich gluten-free diet is recommended, using Reference Nutrient Intake (RNI) values as a guide (see below) depending on the individual case.
1-3 years 350 mg
4-6 years 450 mg
7-10 years 550 mg
11-18 years (female) 800 mg
11-18 years (male) 1000 mg
There are no specific recommendations for lactating mothers who have coeliac disease. An additional 550mg/day are recommended for all women while breastfeeding, so appropriate adjustments for those with coeliac disease should be made on an individual basis.
Dairy products (milk, yoghurt, cheese) provide useful sources of dietary calcium. Where milk-allergy or lactose intolerance is present, patients may obtain calcium from non-dairy sources such as calcium-enriched soya milk, fish with edible bones i.e. salmon and sardines, tofu, baked beans, dried figs.
The treatment of osteoporosis
The management of low BMD in those with coeliac disease should be advised on an individual basis.
People with coeliac disease are recommend to:
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maintain adherence to gluten-free diet
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take adequate dietary calcium, using supplements if necessary
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regular weight bearing exercise
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stop smoking and avoid excess alcohol.
Medications such as bisphosphonates and strontium ranelate, may be used as appropriate.
In cases where the GFD is ineffective at promoting remineralisation, additional secondary causes of osteoporosis should be ruled out - these causes include: corticosteroids untreated hypogonadism, thyroid dysfunction, hyperprolactinemia, medications (anticonvulsants).
References
1 Bianchi ML, Bardella MT (2002) Bone and Celiac Disease. Calcif Tissue Int 71: 465-471
2 Corazza GR, Di Sario A, Cecchetti L et al (1996) Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease. Bone 18: 525-530.
3 Corazza GR et al. Bone mass and metabolism in patients with celiac disease. Gastroenterology 1995;109(1):122-8
4 McFarlane XA et al Osteoporosis in treated adult coeliac disease. Gut 1995;36(5):710-4
5 Pazianas et al. Calcium absorption and bone mineral density in celiacs after long term treatment with gluten-free diet and adequate calcium intake. Osteoporosis International 2005;16(1):56-63
6 Corazza GR et al. Bones in coeliac disease: diagnosis and treatment. 2005;19(3):453-65
8 Mora et al. Effect of gluten-free diet on bone mineral content in growing patients with coeliac disease. American Journal of Clinical Nutrition 1993;57(2):224-8
9 Sugai E et al. Bone specific antibodies in sera from patients with coeliac disease: characterisation and implications in osteoporosis. Journal of Clinical Immunology 2002;22(6):353-62
10 Lewis NR and Scot BB. Should patients with coeliac disease have their bone mineral density measured? European Journal of Gastroenterology and Hepatology 2005;17(10):1065-70
11 Scot BB et al. Guidelines for osteoporosis in coeliac disease and inflammatory bowel disease. British Society of Gastroenterology. Gut 2000;46(S1):i1-8
12. Lewis NR, Scott BB for the British Society of Gastroenterology (2007) Guidelines for osteoporosis in coeliac disease and inflammatory bowel disease. Accessed at www.bsg.org.uk
