Article Outline
Abstract
Osteoporosis is increasingly recognized as a source of significant disability, an awareness that has prompted clinicians to actively pursue the diagnosis among high-risk patients. Fractures have an obvious associated morbidity, a negative impact on quality of life, and both direct and indirect costs. Much of the available clinical information regarding osteoporosis screening, outcomes, and therapeutic interventions is derived from the postmenopausal osteoporosis literature. This position statement summarizes the graded findings and recommendations of a systematic technical review of osteoporosis in 3 common digestive disorders: inflammatory bowel disease (IBD), celiac disease, and postgastrectomy states.
GASTROENTEROLOGY 2003;124:791-794
Abbreviations:
BMD
, bone mineral density,
DXA
, dual-energy X-ray absorptiometry,
GI
, gastrointestinal,
SAP
, serum alkaline phosphatase
Disorders of the gastrointestinal (GI) tract may be associated with osteoporosis. Pathophysiologic factors specific to GI diseases include the frequent onset of IBD and celiac disease in childhood or young adulthood; impaired absorption of nutrients vital to bone health, such as calcium and vitamin D; the use of glucocorticoids in the treatment of IBD; and the chronic inflammatory state of IBD and untreated celiac disease.
The development of bone densitometry has made it possible to measure bone mass and assess its contribution to fracture risk. It is generally accepted that bone mass is the single best predictor of in vitro skeletal strength and of fracture risk. Dual-energy X-ray absorptiometry (DXA) is the current gold standard technique for measuring bone mass. Measurements are usually obtained at the femoral neck and lumbar spine, and less often from the forearm and total body. Bone mass measurements are typically reported as Z score, reflecting the number of standard deviations (SDs) above or below the mean for an age-matched population, or T score, reflecting the number of SDs above or below the mean for a young adult population (corresponding to peak bone mass). Caution must be exercised when extrapolating data from DXA in the postmenopausal state to DXA in GI diseases. There is no consensus on the diagnosis of osteoporosis in men or even on the appropriate reference population for generating the T score. The use of serum and urine measures of bone metabolism is largely confined to research studies. A complete blood count, serum total alkaline phosphatase level, calcium level corrected for serum albumin level, creatinine level, testosterone level (in males), and, in selected cases, 25-(OH)-vitamin D level and protein electrophoresis can be reliably measured in most hospital laboratories and should be obtained in patients with suspected skeletal complications of GI disease to screen for other causes of low bone density.
The single most powerful predictor of a future osteoporotic fracture is the presence of previous such fractures. Such factors as advanced age, family history of osteoporosis, lack of exercise, smoking, and hypogonadal states increase the risk of osteoporosis in patients with GI disease and the general population alike. Other risk factors that warrant consideration in patients with GI disease include malnutrition, low body weight, low intake or absorption of dietary calcium and vitamin D, and corticosteroid use.
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Summary of bone disease in inflammatory bowel disease
1.Osteomalacia and vitamin D deficiency are not common in IBD (including Crohn's disease) and are unlikely to be important causes of most cases of diminished bone mineral density (BMD) in IBD (level B evidence).
2.IBD has only a modest effect on BMD, with a pooled Z score of −0.5 (level A evidence).
3.The overall prevalence of osteoporosis (T score <−2.5) using DXA is approximately 15%, but is strongly affected by age, being higher in older subjects (level A evidence).
4.At diagnosis, the prevalence of diminished BMD is low (level B evidence) and when followed longitudinally, changes in BMD are similar to those expected (level B evidence).
5.DXA is a marker of diminished bone mass and fracture risk, but is not the only marker of fracture risk and should be used to predict fracture risk in concert with other clinical variables (level D evidence).
6.Males and females are at similar risk for osteoporosis (level A evidence).
7.Crohn's disease and ulcerative colitis carry comparable risks for osteoporosis (level B evidence).
8.Corticosteroid use is the variable most strongly associated with osteoporosis (level A evidence). However, it is difficult to distinguish corticosteroid use from disease activity in terms of causal impact on bone density, because the 2 are closely linked.
9.Biochemical bone markers do not correlate sufficiently well with current BMD or rate of bone loss for routine use (level B evidence).
10.The ileoanal pouch procedure after curative colectomy in ulcerative colitis may be associated with an improvement in DXA (level C evidence).
11.Calcaneal ultrasonography has not been as well evaluated as DXA, but possibly could help select patients for DXA (level B evidence).
12.Pediatric DXA should be adjusted for bone age, or else BMD will typically be underestimated (level B evidence).
13.The overall incidence of fractures in a population-based study is 1 per 100 patient-years, but this rate is strongly affected by age, being more common in subjects over age 60 (level A evidence).
14.The overall relative risk of fractures is 40% greater than that of the general population and increases with age (level A evidence).
15.Crohn's disease and ulcerative colitis carry comparable risks for fracture (level A evidence).
16.Males and females share a comparable risk for fracture (level A evidence).
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Summary of bone disease in celiac disease
1.Osteoporosis is more common in patients with untreated celiac disease than in the general population (level A evidence).
2.Vitamin D deficiency is common in celiac disease, but the actual prevalence of osteomalacia in celiac disease is unknown (level B evidence).
3.Among newly diagnosed patients, the prevalence of osteoporosis using DXA is approximately 28% at the spine and 15% at the hip (level B evidence).
4.In adults with a known diagnosis of celiac disease treated with a gluten-free diet, the prevalence of osteoporosis detected using DXA is still increased compared with that in controls (level B evidence).
5.At the time of diagnosis of celiac disease, children and adults have similarly low BMDs; however, children are more likely than adults to have fully restored bone mass after a gluten-free diet (level B evidence).
6.Patients with celiac disease exhibit an increased BMD after initiating a gluten-free diet (level A evidence). The greatest increase occurs in the first year (average of 5%), but final BMD remains below average, with final Z scores of approximately −1.0 for the spine and −0.5 for the hip (level B evidence).
7.Body mass index consistently correlates with BMD at both diagnosis and follow-up (level A evidence).
8.Axial bone mass increases more than appendicular mass during gluten-free diet therapy (level B evidence).
9.Subjects with asymptomatic celiac disease are at increased risk for osteoporosis (level B evidence).
10.The high prevalence of osteoporosis among patients with celiac disease, in asymptomatic subjects, provides a rationale for gluten-free diet therapy for those who do not have overt malabsorption (level D evidence).
11.Males and females are at equal risk for osteoporosis; postmenopausal females are at greatest risk (level B evidence).
12.Typical serological abnormalities that correlate with diminished BMD include elevated parathyroid hormone (PTH) level and 1,25(OH)2-vitamin D and diminished 25-OHD. Levels of 25-OHD, calcium, and possibly PTH should be measured in newly diagnosed celiac disease and in patients where elevated levels warrant increased attention to bone health (level B evidence).
13.The precise incidence of fracture in celiac disease is unknown but is estimated to be 40% by age 70, which is more than twice the expected incidence for the general population (level B evidence).
14.The value of calcaneal ultrasound as a screening test for fracture risk in celiac disease is unknown (level D evidence).
15.DXA is a marker of diminished bone mass but is not a proven marker of fracture risk in patients with celiac disease (level B evidence).
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Summary of bone disease in postgastrectomy states
1.Postgastrectomy patients typically have a number of risk factors for osteoporosis, and bone disease may not necessarily be a sequela of the surgery per se. Nonetheless, postgastrectomy patients are at risk for bone disease (level A evidence).
2.Osteoporosis and osteomalacia may both occur postgastrectomy. The incidence of osteomalacia is approximately 10%–20% (level B evidence). The incidence of osteoporosis is unknown but may be as high as 32%–42% (level B evidence).
3.Postgastrectomy states are associated with an increased risk of fracture and thus patients postgastrectomy should be evaluated for possible underlying bone disease (level B evidence).
4.There is no difference in the risk of postgastrectomy bone disease between patients with a Billroth I procedure and those with a Billroth II procedure (level A evidence).
5.There is no difference in the risk of postgastrectomy bone disease between partial gastrectomy and total gastrectomy (level A evidence).
6.There is no apparent risk of postgastrectomy bone disease associated with acid-reducing procedures such as vagotomy in the absence of gastrectomy (level B evidence).
7.Serum calcium and phosphate levels are most often normal in postgastrectomy states, although calcium levels may be normal as a result of mobilization of calcium from bone (level A evidence).
8.Serum alkaline phosphatase (SAP), vitamin D metabolite, and PTH levels are variable in postgastrectomy states (level A evidence).
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Management
There is a paucity of therapeutic intervention studies specifically aimed at bone health in GI diseases. Most therapy studies of sufficient size are in populations of postmenopausal women or corticosteroid-using patients who do not have GI disease. There is a need for studies that assess interventions directed at improving bone health in patients with GI disease specifically and that use fracture prevention as endpoints.
The following steps outline a possible approach to managing osteoporosis in GI disease:
1.All patients should receive education on the importance of lifestyle changes (e.g., engaging in regular weight-bearing exercise, quitting smoking, avoiding excessive alcohol intake), as well as vitamin D and calcium supplementation (level D evidence).
2.DXA scans should be selectively ordered in IBD patients based on a thorough risk factor assessment (level D evidence).
3.DXA scans are likely unnecessary in patients with newly diagnosed uncomplicated pediatric celiac disease, but should be considered for adults with newly diagnosed celiac disease 1 year after initiation of a gluten-free diet, to allow for stabilization of bone density (level D evidence).
4.Patients who are at least 10 years postgastrectomy, especially postmenopausal females, males over age 50, and patients with low-trauma fractures should undergo DXA testing (level D evidence).
5.In patients with IBD and celiac disease, serum calcium level, corrected for albumin, should be measured at diagnosis. In IBD, celiac disease, and postgastrectomy states in which the patient is found to be osteoporotic or has a low-trauma fracture, screening for other causes of low bone density should be performed through a complete blood count, total SAP level, calcium level, creatinine level, 25-(OH) vitamin D level, protein electrophoresis, and testosterone level (in males) (level D evidence).
6.Serum measurements of PTH are unnecessary unless a patient is found to have an abnormal serum or urinary calcium level (level D evidence).
7.Implementation of a gluten-free diet in celiac disease and correction of nutritional deficiencies is necessary in all GI diseases (level A evidence).
8.Corticosteroid dosing in IBD should be kept to a minimum, and other immunomodulatory agents should be considered to help withdraw patients from corticosteroids once corticosteroid dependence becomes evident (level D evidence in IBD; level A evidence regarding fracture risk reduction by minimizing the corticosteroid dosage for other non-GI diseases).
9.Vitamin D and calcium supplementation should be given to those deemed to be at high risk for osteoporosis or with proven osteoporosis. Younger men and premenopausal women require 1000 mg/day of elemental calcium, whereas men and women over age 50 require up to 1500 mg/day. Vitamin D 400 to 800 IU/day is usually an adequate replacement dose in healthy individuals; it can be obtained from many multivitamin preparations (level D evidence in GI disease, level B evidence regarding nonvertebral and vertebral fracture risk reduction by optimizing calcium and vitamin D intake in older men and women).
10.Estrogen therapy has received FDA approval for the prevention of osteoporosis in postmenopausal or hypogonadal premenopausal women, but must be balanced against the significant risks (level D evidence in GI disease, level A evidence for vertebral and nonvertebral fracture risk reduction in generally healthy postmenopausal women).
11.A selective estrogen receptor modulator (SERM) has been approved by the FDA for the prevention and treatment of osteoporosis in menopausal women (level D evidence in GI disease, level A evidence for vertebral fracture risk reduction in osteoporotic postmenopausal women). A bone disease specialist should participate in the decision to choose a SERM in patients with GI diseases.
12.Testosterone should be used to treat hypogonadism in males (level D evidence).
13.Bisphosphonates are FDA-approved for the prevention and treatment of osteoporosis in patients with known osteoporosis, patients with atraumatic fractures, and patients who cannot withdraw from corticosteroids after 3 months of use (level D evidence in GI disease, level A evidence regarding vertebral and nonvertebral fracture risk reduction in postmenopausal women).
14.Nasal or subcutaneous calcitonin can be considered as an alternative treatment approach when the preceding antiresorptive agents are contraindicated or poorly tolerated (level D evidence in GI disease, level A evidence regarding vertebral fracture risk reduction in postmenopausal women).
15.Fluoride is not recommended as treatment for osteoporosis associated with GI disease (level D evidence in GI disease, no consistent evidence for fracture risk reduction in postmenopausal women).
