Osteoporosis in gastrointestinal diseases

Secondary osteoporosis is common in patients with gastrointestinal diseases (GID), and its pathogenesis is multifactorial. Malabsorption, deficiencies of calcium and vitamin D, secondary hyperparathyroidism, glucocorticoids (GC) use, hypogonadism, low body mass index (BMI) and chronic systemic inflammation are known causes of metabolic bone disease in patients with GID. Patients with celiac disease (CD) frequently have abnormal bone mineral density, even in the absence of symptoms. Adherence to a gluten-free diet increases bone density, following nutritional improvements and reduction of systemic inflammation. Osteoporosis occurs in up to 40% of cases of patients with inflammatory bowel disease (IBD). In those patients, the synergism between GC therapy and disease activity is the main reason for bone loss, which is more intense in Crohn’s disease than in ulcerative colitis. Bariatric surgery, e.g., Roux-en-Y gastric bypass and biliopancreatic diversion, can be associated with bone loss due to intense weight reduction, increased bone turnover and nutritional deficiencies. Recent data have also suggested that osteoporosis and fractures may be enhanced in patients with irritable bowel syndrome (IBS). Osteoporosis and other clinical risk factors for fracture should be investigated in patients with gastrointestinal diseases. Since atraumatic fractures have a high morbid-mortality, appropriated treatment should be offered for those at risk.