A GASTROINTESTINAL LINK TO OSTEOPOROTIC FRACTURES. L. Eck 1 , C. Jachna 1 ; 1 Kansas University Medical Center, Kansas City, KS (Tracking ID #74458) LEARNING OBJECTIVES: To recognize that celiac disease is commonly associated with low peak bone mass and adult osteoporosis leading to disabling fractures. CASE INFORMATION: A 49 year old white male with a history of multiple atraumatic fractures including a hip fracture at age 22, wrist fracture at age 16, multiple rib fractures and a recent wrist fracture presented for evaluation of osteoporosis. Bone mineral density studies revealed a T-score of À3.1 at the spine, consistent with osteoporosis. On clinical history, the patient reported a long-standing history of approximately eight loose bowel movements per day associated with abdominal cramping. He also reported low body weight through young adulthood and lactose intolerance. Lab studies were notable for an elevated IgG antigliadin antibody of 132 Units, with a reference range of >30 Units being strongly postive for a diagnosis of celiac sprue. Follow up small bowel biopsy revealed villous atrophy consistent with the diagnosis of celiac sprue. IMPLICATIONS/DISCUSSION: Celiac disease is caused by a genetically based inability to digest gluten, a major protein commonly found in grains. Due to the availability of new highly sensitive and specific serologic diagnostic tests, it is increasingly recognized in the United States as a cause of malabsorption. Celiac disease is often asymptomatic but symptoms suggesting the diagnosis include bloating, flatulence, chronic diarrhea and lactose malabsorption. Other than gastrointestional symptoms, celiac disease also has a wide spectrum of extraintestinal manifestations including iron deficiency anemia, low bone mineral density, and dermatitis herpetiformis. In a study of North American adults with celiac disease, 70% of subjects had low bone mineral density, predisposing them to fractures. Other studies have suggested that in subjects with celiac disease, bone manifestations may be more severe in men than in women possibly due to estrogen's protective effects on the bone. Historically, initial screening for celiac disease involved detection of antigliadin antibody. However, more specific serologic tests, including antiendomysial and antitissue transglutaminase antibodies, are now available. Histologic identification of gluten sensitive enteropathy, with characteristic small bowel mucosal abnormalities including villous atrophy, crypt heperplasia, and an increased density of inflammatory cells, still remains diagnostic. The pathogenesis of low bone mass and osteoporosis in celiac disease is multifactorial. The reduction in surface area of the intestinal mucosa may contribute to calcium malabsorption and subsequent secondary hyperparathyroidism leading to increased bone resorption. Vitamin D deficiency is also believed to be common. Those who are undiagnosed during childhood and young adulthood may never achieve peak bone mass. In addition, some researchers suspect that systemic effects of inflammatory cytokines involved in the intestinal mucosa inflammation may also contribute to the development of bone disease. Not only should patients with celiac disease be screened for osteoporosis, but patients with low bone mineral density and no evident osteoporosis risk factors should be evaluated for celiac sprue.