Bone mineral metabolism in pediatric inflammatory bowel disease

Abstract

The development of reliable techniques to measure bone densitometry and evolving effective drug treatment have kindled great interest in the diagnosis and treatment of osteoporosis in adults with inflammatory bowel disease. A number of studies have examined the prevalence of abnormal bone mineral metabolism in children and adolescents. Studies, conducted over the past decade, indicate a greater likelihood of clinically significant problems in Crohn's disease than in ulcerative colitis. Corticosteroids have been proven to impair bone mineral status. It is increasingly clear that inflammation and other factors play a bigger role than malabsorbtion of minerals or vitamin D in most patients. As the use of the bisphonate class of drugs is limited in pediatric patient&, there is a need to emphasize the role of diet and exercise in children and teenagers, particularly in those affected by inflammatory bowel disease.

Bone Health in Children With Inflammatory Bowel Disease: Adjusting for Bone Age

“…The interpretation of data pertaining to estimates of BMD is not straightforward in children. In children, the processes of both bone accrual and remodelling are occurring as a result of growth, and therefore, growing bone is more vulnerable to the effects of IBD and any necessary drug treatments (13,14). Clinically, this may result in decreased peak bone mass attained during the adolescent years leading to fracture at an early age, with problems persisting throughout adulthood (4,15).…”

Nutritional concerns in pediatric inflammatory bowel disease patients

“…In addition, corticosteroids reduce calcium absorption, down-regulate calcitriol synthesis, decrease gene expression of calcium-binding protein, inhibit osteoblast proliferation, and stimulate osteoclastic bone resorption [17]. Indeed, the cumulative exposure to corticosteroids is negatively associated with lumbar spine bone mineral density [14,15].…”

Nutrition Support for Pediatric Patients With Inflammatory Bowel Disease: A Clinical Report of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

“…Corticosteroids reduce calcium absorption, downregulate calcitriol synthesis, decrease gene expression of calcium binding protein, inhibit osteoblast proliferation, and stimulate osteoclastic bone resorption (55). Corticosteroid use at >7.5 mg/day, 5 g lifetime cumulative dose, or >12 months of lifetime exposure are risk factors for a low bone mineral density z score (26,53).…”

“…Patients with newly diagnosed Crohn disease exhibit hypercalciuria, indicating negative calcium balance, because of the effects of systemic inflammation (55). Serum from pediatric patients with Crohn disease inhibits osteoblastic activity in bone cell culture that is attributed to the effects of IL-6, TNF-alpha, and cytokines (56).…”