Michael R Rickels1, Susan J Mandel. 1. Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Abstract
OBJECTIVE: To describe a patient who presented with hypocalcemia and hypocalciuria as the initial manifestations of celiac disease, despite a normal vitamin D status. METHODS: We review the diagnostic evaluation, treatment, and biochemical and bone mineral density responses of a patient with asymptomatic celiac disease, which was initially suggested because of a low serum calcium level that became attributable to isolated malabsorption of calcium. RESULTS: A 36-year-old woman presented with hypocalcemia in the presence of normal serum 25-hydroxyvitamin D and high serum 1,25-dihydroxyvitamin D levels. She had hypocalciuria and secondary hyperparathyroidism that were refractory to pharmacologic calcium and cholecalciferol supplementation. Fecal calcium excretion indicated malabsorption of calcium, and biopsy of the small intestine demonstrated pathologic changes characteristic of celiac disease. Bone mineral density, determined by dual-energy x-ray absorptiometry, was in the osteopenic range at the femoral neck. The initiation of a gluten-free diet resulted in correction of all biochemical abnormalities and a substantial increase in bone mineral density. CONCLUSION: Primary intestinal malabsorption of calcium without concomitant vitamin D deficiency is possible in celiac disease because of the preferential involvement of the proximal small intestine early in the disease process. Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal.
OBJECTIVE: To describe a patient who presented with hypocalcemia and hypocalciuria as the initial manifestations of celiac disease, despite a normal vitamin D status. METHODS: We review the diagnostic evaluation, treatment, and biochemical and bone mineral density responses of a patient with asymptomatic celiac disease, which was initially suggested because of a low serum calcium level that became attributable to isolated malabsorption of calcium. RESULTS: A 36-year-old woman presented with hypocalcemia in the presence of normal serum 25-hydroxyvitamin D and high serum 1,25-dihydroxyvitamin D levels. She had hypocalciuria and secondary hyperparathyroidism that were refractory to pharmacologic calcium and cholecalciferol supplementation. Fecal calcium excretion indicated malabsorption of calcium, and biopsy of the small intestine demonstrated pathologic changes characteristic of celiac disease. Bone mineral density, determined by dual-energy x-ray absorptiometry, was in the osteopenic range at the femoral neck. The initiation of a gluten-free diet resulted in correction of all biochemical abnormalities and a substantial increase in bone mineral density. CONCLUSION: Primary intestinal malabsorption of calcium without concomitant vitamin D deficiency is possible in celiac disease because of the preferential involvement of the proximal small intestine early in the disease process. Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal.
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