Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2007
Hypocalcemia after alendronate therapy in a patient with celiac disease.
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Meek Shon E, Nix Kenneth
Аннотация
OBJECTIVE: To describe a patient with osteoporosis who was treated with alendronate and developed hypocalcemia, which ultimately led to the diagnosis of celiac sprue.
METHODS: We present the clinical and laboratory findings in a patient with osteoporosis, in whom hypocalcemia developed after treatment with alendronate. This patient was subsequently diagnosed with celiac sprue. The pertinent literature regarding orally administered bisphosphonate-induced hypocalcemia is reviewed.
RESULTS: A 79-year-old man who was diagnosed with osteoporosis was treated with alendronate. He was subsequently found to have asymptomatic hypocalcemia (serum calcium concentration, 8.3 mg/dL), which resolved after alendronate therapy was discontinued. He was then treated with calcium, vitamin D, and calcitonin nasal spray, which did not cause hypocalcemia. Because of his reduced bone density, however, he was subsequently referred for endocrine consultation. Evaluation at that time showed normal levels of serum calcium, phosphorus, creatinine, alkaline phosphatase, 25-hydroxyvitamin D, thyrotropin, and parathyroid hormone as well as 24-hour urine calcium excretion. An endomysial antibody titer was dramatically elevated. Upper endoscopy showed villous atrophy, and small bowel biopsy confirmed the presence of villous blunting and chronic inflammation, consistent with celiac sprue. He was treated with a gluten-free diet and then subsequently treated with orally administered risedronate, which he tolerated well without evidence of hypocalcemia.
CONCLUSION: To the best of our knowledge, this is the first report of orally administered bisphosphonate-induced hypocalcemia, which subsequently led to the diagnosis of previously unrecognized, otherwise asymptomatic celiac sprue. Patients with unexplained hypocalcemia should be screened for celiac sprue, even in the absence of gastrointestinal symptoms.
METHODS: We present the clinical and laboratory findings in a patient with osteoporosis, in whom hypocalcemia developed after treatment with alendronate. This patient was subsequently diagnosed with celiac sprue. The pertinent literature regarding orally administered bisphosphonate-induced hypocalcemia is reviewed.
RESULTS: A 79-year-old man who was diagnosed with osteoporosis was treated with alendronate. He was subsequently found to have asymptomatic hypocalcemia (serum calcium concentration, 8.3 mg/dL), which resolved after alendronate therapy was discontinued. He was then treated with calcium, vitamin D, and calcitonin nasal spray, which did not cause hypocalcemia. Because of his reduced bone density, however, he was subsequently referred for endocrine consultation. Evaluation at that time showed normal levels of serum calcium, phosphorus, creatinine, alkaline phosphatase, 25-hydroxyvitamin D, thyrotropin, and parathyroid hormone as well as 24-hour urine calcium excretion. An endomysial antibody titer was dramatically elevated. Upper endoscopy showed villous atrophy, and small bowel biopsy confirmed the presence of villous blunting and chronic inflammation, consistent with celiac sprue. He was treated with a gluten-free diet and then subsequently treated with orally administered risedronate, which he tolerated well without evidence of hypocalcemia.
CONCLUSION: To the best of our knowledge, this is the first report of orally administered bisphosphonate-induced hypocalcemia, which subsequently led to the diagnosis of previously unrecognized, otherwise asymptomatic celiac sprue. Patients with unexplained hypocalcemia should be screened for celiac sprue, even in the absence of gastrointestinal symptoms.