HYPOPARATHYROIDISM IN BETA THALASSEMIA MAJOR
AACE ePoster Library. Santana O. 05/13/15; 97765; 506
Omar Santana
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Abstract
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Objective: To report a case of hypoparathyroidism as a cause of hypocalcemia in the setting of transfusion dependent beta thalassemia major.
Methods: Clinical exam, laboratory and hormonal studies, literature review.
Case Presentation: 26 year old male who was admitted to the hospital with complaints of diffuse joint pains with associated numbness and tingling of his feet. He reported a history of beta thalassemia major for which he has required blood transfusions since age 3 and now these are required every 3-5 weeks. Physical examination on admission was remarkable for tachycardia of 110 bpm, tenderness to palpation of knees and elbows, as well as paresthesias of upper and lower extremities, but negative Chvostek’s sign. Laboratory results were remarkable for calcium of 6.4 mg/dL, sodium 129 mEq/L, chloride 95 mEq/L, albumin 3.5 g/dL, ionized calcium 0.90 mmol/L. Electrocardiogram had no QT segment prolongation. He was admitted to the general medical ward for further care. Sodium and chloride abnormalities corrected after hydration with normal saline. He was given IV calcium gluconate with symptomatic improvement but intermittent correction of his serum calcium. Endocrinology service was consulted with further work up revealing a parathyroid hormone level of 11.7 ng/mL, calcium 6.0 mg/dL, ionized calcium 0.89 mmol/L, phosphorus 6.5 mg/dL, magnesium 1.4 mg/dL, 25-hydroxy vitamin D 23.4 ng/mL, and 1,25-hydroxy vitamin D 58 pg/mL. Previous iron studies showed a ferritin of 9999.3 ng/mL, serum iron of 277 mcg/dL, total iron binding capacity of 265.7 mcg/dL, and serum transferrin saturation of 104%. A diagnosis of hypoparathyroidism secondary to potential infiltration of the parathyroid glands from iron overload was made. He was started on scheduled replacement therapy with oral calcium citrate as well as magnesium oxide.
Discussion: Patients with beta thalassemia major undergo frequent blood transfusions as part of their treatment regimen which results in iron deposition of multiple organs leading to potential endocrinopathies. Serum ferritin level has been studied as a predictive marker for progression of endocrine dysfunction in this patient population. Although a rare complication, hypoparathyroidism with resultant hypocalcemia can occur from iron infiltration into the glands. This is an under recognized association in these patients with some studies suggesting a prevalence of 4-10%.
Conclusion: Parathyroid hormone profile should be checked regularly in all patients with transfusion dependent beta thalassemia major as this will allow for earlier detection and management of hypoparathyroidism.
Methods: Clinical exam, laboratory and hormonal studies, literature review.
Case Presentation: 26 year old male who was admitted to the hospital with complaints of diffuse joint pains with associated numbness and tingling of his feet. He reported a history of beta thalassemia major for which he has required blood transfusions since age 3 and now these are required every 3-5 weeks. Physical examination on admission was remarkable for tachycardia of 110 bpm, tenderness to palpation of knees and elbows, as well as paresthesias of upper and lower extremities, but negative Chvostek’s sign. Laboratory results were remarkable for calcium of 6.4 mg/dL, sodium 129 mEq/L, chloride 95 mEq/L, albumin 3.5 g/dL, ionized calcium 0.90 mmol/L. Electrocardiogram had no QT segment prolongation. He was admitted to the general medical ward for further care. Sodium and chloride abnormalities corrected after hydration with normal saline. He was given IV calcium gluconate with symptomatic improvement but intermittent correction of his serum calcium. Endocrinology service was consulted with further work up revealing a parathyroid hormone level of 11.7 ng/mL, calcium 6.0 mg/dL, ionized calcium 0.89 mmol/L, phosphorus 6.5 mg/dL, magnesium 1.4 mg/dL, 25-hydroxy vitamin D 23.4 ng/mL, and 1,25-hydroxy vitamin D 58 pg/mL. Previous iron studies showed a ferritin of 9999.3 ng/mL, serum iron of 277 mcg/dL, total iron binding capacity of 265.7 mcg/dL, and serum transferrin saturation of 104%. A diagnosis of hypoparathyroidism secondary to potential infiltration of the parathyroid glands from iron overload was made. He was started on scheduled replacement therapy with oral calcium citrate as well as magnesium oxide.
Discussion: Patients with beta thalassemia major undergo frequent blood transfusions as part of their treatment regimen which results in iron deposition of multiple organs leading to potential endocrinopathies. Serum ferritin level has been studied as a predictive marker for progression of endocrine dysfunction in this patient population. Although a rare complication, hypoparathyroidism with resultant hypocalcemia can occur from iron infiltration into the glands. This is an under recognized association in these patients with some studies suggesting a prevalence of 4-10%.
Conclusion: Parathyroid hormone profile should be checked regularly in all patients with transfusion dependent beta thalassemia major as this will allow for earlier detection and management of hypoparathyroidism.
Objective: To report a case of hypoparathyroidism as a cause of hypocalcemia in the setting of transfusion dependent beta thalassemia major.
Methods: Clinical exam, laboratory and hormonal studies, literature review.
Case Presentation: 26 year old male who was admitted to the hospital with complaints of diffuse joint pains with associated numbness and tingling of his feet. He reported a history of beta thalassemia major for which he has required blood transfusions since age 3 and now these are required every 3-5 weeks. Physical examination on admission was remarkable for tachycardia of 110 bpm, tenderness to palpation of knees and elbows, as well as paresthesias of upper and lower extremities, but negative Chvostek’s sign. Laboratory results were remarkable for calcium of 6.4 mg/dL, sodium 129 mEq/L, chloride 95 mEq/L, albumin 3.5 g/dL, ionized calcium 0.90 mmol/L. Electrocardiogram had no QT segment prolongation. He was admitted to the general medical ward for further care. Sodium and chloride abnormalities corrected after hydration with normal saline. He was given IV calcium gluconate with symptomatic improvement but intermittent correction of his serum calcium. Endocrinology service was consulted with further work up revealing a parathyroid hormone level of 11.7 ng/mL, calcium 6.0 mg/dL, ionized calcium 0.89 mmol/L, phosphorus 6.5 mg/dL, magnesium 1.4 mg/dL, 25-hydroxy vitamin D 23.4 ng/mL, and 1,25-hydroxy vitamin D 58 pg/mL. Previous iron studies showed a ferritin of 9999.3 ng/mL, serum iron of 277 mcg/dL, total iron binding capacity of 265.7 mcg/dL, and serum transferrin saturation of 104%. A diagnosis of hypoparathyroidism secondary to potential infiltration of the parathyroid glands from iron overload was made. He was started on scheduled replacement therapy with oral calcium citrate as well as magnesium oxide.
Discussion: Patients with beta thalassemia major undergo frequent blood transfusions as part of their treatment regimen which results in iron deposition of multiple organs leading to potential endocrinopathies. Serum ferritin level has been studied as a predictive marker for progression of endocrine dysfunction in this patient population. Although a rare complication, hypoparathyroidism with resultant hypocalcemia can occur from iron infiltration into the glands. This is an under recognized association in these patients with some studies suggesting a prevalence of 4-10%.
Conclusion: Parathyroid hormone profile should be checked regularly in all patients with transfusion dependent beta thalassemia major as this will allow for earlier detection and management of hypoparathyroidism.
Methods: Clinical exam, laboratory and hormonal studies, literature review.
Case Presentation: 26 year old male who was admitted to the hospital with complaints of diffuse joint pains with associated numbness and tingling of his feet. He reported a history of beta thalassemia major for which he has required blood transfusions since age 3 and now these are required every 3-5 weeks. Physical examination on admission was remarkable for tachycardia of 110 bpm, tenderness to palpation of knees and elbows, as well as paresthesias of upper and lower extremities, but negative Chvostek’s sign. Laboratory results were remarkable for calcium of 6.4 mg/dL, sodium 129 mEq/L, chloride 95 mEq/L, albumin 3.5 g/dL, ionized calcium 0.90 mmol/L. Electrocardiogram had no QT segment prolongation. He was admitted to the general medical ward for further care. Sodium and chloride abnormalities corrected after hydration with normal saline. He was given IV calcium gluconate with symptomatic improvement but intermittent correction of his serum calcium. Endocrinology service was consulted with further work up revealing a parathyroid hormone level of 11.7 ng/mL, calcium 6.0 mg/dL, ionized calcium 0.89 mmol/L, phosphorus 6.5 mg/dL, magnesium 1.4 mg/dL, 25-hydroxy vitamin D 23.4 ng/mL, and 1,25-hydroxy vitamin D 58 pg/mL. Previous iron studies showed a ferritin of 9999.3 ng/mL, serum iron of 277 mcg/dL, total iron binding capacity of 265.7 mcg/dL, and serum transferrin saturation of 104%. A diagnosis of hypoparathyroidism secondary to potential infiltration of the parathyroid glands from iron overload was made. He was started on scheduled replacement therapy with oral calcium citrate as well as magnesium oxide.
Discussion: Patients with beta thalassemia major undergo frequent blood transfusions as part of their treatment regimen which results in iron deposition of multiple organs leading to potential endocrinopathies. Serum ferritin level has been studied as a predictive marker for progression of endocrine dysfunction in this patient population. Although a rare complication, hypoparathyroidism with resultant hypocalcemia can occur from iron infiltration into the glands. This is an under recognized association in these patients with some studies suggesting a prevalence of 4-10%.
Conclusion: Parathyroid hormone profile should be checked regularly in all patients with transfusion dependent beta thalassemia major as this will allow for earlier detection and management of hypoparathyroidism.
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