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Symptoms and Signs – Differential Diagnosis of Hypocalcemia
• Renal insufficiency: hypocalcemia caused by:
• Increased calcium deposits in bone and soft tissue secondary to increased serum PO4−3 level
• Decreased production of 1,25-dihydroxyvitamin D
• Excessive loss of 25-OHD (nephrotic syndrome)
• Hypoalbuminemia: each decrease in serum albumin (g/L) will decrease serum calcium by 0.8 mg/dL but will not change free (ionized) calcium.
• Vitamin D deficiency
• Malabsorption (most common cause)
• Inadequate intake
• Decreased production of 1,25-dihydroxyvitamin D (vitamin D–
dependent rickets, renal failure)
• Decreased production of 25-OHD (parenchymal liver disease)
• Accelerated 25-OHD catabolism (phenytoin, phenobarbital)
• End-organ resistance to 1,25-dihydroxyvitamin D
• Hypomagnesemia: hypocalcemia caused by
• Decreased parathyroid hormone (PTH) secretion
• Inhibition of PTH effect on bone
• Pancreatitis, hyperphosphatemia, osteoblastic metastases: hypocalcemia is secondary to increased calcium deposits (bone, abdomen).
• Pseudohypoparathyroidism: autosomal recessive disorder characterized by short stature, shortening of metacarpal bones, obesity, and mental retardation; the hypocalcemia is secondary to congenital end-organ resistance to PTH.
• Idiopathic hypoparathyroidism, surgical removal of parathyroids (e.g., neck surgery)
• “Hungry bones syndrome”: rapid transfer of calcium from plasma into bones after removal of a parathyroid tumor
• Sepsis
• Massive blood transfusion (as a result of ethylenediaminetetraacetic acid [EDTA] in blood)
• Renal insufficiency: hypocalcemia caused by:
• Increased calcium deposits in bone and soft tissue secondary to increased serum PO4−3 level
• Decreased production of 1,25-dihydroxyvitamin D
• Excessive loss of 25-OHD (nephrotic syndrome)
• Hypoalbuminemia: each decrease in serum albumin (g/L) will decrease serum calcium by 0.8 mg/dL but will not change free (ionized) calcium.
• Vitamin D deficiency
• Malabsorption (most common cause)
• Inadequate intake
• Decreased production of 1,25-dihydroxyvitamin D (vitamin D–
dependent rickets, renal failure)
• Decreased production of 25-OHD (parenchymal liver disease)
• Accelerated 25-OHD catabolism (phenytoin, phenobarbital)
• End-organ resistance to 1,25-dihydroxyvitamin D
• Hypomagnesemia: hypocalcemia caused by
• Decreased parathyroid hormone (PTH) secretion
• Inhibition of PTH effect on bone
• Pancreatitis, hyperphosphatemia, osteoblastic metastases: hypocalcemia is secondary to increased calcium deposits (bone, abdomen).
• Pseudohypoparathyroidism: autosomal recessive disorder characterized by short stature, shortening of metacarpal bones, obesity, and mental retardation; the hypocalcemia is secondary to congenital end-organ resistance to PTH.
• Idiopathic hypoparathyroidism, surgical removal of parathyroids (e.g., neck surgery)
• “Hungry bones syndrome”: rapid transfer of calcium from plasma into bones after removal of a parathyroid tumor
• Sepsis
• Massive blood transfusion (as a result of ethylenediaminetetraacetic acid [EDTA] in blood)
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