Causes |
PTH deficiency: hereditary (e.g., isolated congenital hypoparathyroidism, DiGeorge syndrome) or acquired hypoparathyroidism, post-parathyroidectomy and post-thyroidectomy, post-parathyroid glands radiation |
Vitamin D deficiency or resistance [lack of sun exposure, inadequate dietary intake, intestinal malabsorption (steatorrhea), hepatic disease, CKD, osteomalacia, rickets] |
Increased Ca+2 uptake as in rhabdomyolysis, tumor lysis syndrome, hungry bone syndrome (post-parathyroidectomy), or acute pancreatitis |
Ca+2 malabsorption due to small bowel pathologies such as short bowel syndrome and sprue |
Acute hyperventilation (which results in respiratory alkalosis) |
Low dietary intake of Ca+2 (rare in the absence of intestinal malabsorption or vitamin D deficiency) |
Osteoclastic bone metastases as in prostate cancer and small cell lung cancer |
Pseudohypoparathyroidism, which is a rare genetic disorder characterized by resistance to PTH actions |
Hypermagnesemia and profound hypomagnesemia (due to suppression of PTH secretion) |
Acute severe hyperphosphatemia |
Intake of Ca+2-binding ingredients such as oxalate, phosphate, and cellulose |
Medications: bisphosphonate, denosumab, cinacalcet, etelcalcetide |
Massive blood transfusion due to binding of ionized Ca+2 with citrate |
Critical illness |
Pseudohypocalcemia caused by some gadolinium contrast agents (e.g., gadoversetamide) due to interference with total calcium laboratory assay |