21/12/2025
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Alkaline phosphatase (ALP) is an enzyme found mainly in liver and bone. Elevated ALP typically points to either increased osteoblastic activity (bone formation/turnover) or cholestatic liver disease. Serum calcium reflects the balance of bone turnover, parathyroid hormone (PTH), vitamin D, renal handling, and albumin-bound fraction. Interpreting ALP together with calcium (and adding phosphate, PTH, vitamin D, liver enzymes) helps localize the problem to bone vs. hepatobiliary, and clarifies the mechanism driving the abnormality.
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This pairing usually indicates high bone turnover with net bone resorption or PTH-driven hypercalcemia. Two classic causes are:
âĸ Bone metastases: Tumors (breast, prostate, lung, kidney, thyroid) can infiltrate bone, stimulating osteoblasts (raising ALP) and osteoclasts (releasing calcium).
âĸ Typical clues: Bone pain, fractures, mixed lytic/blastic lesions on imaging (blastic lesions often elevate ALP markedly), elevated tumor markers depending on primary.
âĸ Key labs: High ALP, high calcium; phosphate varies; PTH is usually suppressed (non-PTH hypercalcemia).
âĸ Confirmatory steps: Skeletal imaging (X-ray, bone scan, PET/CT), search for primary malignancy, assess PTHrP if suspected humoral hypercalcemia of malignancy.
âĸ Primary hyperparathyroidism: Autonomous PTH secretion increases bone resorption and renal calcium reabsorption; ALP rises if bone turnover is high.
âĸ Typical clues: Stones, bones, abdominal groans, and neuropsychiatric symptoms; may be asymptomatic and found on routine labs.
âĸ Key labs: High or inappropriately normal PTH with high calcium, low-normal or low phosphate; urinary calcium often elevated.
âĸ Confirmatory steps: Repeat serum calcium (corrected for albumin), intact PTH, 25âOH vitamin D, 24âhour urine calcium; neck ultrasound or sestamibi scan if surgical planning.
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This pattern often reflects defective mineralization or impaired renal handling of calcium/phosphate.
âĸ Osteomalacia (adult rickets): Inadequate mineralization of osteoid, commonly due to vitamin D deficiency or malabsorption. Osteoblast activity ramps up (raising ALP), but calcium falls because of poor intestinal absorption and secondary hyperparathyroidism.
âĸ Typical clues: Bone pain, muscle weakness, fractures/pseudofractures, low sun exposure or malabsorption history.
âĸ Key labs: Low or low-normal calcium, low phosphate, high ALP, high PTH (secondary), low 25âOH vitamin D.
âĸ Confirmatory steps: Measure 25âOH vitamin D, phosphate, PTH, consider celiac/IBD workup, radiographs showing Looser zones; respond to vitamin D/calcium repletion.
âĸ Renal failure (chronic kidney diseaseâmineral bone disorder): Reduced 1âalpha hydroxylation lowers active vitamin D, leading to hypocalcemia; phosphate retention further suppresses calcium. Secondary hyperparathyroidism increases bone turnover, elevating ALP.
âĸ Typical clues: Known CKD, pruritus, vascular calcifications, bone pain.
âĸ Key labs: Low or low-normal calcium, high phosphate, high PTH, raised ALP; low 1,25âOHâ vitamin D.
âĸ Confirmatory steps: Assess kidney function (eGFR, creatinine), CKD-MBD panel (calcium, phosphate, PTH, ALP, vitamin D), bone imaging if fractures suspected.
Distinguishing bone vs. liver sources of ALP
âĸ ALP isoenzymes or GGT: Elevated gammaâglutamyl transferase (GGT) points to hepatobiliary origin; normal GGT with raised ALP suggests bone.
âĸ Pattern of liver enzymes: Cholestatic picture (high ALP > ALT/AST) favors biliary obstruction, primary biliary cholangitis, or infiltrative liver disease.
âĸ Clinical context: Bone pain, fractures, skeletal lesions suggest bone; jaundice, pruritus, pale stools suggest hepatobiliary.
