A patient with celiac disease develops hypocalcemia and osteomalacia despite adequate calcium intake. What is the SEQUENTIAL biochemical mechanism of bone disease in this condition?
- A Malabsorption of calcium → hypocalcemia → PTH stimulation → bone resorption (secondary hyperparathyroidism) → osteomalacia from vitamin D deficiency ✓
- B Direct immune-mediated destruction of osteoclasts
- C Reduced dietary protein causing collagen deficiency
- D Hyperphosphatemia from malabsorption forming calcium-phosphate crystals
Explanation
In celiac disease, villous atrophy impairs absorption of both calcium and fat-soluble vitamin D from the proximal small intestine. Vitamin D deficiency prevents Ca2+-binding protein (calbindin) synthesis, reducing intestinal calcium absorption. Hypocalcemia triggers PTH secretion (secondary hyperparathyroidism). PTH promotes bone resorption (RANKL-mediated osteoclast activation) and renal calcium reabsorption, but without 1,25-(OH)2D3, new osteoid cannot mineralize — leading to osteomalacia. The hypophosphatemia from PTH-driven phosphaturia further impairs hydroxyapatite deposition.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
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Written and medically reviewed by the StethoPrep medical team.