SAT-814 - When Bones Speak Louder than Labs: Osteitis Fibrosa Cystica from Primary Hyperparathyroidism Masked by Celiac Disease.

Background:
Primary hyperparathyroidism (PHPT) typically presents with hypercalcemia but celiac disease and other malabsorptive disorders can mask this, delaying diagnosis and allowing severe skeletal complications. Coexistence of PHPT and celiac disease can result in profound osteoporosis, fragility fractures, and skeletal lesions including osteitis fibrosa cystica.

Case Presentation:
A 62-year-old male presented with fatigue and anemia. Labs revealed severe vitamin D deficiency ( < 7 ng/mL), markedly elevated PTH (1600 pg/mL), borderline-normal calcium (9.1mg/dL), hypophosphatemia (2.4 mg/dL), and elevated alkaline phosphatase (784 U/L). DEXA showed severe osteoporosis: lumbar spine T-score −4.8, femoral neck −3.2, forearm −7.7. Sestamibi scan identified a right inferior parathyroid adenoma. Imaging demonstrated marked diffuse osseous demineralization with alternating bands of lucency and sclerosis, focal lucent lesions in the pelvis up to 4.9 cm, and a non-displaced distal radius fracture, consistent with osteitis fibrosa cystica with brown tumors. The patient sustained a pathologic right radial shaft fracture after a ground level fall. Post-parathyroidectomy, PTH normalized to 42 pg/mL. Secondary evaluation revealed positive tissue transglutaminase antibodies, confirming celiac disease. He started a gluten-free diet and vitamin D supplementation (improved to 59 ng/mL).
Follow-up DEXA demonstrated marked skeletal improvement: lumbar spine BMD +74% (T- score −1.0), femoral neck +37% ( −1.9), and forearm +27% (−5.7).

Discussion:
This case shows how primary hyperparathyroidism from a parathyroid adenoma can lead to severe skeletal disease when compounded by celiac-related malabsorption. Vitamin D deficiency masked hypercalcemia, delaying recognition and allowing prolonged PTH elevation with extensive cortical bone loss. Although this patient did not develop hungry bone syndrome, those with markedly elevated PTH and alkaline phosphatase remain at high risk, underscoring the importance of postoperative monitoring. Correction of both the adenoma and underlying malabsorption resulted in dramatic biochemical improvement and marked increases in bone density, highlighting that even advanced osteitis fibrosa cystica can recover.

Conclusion:
Celiac disease and other malabsorptive disorders can mask PHPT and delay diagnosis, increasing the risk of advanced skeletal complications. Screening for celiac disease should be considered in patients with normocalcemic or borderline calcium levels, especially when severe vitamin D deficiency or marked osteoporosis is present. Early parathyroidectomy with correction of vitamin D deficiency and underlying malabsorption can lead to meaningful and sustained skeletal recovery. Even advanced skeletal disease can improve when secondary contributors are identified promptly.

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