Abstract Background: Hepatic osteodystrophy (HOD) is an underrecognized metabolic bone disease that accompanies chronic liver disease and increases fragility-fracture risk. We report a case in which heavy alcohol use and biochemical features of liver involvement created a diagnostic pathway culminating in HOD as the proximate cause of an atraumatic femoral neck fracture, and we summarize a mechanistic framework linking liver injury to skeletal fragility.Case: An adult man with long-standing alcohol use presented with acute right hip pain without high-energy trauma. Radiographs demonstrated a displaced femoral neck fracture. Systemic workup ruled out malignant and infectious etiologies and suggested chronic liver disease. He underwent hip arthroplasty for pain control and early mobilization. Discussion: Contemporary evidence indicates that liver-derived signals (e.g., IGFBP1–FGF21 axis; PP2Ac–LCAT pathway) modulate bone turnover and that vitamin D deficiency, hypogonadism, cytokine-mediated osteoclast activation, and malnutrition converge to decrease bone mass and quality in chronic liver disease. We integrate this liver–bone axis with clinical clues from this patient to explain the insufficiency fracture and outline a diagnostic algorithm emphasizing early identification of HOD.Conclusion: In patients with alcohol use disorder or suspected liver disease presenting with atraumatic fractures, clinicians should actively consider HOD, evaluate reversible contributors (vitamin D/K deficiency, hypogonadism), and address liver disease in parallel with fracture care.
Chiang Chi-ming (Thu,) studied this question.