Jeya Sushimitha Jawahar Kanth, Morrish Obol Okello, Thuparambil M Ravi Anish, Florence Namutebi, Patricia Namawejje, Micheal Collins Segawa, Morris K Rutakingirwa, Phoebe Mbabazi, David Meya
This case demonstrates TDF as a reversible cause of severe osteomalacia and pathological fractures in long-term HIV treatment, emphasizing early recognition, regimen substitution to non-TDF agents, and proactive bone/mineral monitoring to prevent such outcomes in vulnerable populations.
BACKGROUND: People living with HIV on long-term antiretroviral therapy (ART) face increased risks of bone loss and fragility fractures, partly due to tenofovir disoproxil fumarate (TDF), a commonly used nucleoside reverse transcriptase inhibitor. TDF is associated with proximal tubular dysfunction, renal phosphate wasting, osteomalacia, and pathological fractures. This case highlights severe, bilateral femoral fractures as a rare but debilitating manifestation of chronic TDF-induced osteomalacia in a postmenopausal woman.
CASE PRESENTATION: A 43-year-old African woman with HIV (diagnosed >15 years prior) presented with progressive generalized bone pain and inability to bear weight after minor trauma. She had received TDF-based ART for 12 years. One year earlier, her regimen was switched to abacavir/lamivudine/dolutegravir due to emerging bone pain. Examination revealed bilateral hip tenderness, immobility, stage-4 sacral and ischial pressure ulcers, and rectal prolapse secondary to prolonged immobility and constipation. Laboratory findings included severe hypophosphatemia (0.33 mmol/L), elevated alkaline phosphatase (320 U/L), low-normal 25-hydroxy-vitamin D, and upper-normal PTH, with normal renal function and no overt Fanconi syndrome at presentation. Pelvic radiographs confirmed bilateral pathological femoral fractures (right intertrochanteric, left subcapital). Other causes (malignancy, infection, primary metabolic disorders) were excluded. Management involved permanent TDF discontinuation, supplementation with calcium, phosphate, and vitamin D, orthopaedic fixation, and intensive wound care. Serum phosphate and alkaline phosphatase normalized, bone pain resolved, and no new fractures occurred, though full ambulation remained limited due to complications.
CONCLUSION: This case demonstrates TDF as a reversible cause of severe osteomalacia and pathological fractures in long-term HIV treatment, emphasizing early recognition, regimen substitution to non-TDF agents, and proactive bone/mineral monitoring to prevent such outcomes in vulnerable populations.