A patient with longstanding, poorly controlled tophaceous gout developed bilateral Achilles tendon rupture, suggesting that chronic intratendinous monosodium urate crystal deposition may have weakened the tendons and that recent fluoroquinolone exposure may have contributed to rupture in an already compromised tendon.
The report described a 68-year-old male patient with longstanding tophaceous gout who presented with progressively worsening foot deformity over the preceding 2 years. He had been taking allopurinol 100 mg daily for several years without regular follow-up and used colchicine to manage infrequent gout flares. He reported serum urate concentrations above 9 mg/dL. Approximately 1 month prior to presentation, the patient experienced an acute “popping” sensation shortly after completing a short course of levofloxacin for an upper respiratory infection and subsequent difficulty walking and impaired balance. Physical examination revealed multiple tophi and bilateral Thompson tests positivity, prompting magnetic resonance imaging (MRI) of both feet and ankles.
The researchers found MRI-confirmed bilateral Achilles tendon rupture; extensive intratendinous tophaceous deposition involving the Achilles, tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneal tendons; impaired pushoff and gait; and a serum urate concentration of 9.6 mg/dL at presentation. Complete bilateral Achilles tendon ruptures were identified approximately 6 to 6.5 cm proximal to the calcaneal insertion, with tendon retraction and gap formation measuring approximately 4.5 cm on the left and 2 cm on the right. The patient also had impaired pushoff during gait, consistent with the imaging findings. Because of the extensive tophaceous burden and chronic tendon changes, the patient’s allopurinol dose was increased to improve urate control prior to consideration of surgical intervention.
Tendon involvement is an increasingly recognized manifestation of advanced gout. The researchers noted that experimental evidence suggests that monosodium urate crystals may impair tenocyte viability, reduce collagen production, and promote chronic inflammation that weakens tendon structure over time. Fluoroquinolones may contribute to tendon injury through impaired collagen synthesis, oxidative stress, and increased matrix degradation, with the Achilles tendon representing the most commonly affected site.
Based on the clinical course, the researchers proposed a “two-hit” model in which longstanding intratendinous tophaceous gout produced chronic structural tendon degeneration, while recent fluoroquinolone exposure contributed to tendon rupture. They also highlighted MRI as a useful tool for identifying diffuse tendon involvement and defining structural complications that may influence management.
The report’s findings should be interpreted cautiously. The researchers could not establish a causal relationship between fluoroquinolone exposure and tendon rupture or confirm the proposed “twohit” mechanism. The temporal association and imaging findings supported their hypothesis but should not be generalized to all patients with gout or those receiving fluoroquinolones.
“The present case is notable for MRI-confirmed multifocal intratendinous gout associated with bilateral Achilles tendon rupture and highlights a potentially underrecognized population in whom clinicians should maintain a high index of suspicion for tendon complications and exercise caution when prescribing fluoroquinolones,” wrote lead study author Thipsukhon Sathapanasiri, MD, of the Arthritis and Rheumatic Clinic at Bangkok Hospital, and colleagues.
The study authors reported using OpenAI’s language model to improve grammar. Full disclosures of the study authors can be found in the study.
Source: ACR Open Rheumatology
