The Fluoroquinolone Toxicity Research Foundation

 

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QUINOLONE INDUCED MYOTENDINOPATHY

Vasuki Narayanasamy M.D, Harsha Vyas M.D, Guha Krishnaswamy M.D.



The Fluroquinolones is a popular class of antibiotics due to its wide spectrum of activity, favorable pharmokokinetics and relative lack of side effects. They act by inhibiting DNA gyrase and topoisomerase IV resulting in ineffective bacterial DNA synthesis. Myotendinopathy is a major concerning side effect associated with the use of Fluoroquinolones. We are reporting cases of sartorius muscle and achilles tendon ruptures secondary to the use of quinolones.

Case report #1: This is an 82 year old female patient who presented to the clinic with left lower extremity pain and swelling after being treated for bronchitis with levofloxacin in her prior visit. On examination, the calf and dorsum of the left foot was associated with moderate swelling and ecchymosis around the insertion of Achilles tendon. Full range of motion at the ankle was limited due to pain. The pulses were intact. A MRI was performed since a tendon rupture was suspected due to the acute nature of presentation and a history of fluroquinolone use. The MRI showed a near full thickness of the Achilles tendon around 3 cm proximal to the calcaneal insertion. Patient chose the non surgical approach and was treated by non weight bearing cast.

Case report #2: This is a 72 year old male who presented to the clinic with ecchymosis of right lower extremity and intense edema. He was treated with Gatifloxacin 10 days prior to this presentation for COPD exacerbation. Deep vein thrombosis was ruled out by Doppler U/S of the Lower Extremity. Further investigation by MRI showed rupture of the right Sartorius tendon at the insertion to knee. This is the first case to be reported for Gatifloxacin induced tendon rupture. He was treated initially by phonopheresis and continued conservative non surgical management since he was not a surgical candidate.

Conclusion: FQ induced myotendinopathy has been reported extensively in the literature since the 80’s, due to the concern associated with the widespread use of antibiotics in modern medicine. It has been associated with numerous risk factors of which concurrent steroid use and age>60 play a very important role. The exact mechanism by which it occurs is still unclear. There has been data showing an ischemic/vascular insult predisposing the rupture. Also, Quinolones upregulate the expression of Matrix metalloproteinases which are involved in the rapid turn over of the cells thereby causing tendon injury. A thorough physical exam and history is helpful in the diagnosis of most cases. MRI is a sensitive and a specific tool to assess the severity of rupture. Management can be either conservative or involve an aggressive surgical approach based on the age, comorbidities and life style of the patient.