Cephalexin-associated Achilles Tendonitis: Case Report and Review of Drug-induced Tendinopathy

Abstract

Tendon disorders include tenosynovitis or tendonitis, tendinosis, and tendon rupture. Tendinopathy associated with drug administration has been associated with the systemic or local administration of several medications. A 90-year-old man who developed toxic tendinopathy after receiving cephalexin 500 mg twice daily has been described. Unilateral pain of his left Achilles tendon pain during walking appeared three weeks after starting the antibiotic. The drug was stopped after four weeks of treatment; within one week after discontinuing the cephalexin, all tendonitis symptoms spontaneously resolved. Drug-induced tendinopathy has most commonly been associated with fluoroquinolones, statins, glucocorticoids, and aromatase inhibitors. In addition, other systemic agents have caused tendinopathy; they include amlodipine, anabolic steroids, antiretrovirals, isotretinoin, renin-angiotensin II receptor antagonists, rituximab, and sitagliptin. Albeit less frequent, other oral antibiotics, including cephalosporins, azithromycin, and sulfonamides, have also been associated with toxic tendinopathy. Also, injections of collagenase Clostridium histolyticum, corticosteroids, and polidocanol have been followed by tendon rupture. The features of tendinopathy associated with drug treatment are summarized and their postulated mechanisms of pathogenesis are reviewed. The onset of tendon pain following the initiation of treatment with a new medication, especially if the agent has previously been associated with drug-induced tendonitis, tendinosis, or tendon rupture, should prompt the consideration of drug-associated toxic tendinopathy.

Sitagliptin protects liver against aflatoxin B1‐induced hepatotoxicity through upregulating Nrf2/ARE/HO‐1 pathway

“…40,41 Reactive oxygen species (ROS) breaks the bond of Cullin 3-Keap 1 system and further Nrf2 discharge from them and translocates into the nucleus and attaches with a small MAF protein and make a dimer, and the dimer actuates the interpretation of antioxidative genes through ARE binding. [42][43][44] In this, Nrf2 protein expression and antioxidant genes altogether reduced in the AFB1-prompted rats' liver. The Nrf2 signaling downregulation has been affirmed by the decreased expression of NQO-1 and HO-1.…”

“…In the cell cytosol, Nrf2 is set aside neutralized by binding with Cullin 3 and KEAP1 . Reactive oxygen species (ROS) breaks the bond of Cullin 3–Keap 1 system and further Nrf2 discharge from them and translocates into the nucleus and attaches with a small MAF protein and make a dimer, and the dimer actuates the interpretation of antioxidative genes through ARE binding . In this, Nrf2 protein expression and antioxidant genes altogether reduced in the AFB1‐prompted rats' liver.…”

Levofloxacin-induced Achilles Tendinitis in a Steroid User

“…The condition improved by discontinuing levofloxacin ( Picture C ). Drug-induced tendinitis is commonly associated with fluoroquinolones, statins, glucocorticoids, and aromatase inhibitors ( 1 ). Although isolated prednisolone use is a risk factor for tendinopathy through antimitosis and collagenase activation, the combination of prednisolone and fluoroquinolones is 17.5 times more likely to cause tendinopathy than prednisolone used alone ( 2 ).…”

“…Although isolated prednisolone use is a risk factor for tendinopathy through antimitosis and collagenase activation, the combination of prednisolone and fluoroquinolones is 17.5 times more likely to cause tendinopathy than prednisolone used alone ( 2 ). Furthermore, fluoroquinolone-induced tendinopathy typically affects the Achilles tendons within two weeks of fluoroquinolone use, regardless of the class and dosages ( 1 ). Clinicians should therefore consider the risk of fluoroquinolone-associated tendinopathy, especially in steroid users.…”