Atraumatic bilateral Achilles tendon rupture: an association of systemic steroid treatment.

Kotnis, Rohit; Halstead, J C; Hormbrey, Philip

doi:10.1136/emj.16.5.378

Cited by 33 publications

(22 citation statements)

References 5 publications

(1 reference statement)

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“…Glucocorticoids are effective anti-inflammatory agents and give rapid clinical response. However, there have been many case reports of spontaneous tendon rupture, both after local glucocorticoid injections (Chechick et al 1982, Kleinman and Gross 1983, Stannard and Bucknell 1993, Smith et al 1999) and with systemic glucocorticoid therapy (Kotnis et al 1999). Previous studies on histological and mechanical changes after glucocorticoid injections using in vivo animal models have produced conflicting results (Oxlund et al 1981, Kapetanos 1982, McWhorter et al 1991, Wiggins et al 1995, Campbell et al 1996, Tatari et al 2001.…”

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confidence: 96%

Glucocorticoids suppress proteoglycan production by human tenocytes

et al. 2005

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Background The role of glucocortiocid injection therapy in spontaneous tendon rupture is controversial. We hypothesized that glucocorticoids suppress proteoglycan production in tendon and studied the in vitro effects of dexamethasone and triamcinolone on proteoglycan production by cultured human tenocytes.Material and methods We obtained primary cultures of human tenocytes from explants of healthy human patellar tendon. The human tenocytes were treated with 1 µM dexamethasone or 1 µM triamcinolone. The amount of proteoglycan production was measured by 35 S-sulfate incorporation assay and compared with control cultures. The reversibility of the effect of dexamethasone by co-incubation with 10 ng platelet-derived growth factor (PDGFBB) was also tested.Results Treatment with 1 µM triamcinolone reduced the amount of 35 S-sulfate incorporation to 80% of control cultures (p = 0.007), whereas 1 µM dexamethasone reduced it to 72% (p = 0.01). Co-incubation of 10 ng/mL PDGFBB with 1 µM dexamethasone returned the 35 Ssulfate incorporation to a level that was significantly higher than for dexamethasone treatment alone (108%; p = 0.01).Interpretation Glucocorticoids suppressed proteoglycan production in cultured human tenocytes. The suppression by dexamethasone was reversed by simultaneous addition of PDGFBB. Suppressed proteoglycan production may affect the viscoelastic properties of tendon and increase the risk of spontaneous rupture.

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confidence: 96%

Glucocorticoids suppress proteoglycan production by human tenocytes

et al. 2005

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“…Most reported cases of spontaneous tendon ruptures have a patient history significant for systemic disease, such as rheumatoid arthritis, chronic steroid use, and/or injection of steroids to the tendon [7][8][9]. Loss of extensor function will decrease ankle strength [10].…”

Section: Discussionmentioning

confidence: 99%

“…The patient presented in the article has no history of systemic disease, steroids use, or surgical treatment. There seems to be a common theme in the literature of injectable or oral steroids weakening tendons [8,9,11].…”

Section: Discussionmentioning

confidence: 99%

Atraumatic Extensor Hallucis Longus Rupture

Kolodenker¹

2014

JESO

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“…It is said that steroids have the ability to alter the collagen structure of tendons by contributing to dysplasia of collagen fibrils, thus reducing the tensile strength of the tendon (Kelly et al, 2004). Corticosteroids can also interfere with collagen fibre cross-linking which can lead to disruption in the normal healing process of the tendon (Orava et al, 1996;Kotnis et al, 1999;Kelly et al, 2004).…”

Section: Pathogenesismentioning

confidence: 99%

Ciprofloxacin Induced Chondrotoxicity and Tendinopathy

Adikwu

Nelson

2012

American Journal of Pharmacology and Toxicology

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ABSRACTCiprofloxacin is one of the fluoroquinolones with a wide clinical acceptability. Rescently there are increasing reports on Ciprofloxacin induce Chondrotoxicity and Tendinopathy in Animal experiment and clinical experience which is of great clinical concern. A comprehensive survey and review of literaure on reported ciprofloxacin induced Chondrotoxicity and Tendinopathy in Humans and Animals was performed. It was observd that ciprofloxacin is a potential inducer of Chrondrotoxicity and Tendinopathy which could be potentiated by coadministration with corticosteroids.This conditions were reported to be characterised by cartilage lesion, matrix swelling, inhibition of chondrocytes proliferation, secretion of soluble proteoglycan, modification of the metabolism and integrity of extracellular proteins, decrease in epiphyseal growth plate, humerus and femur.The mechanism behind this phenomenon is said to be multifactoral. Ciprofloxacin induced Chrondrotoxicity and Tendinopathy in growing animals is attributed to oxidative stress (lipid peroxidation, Deoxyribonucleic Acid (DNA) oxidative stress). Ciprofloxacin induced cartilage damage may also be attributed to formation of Ciprofloxacin chelates and complexes which possesses the potential to induce a deficiency of functionally available divalent ions resulting in cytoskeletal changes. Animal studies showed that oxidative damage or metabolism of tissues was also found suggesting the involvement of a reactive oxygen species. Administration of magnesium, zinc chloride and vitamin E (α tocopherol) were found to prevent or reverse ciprofloxacin induced Chrondrotoxicity and Tendinopathy. Through excess formation of collagen, increase osteoblastic activity, increase bone growth, inhibition of free oxidation radicals' formation thereby preventing DNA oxidation and oxidative stress. Zinc also directly stimulates DNA synthesis either by enzyme stimulation or altering, the binding of f1 and f3 histones to DNA so as to affect RNA synthesis. Patient medical history should be considered before Ciprofloxacin recommendation. Coadministration with corticosteroid should be done with caution. Further evaluation of antioxidants effect in Ciprofloxacin induce Chonrotoxicity, Tendinopathy in humans could be of clinical importance as observed in Animal studies.

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Atraumatic bilateral Achilles tendon rupture: an association of systemic steroid treatment.

Cited by 33 publications

References 5 publications

Glucocorticoids suppress proteoglycan production by human tenocytes

Glucocorticoids suppress proteoglycan production by human tenocytes

Atraumatic Extensor Hallucis Longus Rupture

Ciprofloxacin Induced Chondrotoxicity and Tendinopathy

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