Deciphering the pathogenesis of tendinopathy: a three-stages process

Our understanding of the pathogenesis of "tendinopathy" is based on fragmented evidences like pieces of a jigsaw puzzle. We propose a "failed healing theory" to knit these fragments together, which can explain previous observations. We also propose that albeit "overuse injury" and other insidious "micro trauma" may well be primary triggers of the process, "tendinopathy" is not an "overuse injury" per se. The typical clinical, histological and biochemical presentation relates to a localized chronic pain condition which may lead to tendon rupture, the latter attributed to mechanical weakness. Characterization of pathological "tendinotic" tissues revealed coexistence of collagenolytic injuries and an active healing process, focal hypervascularity and tissue metaplasia. These observations suggest a failed healing process as response to a triggering injury. The pathogenesis of tendinopathy can be described as a three stage process: injury, failed healing and clinical presentation. It is likely that some of these "initial injuries" heal well and we speculate that predisposing intrinsic or extrinsic factors may be involved. The injury stage involves a progressive collagenolytic tendon injury. The failed healing stage mainly refers to prolonged activation and failed resolution of the normal healing process. Finally, the matrix disturbances, increased focal vascularity and abnormal cytokine profiles contribute to the clinical presentations of chronic tendon pain or rupture. With this integrative pathogenesis theory, we can relate the known manifestations of tendinopathy and point to the "missing links". This model may guide future research on tendinopathy, until we could ultimately decipher the complete pathogenesis process and provide better treatments

Economic evaluation of health consequences of prenatal methylmercury exposure in France

<p>Abstract</p> <p>Background</p> <p>Evidence of a dose–response relationship between prenatal exposure to methylmercury (MeHg) and neurodevelopmental consequences in terms of IQ reduction, makes it possible to evaluate the economic consequences of MeHg exposures.</p> <p>Objective</p> <p>To perform an economic evaluation of annual national benefits of reduction of the prenatal MeHg exposure in France.</p> <p>Methods</p> <p>We used data on hair-Hg concentrations in French women of childbearing age (18–45 years) from a national sample of 126 women and from two studies conducted in coastal regions (n = 161and n = 503). A linear dose response function with a slope of 0.465 IQ point reduction per μg/g increase in hair-Hg concentration was used, along with a log transformation of the exposure scale, where a doubling of exposure was associated with a loss of 1.5 IQ points. The costs calculations utilized an updated estimate of €₂₀₀₈ 17,363 per IQ point decrement, with three hypothetical exposure cut-off points (hair-Hg of 0.58, 1.0, and 2.5 μg/g).</p> <p>Results</p> <p>Because of higher exposure levels of women in coastal communities, the annual economic impacts based on these data were greater than those using the national data, i.e. € 1.62 billion (national), and € 3.02 billion and € 2.51 billion (regional), respectively, with the linear model, and € 5.46 billion (national), and € 9.13 billion and € 8.17 billion (regional), with the log model, for exposures above 0.58 μg/g.</p> <p>Conclusions</p> <p>These results emphasize that efforts to reduce MeHg exposures would have high social benefits by preventing the serious and lifelong consequences of neurodevelopmental deficits in children.</p

Spontaneous bilateral Achilles tendon rupture in a patient treated with oral levofloxacin

A case of bilateral rupture of the Achilles tendon in a patient treated with levofloxacin for cystitis is reported. A 76-year-old woman suddenly developed painful ankles one day after levofloxacin treatment. Drug therapy was switched to amoxicillin/clavulanate on the fourth day. Sonography revealed a serious condition of tendinosis with complete bilateral full-thickness rupture on day 6. Tendons were both repaired in the same surgical session. Pathological anatomy of the specimens reported fatty tissue lobules with panniculitis and histiocytosis. Ankles were immobilized postoperatively with a plaster cast. Achilles tendon rupture may occur as an adverse side effect of short-term use of levofloxacin, a fluoroquinolone antibiotic. This adverse effect is a rare and poorly understood complication of this antibiotic therapy. A review of the literature is provided