Epidemiologic studies indicate that most laminitis cases occur in horses and ponies kept at pasture, hence the term 'pasture-associated laminitis'. Clinical cases of laminitis most often occur under conditions that favor accumulation of rapidly fermentable nonstructural carbohydrates (fructans, simple sugars, or starches) in pasture, and animals with an equine metabolic syndrome (EMS) phenotype (insulin resistance, abnormal insulin dynamics, +/- obesity) seem to be at highest risk for developing the condition. Although the mechanisms linking consumption of pasture forage with development of lamellar failure have not been fully elucidated, a systemic inflammatory response that accompanies hindgut carbohydrate overload likely initiates lamellar inflammatory events (including infiltration and activation of leukocytes) that contribute to destruction of lamellar epithelium and extracellular matrix. This article reviews current knowledge on the epidemiology and risk factors for pasture-associated laminitis, including the role of forage carbohydrates and metabolic/endocrine predispositions, and also discusses the pathophysiology of this condition.
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