Glucocorticoid therapy and the risk of equine laminitis

Abstract

Summary Although glucocorticoids have been used successfully for the treatment of noninfectious inflammatory diseases of horses for more than 35 years, their use has been attended by a fear of the induction of laminitis. This paper reviews the evidence for this fear and the possible mechanisms whereby glucocorticoids could participate in laminitis induction. Although the association of laminitis with elevated serum cortisol in pituitary pars intermedia dysfunction suggests that chronic exposure to glucocorticoids may be part of laminitis pathogenesis, review of published reports and databases suggests that glucocorticoid‐induced laminitis is a relatively rare occurrence. However, several of the actions of glucocorticoids are similar to those known to be involved in laminitis pathogenesis. Glucocorticoid administration can induce insulin resistance, lead to vascular dysfunction that potentiates vasoconstriction, and interfere with keratinocyte proliferation and differentiation as well as matrix integrity, all mechanisms that could possibly induce laminitis. Drug formulation, dose and route of administration, and the systemic and hoof disease history of the horse must all be considered when assessing laminitis risk during glucocorticoid treatment. Generally, local glucocorticoid administration presents little risk as does systemic treatment of recurrent airway obstruction without concurrent disease. Caution should be used however in horses that are overweight and/or insulin resistant, or have had a recent bout of acute laminitis of alimentary or endotoxic origin. Overall, however, the risk of laminitis after glucocorticoid treatment, especially local use, is acceptable compared to the many benefits of these drugs.

Does oral prednisolone treatment increase the incidence of acute laminitis?

“…Similarly, glucocorticoids may cause hyperinsulinaemia and insulin resistance due to inhibition of glucose uptake into muscle and adipose tissue, as well as by stimulation of gluconeogenesis [2,30]. Hence, the risk of prednisolone-associated (and possibly other glucocorticoid-associated) laminitis may be higher in patients with underlying endocrine disease [3]. Hence, the risk of prednisolone-associated (and possibly other glucocorticoid-associated) laminitis may be higher in patients with underlying endocrine disease [3].…”

“…However, their use has been accompanied by a perception of risk of inducing laminitis [1][2][3]. Explanations of the mechanism by which laminitis may be induced have included potentiation of the vasoconstrictive actions of catecholamines on large digital vessels [4,5], lamellar weakening due to protein catabolism [3], insufficient glucose supply to keratinocytes [2,6] and increased intestinal permeability to toxins [7]. Explanations of the mechanism by which laminitis may be induced have included potentiation of the vasoconstrictive actions of catecholamines on large digital vessels [4,5], lamellar weakening due to protein catabolism [3], insufficient glucose supply to keratinocytes [2,6] and increased intestinal permeability to toxins [7].…”

Review of glucocorticoid therapy in horses. Part 1: Pharmacology

“…Laminitis is a reported complication of glucocorticoid administration in horses (Bailey and Elliott 2007); however, there is as yet no scientific evidence proving a clear causative link between the two (Cornelisse and Robinson 2013). The clinical incidence of laminitis reported in horses that receive glucocorticoids is very lowe.g.…”

Musculoskeletal Pathology

“…92 Contrary to historical and widely held beliefs, there is no strong scientific evidence that intra-articular administration of normal doses of exogenous corticosteroids increases the risk of laminitis in systemically healthy horses. [93][94][95] Supporting limb laminitis Supporting limb laminitis occurs in the contralateral limb because of a separate musculoskeletal condition that has resulted in persistent, unilateral lameness with minimal weight bearing. Loss of a normal cyclic pattern of loading, rather than merely an increase in load, is thought to cause hypoperfusion, hypoxia, and energy failure within the lamellar dermis of the weight-bearing foot.…”