Glucocorticoids and laminitis in the horse.
The administration of exogenously administered GCs and syndromes associated with GC excess are both attended by increased risk for the development of laminitis in adult horses. However, there exists substantial controversy as to whether excess GCs cause laminitis de novo. If true, the pathogenesis of laminitis arising from the effects of GC excess is probably different from that associated with diseases of the gastrointestinal tract and endotoxemia. Although a satisfactory explanation for the development of laminitis as a consequence of GC action is currently lacking, numerous possible and plausible theoretical mechanisms do exist. Veterinarians must exert caution with respect to the use of GCs in adult horses. The extent to which individual horses are predisposed to laminitis as a result of GC effect cannot be predicted based on current information. However, the administration of systemic GCs to horses that have been previously affected by laminitis should be used only with extreme caution, and should be accompanied by careful monitoring for further signs of laminitis. The risk of laminitis appears to be greater during treatment using some GCs (especially dexamethasone and triamcinalone) compared with others (prednisone and prednisolone). Whenever possible, to reduce the risk of laminitis, GCs should be administered locally. For example, the risk of GC-associated laminitis is evidently considerably reduced in horses affected with chronic obstructive pulmonary disease (COPD) if GC treatment is administered via inhalation. We have hypothesized that structural changes in the equine hoof that resemble laminitis may arise as a consequence of excess GC effect. Although these changes are not painful per se, and are not associated with inflammation, they could likely predispose affected horses to the development of bona fide laminitis for other reasons. Moreover, the gross morphological appearance of the chronically GC-affected hoof resembles that of a chronically foundered hoof in some respects. Further investigation into the effect of GC on the hoof lamellar interface is clearly needed.
Johnson
Philip J
PJ
Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Clydesdale Hall, Columbia, MO 65211, USA. johnsonpj@missouri.edu
Slight
Simon H
SH
Ganjam
Venkataseshu K
VK
Kreeger
John M
JM
D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D005260:Female; D005534:Foot Diseases / Q000139:chemically induced / Q000473:pathology / Q000662:veterinary*; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects*; D006724:Hoof and Claw / Q000187:drug effects / Q000473:pathology*; D006734:Horse Diseases / Q000139:chemically induced* / Q000473:pathology; D006736:Horses; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology / Q000662:veterinary; D007794:Lameness, Animal; D008297:Male; D012307:Risk Factors
D005938:Glucocorticoids; D042842:11-beta-Hydroxysteroid Dehydrogenases