Dexacortone

Anti-inflammatory corticosteroids, such as dexamethasone, are known to exert a wide range of side effects. Whilst single high doses are generally well tolerated, they may induce severe side-effects in long-term use. Long-term use should therefore be avoided. Should long-term use be indicated, a corticosteroid with a shorter duration of action e.g. prednisolone is more appropriate (see section 4.5).

The significant dose related cortisol suppression noticed during therapy is a result of effective doses suppressing the hypothalamic-pituitary-adrenal axis. Following cessation of treatment, signs of adrenal insufficiency extending to adrenocortical atrophy can arise and this may render the animal unable to deal adequately with stressful situations. Consideration should therefore be given to means of minimising problems of adrenal insufficiency following the withdrawal of treatment.

The significant increase in triglycerides noticed can be a part of possible iatrogenic hyperadrenocorticism (Cushings disease) involving significant alteration of fat, carbohydrate, protein and mineral metabolism, e.g. redistribution of body fat, increase in body weight, muscle weakness and wastage and osteoporosis may result. Cortisol suppression and an increase in plasma triglycerides is a very common side-effect of medication with corticoids (more than 1 in 10 animals treated). The increase of alkaline phosphatase by glucocorticoids could be related to enlargement of the liver (hepatomegaly) with increased serum hepatic enzymes. Other changes in blood biochemical and haematological parameters probably associated with the use of glucocorticosteroids were significant effects noticed on lactate dehydrogenase (decrease) and albumin (increase) and on eosinophils, lymphocytes (decrease) and segmented neutrophils (increase).

A decrease in aspartate transaminase is also noticed.

Systemically administered corticosteroids may cause polyuria, polydipsia and polyphagia, particularly during the early stages of therapy. Some corticosteroids may cause sodium and water retention and hypokalaemia in long-term use. Systemic corticosteroids have caused deposition of calcium in the skin (calcinosis cutis). Corticosteroid use may delay wound healing and the immunosuppressant actions may weaken resistance to or exacerbate existing infections. In the presence of viral infections, corticosteroids may worsen or hasten the progress of the disease. Gastrointestinal ulceration has been reported in animals treated with corticosteroids and gastrointestinal ulceration may be exacerbated by steroids in animals given nonsteroidal anti-inflammatory drugs and in animals with spinal cord trauma. Other adverse reactions that may occur are: inhibition of longitudinal growth of bones, skin atrophy, diabetes mellitus, euphoria, pancreatitis, decrease in thyroid hormone synthesis, increase in parathyroid hormone synthesis. See also section 4.7.