Steroids themselves, during treatment, may cause Cushingoid symptoms involving significant alteration of fat, carbohydrate, protein and mineral metabolism, . redistribution of body fat, muscle weakness and wastage and osteoporosis may result. During therapy, effective doses suppress the Hypothalamo-Pituitreal-Adrenal axis. Following cessation of treatment, signs of adrenal insufficiency extending to adrenocorticol 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, . dosing to coincide with the time of the endogenous cortisol peak (. in the morning with regard to dogs and the evening with regard to cats) and a gradual reduction of dosage (for further discussion see standard texts). 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 longer term use. Systemic corticosteroids have caused deposition of calcium in the skin (calcinosis cutis). Corticosteroids may delay wound healing and the immunosuppressant actions may weaken resistance to or exacerbate existing infections. In the presence of bacterial infection, anti-bacterial drug cover is usually required when steroids are used. In the presence of viral infections, steroids may worsen or hasten the progress of the disease.