While Cushing’s disease is caused by too many corticosteroids circulating within the body, Addison’s disease is caused by the exact opposite: inadequate amounts of circulating corticosteroids. This includes not only the glucocorticosteroids produced by the adrenal glands but the mineralocorticoids as well. Because the latter are so vital at maintaining a fluid and electrolyte balance within the body, Addison’s disease can be acutely life-threatening in the affected individual. Like Cushing’s disease, Addison’s disease is primarily a disease of dogs; it is rare in cats.
Causes of this disease in dogs can include tumors, infections, autoimmune diseases, and toxins. It can also occur secondarily to overtreatment with corticosteroids.
The clinical signs seen resemble those exhibited by pets afflicted with viral or parasitic gastroenteritis—namely vomiting, diarrhea, and dehydration. Loss of appetite and weight loss accompany these signs as well, yet there might be an increase in water consumption. Because the levels of sodium and potassium, two electrolytes vital to proper muscle contraction, are disrupted, profound muscle weakness, including a slowing of the rate at which the heart muscle contracts, are also observed. In severe cases, collapse of the entire circulatory system, with shock and then death, has been documented.
Diagnosis of Addison’s disease can made based on the history (i.e., long-term corticosteroid therapy), clinical signs seen, and determining the ratio of sodium to potassium in the bloodstream. Marked increases in potassium and decreases in sodium are indicative of primary Addison’s disease. Physical examination and electrocardiograms will reveal abnormal heart activity in these patients as well.
If Addison’s disease is diagnosed or suspected, treatment should be instituted immediately. Dehydration is combated with intravenous fluids, and injections of mineralocorticoids are administered to stabilize fluid and electrolyte levels.
For cases of primary Addison’s disease, periodic injections with mineralocorticoids will be required throughout the dog’s life to prevent relapses from occurring. If the condition was caused by the sudden cessation of glucocorticosteroid therapy, such therapy is reinstituted and then gradually tapered off over weeks to months.
Causes of this disease in dogs can include tumors, infections, autoimmune diseases, and toxins. It can also occur secondarily to overtreatment with corticosteroids.
The clinical signs seen resemble those exhibited by pets afflicted with viral or parasitic gastroenteritis—namely vomiting, diarrhea, and dehydration. Loss of appetite and weight loss accompany these signs as well, yet there might be an increase in water consumption. Because the levels of sodium and potassium, two electrolytes vital to proper muscle contraction, are disrupted, profound muscle weakness, including a slowing of the rate at which the heart muscle contracts, are also observed. In severe cases, collapse of the entire circulatory system, with shock and then death, has been documented.
Diagnosis of Addison’s disease can made based on the history (i.e., long-term corticosteroid therapy), clinical signs seen, and determining the ratio of sodium to potassium in the bloodstream. Marked increases in potassium and decreases in sodium are indicative of primary Addison’s disease. Physical examination and electrocardiograms will reveal abnormal heart activity in these patients as well.
If Addison’s disease is diagnosed or suspected, treatment should be instituted immediately. Dehydration is combated with intravenous fluids, and injections of mineralocorticoids are administered to stabilize fluid and electrolyte levels.
For cases of primary Addison’s disease, periodic injections with mineralocorticoids will be required throughout the dog’s life to prevent relapses from occurring. If the condition was caused by the sudden cessation of glucocorticosteroid therapy, such therapy is reinstituted and then gradually tapered off over weeks to months.
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