Pearls
- Endocrinopathies are particularly common in small animals. However, HAC may also be seen in older horses or ponies with PPID, caused by hyperplasia or adenomas of the pars intermedia of the pituitary gland.
- Many pets with endocrine disorders are older. Hypoadrenocorticism, however, can be seen in relatively young dogs if congenital rather than acquired.
- In dogs, we see hypothyroidism, HAC, hypoadrenocorticism, and DM.
- In cats, we see hyperthyroidism, DM, and HAC (not very commonly, but may complicate DM).
- CBC findings can be useful in many of these disorders.
- Cats with hyperthyroidism often have a stress leukogram. The Hct is variable and some may have accompanying disease, such as renal failure, because they are often aged cats and concurrent disease would not be unusual in these cases. Cardiac disease, directly related to hyperthyroidism, as well as direct effects of excess thyroid hormone, can result in hematocrit elevations (absolute erthrocytosis).
- Dogs with hypothyroidism may have a mild nonregenerative anemia due to lack of thyroxine effect on the bone marrow.
- Dogs with HAC may have a mild erythrocytosis due to steroid influence on the bone marrow. They may also have a stress leukogram (in a patient that is not particularly ill/stressed) resulting from high levels of endogenous cortisol.
- Dogs with hypoadrenocorticism may have a mild nonregenerative anemia and lack of stress leukogram (in a patient that is often extremely ill and should have a stress response). These patients occasionally have an absolute lymphocytosis and/or eosinophilia, again from glucocorticoid lack.
- Animals with DM may have normal CBCs or there may be a mild anemia from underlying disease and/or stress leukogram if the animal is particularly ill when presented (e.g. in a state of ketoacidosis).
- Biochemical findings seen in endocrinopathies:
- Cats with hyperthyroidism usually have increases in ALP and ALT activities due to a degree of hepatotoxicosis from the hyperthyroid state and increased metabolic activity by the liver. Some of the ALP elevation is from increased bone turnover, again from the heightened metabolic state. Cholesterol is often mildly elevated.
- Dogs with hypothyroidism may have a moderate to marked hypercholesterolemia and little else on the biochemical panel.
- Dogs with HAC are often PU/PD and may have low urea and creatinine from diuresis. ALP (especially), ALT, GLDH, and GGT activities are often elevated due to steroid induction (particularly ALP) as well as glucocorticoid hepatopathy. Cholesterol may be elevated. Urine is often hyposthenuric and UTI may be present without an appropriate local leukocyte response (detected on urine sediment examination) due to a state of immunosuppression.
- Dogs with hypoadrenocorticism may be deficient in glucocorticoid, mineralocorticoid, or both. Glucocorticoid lack will result in hypoglycemia. Hypoglycemia may result in presentation in a very weak condition, comatose state, or seizuring. Mineralocorticoid lack will result in hyperkalemia, hyponatremia, and hypochloremia, and causes hypovolemia, poor renal perfusion, occasional GI bleeding, and often a collapsed state. There is usually azotemia and metabolic acidosis which mimics renal failure because of an inability to concentrate urine due to the severe, sustained hyponatremia. Look for other clues on the CBC and biochemical panel suggesting that you are not dealing with a primary renal problem. Urine concentrating ability may not return until fluid balance and sodium/chloride are replenished. Other findings that may accompany hypoadrenocorticism are hypercalcemia and hypoproteinemia.
- Animals with DM have hyperglycemia and usually elevations of hepatic enzyme activities due to fatty liver. Hypercholesterolemia is also present. If in ketoacidosis, there is often a high anion gap metabolic acidosis. Serum potassium concentration can drop dramatically once insulin therapy is initiated which allows potassium to move into cells. Potassium concentrations must be monitored closely and supplementation is often required shortly following initiation of insulin therapy. There will be glucosuria and ketonuria (if ketoacidotic). Diabetic patients may also have urinary tract infections, sometimes without an adequate local leukocyte response (detected on urine sediment examination).
- DO NOT DIAGNOSE DIABETES MELLITUS IN CATS BASED ON BLOOD GLUCOSE ELEVATION ALONE. Very excited, fractious cats can raise their blood glucose concentration quickly and dramatically. We have seen blood glucose concentrations of 22 mmol/L in excited cats that did not have DM. Always interpret laboratory findings in relation to history and clinical findings. If the history is suggestive of DM and the patient is not particularly stressed/excited, then the hyperglycemia is probably significant (particularly if there is ketonuria). If you are not sure, repeat the testing when the cat is more relaxed. If this is not possible, fructosamine can be measured to assess the blood glucose concentration over the prior 2 weeks. Alternatively, the owner could collect 2 or 3 urine samples over a few days to see if glucosuria is persistent (this is not always easy to do in cats).
definition
Increase in the number of eosinophils in peripheral blood.
