Peter P. Kintzer’s research while affiliated with Tufts Medical Center and other places

Survey radiographs often are obtained in dogs with primary hypoadrenocorticism in adrenal crisis as part of the routine evaluation of a critically ill dog. In this study, standardized methods of cardiac, pulmonary vasculature, and vena cava mensuration were used in 22 dogs with naturally-occurring primary hypoadrenocorticism, and the findings were compared with those in 22 breed-matched, clinically normal dogs. Most (81.8%) untreated dogs with primary hypoadrenocorticism had one or more radiographic abnormalities, including small size of the heart (45.5%), cranial lobar pulmonary artery (36.4%), caudal vena cava (54.5%), or liver (36.4%). Megaesophagus was not found in any of the dogs with hypoadrenocorticism, and therefore, compared to the other common radiographic findings, should be considered a rare finding.

Many insulin preparations are available for use in the diabetic dog or cat. Appropriate selection of an insulin preparation must take into account several factors. These include species of patient, type of diabetes, duration of action of insulin, client preferences, and, sometimes, species of origin of the insulin preparation.

Mitotane (o,p'-DDD; Lysodren) is the drug most commonly used to treat dogs with pituitary-dependent hyperadrenocorticism. Although variations of the original protocol, suggested more than 20 years ago, have been reported, most clinicians still use an initial loading dose of mitotane followed by a weekly maintenance dose. Although a gratifying response to treatment is seen in most dogs, some dogs are neither easy nor straightforward to treat and present the practitioner with one or more therapeutic challenges, including failure to respond adequately, development of adverse effects, or development of relapse during treatment. Nevertheless, with careful management and follow-up, such problems can be overcome and a successful outcome achieved in most cases.

Hypoadrenocorticism (primary or secondary) is an uncommon endocrine disorder seen most commonly in young-to-middle-aged female dogs. This article reviews the various clinical manifestations of this disorder, recommended testing protocols for definitive diagnosis, and current therapeutic protocols. The long-term prognosis is good-to-excellent for most dogs receiving appropriate replacement therapy.

Cortisol-secreting adrenal tumors are responsible for 10% to 15% of all cases of naturally occurring canine hyperadrenocorticism. Differentiation of adrenal-dependent hyperadrenocorticism from pituitary-dependent hyperadrenocorticism is very important because the recommended therapeutic approaches for each are different, and the prognosis also may be different. A stepwise approach to diagnosing and staging the disease is needed. Treatment options include surgery and administration of mitotane or ketoconazole.

Results of long-term treatment were evaluated in 200 dogs with primary hypoadrenocorticism and 5 dogs with spontaneous secondary hypoadrenocorticism. Fludrocortisone acetate initially was used for mineralocorticoid replacement in 190 of the dogs with primary hypoadrenocorticism. The daily dose of fludrocortisone required in these dogs increased significantly during the treatment period (median, 2.6 years) from an initial median dose of 13.1 μg/kg to a final dose of 22.6 μg/kg. In 27 of the 200 dogs, mineralocorticoid therapy was changed from fludrocortisone to desoxycorticosterone pivalate (DOCP) because of adverse effects, poor response, or financial considerations. The dose of DOCP required in the 33 dogs (27 dogs plus 6 dogs initially given DOCP) increased significantly during the treatment period (median, 3.5 years) from an initial median dose of 1.56 mg/kg to a final dose of 1.69 mg/kg; the interval between DOCP injections ranged from 14 to 35 days (median, 30 days). The dose of prednisone administered to the dogs with primary hypoadrenocorticism decreased significantly from an initial median dose of 0.3 mg/kg to a final dose of 0.2 mg/kg; the drug was discontinued in 22 dogs due to adverse effects. The 5 dogs with secondary hypoadrenocorticism received only glucocorticoid replacement therapy (prednisone) at initial and final daily dosages of 0.41 mg/kg and 0.25 mg/kg, respectively, during a median treatment period of 4.4 years. More than 80% of the dogs were considered to have a good to excellent response to therapy. The median survival time of all 205 dogs was 4.7 years. There were no differences in response to treatment or survival between dogs treated with fludrocortisone and those receiving DOCP, or between dogs with primary hypoadrenocorticism and those with secondary hypoadrenocorticism.

To evaluate clinical and laboratory findings in 225 dogs with naturally occurring hypoadrenocorticism diagnosed over a 14-year period. Retrospective case series. 220 dogs with primary hypoadrenocorticism and 5 dogs with secondary hypoadrenocorticism (primary ACTH deficiency). We reviewed medical records of all dogs with naturally occurring hypoadrenocorticism examined at The Animal Medical Center between 1979 and 1993 or at Tufts University, Foster Hospital for Small Animals, between 1987 and 1993. Dogs ranged from 4 months to 14 years old. Most (71%) were female, and female dogs had a significantly higher relative risk of developing hypoadrenocorticism than did males. Great Danes, Portuguese Water Dogs, Rottweilers, Standard Poodles, West Highland White Terriers, and Wheaton Terriers had a significantly higher relative risk of developing hypoadrenocorticism than did dogs of other breeds. Common owner complaints included lethargy, poor appetite, and vomiting, whereas lethargy, weakness, and dehydration were common abnormalities detected on physical examination. Serum biochemical testing at the time of diagnosis revealed moderate-to-severe azotemia and hyperphosphatemia in most dogs. In 99 of 172 (57.6%) dogs that had a pretreatment urinalysis performed, urine specific gravity was < 1.030 even though dogs were azotemic. Serum electrolyte changes included hyperkalemia (n = 215), hyponatremia (183), hypochloremia (94), and hypercalcemia (69). Five of the 220 dogs with primary hypoadrenocorticism and the 5 dogs with secondary hypoadrenocorticism did not have hyperkalemia at time of diagnosis. In all dogs, ACTH stimulation testing revealed a low to low-normal baseline serum cortisol concentration with little to no rise after ACTH administration. Endogenous plasma ACTH concentration measured in 35 dogs with primary hypoadrenocorticism was markedly high; whereas ACTH concentration was undetectable to low in the 5 dogs with secondary hypoadrenocorticism. hypoadrenocorticism is a rare disease in dogs, most commonly affecting young to middle-aged females; some breeds are at greater risk of developing the disease than others. In general, clinical signs are nonspecific and similar to manifestations of more common diseases. Serum electrolyte disturbances of hyperkalemia and hypernatremia are characteristic in dogs with primary hypoadrenocorticism, but concentrations may be normal in dogs with early or mild primary or secondary hypoadrenocorticism. Diagnosis of hypoadrenocorticism is best confirmed by demonstration of a low baseline serum cortisol concentration with a subnormal or negligible response to ACTH administration. Determination of endogenous plasma ACTH concentrations is valuable in differentiating primary from secondary hypoadrenocorticism, particularly in dogs with normal serum electrolyte concentrations.