Unusual feline endocrinopathies (Proceedings)


Understanding hyperadrenocorticism and hyperaldosteronism

I. Thyroid Storm – see previous notes

II. Hyperadrenocorticism

A. a rare disorder in cats

B. Etiology

1. Pituitary adenoma (85%)

2. adrenal adenoma

3. adrenal carcinoma

C. Clinical presentation

1. Middle-older aged cats (5-16 years), no breed or sex predilection

2. Most cats have concurrent insulin-resistant diabetes mellitus

3. Thin, fragile skin

4. Large non-healing cutaneous wounds

5. Polyuria/polydipsia

6. Polyphagia

7. Recurrent cutaneous, upper respiratory, and urinary tract infections

8. Lethargy

9. Muscle atrophy

10. Weakness

11. abdominal enlargement

12. alopecia/failure to regrow hair

D. Clinicopathologic Findings

1. Elevated ALP and ALT

2. hypercholesterolemia

3. hyperglycemia

4. mature neutrophilia, lymphopenia, eosinopenia (stress leukogram)

5. glucosuria

6. lack of urine concentrating ability

7. proteinuria

8. bacteriuria, pyuria

E. Diagnosis

1. Screening tests

a. Low-dose dexamethasone suppression test

(1) use 10 x dexamethasone dose as for dogs

(2) 0.1 mg/kg dexamethasone IV

(3) serum cortisol measured 0, 4, 8 hr

(4) cortisol not suppressed at 4 and/or 8 hr – supports diagnosis of hyperadrenocorticism

(5) cannot be used as a differentiating test as in dogs

b. ACTH-stimulation test

(1) 40-50% of cats with hyperadrenocorticism will show a normal response to ACTH

(2) synthetic ACTH (cortrosyn)

-125 mcg IM, serum cortisol samples 0, 30, 60 min.

-125 mcg IV, serum cortisol samples 0, 60, 90 min.

(3) ACTH gel – 2.2 U/kg IM, serum cortisol samples 0, 60, and 120 min

(4) an exaggerated response to ACTH of > 19 mcg/dl is consistent with a diagnosis of hyperadrenocorticism

2. Differentiating tests

a. plasma endogenous ACTH concentration

(1) single plasma sample submitted

(2) special handling of plasma depending on laboratory used

(3) pituitary-dependent disease: ACTH concentrations normal to high

(4) adrenal-dependent disease: ACTH concentrations low or nondetectable

b. abdominal ultrasonography

(1) unilaterally enlarged or calcified adrenal gland supports adrenal-dependent hyperadrenocorticism

(2) bilaterally enlarged adrenal glands support pituitary- dependent hyperadrenocorticism

c. magnetic resonance imaging – pituitary tumor

F. Treatment

1. Medical

a. mitotane (Lysodren)

(1) not effective in cats

(2) deleterious side effects

b. trilostane

(1) begin with 5 mg/kg PO q 24 and increase or decrease as necessary

(2) monitor with ACTH-stimulation test with the goal of having pre- and post- ACTH cortisol concentrations between 1-4 mcg/dl

(3) monitor serum Na/K levels

(4) in cats with diabetes mellitus, reduce insulin by at least 25% before starting trilostane as insulin requirements will decrease

2. Surgical

a. unilateral adrenalectomy

b. bilateral adrenalectomy in cats that cannot be medicated orally

c. control clinical signs of hyperadrenocorticism with trilostane for at least 2 weeks before surgery to heal skin lesions and control diabetes mellitus if present. Insulin dose should be decreased by at least 25% before initiating trilostane

d. If bilateral adrenalectomy, glucocorticoid and mineralocorticoid therapy will be necessary for life.

(1) desoxycorticosterone pivalate (DOCP; Percorten-V, Novartis Animal Health) – 2.2 U/kg IM q 30 days

(2) prednisolone 0.4 mg/kg PO sid

(3) methylprednisolone acetate, Depomedrol, 10 mg IM q 30 days

e. With unilateral adrenalectomy, glucocorticoid and mineralocorticoid therapy may be necessary for several weeks while the healthy adrenal gland regenerates.

II. Hyperaldosteronism (Conn's Syndrome)

A. An uncommon disease in cats

B. Etiology

1. oversecretion of aldosterone

2. unilateral or bilateral adrenocortical tumors

3. may be benign or malignant

C. Clinical presentation

1. Signalment

a. middle-older aged cats (range 6-20 years)

b. no breed/sex predilection

2. History

a. episodic lameness or muscle weakness

b. polyuria/polydipsia

c. vision loss

d. polyphagia

e. weight loss

3. Clinical signs

a. hypokalemic polymyopathy

(1) ventroflexion of neck

(2) hindlimb weakness

(3) paresis

b. retinal abnormalities

(1) detachment

(2) tortuous vessels

(3) hemorrhages

(4) bullae

(5) edema

c. hypertension

4. Clinicopathologic changes

a. hypokalemia (common)

b. hyponatremia (uncommon)

c. azotemia

d. elevated CK

e. elevated plasma aldosterone

5. Abdominal Ultrasound

a. unilateral or bilateral adrenal mass(es)

b. mass extension into the vena cava

D. Diagnosis

1. appropriate history and clinical signs

2. appropriate biochemical data, hypokalemia most important

3. elevated plasma aldosterone levels

4. presence of uni- or bilateral adrenal masses

E. Treatment

1. correction of hypokalemia

a. oral potassium gluconate: 0.5 mEq/kg PO

b. potassium chloride IV not to exceed 0.5 mEq/kg/hr

2. blockage of aldosterone: spironolactone: 2-3 mg/kg PO q 12 hr

3. treatment of hypertension

a. enalapril or benazepril: 0.5 to 2 mg/kg PO q 12 hr

b. amlodipine: 0.625 to 1.25 mg PO or rectally q 12-24 hr

c. nitroprusside: 0.5-5 mcg/kg/min as a constant rate infusion

4. definitive treatment

a. surgical removal of tumor

b. ultrasound or MRI should be performed to determine whether tumor has invaded vessels.

F. Prognosis

1. medical treatment improves clinical signs, but will not normalize blood values

2. medical treatment can preserve quality of life for 1-3 years; euthanasia usually due to chronic renal failure

3. surgical removal of non-malignant tumor yields good response of up to 6 years.

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