Endocrinology

Canine Hypoadrenocorticism: Overview, Diagnosis, & Treatment

Canine Hypoadrenocorticism: Overview, Diagnosis, & Treatment
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Maya Lottati DVM, PhD, and David Bruyette, DVM, Diplomate ACVIM (Internal Medicine)

Addison’s disease has an overall low disease prevalence, and when combined with vague clinical signs and nonspecific clinicopathologic abnormalities, diagnosis is challenging. The authors identify the function of the adrenal cortex, forms of the disease, diagnostics, acute therapy, and long-term maintenance.


Canine hypoadrenocorticism, or Addison’s disease, results from adrenocortical hormone insufficiency. An overall low disease prevalence combined with vague clinical signs and nonspecific clinicopathologic abnormalities makes diagnosis challenging. Ultimately, specialized laboratory testing is required for definitive diagnosis.

Early identification and treatment can result in an overall excellent long-term prognosis; therefore, it is essential that clinicians be familiar with the various forms and potential presentations of canine hypoadrenocorticism.

ADRENAL CORTEX PHYSIOLOGY

The adrenal cortex is composed of 3 distinct functional layers (Figure):

  • Outer zona glomerulosa: Primarily involved in production of mineralocorticoids (ie, aldosterone)
  • Middle zona fasciculata: Responsible for production of glucocorticoids (ie, cortisol)
  • Inner zona reticularis: Primarily involved in production of sex hormones (ie, androgens, estrogens).
SepOct14 Addison's Disease Figure

Figure. The adrenal gland is composed of an outer cortex and inner medulla. Each functional zone of the cortex is responsible for the synthesis of a specific hormone.

Glucocorticoids

Glucocorticoids (cortisol) influence nearly every tissue in the body and are vital for metabolism, immunity, and stress counter—regulation.

  • Production is regulated by an elaborate hypothalamic—pituitary—adrenal axis, which uses a series of positive and negative feedback loops for precise moment-to-moment control of cortisol production from the adrenal cortex.
  • Pituitary-derived adrenocorticotropic hormone (ACTH) binds to ACTH receptors in the adrenal cortex, resulting in glucocorticoid synthesis and secretion.
  • Glucocorticoids are subject to a feedback mechanism that stimulates or inhibits their production.

Aldosterone

Aldosterone is the primary mineralocorticoid that promotes sodium resorption and potassium excretion in the distal renal tubules.

  • Water passively follows sodium, facilitating movement of fluid from the glomerular filtrate into the renal medullary interstitium.
  • Synthesis and release of aldosterone are primarily regulated by the renin—angiotensin—aldosterone system, which is upregulated in states of hypotension and hypovolemia.
  • To a lesser extent, the release of aldosterone is regulated by elevated serum potassium concentrations.

FORMS OF HYPOADRENOCORTICISM

Primary Hypoadrenocorticism

Primary hypoadrenocorticism, the classic form of the disease, is characterized by a lack of glucocorticoids and mineralocorticoids.

Causes. Primary hypoadrenocorticism typically results from immune-mediated destruction of adrenal cortical tissue; nearly 85% to 90% of adrenal tissue must be destroyed before substantial biochemical and clinical manifestations occur. Less common causes of adrenocortical destruction include:1,2

  • Iatrogenic administration of mitotane or trilostane for hyperadrenocorticism treatment
  • Neoplasia, infection, or infarction of the adrenal glands.

Autoantibodies. Although the specific immunologic antigen is not yet known in dogs, the presence of 21-hydroxylase autoantibodies characterizes most human cases.3,4 Recently, autoantibodies for a P450 side-chain cleavage enzyme were more commonly identified in canine patients with hypoadrenocorticism as compared to control patients.5 However, further studies are required to elucidate the role of antibodies to this enzyme in the pathogenesis of hypoadrenocorticism.

Atypical Hypoadrenocorticism

In a small population of “atypical” dogs—approximately 5% to 10%—adrenal destruction is purported to spare the glomerulosa layer, resulting in an isolated glucocorticoid deficiency.6Most dogs with isolated glucocorticoid insufficiency do not progress to clinically significant mineralocorticoid deficiency,6,7 although a recent paper showed that these dogs may have low or undetectable levels of aldosterone despite apparently normal electrolyte concentrations.8

Secondary Hypoadrenocorticism

Secondary hypoadrenocorticism refers to a central (anterior pituitary) deficiency of ACTH, resulting in isolated glucocorticoid insufficiency. Mineralocorticoids are spared because ACTH does not directly influence their release.

Causes. This condition most commonly results from abrupt discontinuation of long-term exogenous administration of corticosteroids or progesterone analogs. Rarely, congenital defects of the pituitary gland, such as a cystic Rathke’s pouch, neoplasia, or trauma9 affecting the hypothalamus or pituitary gland, result in secondary hypoadrenocorticism.

Critical Illness-Related Corticosteroid Insufficiency

Critical illness-related corticosteroid insufficiency (CIRCI) is also referred to as relative adrenal insufficiency and has been associated with severe illness, such as sepsis, septic shock, or trauma. The syndrome is typically transient, and adrenal function normalizes following correction of the underlying condition. Critically ill patients exhibiting refractory hypotension despite aggressive fluid therapy and the use of pressor agents should be evaluated for CIRCI.

SIGNALMENT

Age & Sex

Primary hypoadrenocorticism is most commonly reported in young to middle-aged female dogs,10while atypical hypoadrenocorticism generally occurs at older ages than those seen with primary hypoadrenocorticism.7

Table 1: Common Breeds Affected by Hypoadrenocorticism
  • Great Dane
  • Poodle12
  • Portuguese water dog11
  • Rottweiler
  • Wheaten terrier
  • West Highland white terrier

Breeds

Although dogs of any sex, age, or breed (including mixed breeds) can develop the disease, certain breeds are overrepresented (Table 1),10 and strong evidence suggests the disease is heritable in certain breeds.11-13 A study underway at North Carolina State University is attempting to identify genetic factors involved in Addison’s disease in standard poodles (ncstatevets.org/addisonsstudy).

DIAGNOSIS

Hypoadrenocorticism is diagnosed on the basis of a compatible history, clinical signs, laboratory abnormalities, imaging studies, and ACTH stimulation test results. With the exception of the ACTH stimulation test—which has narrow values that define hypoadrenocorticism—there is a vast continuum of potential findings on the initial screening tests.

History & Clinical Signs 

The clinical presentation of hypoadrenocorticism can vary in severity (Table 2), with waxing and waning episodes of illness that classically worsen during times of stress. The Addisonian crisis is the life-threatening culmination of combined hormone deficiencies that can be fatal if not appropriately treated.

Based on the signs noted in Table 2, it is understandable that atypical hypoadrenocorticism is more challenging to diagnose because signs related to isolated glucocorticoid deficiency are more insidious.

Table 2. Clinical Signs of Mineralocorticoid & Glucocorticoid Insufficiency
MINERALOCORTICOID INSUFFICIENCY GLUCOCORTICOID INSUFFICIENCY
Results in:
  • Low sodium concentrations
  • High potassium concentrations
  • These changes may manifest as:
    • Dehydration
    • Hypovolemic shock
    • Collapse
Results in vague signs:
  • Lethargy/weakness
  • Shaking
  • Polyuria/polydipsia
  • Vomiting/diarrhea
  • Abdominal pain
  • Inappetence/weight loss

Laboratory Abnormalities

Patients with hypoadrenocorticism may present with myriad laboratory abnormalities related to glucocorticoid and/or mineralocorticoid insufficiency (Table 3). The serum biochemical profile may reveal hypoglycemia, eosinophilia, lymphocytosis, hypercalcemia, hypocholesterolemia, hyperphosphatemia, hypochloremia, and elevated liver enzymes.10

GI Abnormalities. Anorexia, vomiting, and diarrhea are common. Anemia—from chronic disease or gastrointestinal (GI) bleeding—may be identified, although relative polycythemia may also result from dehydration. Depending on the degree of vomiting and diarrhea, hypoalbuminemia, hypoglobulinemia, or acidemia may be identified.

Na/K Ratio. When hyponatremia, hyperkalemia, or both are noted, mineralocorticoid insufficiency is identified. A sodium/potassium (Na/K) ratio < 27:1 is strongly suggestive for hypoadrenocorticism, and lower ratios are associated with higher specificity.14,15 However, low Na/K ratios as severe as < 20:1 can also occur with other disorders, such as acute kidney injury, diabetic hyperosmolar syndrome, gastroenteritis, and various causes of abdominal and thoracic effusions.

A recent study demonstrated that the combination of Na/K ratio with lymphocyte count is a better screening test for hypoadrenocorticism than either variable alone,15 but this also can be subject to misinterpretation.

Renal Abnormalities. Azotemia in the presence of an inappropriately low specific gravity (typically < 1.030) can easily be confused with primary renal insufficiency, but hypoadrenocorticism can coexist with renal insufficiency.

Atypical Hypoadrenocorticism. Patients with atypical hypoadrenocorticism are more likely to exhibit hypoalbuminemia, hypocholesterolemia, and anemia on routine bloodwork (Table 3).7

Table 3. Comparison of Typical Versus Atypical Hypoadrenocorticism in Dogs
PARAMETER HYPOADRENOCORTICISM
TYPICAL ATYPICAL
Age Young to middle age Middle to older age
LABORATORY ANALYSIS
Anemia
Present Present*
Azotemia
Present* Present
Eosinophilia/lymphocytosis
Present Present
Hypercalcemia
Present* Absent
Hyperkalemia/hyponatremia
Na:K ratio < 27
Present* Absent
Hypoalbuminemia
Present Present*
Hypocholesterolemia
Absent Present*
Hypoglycemia
Present Present
Urine specific gravity < 1.030 Present Present
THERAPY
Glucocorticoid replacement
Required Required
Mineralocorticoid replacement Required Not required
* Significant difference between typical and atypical groups7

Diagnostic Imaging

Thoracic radiographs may reveal a small heart and caudal vena cava, which signifies hypovolemia;16 rarely, megaesophagus may be seen in association with hypoadrenocorticism.17

On abdominal ultrasonography, atrophy of the adrenal glands should result in a measurable reduction in adrenal size. In the hands of experienced ultrasonographers, the adrenal glands may appear thin and short when compared with adrenal glands in healthy dogs;18 however, in a few cases of hypoadrenocorticism, normal size adrenal glands have been reported.14

An electrocardiogram may reveal a bradyarrhythmia with absent P waves, tented T waves, prolonged QRS complexes, and decreased R wave amplitude, depending on the degree of hyperkalemia.

ACTH Stimulation Test

A baseline serum cortisol level > 2 mcg/dL can be used to rule out hypoadrenocorticism, while a cortisol level ≤ 2 mcg/dL necessitates an ACTH stimulation test.19 The ACTH stimulation test remains the gold standard for diagnosis of all forms of hypoadrenocorticism; it should be performed in any patient suspected of having the disease.

Cortisol is measured at baseline and then one hour following an IV or IM injection of synthetic ACTH (5 mcg/kg).20 Typical and atypical hypoadrenocorticism are defined by a pre- and postcortisol concentration of ≤ 2 mcg/dL.7

Differentiation between primary and secondary hypoadrenocorticism requires demonstration of elevated or low/absent endogenous ACTH.

Currently, the diagnosis of CIRCI is controversial, and the following guidelines have all been used to evaluate adrenal function in critically ill patients21-23

  • A change in cortisol concentration (delta cortisol) of < 3 mcg/dL following exogenous ACTH administration
  • A post ACTH cortisol concentration < the top end of the normal reference range, with a normal to high baseline cortisol concentration.
  • A normal or elevated baseline cortisol concentration and < 5% increase in cortisol following ACTH administration.

TREATMENT

Addisonian Crisis

  1. As soon as possible, collect samples for a minimum database (complete blood count, serum biochemical profile, urinalysis) and baseline cortisol level—before starting any therapy.
  2. Initiate an ACTH stimulation test and begin aggressive IV fluid therapy with isotonic crystalloids (0.9% sodium chloride, Ringer’s lactate solution).
  3. Incrementally and rapidly administer shock fluid doses (up to 90 mL/kg) until perfusion parameters noticeably improve. Proceed cautiously if the serum sodium concentration is < 120 mEq/L to avoid demyelinating certain parts of the brain.
  4. Once hemodynamic stability has been reached, correct dehydration and ongoing losses over the next 12 to 24 hours.
  5. Monitor packed cell volume/total solids, serum electrolytes, and blood glucose every 6 to 8 hours until values have normalized and the patient is clinically stable.

If hyperkalemia persists despite fluid resuscitation and mineralocorticoid replacement therapy, suspect renal failure and monitor patient for oliguria or anuria. Additionally, to correct life-threatening hyperkalemia:

  • Consider treatment with dextrose and regular insulin, addressing metabolic acidosis, or
  • Treatment with a beta-adrenergic drug, such as terbutaline or albuterol.

If primary hypoadrenocorticism is highly suspected, then replacement of glucocorticoids and mineralocorticoids in the acute setting can help improve clinical signs and clinicopathologic abnormalities.

  • Administer IV dexamethasone after fluid resuscitation (Table 4) because it does not interfere with the ACTH stimulation test.
  • After the ACTH stimulation test, if documented hyperkalemia is a concern, administer an IM injection of the synthetic mineralocorticoid desoxycorticosterone pivalate (DOCP) (2.2 mg/kg), which is safe in the emergency setting even if primary hypoadrenocorticism is not the final diagnosis. Studies have shown that DOCP administered to healthy dogs at these doses does not produce adverse effects.24

In the emergency setting, avoid:

  • Administration of prednisone, prednisolone, and cortisone acetate because they interfere with the cortisol assay and artificially alter test results
  • SC administration of DOCP or any other medication due to poor absorption in the dehydrated patient
  • PO administration of any medication, including fludrocortisone, in patients exhibiting GI signs or poor GI tract perfusion.

In the acute setting, IV fluids are lifesaving and—through dilution and renal excretion—restore blood volume, improve renal perfusion, and decrease potassium concentrations.

Table 4. Recommended Starting Doses for Glucocorticoid & Mineralocorticoid Replacement
MEDICATION MECHANISM OF ACTION DOSE SPECIAL CONSIDERATION
Acute (Addisonian Crisis)
Dexamethasone or Dexamethasone sodium phosphate
Glucocorticoid
0.1—0.2 mg/kg IV Q 24 H
Prednisone or Prednisolone
Glucocorticoid
0.5—1 mg/kg PO Q 24 H,
or SC (prednisone only)
PO/SC steroids notrecommended in dehydrated patients or those with GI signs
Desoxycorticosterone pivalate Mineralocorticoid 2.2 mg/kg IM Q 28 D,
or as necessary
SC administration not recommended in dehydrated patients
Maintenance Phase
Prednisone or Prednisolone
Glucocorticoid
0.25—0.5 mg/kg PO Q 24 H
Titrate dose to effect
Cortisone acetate
Glucocorticoid
0.25—0.5 mg/kg PO Q 24 H
Titrate dose to effect
Fludrocortisone acetate
Mineralocorticoid & glucocorticoid
0.02 mg/kg PO Q 24 H,
or divided
Titrate dose to effect
Desoxycorticosterone pivalate Mineralocorticoid 2.2 mg/kg SC or IM Q 28 D,
or as necessary
Frequency of administration/required dose vary among dogs

Long-Term Maintenance 

Patients with primary hypoadrenocorticism require life-long glucocorticoid and mineralocorticoid replacement, while those with atypical or secondary hypoadrenocorticism require only glucocorticoid replacement.

Replace glucocorticoids daily at physiologic doses (Table 4).

  • Prednisone, prednisolone, and cortisone acetate are all reasonable choices; titrate doses to the lowest effective dose that controls clinical signs and minimizes adverse effects.
  • Determine which steroid to use based largely on availability, cost, and adverse effects seen in a given patient.
  • Consider increasing the initial dose if, during the course of treatment, GI signs, malaise, or weight loss continue.
  • Conversely, consider decreasing the dose, or switching to another corticosteroid, if there are clinical signs of glucocorticoid excess, such as polyuria/polydipsia. Note: it might be difficult to distinguish these signs from the polydipsia/polyuria that can accompany DOCP treatment.
  • The maintenance dose should be increased (2—3 times) during times of stress, such as illness, injury, or surgery, including elective procedures that require anesthesia.
  • Parenteral steroid administration may be necessary in patients that cannot tolerate oral medications or are dehydrated (Table 4).

Clinical signs of secondary hypoadrenocorticism in veterinary patients on long-term steroid therapy are uncommon. Rarely, some patients may experience GI signs secondary to glucocorticoid withdrawal following abrupt cessation of steroid therapy. To avoid signs of adrenal insufficiency, it is recommended to taper steroids to physiologic replacement doses over several weeks.

Treatment of CIRCI

Glucocorticoid treatment of veterinary patients with CIRCI is controversial, and limited data is available to support use, dosage, or route of administration. In patients that meet the criteria of CIRCI and display refractory hypotension (despite aggressive medical management), we suggest the use of supplemental glucocorticoids at doses similar to those used in an Addisonian crisis (Table 4). Following resolution of critical illness, corticosteroid therapy may be tapered and discontinued depending on the patient’s clinical response. A repeat ACTH stimulation test can be performed 4 to 6 weeks following discontinuation of steroid therapy to document adrenal recovery.

Replace mineralocorticoids in the form of IM or SC DOCP (2.2 mg/kg Q 25 days25)—the most common form of replacement; these patients also require daily glucocorticoid replacement therapy.

  • Check patient electrolyte levels at 2 and 3 weeks after initial DOCP administration; then every 3 to 4 days until abnormal shifts in Na or K are detected.
  • The dosing interval lasts 28 days on average, but range varies widely among patients. It is not uncommon for veterinarians to successfully extend the dosing interval.
  • See Dosing & Financial Considerations for DOCP.

Combined glucocorticoid and mineralocorticoid activity is provided by fludrocortisone acetate, a PO daily medication, which abolishes the requirement for a separate corticosteroid and can be substituted if DOCP is not available. However, compared with DOCP, disadvantages of fludrocortisone include increased cost (especially in larger dogs), more frequently recognized adverse effects (eg, polyuria/polydipsia), and less control of hyponatremia.27

Dosing & Financial Considerations for DOCP

A recent paper demonstrated that, in canine patients with hypoadrenocorticism, lower initial doses of DOCP are equally efficacious in controlling electrolytes and clinical signs compared with the recommended starting dose (Table 4).26

DOCP is relatively expensive, particularly in large breed dogs; thus, these findings have important financial implications for veterinarians and pet owners. If finances are of concern, after the first dose, it is reasonable to attempt incremental lowering of the subsequent DOCP doses by approximately 25%. Clients can also be taught to administer DOCP at home, which has potential cost savings.

When an attempt is made to reduce the dose or extend the interval between injections, more frequent monitoring of serum electrolytes is required, and clients should be informed that—in addition to the cost of DOCP—initial cost will increase accordingly.

PROGNOSIS

All patients with primary hypoadrenocorticism require life-long medical therapy. Once patients are well regulated, evaluate them at least 2 times each year, with a physical examination and routine bloodwork. Although canine hypoadrenocorticism is serious and, sometimes, life-threatening, early identification and proper treatment can result in an excellent long-term prognosis in most patients.27

ACTH = adrenocorticotropic hormone; CIRCI = critical illness-related corticosteroid insufficiency; DOCP = desoxycorticosterone pivalate; GI = gastrointestinal; K = potassium; Na = sodium

References

  1. Feldman EC, Nelson RW. Canine and Feline Endocrinology and Reproduction, 3rd ed. St. Louis: WB Saunders, 2004. pp 394-439.
  2. Kook PH, Grest P, Raute-Kreinsen U, et al. Addison’s disease due to bilateral adrenal malignancy in a dog. J Small Anim Pract 2010; 51(6):333-336.
  3. Erichsen MM, L++v+�s K, Skinningsrud B, et al. Clinical, immunological, and genetic features of autoimmune primary adrenal insufficiency: Observations from a Norwegian registry. J Clin Endocrinol Metab 2009; 94(12):4882-4890.
  4. Winqvist O, Karlsson FA, Kampe O. 21-Hydroxylase, a major autoantigen in idiopathic Addison’s disease. Lancet 1992; 339:1559-1562.
  5. Boag AM, McLaughlin K, Christie M, et al. Analysis of P450 side-chain cleavage enzyme autoantibodies in dogs affected with hypoadrenocorticism (abstract). J Vet Intern Med 2014; 28:1027.
  6. Lifton SJ, King LG, Zerbe CA. Glucocorticoid deficient hypoadrenocorticism in dogs: 18 cases (1986-1995). JAVMA 1996; 209(12):2076-2081.
  7. Thompson AL, Scott-Moncrieff JC, Anderson JD. Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005). JAVMA 2007; 230(8):1190-1194.
  8. Baumstark ME, Sieber-Ruckstuhl NS, M++ller C, et al. Evaluation of aldosterone concentrations in dogs with hypoadrenocorticism. J Vet Intern Med 2014; 28(1):154-159.
  9. Platt SR, Chrisman CL, Graham J, Clemmons RM. Secondary hypoadrenocorticism associated with craniocerebral trauma in a dog. JAAHA 1999; 35(2):117-122.
  10. Peterson ME, Kintzer PP, Kass PH. Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). JAVMA 1996; 208(1):85-91.
  11. Oberbauer AM, Bell JS, Belanger JM, Famula TR. Genetic evaluation of Addison’s disease in the Portuguese Water Dog. BMC Vet Res 2006; 2:15.
  12. Famula TR, Belanger JM, Oberbauer AM. Heritability and complex segregation analysis of hypoadrenocorticism in the standard poodle. J Small Anim Pract 2003; 44:8-12.
  13. Oberbauer AM, Benemann KS, Belanger JM, et al. Inheritance of hypoadrenocorticism in bearded collies. Am J Vet Res 2002; 63:643-647.
  14. Adler JA, Drobatz, KJ, Hess RS. Abnormalities in serum electrolyte concentrations in dogs with hypoadrenocorticism. J Vet Intern Med 2007; 21(6):1168-1173.
  15. Seth M, Drobatz KJ, Church DB, Hess RS. White blood cell count and the sodium to potassium ratio to screen for hypoadrenocorticism in dogs. J Vet Intern Med 2011; 25(6):1351-1356.
  16. Melián C, Stefanacci J, Peterson ME, Kintzer PP. Radiographic findings in dogs with naturally-occurring primary hypoadrenocorticism. JAAHA 1999; 35(3):208-212.
  17. Whitley NT. Megaoesophagus and glucocorticoid-deficient hypoadrenocorticism in a dog. Small Anim Pract 1995; 36(3):132-135.
  18. Wenger M, Mueller C, Kook PH, Reusch CE. Ultrasonographic evaluation of adrenal glands in dogs with primary hypoadrenocorticism or mimicking diseases. Vet Rec 2010; 167(6):207-210.
  19. Lennon EM, Boyle TE, Hutchins RG, et al. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). JAVMA 2007; 231(3):413-416.
  20. Behrend EN, Kemppainen RJ, Bruyette DS, et al. Intramuscular administration of a low dose of ACTH for ACTH stimulation testing in dogs. JAVMA 2006; 229(4):528-530.
  21. Burkitt JM, Haskins SC, Nelson RW, Kass PH. Relative adrenal insufficiency in dogs with sepsis. J Vet Intern Med 2007; 21(2):226-231.
  22. Martin LG, Groman RP, Fletcher DJ, et al. Pituitary-adrenal function in dogs with acute critical illness. JAVMA 2008; 233(1):87-95.
  23. Martin LG. Critical illness-related corticosteroid insufficiency in small animals. Vet Clin North Am Small Anim Pract 2011; 41(4):767-782.
  24. Chow E, Campbell WR, Turnier JC, et al. Toxicity of desoxycorticosterone pivalate given at high doses to clinically normal beagles for six months. Am J Vet Res 1993; 54(11):1954-1961.
  25. McCabe MD, Feldman EC, Lynn RC, et al. Subcutaneous administration of desoxycorticosterone pivalate for the treatment of canine hypoadrenocorticism. JAAHA 1995; 31(2):151-155.
  26. Bates JA, Shott S, Schall WD. Lower initial dose desoxycorticosterone pivalate for treatment of canine primary hypoadrenocorticism. Aust Vet J 2013; 91(3):77-82.
  27. Kintzer P, Peterson M. Treatment and long-term follow-up of 205 dogs with hypoadrenocorticism. J Vet Intern Med 1997; 11(2):43-49

F04_bMaya Lottati, DVM, PhD, is a resident in internal medicine at VCA Veterinary Specialists of the Valley in Woodland Hills, California. She received her DVM from University of California—Davis and completed a small animal internship at VCA West Los Angeles Animal Hospital.

 

F04_cDavid Bruyette, DVM, Diplomate ACVIM, is the medical director at West Los Angeles Animal Hospital and a clinical professor in the Department of Radiation Oncology at University of California—Los Angeles. He received his DVM from University of Missouri and completed an internship at Purdue University and residency in internal medicine at University of California—Davis. He then became a staff internist at West Los Angeles Veterinary Medical Group and member of the Department of Comparative Medicine at Stanford University.

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