Treatment of Canine Hypothyroidism: Current Recommendations
By Peter Kintzer, DVM, Diplomate ACVIM
Friday, June 12, 2009 :: Published in the 5 Minute Veterinary Consult
MODULE 1-Signalment
Today, we will discuss some of the current treatment recommendations for canine hypothyroidism, highlighting certain aspects of use in clinical practice. Canine hypothyroidism is a common, well-recognized endocrine disorder. Given the pervasive effects of thyroid hormones on the body, multiple systems can be affected by thyroid hormone deficiency. Nevertheless, the number and degree of clinical signs in a given patient is quite variable. These patients typically respond quite well to therapy, so the proper diagnosis and proper therapy are important.
Canine hypothyroidism is typically seen in middle-aged dogs, but older dogs can be affected and congenital hypothyroidism is rarely reported. There is no strong sex predilection. The patients are typically mid-sized to larger dogs and often purebred.
The literature describes certain breeds of dog that seem to be at increased risk of developing hypothyroidism. These include golden retrievers, cocker spaniels, Dobermans, dachshunds, beagles, Irish setters, miniature schnauzers, poodles, boxers, Labrador retrievers, and great Danes.
This is Sammy, a patient of mine, a 7-year-old male castrated boxer demonstrating many of the clinical manifestations of hypothyroidism. He’s overweight, has a dry haircoat with increased shedding, some areas of increased pigmentation, and a slightly “tragic” expression. Sammy responded dramatically to thyroid hormone replacement therapy, much to the delight of his owner.
MODULE 2- Clinical Sign
As previously stated, canine hypothyroidism is a multisystem disorder having variable clinical signs, with few to many signs being manifested in a given patient. Symptoms in some dogs are quite vague. It’s important to keep in mind that these clinical signs can be seen in other common medical conditions.
Several unusual manifestations of canine hypothyroidism have been described, some documented, others not-so-well documented. There may be neuropathy, primarily related to the peripheral nervous system (lower motor neuron). Abnormalities of the cardiac system, such as sinus bradycardia, weak apex beats, low QRS voltages, and inverted T waves may be seen in hypothyroid dogs. Gastrointestinal symptoms may manifest as either constipation or diarrhea.
Hypothyroid dogs can be lethargic, dull, and show decreased activity. It is not unusual for weight gain to be seen. Behavioral changes, such as cold avoidance, decreased exercise tolerance, or sleeping more can be seen, but other more serious changes, such as aggression, have been reported in the literature. Reproductive abnormalities have also been attributed to hypothyroidism.
Skin changes are not uncommon and many have been described. In fact, dermatologic abnormalities have been reported in 60% to 80% of hypothyroid dogs. Hyperpigmentation and increased skin thickness may be found. Accumulation of mucopolysaccharides in the dermis (myxedema) is noted in some patients. In the facial area, this contributes to the “tragic facies” (tragic facial expression) seen in some hypothyroid dogs. One important point to make here is that endocrine dermatoses are classically nonpruritic. However, if there is significant seborrheic change, or a bacterial or yeast infection is present, these dogs can be quite itchy. Hypothyroid dogs may be more prone to skin and ear infections.
Other dermatologic abnormalities include varying degrees of hair coat abnormalities, ranging from increased shedding and easily epilated hair to bilaterally symmetrical alopecia. Owners will often report that the dog has a dull, dry hair coat. Another abnormality that may be reported is poor regrowth of hair following clipping.
Because thyroid hormones influence the function of almost every organ in the body, there are additional clinical manifestations that may be seen less frequently or rarely. Vestibular disease has been reported, sometimes with a concurrent cranial nerve VII deficit. Generalized myopathy is rare, but has been documented. Megaesophagus, laryngeal paralysis, and Horner’s syndrome have been reported to occur in association with canine hypothyroidism, but a causal relationship has not been definitively proven. Although rare, there have also been reports of insulin-resistant diabetes mellitus. Other uncommon clinical signs include congestive heart failure, cerebral vascular accidents, and galactorrhea. Rarely, congenital hypothyroidism has been reported with cretinism and dwarfism resulting.
I recommend that a complete blood count, serum chemistry panel with electrolytes, and urinalysis be run on all dogs being evaluated for hypothyroidism. Demonstration of classic laboratory abnormalities of a mild normocytic-normochromic anemia and hypercholesterolemia is further evidence for the diagnosis. Hypothyroid dogs may also have hypertriglyceridemia. The lipid levels in the blood may be high enough to interfere with other tests in some cases. This minimum database also allows the clinician to evaluate the patient for the presence of nonthyroidal illness, which can significantly interfere with thyroid testing.
MODULE 3-Treatment
Treatment of canine hypothyroidism involves daily life-long hormone replacement therapy using L-thyroxine. The usual recommended starting dose is 0.1 mg/10 pounds of body weight with a maximum dose of 0.8 to 1 mg unless the dog is very large. Therapy is administered once or twice daily, typically twice daily with the standard tablet formulations. The use of a name-brand preparation is recommended when using tablets and a new liquid formulation is available.
The liquid thyroxine formulation available is called Leventa®. It has appeared efficacious and safe in studies in normal and hypothyroid dogs. When Leventa® is used usual therapeutic monitoring and dose adjustments are made during therapy. Leventa® should be efficacious when administered once daily in a higher percentage of cases and is a viable alternative to tablet formulations.
A pharmacokinetic study showed that Leventa® had significantly greater bioavailability than a standard tablet formulation. Another pharmacokinetic study showed that the bioavailability of Leventa® was decreased in the presence of food. Therefore clients should be counselled to consistently give Leventa® either with food or without food to remove this variable. When Leventa® is used, the usual therapeutic monitoring and dose adjustments during therapy are made.
In dogs with concurrent heart disease, diabetes, and Addison’s disease, we institute thyroid hormone replacement therapy at a lower dosage. Gradual incremental replacement is then used to avoid abrupt increases in the metabolic rate. In addition, in dogs with concurrent Addison’s disease adrenal hormone replacement is given first, followed by the institution of thyroid hormone replacement.
In dogs with hypothyroidism receiving appropriate thyroid hormone replacement therapy, clinical signs should resolve. We can see improved attitude and activity in the first week or two. Weight loss and neurologic improvement can be seen within the first few weeks. Dermatologic and reproductive abnormalities will resolve over a few to several months. In addition to monitoring response to therapy with resolution of clinical signs, therapeutic monitoring is recommended.
MODULE 4-Monitoring
Monitoring the thyroid hormone levels during therapy is recommended to ensure that a proper dosage of thyroid hormone replacement is being given and to avoid both undertreatment and overtreatment of the patient.
Usually only total T4 levels are measured. We can measure peak and/or trough levels. In selected cases, serum TSH levels are measured to help us adjust the dose of thyroid hormone replacement therapy. Thyroid hormone levels are checked 6 weeks after starting replacement therapy, 4 to 6 weeks after any change in dosage or brand, and every 3 to 6 months during therapy.
Peak T4 levels are checked 4 to 6 hours after the dose is given. Trough T4 levels are determined just prior to the next dose. Peak T4 levels should be high-normal to slightly increased; whereas trough T4 levels should be in the low-normal range. If once-daily therapy is being used, for example with Leventa®, I would recommend determining both trough and peak levels, at least initially; this will allow one to determine both that the dosage is adequate and that the duration of action is sufficient.
Daisy is an example of how monitoring T4 levels during thyroid hormone replacement therapy can be useful. Daisy was an 8-year-old female spayed miniature poodle. She’d been appropriately diagnosed with hypothyroidism and placed on an appropriate dose of Leventa®. I saw Daisy a few months after this because she was continuing to be lethargic and continuing to have skin problems.
On physical exam, Daisy was obese, had a thin hair coat, and secondary infection. Her CBC, blood chemistry, and urinalysis were unremarkable. Her trough T4 level was 0.9 µg/dL, which is the low end of the normal range for the lab we use. Her peak T4 level, drawn at 4 hours after dosing, was 2.1 µg/dL, which is a little lower than I like to see in a dog on adequate replacement therapy.
Therefore we increased Daisy’s Leventa® dosage to 0.2 mg, once daily. When rechecked in 6 weeks, the owner reported that she was clinically improving. Her trough level at this time was 1.6 µg/dL and the peak T4 level, again drawn 4 hours after dosing, was 4.1 µg/dL. And these are appropriate levels for thyroid hormone replacement therapy.
If an inadequate response to therapy is seen, there are several potential reasons. First, the dog may not be hypothyroid. Another potential cause is that the wrong dose or frequency of thyroid hormone replacement is being used for that particular patient. Poor absorption of the particular product being used is another possibility. Poor owner compliance will lead to inadequate response to therapy. In this situation, use of a thyroid hormone replacement product that is efficacious given once daily can be of particular benefit.
The prognosis for canine hypothyroidism is excellent with proper therapy. The key is both in making the proper diagnosis and following up to make sure that the therapy is working well, and adjusting as necessary.
<<Back to more articles
