Thyroid Function in Canine Megaesophagus
by
W. Jean Dodds, DVM
HEMOPET m 938 Stanford Street m Santa Monica, CA 90403
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What role does thyroid function (and dysfunction) play in the development and clinical signs of megaesophagus in dogs? Before addressing this question, we need to first review the types and causes of megaesophagus.
Background
The most common cause of regurgitation in dogs is idiopathic megaesophagus, where the cause of the problem is unclear. The condition is characterized by moderate to severe dilation of the esophagus and ineffective esophageal muscle contractility (peristalsis). Several forms of the syndrome have been described:
Congenital idiopathic megaesophagus is a generalized dilation and hypomotility of the esophagus causing regurgitation and failure to thrive in puppies shortly after weaning. An increased breed incidence has been reported in the Boston Terrier, Chinese Shar-Pei, Great Dane, German Shepherd, White German shepherd, Golden Retriever, Greyhound, Irish Setter, Labrador Retriever, Mastiff, Newfoundland, and Rhodesian Ridgeback breeds, but heritability has been proven only in the Miniature Schnauzer and Wire-haired Fox Terrier breeds. The underlying cause is not completely understood, but appears to be a defect in the sympathetic (vagal) nerve supply to the esophagus.
Acquired secondary megaesophagus may occur in association with a number of other conditions. Myasthenia gravis accounts for at least 25% of these cases. In some Myasthenia gravis cases, regurgitation and weight loss may be the only presenting signs of the disease.
Acquired idiopathic megaesophagus is the form of disease seen in most adult onset cases. It appears spontaneously in adult dogs between 7-15 years of age, and there is no sex or breed predilection. The disorder is not the same as esophageal achalasia in humans. While the responses of the upper and lower esophageal sphincters to swallowing appear to be intact, esophageal distension does not initiate peristaltic contractions in affected animals. The exact site of this abnormality in the nerve response has not yet been determined.
Diagnosis
Routine laboratory testing should be performed to investigate possible secondary causes of megaesophagus such as hypothyroidism, polymyositis, and hypoadrenocorticism (Addison’s disease). X-rays including contrast studies should be made to confirm the diagnosis, evaluate motility, and exclude foreign bodies or obstruction as the cause of the megaesophagus.
For the proper diagnosis of thyroid dysfunction, a complete baseline thyroid profile is measured and typically includes total T4, total T3, free T4, free T3, T3AA,T4AA, and TgAA. The cTSH assay is a relatively poor predictor of primary hypothyroidism in dogs (~70%) versus people (95%), so it is rarely needed or relied upon in making the diagnosis. The TgAA assay is especially important in screening breeding stock for heritable autoimmune thyroid disease.
The normal reference ranges for thyroid analytes of healthy adult animals tend to be similar for most breeds of companion animals. Exceptions are the sighthound and giant breeds of dogs which have lower basal levels.
The autoimmune form of canine thyroid disease is similar to Hashimoto’s thyroiditis of humans, which has been shown to be associated with human major histocompatibility complex (MHC) tissue types. A similar association with canine MHC genes in hypothyroid dogs has recently been reported in Doberman Pinschers, English Setters and Rhodesian Ridgebacks, who share a rare dog leukocyte antigen (DLA) genetic marker. The presence of this determinant doubles the risk of a dog developing hypothyroidism. This exciting finding should lead to development of a genetic marker test to identify affected breeding stock and allow for selective breeding.
Treatment
Animals with secondary acquired megaesophagus should be treated for the associated underlying condition. For hypothyroid dogs therapy with thyroxine should be given twice daily at least an hour before or three hours after a meal to ensure proper absorption. If the thyroid condition is autoimmune thyroiditis, the animal should not be used for breeding, although having megaesophagus is another reason to not breed the dog.
Affected animals should be fed a high-calorie diet, in small frequent feedings, from an elevated or upright position to take advantage of gravity drainage through a non-peristaltic esophagus. [For more information on dietary issues, please refer to the article, Megaesophagus - Nutritional Rewards & Challenges, by Monica Segal.]
While medical therapies have been advocated for treating dogs with megaesophagus, clinical results have failed to show efficacy in improving esophageal peristalsis in affected dogs.
Prognosis
Animals with congenital idiopathic megaesophagus have a fair prognosis if adequate nutrition is provided and every effort is made to prevent aspiration pneumonia. Many of these dogs will develop improved esophageal motility over the course of several months.
By contrast, the morbidity and mortality of acquired idiopathic megaesophagus remain unacceptably high, and lead to a poor overall prognosis. Many animals eventually succumb to the effects of chronic malnutrition and repeated episodes of aspiration pneumonia. Animals with acquired secondary megaesophagus have a more favorable prognosis if the underlying disease (e.g. hypothyroidism) can be promptly identified and successfully managed. In a retrospective study of 29 dogs with neurologic signs and hypothyroidism, four cases had megaesophagus. Of these. three dogs had good clinical remission with occasional regurgitation and one dog did not improve. In one published case study, the treatment for concomitant hypothyroidism resulted in total regression of the megaoesophagus, which completely disappeared clinically and radiographically for at least two years of followup. However, although resolution following therapy with thyroxine is highly suggestive of a causal relationship between megaesophagus and hypothyroidism, it does not prove it.
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References
Jaggy A, Oliver JE, Ferguson DC, et al. Neurological manifestations of hypothyroidism: a retrospective study of 29 dogs. JVIM 8: 328-336, 1994.
Dodds WJ. Estimating disease prevalence with health surveys and genetic screening. Adv Vet Sci Comp Med 39: 29-96, 1995.
Dodds WJ. Autoimmune thyroiditis and polyglandular autoimmunity of purebred dogs. Can Pract 22: 18-19, 1997.
Gaynor, AR, Shofer ES, Washabau,RJ. Risk factors for aquired meagoesophagus in dogs. JAVMA 211:1406-1412, 1997.
Huber E, Armbrust W, Forster JL et al. Resolution of megaesophagus after treatment of concurrent hypothyroidism in a dog [in French]. Sch Arch Tier 148: 512-514,2001
Kennedy LJ, Quarmby S, Happ GM et al. Association of canine hypothyroid disease with a common major histocompatibility complex DLA class II allele. Tissue Antigens 68: 82-86, 2006.
Nachreiner RF, Refsal KR, Graham PA et al. Prevalence of serum thyroid hormone autoantibodies in dogs with clinical signs of hypothyroidism. JAVMA 220: 466-471, 2002.
Washabau, RJ. Canine idiopathic megaesophagus.: pathogenesis, diagnosis, and therapy. Proc. WSAVA Congress, Vancouver, BC, 2001, 5 pp.
-- Edited by Moderator Peg on Wednesday 13th of May 2009 10:18:24 AM
