Reversible megaoesophagus associated with primary hypothyroidism in a dog

Hypothyroidism has historically been cited as a possible cause of megaesophagus. However, a definitive association between hypothyroidism and megaesophagus has not been proved. A 7-year old entire female German Shepherd dog was presented with a ten day history of regurgitation a few minutes after feeding. It was also reported that the dog was weak and had nonpruritic dermatological abnormalities since months: poor and dull hair coat and hair loss. On the physical examination, the dog had a body condition score of 6/9 and a diffusely poor, dull and dry hair coat with bilaterally symmetric rarefaction in the truncal area, alopecia and hyperpigmentation in the friction areas and on the tail was evidenced. The remainder of the physical examination was unremarkable. The blood results showed a moderate non regenerative normochromic and normocytic anaemia and a mild increase in serum cholesterol concentration. On survey radiographies (figure 1) of the thorax, pre and post barium PO administration, a consistently diffuse megaesophagus was evident. Further diagnostic work-up included: measurement of serum canine thyroid stimulating hormone (cTSH), recombinant human thyroid stimulating hormone (rhTSH) stimulation test to investigate hypothyroidism, measurement of Acetylcholine (Ach) receptor antibodies to investigate MG and skin scraping to investigate demodicosis. There was a high concentration of cTSH associated with low basal total thyroxine (T4) which did not increase six hours post stimulation. These findings allowed to diagnose a primary hypothyroidism. The serology for Ach receptors antibodies was negative and, therefore, a focal MG was considered less likely. The final diagnosis was hypothyroidism associated with most likely secondary megaesophagus. Treatment was initiated with levothyroxine 20 μg/kg body weight q12h PO and specific feeding instructions for the megaesophagus were recommended. One week later the owner was telephonically contacted, he reported that the dog was much more active and not regurgitating anymore. Twenty five days after treatment the dog was in a good general condition, the haircoat was less dull, with new areas of hairgrowth. Follow up blood results and chest radiographies (figure 1) were within normal limits. Two years after the diagnosis, the dog is clinically well and no further dermatological signs or regurgitations are reported. The association between hypothyroidism and megaesophagus is controversial. In a retrospective study by Jaggy and others (1994) of 29 hypothyroid dogs, four had megaesophagus; one dog showed an improvement of the esophageal clinical signs after therapy but radiological evidence of megaesophagus persisted in all dogs. As previously reported, complete resolution of clinical and radiographic signs was achieved in our case. Although concurrent MG was unlikely, it was not possible to completely exclude spontaneous recovery from a focal MG at the same time of levothyroxine supplementation. Finally, only the suspension of levothyroxine therapy, with a recrudescence of the megaesophagus, could have proven irrefutably the connection between hypothyroidism and megaesophagus, however, such procedure was not performed for ethical reasons.