Challenging cases in internal medicine: An underweight Gordon setter with brittle claws

This dog's clinical signs suggested a problem that was more than skin-deep. A variety of tests were necessary to discover the underlying internal disorder.
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Jun 01, 2004


1. The 4-year-old Gordon setter at presentation. Comparing the dog's size with that of the book illustrates the dog's small stature for its breed.
A 4-YEAR-OLD, female spayed Gordon setter was evaluated at the Veterinary Medical Teaching Hospital at the University of Wisconsin-Madison because of brittle claws of about one year's duration. Eighteen months earlier, the referring veterinarian had examined the dog because of a flaky, dry coat that had progressed to abnormal claw integrity. The dog frequently had broken claws requiring cauterization. All four feet were affected at different times throughout the year. The referring veterinarian had performed a premium thyroid panel, consisting of total T4 and T3 concentrations, free T4 and T3 concentrations, the TSH concentration, and T4, T3, and thyroglobulin autoantibody concentrations. The results had been normal with the exception of an increase in thyroglobulin autoantibody (1,159%, normal < 200%). The results of aerobic bacterial and fungal cultures of the claw beds had been negative. The dog had been treated with cephalexin multiple times (dose and duration unknown), and fatty acid supplementation had been initiated.

Physical examination findings and initial diagnostic procedures

On physical examination, the dog was small and thin for its breed ( Figure 1 ), weighing 33 lb (15 kg) (normal = 55 to 66 lb [25 to 30 kg]). The dog's coat was thin, dull, and dry. The claw beds were normal, but the claws on all four feet were brittle and splitting; the hair keratin easily split longitudinally. On further questioning, the owners mentioned that the dog was occasionally lethargic and quiet and intermittently had loose stools and a poor appetite.

Because of this dog's small stature, poor coat, and dry, splitting claws, a systemic disease was suspected rather than a primary claw disorder (e.g. onychomycosis). Primary claw disorders, with no other dermatologic manifestations, are rare in dogs and cats. Most commonly, claw diseases are asymmetric and result from trauma (either physical or chemical) and secondary bacterial infection. Systemic diseases with claw bed involvement include lupoid dermatoses and drug reactions.1 The differential diagnosis list at this point included hypothyroidism, hypoadrenocorticism, and maldigestion or malnutrition secondary to intestinal disease.

The results of a complete blood count and serum chemistry profile were normal. A total T4 concentration was rechecked because increased thyroglobulin autoantibodies can predispose a dog to hypothyroidism. The total T4 concentration was normal. No abnormalities were noted on cytologic examination of claw bed samples.

The patient was discharged, and the owner was instructed to administer fenbendazole (50 mg/kg once a day for three days, repeated in three weeks) and to return in one week for additional diagnostic tests that required fasting.

Further diagnostic testing

One week later, an ACTH stimulation test was performed to rule out hypoadrenocorticism, because the dog had intermittent gastrointestinal signs, lethargy, and depression. The results were normal (cortisol concentration before ACTH administration = 7.4 ng/ml, normal = 2 to 10 ng/ml; cortisol concentration one hour after ACTH administration = 167 ng/ml, normal = 55 to 280 ng/ml). Fasting trypsin-like immunoreactivity and folate and cobalamin concentrations were measured to screen for exocrine pancreatic insufficiency, malabsorption or maldigestion, and small intestinal bacterial overgrowth. The trypsin-like immunoreactivity results were normal. The folate concentration was 3.3 µg/L (normal = 6.5 to 11.5 µg/L), which is consistent with disease affecting the proximal small intestine. The cobalamin concentration was 312 ng/L (normal = 249 to 733 ng/L). The differential diagnosis list now included inflammatory bowel disease (IBD), gastrointestinal lymphoma, and, less likely because of our geographic area, fungal infection (e.g. histoplasmosis). Endoscopy was performed to further evaluate the upper gastrointestinal tract.

On endoscopic examination, the esophagus and fundic region of the stomach looked normal, whereas the pylorus appeared hyperemic. Many areas of the proximal small intestinal mucosa had a cobblestone appearance. Biopsy samples of the stomach and duodenum were submitted for histopathologic examination.