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Spontaneous primary hypothyroidism in 7 adult cats

Thyroid scintigraphy illustrating scans of (A) clinically normal cat; (B) cat with goitrous hypothyroidism; and © cat with atrophic hypothyroidism.

Spontaneous primary hypothyroidism appears to be an extremely rare clinical disorder in adult cats, with only 4 reported cases over the last 25 years.

Most hypothyroid cats are younger (generally kittens, aged 2–4 months) and suffer from congenital hypothyroidism, which typically results in disproportionate dwarfism (cretinism).

Of approximately 60 cats with congenital hypothyroidism that have been reported, only 3 were older than 12 months of age at time of diagnosis, but these 3 cats were stunted since kittenhood, consistent with the diagnosis of congenital hypothyroidism.

In dogs and humans, almost all naturally occurring hypothyroidism is attributable to irreversible destruction of the thyroid gland. Histologically, primary hypothyroidism in humans and dogs presents as either lymphocytic thyroiditis or idiopathic thyroid degeneration (idiopathic follicular atrophy).

Of the 4 reported adult cats with naturally occurring primary hypothyroidism, 2 had lymphocytic thyroiditis, 1 had idiopathic atrophy, and 1 had a goitrous form of hypothyroidism associated with diffuse thyroid follicular hyperplasia of both thyroid lobes.

Goitrous hypothyroidism is extremely rare in dogs, with iatrogenic, drug‐induced thyroid goiter being the most common cause. However, a subset of adult hypothyroid humans have goiter secondary to iodine deficiency, environmental goitrogens, or ineffective thyroid hormone synthesis caused by biosynthetic defect (dyshormonogenesis).

Given the paucity of data regarding adult‐onset feline hypothyroidism, we sought to describe the history, clinical features (including presence or absence of goiter), diagnostic testing, treatment, and long‐term outcome of 7 adult cats with spontaneous primary hypothyroidism. For these cats, we used the serum concentrations of T4, free T4 (fT4), and thyroid stimulating hormone (TSH), and results of thyroid scintigraphy to aid in both the diagnosis and long‐term monitoring of thyroid hormone replacement treatment.

Prospective case series. We collected data on cats’ signalment, clinical signs, results of physical examination, routine laboratory and thyroid hormone testing, and thyroid imaging (thyroid scintigraphy or ultrasound). We subsequently treated cats with levothyroxine and evaluated their response to treatment.

Cats ranged from 3.5 to 11 years, with no apparent breed predilection; 6/7 cats were male. Only 2/7 cats were initially tested because of signs of hypothyroidism (hair‐coat changes, lethargy, obesity); others were tested for routine thyroid monitoring or palpable thyroid nodules. Four were azotemic (serum creatinine, 2.2‐3.4 mg/dL). Six of the cats had low serum thyroxine (T4) and free T4 (fT4) concentrations, whereas all 7 cats had high thyroid‐stimulating hormone (TSH) concentrations. In 6/7 cats, thyroid scintigraphy revealed bilateral goiter with intense radionuclide uptake; imaging showed no visible thyroid tissue in the other. After levothyroxine (L-T4) treatment, serum concentrations of T4 and fT4 increased and TSH fell; high serum creatinine normalized in azotemic cats; and repeat imaging showed reduction in goiter size.

Primary hypothyroidism develops in adult cats, with a higher prevalence than previously thought. Most cats appear to develop a goitrous form of hypothyroidism associated with thyroid hyperplasia, whereas thyroid atrophy appears to be less common. With levothyroxine (L-T4) replacement, clinical and laboratory abnormalities improve or resolve.

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