To describe the clinicopathological findings and outcomes of cases of feline congenital hypothyroidism diagnosed in a single veterinary hospital in Santiago, Chile. Materials and MethOds: Medical records were searched for cases of congenital hypothyroidism over an 18-month period. Inclusion criteria were a diagnosis of congenital hypothyroidism based on consistent historical and clinical findings, a low or low-normal serum total T4 and elevated serum canine TSH (cTSH). results: Six unrelated cats ranging in age from 4 to 19 months met the inclusion criteria. The most common historical signs were small stature and lethargy. All cats had disproportionate dwarfism, delayed tooth eruption, retained deciduous teeth, bilateral palpable goitres and low rectal temperatures. Other findings were bradycardia, obesity, poor hair coat and focal alopecia on the ventral aspects of the elbows and hocks. In all cases, cTSH was markedly elevated. Sequential changes noted after the initiation of therapy included normal T4 after 6 weeks, improved hair coat and increased physical activity by 8 weeks, normal cTSH by 10 weeks and normal physical appearance and dentition after 4 months. Goitres shrank markedly but remained palpable. Hypothyroidism was well managed clinically in all cases 2 years after diagnosis except for one cat that died of unrelated causes. clinical significance: This is the first report to describe a cluster of congenital hypothyroidism cases in non-related cats that were presented over a short period of time. Growth defects resolve with treatment, even in cats diagnosed after puberty. Larger, prospective multi-centre studies are warranted to determine the incidence of congenital hypothyroidism in cats.

Cyclooxygenase (COX)-2 expression is positively correlated with malignant features in canine mammary carcinomas. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit COX activity and may therefore possess anticancer effects. Meloxicam is an NSAID that is widely used in human and veterinary medicine. High concentrations of meloxicam have been reported to be antitumorigenic in vitro; however, the effect of meloxicam at concentrations that are equivalent to those that can be obtained in vivo remains unknown. In the current study, the in vitro effects of low-dose meloxicam (0.25 µg/ml) on CF41.Mg canine mammary carcinoma cells were evaluated. The effects on cell proliferation, apoptosis, cell migration and invasion, in addition to the expression of different molecules associated with tumor invasiveness were analyzed. No effect on cell viability and apoptosis were observed. However, cell migration and invasion were significantly reduced following treatment with meloxicam. MMP-2 expression and activity were similarly reduced, explaining the impaired cell invasion. In addition, β-catenin expression was downregulated, while its phosphorylation increased. These results indicate that 0.25 µg/ml meloxicam reduces cell migration and invasion, in part through modulating MMP-2 and β-catenin expression. Additional studies are required to elucidate the mechanism associated with the anti-invasive effect of meloxicam on CF41.Mg cells. The results of the present study suggest that meloxicam has a potential adjunctive therapeutic application, which could be useful in controlling the invasion and metastasis of canine mammary carcinomas.

Mammary cancer is a frequent neoplasia in female dogs, in which most important risk factors are hormonal. Sexual hormones as estradiol play an important role in mammary carcinogenesis, being able to induce carcinogenic initiation, promotion and progression. However, the molecular mechanisms involved are incompletely understood. Estradiol is synthesized mainly in the ovaries, nevertheless, high concentrations of estradiol and some of its hormonal precursors have also been described in malignant mammary tumor tissue. The mechanisms of action of estradiol include the classic genomic effects that modulate gene transcription, and non-genomic effects, which trigger quick effects after estradiol binds to its specific receptors. These responses modulate various intracellular signaling pathways, triggering post-translational modification of several proteins. This review will discuss the well-known underlying mechanisms associated with the action of estradiol in the malignant progression of canine mammary tumors.

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