Adult-onset hypothyroidism has previously been reported in a chimpanzee (Pan troglodytes), a western lowland gorilla (Gorilla gorilla gorilla), and two Bornean orangutans (Pongo pygmaeus).1-5 To the authors’ knowledge, primary congenital hypothyroidism (CH) has not been described in great apes. In humans, CH is most commonly due to thyroid dysgenesis (athyreosis, ectopy, or hypoplasia). The remaining cases are caused by inherited defects in thyroid hormone biosynthesis (dyshormonogenesis).6 The first case is a 9-month-old male Bornean orangutan presented with delayed development, myxedematous facies, hypotonia, macroglossia, and abdominal distension. Genetic testing including karyotype, fluorescence in situ hybridization (FISH) analysis, and chromosome microarray analysis (CMA) was utilized to rule out Down syndrome and other inherited disorders with similar clinical signs. Thyroid sonography performed by a board-certified pediatric radiologist showed that there was no discernible thyroid tissue present. Thyroid scintigraphy using technetium-99m detected only minimal radionuclide uptake in the anatomic region of the thyroid gland consistent with severe hypoplasia. The second case is a 6-week-old female Sumatran orangutan (Pongo abelii) presented with a poor feeding response, lethargy, impaired thermoregulation, jaundice, and anemia. While commercially available thyroid hormone assays for humans are not validated for use in orangutans, when compared to clinically healthy orangutans of similar age, serum thyroxine (T4) level was significantly decreased, and thyroid stimulating hormone (TSH) level was markedly elevated in both cases. Oral supplementation with levothyroxine sodium resulted in noticeable clinical improvement in both cases with near resolution of all clinical signs in the Bornean orangutan within 30 days of initiating treatment.
The authors would like to thank Dr. Michael Trautman and Dr. Brandon Brown for their assistance with the case of the Bornean orangutan.
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