ABSTRACT
Congenital hypothyroidism (CH) in humans is most commonly caused by disruption of thyroid gland development (dysgenesis) or an inherited defect in thyroid hormone biosynthesis (dyshormonogenesis). CH has not been previously documented in great apes. This report describes the clinical presentation, diagnosis, and treatment of CH in a 9-mo-old male Bornean orangutan (Pongo pygmaeus) and a 6-wk-old female Sumatran orangutan (Pongo abelii). Primary CH due to thyroid dysgenesis was confirmed in the Bornean orangutan using sonography and radioisotope scintigraphy. Although commercial thyroid immunoassays are not validated for use in orangutans, in comparison to age-matched controls, thyroid-stimulating hormone level was markedly elevated, and serum thyroxine (T4) and free T4 levels were markedly decreased in both cases. Oral supplementation with levothyroxine sodium resulted in noticeable clinical improvement in both orangutans within 30 days of initiating treatment.
Subject(s)
Ape Diseases/congenital , Congenital Hypothyroidism/veterinary , Pongo/classification , Thyroxine/therapeutic use , Aging , Animals , Ape Diseases/drug therapy , Ape Diseases/pathology , Congenital Hypothyroidism/diagnosis , Congenital Hypothyroidism/drug therapy , Female , Male , Species Specificity , Thyrotropin/blood , Thyroxine/bloodABSTRACT
OBJECTIVE: We report the first case of cleft palate in a newborn male gorilla (Gorilla gorilla gorilla). CASE HISTORY AND RESULTS: The full-term infant was born to clinically healthy, wild-caught parents and survived 5 days. Autopsy disclosed a unilateral cleft palate, moderate scalp hemorrhage (birth versus postnatal trauma), cerebral edema, and a sterile fibrin vegetation in the heart. The palate was also shorter and narrower than expected, and the biorbital breadth was reduced; otherwise, growth and development appeared normal. Standard cranial and intraoral radiographs and three-dimensional reconstructions of computerized tomographic (CT) scans provided thorough and noninvasive methods of studying the craniofacial complex and extracranial skeleton. By this technique, major findings were: intact premaxilla, interpremaxillary, and premaxillary/maxillary sutures; intramaxillary cleft with ipsilateral choanal atresia; mildly asymmetric inferior turbinates; and normal nasal septum and vomer. CONCLUSIONS: Except for choanal atresia, cleft palate was not associated with other major craniofacial or extracranial anomalies in this case. Choanal atresia has been observed at times with cleft palate, but to our knowledge, the association has not been reported in nonhuman primates. Cleft palate, with or without cleft lip, has been recognized in a variety of nonhuman primates, including the lemur, marmoset, tamarin, squirrel monkey, and macaque. Some occurrences are spontaneous, while others are syndromic and/or arise from genetic or teratogenic influences. Each mode of presentation is poorly understood in nonhuman primates, but in this case, the absence of relevant environmental or parental history suggests that the occurrence was spontaneous. Anatomic studies of nonhuman primates are particularly valuable when they involve endangered species and will hopefully increase our understanding of the pathogenesis and etiology of congenital disorders, as well as other relationships between nonhuman primates and humans.
