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A two-year-old intact male Bearded Dragon was presented for vomiting and regurgitation of 3-4 weeks duration. Signs began as the patient came out of brumation, and were accompanied by mild lethargy and inappetence. Blood work revealed elevated WBC (32.2 K/uL) and severe hyperglycemia (1339 mg/dL). Fecal flotation tests returned negative. On the day of admission, dark red blood was present in his vomit. A CT was performed. Administration of contrast failed – only native images are available.
The liver is enlarged with lobular margins and is diffusely hypoattenuating (approximately -50 HU), containing several well-defined soft tissue attenuating nodules up to 6mm in diameter. Along the lesser curvature of the stomach is an ill-defined, soft-tissue attenuating, contrast-enhancing mass (15mm x 8mm), and luminal margins are undulating and irregular. In the colon is a small amount of punctate mineral and fecal material, otherwise the gastrointestinal tract is empty. The abdominal fat bodies are severely, symmetrically enlarged encompassing a large portion of the coelomic cavity. There is a mild reduction in lung volume, with a concurrent mild ground glass attenuation present ventrally. The remaining coelomic and musculoskeletal structures are normal.
1. Gastric mass Given the severe hyperglycemia, gastric neuroendocrine carcinoma is prioritized. Other neoplasia are also possible, such as adenocarcinoma.
2. Hypoattenuating hepatomegaly, hepatic nodules Hepatic lipidosis is prioritized, and liver nodules are most consistent with metastatic disease (from the gastric mass).
3. Reduced pulmonary volume, mild ventral ground glass opacity This is attributed to atelectasis secondary to hepatomegaly
The patient was euthanized.
Necropsy results indicated:
1. Gastric neuroendocrine carcinoma with hepatic metastases
Immunohistochemistry was performed. Approximately 5% of the neoplastic cells demonstrated strong cytoplasmic immunoreactivity for somatostatin.
2. Diffuse, severe hepatic lipidosis No pathological changes were observed in the lung.
Gastric neuroendocrine carcinomas are a highly malignant neoplastic entity of young bearded dragons (1). While these tumors may exhibit multihormonal expression, somatostatin production predominates despite variable immunoreactivity for somatostatin (1, 2). In people, somatostatinoma syndrome consists of a triad of diabetes mellitus (by limiting insulin release), diarrhea and gallstones. Weight loss and anemia may also be encountered (3). In this bearded dragon, no symptoms other than hyperglycemia and weight loss were observed.
In people, somatostatinomas are commonly associated with neurofibromatosis type 1 (Von Recklinghausen\’s disease), caused by a mutation in the tumor suppressor gene NF1, which results in decreased expression of neurofibromin. In all 5 dragons examined in the Ritter et al case series, neoplasms exhibited decreased neurofibromin expression compared with control tissues, suggesting that decreased functional neurofibromin may play a role in the pathogenesis of somatostatinomas in bearded dragons. Hepatic lipidosis is commonly recognized in reptiles, as a pathologic process related to chronic disease, associated with obesity and sedentarity, or as a pre-reproduction physiologic increase in intrahepatic fat in females (4).
1. Ritter JM, Garner MM, Chilton JA et al. Gastric Neuroendocrine Carcinomas in Bearded Dragons (Pogona vitticeps). Vet Pathol 2009; 46: 1109-1116.
2. Lyons JA, Newman SJ, Greenacre CB et al. A gastric neuroendocrine carcinoma expressing somatostatin in a bearded dragon. J Vet Diagn Invest 2010; 22 (2): 316-320.
3. Vinik A, Pacak K, Feliberti E et al. Somatostatinoma. www.endotext.org https://www.ncbi.nlm.nih.gov/books/NBK279034/
4. Divers S and Stahl S (eds). Mader’s Reptile and Amphibian Medicine and Surgery, 3rd Ed. Elsevier 2019.