Blackwell's Five-Minute Veterinary Consult: Reptile and Amphibian. Javier G. Nevarez

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Blackwell's Five-Minute Veterinary Consult: Reptile and Amphibian - Javier G. Nevarez

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cases of visceral gout, allopurinol should also be avoided as it increases uric acid excretion by the kidneys and could theoretically make the condition worse.

      PRECAUTIONS/INTERACTIONS

      Allopurinol and probenecid may potentially interact, although the clinical significance of this interaction in reptiles is unknown.

FOLLOW‐UP

      PATIENT MONITORING

       Response to therapy is usually monitored by physical examination findings (e.g., increase in activity levels or no progression in joint swellings).

       Repeat blood samples can also be taken to recheck uric acid levels which would be expected to start reducing within 7 days of allopurinol treatment.

      EXPECTED COURSE AND PROGNOSIS

       The prognosis for patients with severe widespread disease is poor, but if diagnosed early the condition could be managed successfully.

       If left untreated, the disease will progress with widespread uric acid deposition ultimately resulting in organ failure and death.

MISCELLANEOUS

      COMMENTS

      N/A

      ZOONOTIC POTENTIAL

      N/A

      SYNONYMS

      N/A

      INTERNET RESOURCES

      Veterinary Information Network: www.vin.com

      1 Casimire‐Etzioni AL, Wellehan JF, Embury JE et al. Synovial fluid from an African spur‐thighed tortoise (Geochelone sulcata). Vet Clin Path 2004;33(1):43–46.

      2 Dallwig R. Allopurinol. J Exot Pet Med 2010;19(3):255–257.

      3 Mader DR. Gout. In: Mader DR, ed. Reptile Medicine and Surgery. 2nd ed. St. Louis, MO: Elsevier Saunders; 2006:374–379.

      Author Joanna Hedley, BVM&S, DZooMed (Reptilian), DECZM (Herpetology), MRCVS

      Hepatic Lipidosis

      

BASICS

      DEFINITION/OVERVIEW

      Hepatic lipidosis is the excessive accumulation of triglycerides in the hepatocytes and can result in altered hepatic function. It is expected to be a reversible lesion if the underlying cause is corrected. It is a common lesion diagnosed in reptiles.

      ETIOLOGY/PATHOPHYSIOLOGY

       Triglyceride accumulation in hepatocytes can occur due to disturbances of lipid metabolism from primary metabolic liver disease, toxins, protein malnutrition, diabetes mellitus, obesity, anorexia (increased fatty acid mobilization from peripheral stores), extrahepatic visceral inflammation, and anoxia (inhibits fatty acid oxidation).

       In female reptiles, the change can be associated with folliculogenesis.

       The common factor for each of these possible etiologies is a negative balance between the rates of deposition and dispersal of fat from the liver, resulting in an accumulation of triglycerides in the liver.

       In reptiles, obesity from rich diets can result in hepatic lipidosis and enlargement of the coelomic fat bodies.

       Reduced activity will also contribute to increased fat deposits and is not uncommonly reported condition in monitors and turtles.

       In tortoises, a lack of normal hibernation and reproductive activity can lead to hepatic lipidosis.

      SIGNALMENT/HISTORY

       Hepatic lipidosis is reported to be more common in turtles. Data from one laboratory (D Reavill, unpublished) found the percentages of hepatic lipidosis in the reptile groups with the liver submitted for evaluation, as follows:chelonians (turtles and tortoises) (97/676) 14%lizards (304/1485) 20%snakes (91/1672) 5.4%

       There is a reported difference in tolerance to the condition, with turtles being more resistant to metabolic derangements.

      CLINICAL PRESENTATION

       The clinical signs are generally non‐specific.

       Signs include weakness, depression, pale oral mucous membranes, and non‐specific neurologic signs.

       Green to blue urates are reported, and clay‐like, tan, or watery feces may also be noted.

      RISK FACTORS

       Husbandry

       Inappropriate diet and overfeeding, such as chelonians fed only canned dog food.

       Chronic stress: inappropriate captive husbandry conditions (POTZ, cage size, feeding strategies).

       Inactivity: restricted physical activity due to space or adequate stimulation.

       Inappropriate support for reproduction

       Inappropriate hibernation conditions

       Anorexia/hyporexia: desert and sulcata tortoises that have failed to eat for more than 1 week.

       Others

      N/A

DIAGNOSIS

      Although the presumptive diagnosis is based on history, clinical signs, laboratory data, and imaging, the definitive diagnosis is made by microscopic evaluation of a liver biopsy or necropsy examination.

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