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Оглавление

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 Data from one laboratory (D Reavill, unpublished) found the percentages of hepatic lipidosis in the reptile groups with the liver submitted for evaluation, as follows:chelonians (turtles and tortoises)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.

DIFFERENTIAL DIAGNOSIS

Hepatic lipidosis needs to be distinguished from other causes of hepatomegaly.

Vascular congestion: underlying cardiovascular disease.

Toxins: mycotoxins, pesticides, heavy metals

Infectious diseases: herpesvirus, adenovirus, Salmonellaspp., mycobacteria, Gram‐ negative bacterial infections, abscesses/ granulomas, protozoa.

Tumor: lymphoma, hepatoma

DIAGNOSTICS

Imaging

Radiographs ± contrast, ultrasound, CT, and MRI.

There may an enlarged hepatic silhouette on radiography.

Ultrasound may reveal a brightly reflective, enlarged, rounded liver.

CT provides measurements of radiodensity of the liver.

CT values lower than 20 HU are compatible with hepatic lipidosis in red‐footed tortoises (Chelonoidis carbonaria).

Hematology and Biochemistry

Serum biochemistry: lack of species‐specific reference ranges make interpretation challenging.

In general, decreased plasma proteins; increased triglycerides, cholesterol, AST, and LDH; glucose and bile acid levels vary; blood is often noticeably lipemic.

PATHOLOGICAL FINDINGS

The gross appearance is of an enlarged, friable liver, pale tan to yellow, and typically has a greasy feel.

Biopsy and/or necropsy histopathology: the hepatocytes will be variably enlarged, and supporting cytoplasmic vacuolization with HE stain.

Additional stains will demonstrate the prominent oil red O‐positive lipid droplets in all the hepatocytes.

TREATMENT

APPROPRIATE HEALTH CARE

Administration of oral medications is recommended.

NUTRITIONAL SUPPORT

Placement of an esophagostomy tube for feeding is recommended.

Maintain at appropriate temperature and humidity; exercise.

Caloric reduction with a nutritionally complete, low‐fat, high‐quality protein, liquid diet (Lafeber’s Emeraid®, EmerAid, LLC, Cornell, IL; Oxbow Critical Care®, Oxbow Animal Health, Omaha, NE; or Oxbow Carnivore Care®, Oxbow Animal Health, Omaha, NE).

Hydration

CLIENT EDUCATION/HUSBANDRY RECOMMENDATIONS

N/A

MEDICATIONS

DRUG(S) OF CHOICE

Antibiotic of choice in reptiles if needed: ceftazidime.

Nutriceuticals such as silymarin and milk thistle are reported to be an anti‐ inflammatory and antioxidant; however, there are no studies to support claims for hepatic benefits.

PRECAUTIONS/INTERACTIONS

Avoid hepatotoxic agents in reptiles:

antibiotics: doxycycline, clindamycin, erythromycin

antivirals: acyclovir

antifungals: itraconazole, ketoconazole

antiparasitic: metronidazole, dichlorvos, tiabendazole, ivermectin

FOLLOW‐UP

PATIENT MONITORING

Regular checkups to assess body weight, change in serum biochemistries, and possibly rebiopsy.

EXPECTED COURSE AND PROGNOSIS

After support through any acute crisis, the long‐term prognosis depends on associated conditions and whether these can be changed.

MISCELLANEOUS

COMMENTS

N/A

ZOONOTIC POTENTIAL

N/A

SYNONYMS

Fatty liver

Vacuolar hepatopathy

ABBREVIATIONS

AST = aspartate aminotransferase

CT = computed tomography

HE = hematoxylin and eosin

LDH = lactate dehydrogenase

MRI = magnetic resonance imaging

POTZ = preferred optimal temperature zone