Evidence map›Paper›PMID 40530035›Full record

ArticleFrontiers in veterinary science2025

Hepatic lipidosis in nine African white-bellied pangolins (

Molly Horgan, Jennifer Landolfi, Nicole I Stacy, Jennifer Watts, Copper Aitken-Palmer

Abstract read
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Article in Frontiers in veterinary science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Molly HorganDepartment of Comparative, Diagnostic, and Population Medicine, College of Veterinary Medicine, University of Florida, Gainesville, FL, United States.
Jennifer LandolfiZoological Pathology Program, University of Illinois, Brookfield, IL, United States.
Nicole I StacyDepartment of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, United States.
Jennifer WattsBrookfield Zoo Chicago, Brookfield, IL, United States.
Copper Aitken-PalmerBrookfield Zoo Chicago, Brookfield, IL, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The African white-bellied pangolin ( Methods: This report describes hepatic lipidosis in these pangolins (clinical presentation, diagnostic imaging, clinicopathologic and postmortem findings) and summarizes clinically relevant predictors of disease. Results: The time from the onset of illness to death ranged from 2 to 75 days (median 23 days). Obesity was noted prior to clinical presentation for illness in 4/9 animals. All pangolins had anorexia and lethargy; other common clinical signs included constipation (6/9), vomiting or regurgitation (6/9), and/or dyspnea (5/9). Increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were observed in 7/9 animals, hyperbilirubinemia in 5/9, and increased bile acids in 5/9. Serum selenium was low in 3/9 animals, but vitamin E concentrations were normal. Hypertriglyceridemia was uncommon during illness (1/9). Evidence of renal dysfunction was also common, and included glucosuria (6/6), proteinuria (7/7), and azotemia (6/9). Ultrasound was the most reliable imaging technique at identifying hepatic lipidosis as evidenced by hepatomegaly and increased echogenicity. Despite variable treatment including assisted feeding, hepatoprotectants, fluid therapy, gastroprotectants, antibiotics, and/or antiemetics, all cases were ultimately fatal. Each of the animals had comorbidities or an inciting reason for anorexia that led to negative energy balance. In 5/9, resultant hepatic lipidosis was severe and deemed the primary cause of death or euthanasia. Discussion: This case series suggests that white-bellied pangolins are prone to developing hepatic lipidosis following a period of anorexia secondary to other underlying disease processes. Elevated AST, ALT, bilirubin, and bile acids in an anorectic and lethargic pangolin should provide a high index of suspicion for hepatic lipidosis. Further study is needed to evaluate pangolins for potential unique polyunsaturated fatty acid or other species-specific dietary requirements.

Indexed as

anorexiahepatic lipidosisliverobesitypangolinPhataginus tricuspis

Identifiers

PMID40530035
PMCPMC12170562

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.