Evidence map›Paper›PMID 41742491›Full record

ArticleJournal of veterinary internal medicine2026

Hyperbilirubinemia and neurologic signs in dogs with non-associative immune-mediated hemolytic anemia: 81 cases (2015-2024).

Sasha Chapman, John M Angles, Christine Griebsch, Jane Yu

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Article in Journal of veterinary internal medicine, 2026. 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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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Sasha ChapmanAnimal Referral Hospital Canberra, Internal Medicine Department, Pialligo, Australian Capital Territory, 2609, Australia.
John M AnglesAnimal Referral Hospital Canberra, Internal Medicine Department, Pialligo, Australian Capital Territory, 2609, Australia.
Christine GriebschSydney School of Veterinary Science, Faculty of Science, The University of Sydney, Sydney, New South Wales 2006, Australia.
Jane YuAnimal Referral Hospital Canberra, Internal Medicine Department, Pialligo, Australian Capital Territory, 2609, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBilirubin encephalopathy is a poorly recognized complication in dogs with immune-mediated hemolytic-anemia (IMHA). HYPOTHESIS/

objectivesAssess serial trends of hyperbilirubinemia and the association between bilirubin concentrations and neurologic signs in dogs with IMHA. ANIMALS: Eighty one dogs with non-associative IMHA and hyperbilirubinemia.

methodsMulticenter retrospective cohort study. The signalment, clinical signs, clinicopathological data, treatment, and outcome were evaluated. Bilirubin concentrations were recorded at the baseline, peak, initial decrease, and normalization. Univariable logistic regression was used to determine the association between neurologic signs and hyperbilirubinemia.

resultsThe median bilirubin concentrations at the baseline, peak, and initial decrease were 2.5 (IQR, 1.4-4.8), 3.7 (IQR, 1.8-24.2), and 1.1 mg/dL (IQR, 0.5-4.3; 43, 64, and 19 μmol/L), respectively. Twenty percent (16/81) of dogs developed neurologic signs. Neurologic signs included stupor, non-ambulatory tetraparesis, and generalized seizures. A significant association was found between the presence of neurologic signs and the baseline, peak, and fold-change of bilirubin concentration (P < .001). The odds of having neurologic signs were 12.2 (95% CI, 3.1-48.2) for dogs with baseline bilirubin concentrations ≥3.3 mg/dL (≥57.5 μmol/L), and 93.3 (95% CI, 11.0-795.5) for dogs with peak bilirubin concentrations ≥13.9 mg/dL (≥239.5 μmol/L). CONCLUSIONS AND CLINICAL IMPORTANCE: Although the causation of the neurologic signs cannot be attributed solely to bilirubin based on our study, these findings emphasize the importance of monitoring serum bilirubin concentrations and the development of neurologic signs in dogs with IMHA. The results reflect findings in our study population and may not be directly applicable to all dogs with IMHA.

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kernicterusneurologicplasmapheresisprognosis

Identifiers

PMID41742491
PMCPMC12881973

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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.