# A Case of Canine Hepatitis with Hepatocellular Attack by Non-Neoplastic Perforin-Laden Lymphocytes

## TL;DR

A dog with chronic hepatitis showed signs of an autoimmune attack on the liver, similar to human autoimmune hepatitis, but with a different immune cell pattern.

## Contribution

The study presents a canine case of chronic hepatitis with evidence of T-cell-mediated hepatocellular damage, suggesting an autoimmune mechanism.

## Key findings

- Liver biopsy showed infiltration of CD3-positive, perforin-containing T lymphocytes causing hepatocellular apoptosis.
- Immunosuppressive therapy improved some blood parameters but did not normalize liver enzymes.
- The dog's death 11 months later supports the role of autoimmune mechanisms in canine chronic hepatitis.

## Abstract

The cause of canine chronic hepatitis (CH) remains unknown, but an autoimmune basis is suspected in some cases. An 11-year-old spayed female Norwich Terrier presented with elevated liver enzymes, hyperbilirubinemia, regenerative anemia, and thrombocytopenia. Bacterial cultures of liver tissue and bile were negative. Liver histology resembled human autoimmune hepatitis, except for a lack of plasma cells. Immunohistochemistry revealed the infiltration of CD3-positive, perforin-containing T lymphocytes, causing hepatocellular apoptosis, suggesting an autoimmune attack. Treatment with prednisolone and cyclosporine improved the dog’s overall condition, normalizing platelet and total bilirubin levels, though liver enzymes remained elevated. The dog died 11 months after starting treatment. These findings suggest that an autoimmune mechanism may contribute to canine CH.

The etiology of canine chronic hepatitis (CH) is unknown, although an autoimmune background has been suggested in some cases of canine CH. An 11 y old spayed female Norwich Terrier showed a marked elevation of liver enzymes with hyperbilirubinemia, regenerative anemia, and thrombocytopenia. A bacterial culture of the surgically excised liver tissue and bile was negative. The histological features of the liver biopsy resembled those of human autoimmune hepatitis except for a paucity of intralesional plasma cells. It was established through immunohistochemistry that CD3-positive perforin-containing T lymphocytes had actively infiltrated the patient’s liver causing hepatocellular apoptosis, implying an autoimmune attack on hepatocytes. The patient’s general condition improved, with normalization of platelet and serum total bilirubin levels, after immunosuppressive therapy with prednisolone and cyclosporine, whereas liver enzymes did not reach the reference interval. The dog died 11 months after the initiation of immunosuppressive therapy. These pathological findings may be one aspect of autoimmune mediation in canine CH.