A Collaborative Effort to Fight Immune Thrombocytopenia

A Collaborative Effort to Fight Immune Thrombocytopenia

A collaborative effort is underway to improve our understanding and treatment of immune thrombocytopenia (ITP) in dogs. Thanks to funding from the Old English Sheepdog Club of America and the English Cocker Spaniel Club of America Health and Rescue Organization, canine health researchers at Cornell University and Iowa State University have been working to expand what we know about this deadly disease. With oversight through AKC Canine Health Foundation (CHF) Grant 02536-MOU: Immunoprofiling to Combat Canine Immune Thrombocytopenia, their research has explored the genetics that underlie this disease, examined biomarkers that help to predict disease severity, and suggested new treatment strategies.

In ITP, the immune system malfunctions and destroys platelets, the small blood cells that bind together and plug holes in damaged blood vessels. It is often diagnosed in middle-aged, female dogs. Any breed can be affected, but the disease is most common in mixed breeds, Cocker Spaniels, Poodles, and Old English Sheepdogs. Clinical signs of ITP include spontaneous bruising, bleeding, decreased energy, decreased appetite, pale gums, fever, rapid breathing, and anemia. Seventy to ninety percent of dogs will recover, but relapses are common and up to 30 percent of affected dogs will not survive. Treatment involves the long-term use of drugs that suppress the immune system.

As part of this research, investigators developed a test to measure anti-platelet antibody concentrations in dogs. These molecules attack and coat platelets, setting them up for destruction by the immune system. Measuring them in the bloodstream may aid in diagnosis and provide a more accurate picture of disease severity.

Investigators also described a suite of test results and clinical findings that more accurately identify dogs with primary ITP, a form of the disease where no underlying or inciting cause is known, or more severe ITP. This will provide a more accurate prognosis and help to guide treatment decisions for affected dogs. Aggressive therapies can be started earlier for dogs with severe disease, while the side effects of long-term immunosuppressive therapy can be limited in dogs with milder disease.

The latest findings from this collaborative research provide even more information on how ITP develops in dogs. The primary mechanism of this disease is increased platelet destruction. However, in humans, decreased platelet production also contributes to low platelet levels. Could the same be true in dogs?

Thrombopoietin (TPO) is a hormone produced in the liver that regulates platelet production. Since canine TPO molecules differ enough from human TPO, existing human testing methods will not accurately measure TPO levels in dogs. CHF-funded investigators developed a dog-specific test to measure canine TPO levels in the blood and used it to explore the role of TPO in canine ITP. If platelets are being destroyed, TPO should be elevated, signaling the bone marrow to make more of them. However, dogs with ITP in this study had unexpectedly low TPO levels. This suggests that ineffective platelet production may also contribute to low platelet levels in affected dogs.

The good news is that drugs that bind to TPO receptors and increase platelet production are being used to successfully treat ITP in humans. This opens a new avenue for future studies to explore their use in veterinary medicine, providing another treatment option for dogs with ITP.

Thanks to the collaborative passion and dedication of these dog clubs and CHF-funded investigators, we have significantly increased our understanding of the disease mechanisms involved in canine ITP. Clinicians can now provide a more accurate prognosis, start more aggressive therapy if needed, and may have a whole new treatment approach to help affected dogs make and maintain adequate platelets. All of this means healthier, longer lives for dogs. Learn more about this important research at: akcchf.org/bloodRPA.