A small French study found the inflammation marker helped separate some causes of breathing trouble in cats. A larger German study found it could not clearly tell respiratory conditions apart.
Can a blood test for inflammation help sort out what is behind respiratory disease in a cat? Two studies published in 2026 asked that question about serum amyloid A (SAA), the major acute-phase protein in cats. The 2 research teams came away with different answers.1,2
In the Journal of Small Animal Practice, a team at Centre Hospitalier Vétérinaire AniCura Nordvet in La Madeleine, France, reported that SAA was significantly higher in cats with inflammatory lower respiratory tract disease than in cats with cardiac or neoplastic respiratory disease.1 In Frontiers in Veterinary Science, a team at Ludwig-Maximilians-University of Munich in Germany concluded that SAA and haptoglobin cannot be used to clearly distinguish between different respiratory diseases in cats.2
Eva Berro, DVM, an internal medicine resident at the French hospital, conducted the study with Aline Fastrès, DVM, PhD, DipECVIM-CA, and Anaïs Lamoureux, DVM, DipECVIM-CA, both internal medicine specialists at AniCura Nordvet. The team went back through the records of cats seen in the hospital's emergency unit for respiratory distress between October 2021 and December 2024.1 The study included 22 cats that had SAA measured within 48 hours after admission.1
Two board-certified internal medicine specialists sorted the cats into 2 groups without knowing the SAA results.1 The inflammatory group had 15 cats: 7 with aspiration pneumonia, 7 with feline lower airway disease and 1 with pulmonary toxoplasmosis. The cardiac/neoplastic group had 7 cats: 3 with left-sided congestive heart failure (CHF) and 4 with neoplastic disease.1
Median SAA was 57.5 μg/mL in the inflammatory group and 5 μg/mL in the cardiac/neoplastic group.1 The assay could not measure below 5 μg/mL, so any lower result was recorded as 5 μg/mL.1 The best cutoff for telling the 2 groups apart was 8.6 μg/mL, which had a sensitivity of 80% and a specificity of 100%.1
Berro and colleagues wrote that SAA may have potential as a supportive tool for quickly separating inflammatory lower respiratory tract disease from cardiac or neoplastic respiratory disease.1 The French team also urged restraint. The results “should be interpreted with caution given the small sample size,” the authors wrote, and the proposed cutoff cannot yet serve as a definitive rule-out threshold.1
Hannah Gareis, DVM, Dr med vet, and Bianka Schulz, Dr med vet, DipECVIM-CA, tested serum from 102 cats with respiratory signs and 20 healthy control cats.2 The diseased cats fell into 5 groups: feline lower airway disease (n = 26), infectious lower airway or pleural space disease (n = 12), neoplastic lower airway or pleural space disease (n = 17), CHF (n = 29) and upper airway disease (n = 18).2
Only 1 comparison between disease groups stood out. Median SAA was significantly higher in cats with infectious lower airway or pleural space disease (2.61 μg/mL) than in cats with feline lower airway disease (0.14 μg/mL).2 SAA did not differ significantly between any other disease groups or between diseased and healthy cats. The median in every group was within the laboratory reference range of less than 6.7 μg/mL.2
Even within the infectious group, the picture was mixed. The higher SAA values were mainly in cats with pyothorax. Most cats with other infections had values within the reference range.2 In the neoplastic group, the 3 cats with SAA values above 15 μg/mL all had pleural effusion secondary to intrathoracic neoplasia.2
Gareis and Schulz wrote that a normal SAA value does not rule out an infectious cause and that SAA “should be used as supporting diagnostic information only.”2
The 2 studies were set up differently in several ways.
The test. The French team ran SAA in-house on fresh serum with a feline-specific immunofluorescence assay. Berro and colleagues noted that peer-reviewed validation data for the in-house assay are lacking.1 The German team sent samples to an external laboratory for an immunoturbidimetric assay.2
The groups. The French inflammatory group mixed infectious and noninfectious disease. Berro and colleagues wrote that the retrospective data did not allow the 2 to be separated.1 The German study did separate the 2, which is where its only significant SAA difference between disease groups appeared.2
The patients. Every French cat was in respiratory distress.1 In the German study, 71 of 102 cats were. The German cats in respiratory distress had significantly higher SAA than the German cats without it, although both medians were within the reference range.2
The timing. SAA was measured right at admission in 17 of the 22 French cats. The other 5 were tested within the following 48 hours, after receiving drugs.1 The German cats were sampled at initial presentation before treatment. Gareis and Schulz noted that many cats were likely not sampled at the peak of the acute-phase response.2
Survival. The French study found no significant difference in SAA between cats that survived to discharge and cats that died.1 In the German study, cats that died or were euthanized had significantly higher SAA at admission than survivors. Gareis and Schulz cautioned against using acute-phase proteins for prognosis.2
The studies also touch on heart failure. Berro and colleagues wrote that normal SAA in the cats with cardiac disease could be explained by SAA being a marker of acute rather than chronic inflammation and by the small number of cardiac cases in the study.1 In the German study, median SAA in cats with CHF was 0.70 μg/mL, within the reference range.2 A 2020 study in the Journal of Veterinary Internal Medicine reported significantly higher SAA in cats with CHF caused by primary cardiomyopathy than in cats with preclinical cardiomyopathy or healthy control cats.3
On one point, the French and German teams agree: larger prospective studies are needed.1,2
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