Feline pancreatitis can be a very difficult disease to diagnose and often requires a combination of clinical suspicion, appropriate physical examination findings, elevations in serum feline pancreatic lipase immunoreactivity, and changes on abdominal ultrasonography consistent with pancreatic disease. The diagnostic difficulties encountered are related to a lack of specific and readily attributable clinical signs in cats. Serum lipase may be increased early in acute pancreatitis, but amylase and lipase were recently found to be of little diagnostic value in distinguishing normal cats from those with pancreatitis. Amylase is of no use in cats for the diagnosis of pancreatitis, partly because cats make very little amylase, and serum amylase levels are often low in cats with confirmed pancreatitis. Specific tests of GI and pancreatic function (e.g., cobalamin, folate) are very useful in the diagnosis of pancreatitis and in assessing the role of concurrent GI diseases in cats.

To provide a more accurate test of pancreatic inflammation, an enzyme-linked immunosorbent assay (ELISA) specific for pancreatic lipase immunoreactivity (PLI) was developed and validated in cats, and is the most reliable measurement of elevations in pancreatic lipase, a condition consistent with acute pancreatitis. In a recent study of cats with acute pancreatitis, the assay was highly sensitiveand specific (80% sensitivity in severe pancreatitis, 80% specificity). Overall, the sensitivity and specificity of the diagnosis of pancreatitis are highest when a combination of tests is utilized; but even when such tests are employed, the diagnosis is still problematic, especially in cats with chronic pancreatitis. Therapy is symptomatic and focuses on maintaining fluid volume, controlling pain and vomiting, preventing infection, and adjusting to changes in the cat's condition as they occur.

Reference: Zoran Dl, JAAHA 42:1-9, 2006.

A retrospective study of 91 dogs with pemphigus foliaceus was performed. The most commonly affected breeds were: mixed (40), Akita (10), Labrador retriever (9), cocker spaniel (5) and 3 each of German shepherd dog and Chinese shar pei, and 2 each of chow chow, Boston terrier, Shih tzu, and Australian cattle dog. Clinical signs of the disease included crusts (n=79), pustules (n=36), and alopecia (n=33). Lesions were most common on the trunk (n=53), inner pinnae (n=46), face (n=37), and foot pads (n=32). Cytological evaluation revealed acantholytic keratinocytes in 37 of 48 dogs. Results of combination treatment with prednisolone and azathioprine were comparable to results with prednisolone therapy alone. More than half of the dogs achieved remission with appropriate therapy, and another 25% significantly improved.

Of the 88 dogs treated for the disease, 46 went into remission with treatment, 31 improved greatly with treatment but still had mild focal lesions, and 11 were euthanized. Four dogs were euthanized because they had severe disease that did not respond to treatment. Two dogs were euthanized because of adverse effects from medications, and four were euthanized for other diseases or unrelated causes. In one dog, the reason for euthanasia was unknown.

The average time to remission for dogs that received prednisolone and azathioprine (n=33) was 11.7 mos (range 2-29 mos). There was no significant difference between time to remission for dogs treated with glucocorticoids alone and those treated with azathioprine and prednisolone. Adverse effects seen with combination therapy of prednisolone and azathioprine included iatrogenic hyper-adrenocorticism (n=13), hepatotoxicity (n=3), anemia (n=1), demodicosis (n=1), and gastrointestinal bleeding (n=1). Adverse effects occurred more often with this combination than with prednisolone alone. Eight dogs were initially treated with tetracycline and niacinamide, and the disease was controlled in three of them, although adverse effects were not seen with this therapy.

Reference: Mueller RS et al, JAAHA 42:189-196, 2006.