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53 NOVEMBER/DECEMBER 2017 ■ TVPJOURNAL.COM CONTINUING EDUCATION also can be seen in normal cats or those with IBD. 27 Additionally, loss of intestinal wall layering, mass- like lesions, and/or reduced wall echogenicity have been associated with lymphoblastic lymphoma. 27 Markers of Dysbiosis, Vitamin Deficiency, and Pancreatic Inflammation Hypocobalaminemia is present in 61% of cats with primary GI disease, 28 and vomiting has been reported as the only clinical sign in some cats with hypocobalaminemia. 29 Hypocobalaminemia also has been reported in cats with extragastrointestinal disease, such as hepatitis and hyperthyroidism. 27,30,31 It is important that cobalamin deficiency be detected and addressed because failure to do so can result in persistence of clinical signs despite treatment of the primary disease. 27 Some cats have been diagnosed with clinical cobalamin deficiency based on the presence of increased methylmalonic acid concentrations without hypocobalaminemia. 28 Consequently, supplementation should be considered for cats with values in the low end of the reference range. Folate is absorbed in the proximal small intestine only. Elevated serum folate concentrations can be secondary to small intestinal bacterial overgrowth (resulting from GI disease or dysbiosis) or coprophagia (feces have high folate concentrations). 32 Decreased serum folate concentrations can be secondary to focal proximal or diffuse small intestinal disease, but they also have been noted in cases of pancreatitis or cholangiohepatitis. 27 Low serum folate concentrations also can be seen in clinically healthy cats. 27 Concurrent low cobalamin and folate concentrations have been associated with severe diffuse GI disease. 33 Some patients with high serum folate and low cobalamin concentrations experience normalization of folate concentrations after cobalamin supplementation. 29 Reevaluation of folate concentration after correction of hypocobalaminemia might, therefore, be prudent in some cases. Exocrine pancreatic disease can be divided into exocrine pancreatic insufficiency (EPI) and pancreatitis. EPI is diagnosed based on decreased serum trypsin- like immunoreactivity concentration. Although feline EPI historically has been considered rare, the apparently low prevalence could reflect inadequate surveillance for the disease, according to a recent report. 34 Clinical signs in cats with EPI in that report included poor body condition, weight loss, loose stools or diarrhea, and polyphagia, but also lethargy, anorexia, and vomiting. The study found a high frequency of low cobalamin and high folate concentrations. Elevated trypsin-like immunoreactivity also can be seen in cats with small intestinal disease, pancreatitis, and kidney failure. Sensitivities (42% to 80%) and specificities (63% to 100%) of the validated lipase assays for pancreatitis vary dramatically, depending on the criteria for diagnosis (histologic inflammation, clinical signs and ultrasonographic changes, or some combination thereof ). 35–38 A semiquantitative point-of-care feline pancreatic-specific lipase test is available, but its sensitivity, specificity, and accuracy have not been independently validated. None of the biomarkers for pancreatic inflammation are a substitute for clinical judgment, and clinical signs and other diagnostic test results should be integrated into the diagnosis of feline pancreatitis. Urine Histoplasma Antigen Histoplasma urine antigen concentration ( miravistalabs.com ) should be quantitated in cases with appropriate clinical history and exposure, laboratory findings, and abdominal imaging changes. Histoplasma infections primarily occur in the Ohio River Valley and southeastern United States. The assay has good sensitivity (94.4%), although negative test results do not rule out infection. 39 Cross-reactivity with other systemic infectious agents is possible. 39 Helicobacter Species Testing Helicobacter species have been identified in biopsy specimens from both clinically ill and healthy cats. 40–44 Prevalence increases with age, 43 although the organisms have been noted in animals as young as 6 weeks. 45 Because of the high prevalence of Helicobacter species within healthy populations, treatment is generally withheld unless concurrent histopathologic abnormalities have been identified and other causes of gastritis have been ruled out. 45 Treatment consists of multimodal antibiotics with or without gastric acid suppression. 45–47 WHEN TO RECOMMEND ENDOSCOPY Direct evaluation of the GI tract should be considered when the preceding testing does not reveal a systemic cause for vomiting and diet trials have failed or the cat has evidence of focal disease that warrants focused