Routine laboratory results may be normal. Panhypoproteinemia, hypoalbuminemia or hypergammaglobulinemia can be found in moderate to more severe cases. Liver enzymes may be elevated due to GI tract flora and toxins entering the portal venous circulation, from immune-mediated liver disease, or from ascending cholangiohepatitis secondary to small intestine bacterial overgrowth (SIBO) and changes in GI motility. Eosinophilia may be present, but leukocytosis is not typical, and if found, would be suggestive of a significant bowel inflammatory response or fungal infection. With GI hemorrhage, anemia may be seen.

Chronic GI hemorrhage results in microcytic, hypochromic anemia from iron deficiency. Other laboratory tests that are important to consider in animals with GI signs include: fecal tests (fecal flotation, direct smear, giardia screen (ELISA) method, Clostridium perfringens enterotoxin, and FA for cryptosporidiosis); serum thyroid profile (especially in cats); FeLV and FIV screen; FIP-specific ELISA (FIPSE, if the "dry" form of FIP is suspected); toxoplasma titers; serum cobalamin/folate levels (significance of SIBO is questionable in cats); and fasting trypsin-like immunoreactivity (TLI) levels. In feline, but not canine IBD patients, the TLI is often elevated, as it is in canine and feline pancreatitis.

In certain locations, screening for histoplasmosis or other fungi may be indicated. In canines, consider an ACTH stimulation test to rule-out Addison's disease. Lead poisoning is another possible cause of chronic GI signs. With hypoalbuminemia, determining pre- and post-prandial bile acids and urine protein:creatinine ratio can be helpful. Radiographs may be normal. A barium series also may be normal or reveal mucosal irregularity and narrowed dye columns or strictures. Ultrasound examination may be unremarkable or reveal thickened bowel loops. Marked lymphadenopathy with hepatomegaly and/or splenomegaly should raise suspicions of lymphosarcoma, mastocytosis or hypereosinophilic syndrome in cats. Fine needle aspirate cytology of the liver, spleen and/or lymph nodes may provide a diagnosis (fungal or neoplasia).

A diagnosis of IBD is confirmed by intestinal biopsy. Multiple sites of the GI tract should be biopsied, even if the intestine looks grossly normal.

Management of IBD varies widely. Lasting remission (oral tolerance) cannot be regained until the memory of GI hypersensitivity is lost. For "primed" circulating immunoglobulins, at least one month without ongoing antigenic stimulation is necessary for that stimulus to wane. When T-lymphocytes are involved, at least three months are required for immune stimulation to wane.

Dietary management and drug therapy are the hallmarks of therapy. Feeding "novel" and/or a highly digestible protein source is recommended (i.e. elimination diet). "Bulking" agents are an adjunct therapy for colitis; various fiber sources, including sweet potatoes, yams or canned pumpkin sometimes produce good clinical results. Empirical use of immunosuppressive drugs and prednisolone without performing GI tract biopsies is generally not advisable. Misdiagnosis could lead to disastrous consequences as well as alter the appearance of histopathological biopsies done at a later time. Prednisolone (in decreasing dosages), metronidazole (antiprotozoal, inhibits cell-mediated immunity, treats SIBO), azathioprine, sulfasalazine (large bowel diarrhea only), and chlorambucil have been utilized to control confirmed cases of IBD. Depending on the severity of the lesions, different protocols and drug dosages are recommended. Judicious use of motility modifiers also can be beneficial.

Prognosis is good for most patients except those with severe mucosal distortion and fibrosis, eosinophilic enteritis/hypereosinophilic syndrome of cats, and granulomatous IBD. Treatment failures may reflect misdiagnosis, poor client compliance, and lack of perserverance with treatment regimens.