Page 585 - Clinical Small Animal Internal Medicine

51 Gastritis and Gastric Ulceration in Dogs and Cats 553

ulcerative lesions in dogs. Gastrointestinal disease sec- nosed by endoscopic visualization and histopathology).
VetBooks.ir ondary to infectious etiologies often requires histopatho- Evidence of protein‐losing enteropathy is variably
present on bloodwork. It has been hypothesized that
logic or immunohistochemical identification of the
organism. Helicobacter‐associated gastritis in cats and
carcinoma as a result of chronic, severe gastritis.
dogs is definitively diagnosed by identification of the this syndrome can also lead to development of gastric
organism in gastric biopsies using fluorescence in situ
hybridization (FISH) or polymerase chain reaction
(PCR). Increased tissue urease activity and positive urea
breath tests have been correlated with the presence of Treatment of Gastritis and Gastric
Helicobacter, but are also identified in the presence of Ulceration
other urease‐producing bacteria and thus lack specific-
ity. Special staining methods (Steiner staining) and The best course of therapy for animals with gastritis or
immunohistochemistry methods can aid in species gastric ulceration is removal of the offending agent, if
differentiation. possible, and amelioration of mucosal injury. Specific
Gastritis and/or gastric ulceration secondary to gastric therapies will depend on the identified cause (e.g., azole
neoplasms (carcinomas, lymphoma, mast cell tumors) or treatment for Histoplasma infection, chemotherapy/
gastrinomas can be identified via histopathologic surgery for neoplasia).
examination of tissue (e.g., stomach, pancreas) biopsies. Nonspecific, supportive treatment for animals with
Serum gastrin measurement provides a noninvasive test gastritis and vomiting should begin with restoration of
when gastrinoma is suspected. Marked hypergastrine- fluid deficits and normalization of electrolyte imbal-
mia in the presence of gastroduodenal ulceration is sug- ances, if present. A list of commonly used medications
gestive of a pancreatic gastrinoma. Thus, a serum gastrin for gastritis and gastric ulceration is provided in
measurement should be performed in any patient pre- Table 51.3.
senting for chronic gastritis and gastroduodenal ulcera- Acid suppressants (e.g., histamine‐2 receptor antago-
tion where other systemic diseases are eliminated as nists [H 2 RAs] and proton pump inhibitors [PPIs]) are
causes. Serum gastrin concentration should be inter- recommended in vomiting animals with clinical signs of
preted cautiously in the face of acid suppressant treat- vomiting‐induced esophagitis but should not be used
ment, which can result in increased serum gastrin prophylactically. H 2 RAs are competitive inhibitors for
concentrations. the interaction of histamine with its receptor on the gas-
tric parietal cell but differ in potency (famotidine > ran-
itidine > cimetidine). In contrast, PPIs (e.g., omeprazole,
Ancillary Diagnostic Testing in Gastric pantoprazole, esomeprazole) are inactivators of the pro-
Disease Patients
ton pump and are more effective than H 2 RAs in raising
Testing for the presence of bacterial enteropathogens both feline and canine intragastric pH. Thus, PPIs,
such as E. coli, Clostridium, Campylobacter and administered twice-daily, are considered the treatment
Salmonella spp. might be considered as an ancillary of choice when concern for acid‐induced tissue injury
diagnostic test for dogs presenting with fever, acute hem- exists. Preliminary evidence suggests that PPIs are more
orrhagic diarrhea, and vomiting. However, results should effective when given alone than in combination with
be interpreted with caution, as these organisms have H 2 RAs in dogs for the treatment of upper GI ulceration.
been isolated from the feces of healthy dogs and cats. Antiemetics (e.g., 5‐HT 3 and neurokinin receptor antag-
In cases where there is a high suspicion of gastrointes- onists) may be administered to vomiting animals once
tinal mycosis or oomycete disease, multiple diagnostics mechanical obstruction has been ruled out as a cause of
are available for antemortem diagnosis. Pythium testing the clinical signs.
includes serology, enzyme‐linked immunosorbent assay Cytoprotective agents (e.g., sucralfate) can be given,
(ELISA), PCR or immunohistochemistry (IHC) of once vomiting is controlled, if there is evidence or sus-
infected tissues or blood. A quantitative urine antigen picion of gastrointestinal bleeding. Sucralfate is most
enzyme immunoassay is available for Histoplasma effective at an acidic pH and can interfere with appro-
detection. Pyogranulomatous lesions and visualization priate absorption of pH‐dependent drugs. Thus,
of fungal organisms can be noted in biopsies obtained sucralfate should be administered as a slurry at least
from dogs with fungal gastritis within the liver, spleen, 1–2 hours before or after administration of meals and
lymph nodes, or gastrointestinal tract. If present, biopsies other medications. The PGE 1 analog misoprostol is
of cutaneous lesions should be submitted for histopa- indicated for use in NSAID‐induced toxicoses but does
thology and fungal culture. Gastritis in the Norwegian not promote healing in non‐NSAID‐induced causes of
lundehund is often secondary to lymphangiectasia (diag- GI ulceration.