Therapeutics
Specific therapy is directed at the underlying cause. Bilious vomiting syndrome, is usually managed by feeding the dog late at night and a combination of prokinetics and H2- blockers (Webb and Twedt 2003).
Gastric parasites are treated with tetramisole (2.5% formulation at 5 mg/kg) or fenbendazole (10 mg/kg, orally for two days) for Ollulanus tricuspis infections, and pyrantel pamoate (15 mg/kg orally and repeated twice every 2-3 weeks) for Physaloptera spp infections. Gastroscopic removal of the adult worm in the case of Physaloptera infection is also recommended. Recurrence of Physaloptera- infection is likely if paratenic hosts are ingested. A combination of aggressive surgical resection with 3-4 cm margins and prolonged antifungal therapy (itraconzaole at 10 mg/kg, orally, once daily or terbinafine, 5-10 mg/kg orally once daily) is indicated for treating gastrointestinal pythiosis (Grooters and Foil 2012). Serology can be used to monitor for recurrence, starting at 2-3 months postoperatively.Supportive care for chronic gastritis includes antacid therapy, including H2-block- ers, proton-pump inhibitors, and the mucosal binder, sucralfate, which are often used empirically. H2-blockers like famotidine are favored due to ease of dosing, where administering the drug with food improves bioavailability in contrast to omeprazole, which requires dosing on an empty stomach. Omeprazole is, however, considered to be superior. There is strong evidence to demonstrate that sucralfate binds to gastrointestinal mucosa in cats (Clark et al. 1987). Whether these drugs should be dosed empirically in gastritis in cats or dogs remains to be elucidated, considering that many forms of chronic gastritis do not manifest in gastric ulceration or erosions and in some instances actually atrophic gastritis is associated with achlorhydria and luminal alkalosis.
It is certainly warranted in cases of hematemesis, and ultrasonographic or endoscopic evidence of ulcers.Most of the therapeutic guidelines for treating HLO in companion animals are extrapolated from the American National Institutes of Health. No therapy is recommended for asymptomatic humans. Treatment in dogs and cats has had mixed success. An uncontrolled treatment trial reported >90% improvement of clinical signs in dogs and cats treated with amoxicillin, metronidazole, and famotidine with confirmed colonization of HLO and 74% of the dogs and cats re-biopsied were free of colonization after treatment (DeNovo and Magne 1995). Amoxicillin, metronidazole, and bismuth subsalicylate, with or without famotidine therapy for 14 days, resolved clinical signs of all dogs that had HLO colonization (Leib, Duncan, and Ward 2007). Eradication of HLO was also associated with improved gastritis on histopathology (Leib et al. 2007). There are studies that demonstrate antibiotics suppress colonization but are not effective in long-term elimination (Leib et al. 2007; Jergens et al. 2009; Simpson et al. 1999; Simpson et al. 2000).
After exclusion of potential causes of chronic gastritis a diagnosis of idiopathic chronic gastritis is made and immunosuppressive therapy is warranted. Prednisolone, at 1-2 mg/kg dosed orally, BID for 1-2 weeks followed by reducing the doses over 2-3 months. Steroid sparing drugs, or drugs that will substitute steroid use as they are contraindicated for example diabetes mellitus or gastric ulceration include azathioprine in the dog, and chlorambucil in the cat. Azathioprine, which is usually more effective when dosed together with prednisolone, is started at 2 mg/kg, orally, OID, for 7 days then dosed every other day, with hematology and biochemistry to monitor for potential side-effects of neutropenia or hepatotoxicity (Richter 2014). Azathioprine is extremely myelotoxic in cats. Chlorambucil is a good choice for cats and is combined with prednisolone, which is started at a dose at 5-10 mg per cat, OID.
The identical chlorambucil protocol used in feline gastrointestinal lymphoma is employed (Richter 2014), dosed either at a high pulse dose at 15mg∕m2 of body weight, orally daily for 4 days, which is repeated every 3 weeks or 20 mg∕m2 of body weight every 2 weeks or low dose high frequency, at 2 mg per cat daily. Side effects include vomiting, diarrhea, anorexia, and lethargy.Standard medical therapy for hypertrophic gastritis includes antacids and H2-blockers and proton-pump inhibitors. Once again, the role of proton pump inhibitors is controversial since it causes hypergastrinemia, which is proposed as part of the etiopathogenesis of acquired antral pyloric hypertrophy and hyperplastic gastritis. Considering the potential complications of Menetrier's disease (gastric carcinoma), it may be worth considering the use of tyrosine kinase inhibitors in these patients. In medical refractory cases, partial gastrectomy is justified (Lecoindre et al. 2012). Most cases of acquired antral pyloric hypertrophy have resolved clinical signs after surgical resection of the outflow obstruction.
Due to the differences in pathology noted between the human and the canine and feline form of uremic gastropathy, often with the lack of identifiable gastric ulceration and hemorrhage in small animal patients, there is no evidence to support the empirical use of antacid therapy. In fact, it is speculated that many of these patients would have increased intra- gastric pH due to glandular atrophy (Peters et al. 2005). Cats, which have fibrosis and mineralization with atrophic non-inflammatory gastropathy therapy should focus on addressing the uremic toxin phosphate, with phosphate binders and phosphate-restricted diet.