BackgroundAlthough gastroesophageal reflux (GER) often is assumed to be causative for upper gastrointestinal and respiratory signs in dogs, no attempts have been made to verify this assumption.ObjectivesTo monitor esophageal pH with the Bravo pH system in healthy dogs and client‐owned dogs displaying signs commonly attributed to GER.AnimalsSeven healthy and 22 client‐owned dogs.MethodsAfter routine esophagogastroduodenoscopy, radiotelemetric pH capsules were placed in distal esophagus for continuous pH recording. Reflux was defined as single pH measurement <4. At discharge, owners were instructed to press individually predefined clinical sign‐buttons on the receiver whenever indicated. Results between groups were compared using Mann–Whitney U‐test.ResultsThe median (range) number of refluxes in client‐owned and healthy dogs, respectively, was 17 (1–205) and 10 (1–65), the number of refluxes >5 minutes in duration was 1 (0–14), and 1 (0–4), duration of longest reflux (min) was 10 (0–65) and 8 (0–27), and fractional time pH <4 (%) was 0.76% (0.01–6.28), and 0.3% (0–3.1). No differences were found between groups. The median of 7 (1–35) clinical sign‐button pushes were recorded in 21 dogs. Median of 12.5% (2.8% [1/35]–50% [2/4]) reflux‐positive clinical sign‐button pushes was found in 10 dogs with reflux‐positive pushes. Five (22.7%) dogs had increased esophageal acid exposure, and mild esophagitis was noted in 1 dog.Conclusion and Clinical ImportanceDespite evidence of increased GER in some dogs, the clinical sign‐reflux association remained poor. Future investigation should focus on dogs with esophagitis.

Results suggested that orally administered cisapride may be of benefit in canine patients for which an increase in LES pressure is desirable, whereas orally administered metoclopramide did not affect LES resting pressures in dogs.

HRM was feasible for evaluation of esophageal function in most awake dogs. Although sedation in uncooperative patients may minimally influence results of some variables, an overall assessment of swallowing should be possible.

BackgroundEffects and duration of commonly used protocols for cobalamin (Cbl) supplementation on cellular Cbl deficiency have not been determined in hypocobalaminemic cats.Hypothesis/ObjectivesTo evaluate effect of Cbl supplementation on clinical signs, serum and urine methylmalonic acid (MMA) concentrations over 16 weeks.AnimalsTwenty client‐owned hypocobalaminemic cats with enteropathy.MethodsProspective study. Serum Cbl and serum and urine MMA concentrations were determined prospectively in cats at enrollment (t0), immediately before (t6), and 4 (t10) and 10 weeks (t16) after 6th Cbl injection (250 μg, IM q 7 days). Clinical signs severity (activity, appetite, vomiting, diarrhea, body weight) graded at each time point and expressed as clinical disease activity score.ResultsClinical disease activity score decreased during supplementation and increased after treatment discontinuation. Median serum Cbl concentration increased significantly from t0 (111 pmol/L, range 111–212) to t6 (2,332.5 pmol/L, range 123–22,730) (P < 0.01). Values at t10 were 610.5 pmol/L (range, 111–2,527) and 180.5 pmol/L (range, 111–2,262) at t16 (P < 0.01). Median baseline serum MMA concentration (372 μmol/L, range 0.39–147,000) decreased significantly to 1.62 μmol/L (range, 0.18–806) at t6 (P < 0.01) and gradually increased to 5.34 μmol/L (range, 0.13–1,730) at t10 and 189 μmol/L (range, 0.4–983) at t16. Similar, nonsignificant, pattern observed for urine MMA concentration. Serum and urine MMA concentrations had not normalized in 12 and 6 cats, respectively, at t6.Conclusion and Clinical ImportanceThe Cbl supplementation protocol used here did not lead to complete normalization of cellular Cbl deficiency in all examined cats, and biochemical improvements were transient.

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OBJECTIVE To evaluate the effects of storage conditions and duration on cobalamin concentration in serum samples from dogs and cats. DESIGN Experiment. SAMPLE Serum samples from 9 client-owned cats and 9 client-owned dogs. PROCEDURES Serum harvested from freshly obtained blood samples was separated into 11 aliquots/animal. One aliquot (baseline sample) was routinely transported in light-protected tubes to the laboratory for cobalamin assay; each of the remaining aliquots was stored in a refrigerator (6°C; n = 5) or at room temperature (20°C) with exposure to daylight (5) for 24, 48, 72, 96, or 120 hours. Aliquots were subsequently wrapped in aluminum foil, frozen (-20°C), and then transported to the laboratory for measurement of cobalamin concentration, all in the same run. Percentage decrease in cobalamin concentration from baseline was analyzed by means of linear mixed modeling. RESULTS No differences in cobalamin values were identified between cats and dogs; therefore, data for both species were analyzed together. Median baseline serum cobalamin concentration was 424 ng/L (range, 178 to 1,880 ng/L). Values for serum samples stored with daylight exposure at room temperature were significantly lower over time than were values for refrigerated samples. Although values for refrigerated samples did not decrease significantly from baseline values over time, values for the other storage condition did; however, the mean percentage decrease for serum samples stored at room temperature was small (0.14%/h; 95% confidence interval, 0.07% to 0.21%/h). CONCLUSIONS AND CLINICAL RELEVANCE Overall, serum cobalamin concentration appeared stable for 5 days when feline and canine serum samples were refrigerated at 6°C. The effect of light and room temperature on serum cobalamin concentration, although significant, was quite small for samples stored with these exposures for the same 5-day period.

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ZusammenfassungBei einer 7-jährigen männlich-kastrierten Europäisch-Kurzhaar-Katze, vorgestellt aufgrund von akut reduziertem Allgemeinbefinden und einer vestibulären Ataxie, wurde die Diagnose Polycythaemia vera gestellt. Im weiteren Verlauf zeigte die Katze intermittierend orofaziale Zuckungen, Aggressivität, Speicheln, Kreiswandern und Kopfschiefhaltung. Bei der weiterführenden Diagnostik mittels Magnetresonanztomografie ließen sich Veränderungen im Bereich des Hippocampus nachweisen, die mit einer Hippocampussklerose vereinbar waren. Der Fallbericht beschreibt zum einen die klinischen und hämatologischen Befunde einer Polyzythämie und den Krankheitsverlauf während der Therapie. Zum anderen wird der Zusammenhang zur Hippocampusveränderung diskutiert. Diese könnte sekundär zu einer durch die Polyzythämie verursachten zerebralen Hypoperfusion entstanden sein.