OBJECTIVE To evaluate the effects of storage conditions and duration on cobalamin concentration in serum samples from dogs and cats.
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.
Objective—To evaluate the use of high-resolution manometry (HRM) in awake and sedated dogs and to assess potential effects of a standard sedation protocol.
Procedures—An HRM catheter with 36 pressure sensors was inserted intranasally in each dog. After an adaption period of 5 minutes, each set of measurements included 5 swallows of a liquid and 5 swallows of a solid bolus. Measurements were repeated 30 minutes after IM administration of buprenorphine and acepromazine.
Results—HRM was successfully performed in 14 dogs. Data sets of 8 dogs were adequate for analysis. For the upper esophageal sphincter, median values of baseline pressure, residual pressure, relaxation time to nadir, and relaxation duration were determined for awake and sedated dogs for liquid and solid swallows. For the tubular portion of the esophagus, median values of peristaltic contractile integral, bolus transit time, and contractile front velocity were determined for awake and sedated dogs for liquid and solid swallows. For the lower esophageal sphincter, median values of baseline pressure and residual pressure were determined for awake and sedated dogs for liquid and solid swallows. Significant differences (awake vs sedated) were found for the upper esophageal sphincter residual pressure (liquid swallows), relaxation time to nadir (liquid swallows), bolus transit time (solid swallows), and contractile front velocity (solid swallows).
Conclusions and Clinical Relevance—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.
Objective—To characterize the ultrasonographic appearance of the canine esophagus.
Animals—14 healthy Beagles.
Procedures—Endoscopic ultrasonography (EUS) examinations were performed with a radial ultrasonographic gastrovideoscope in anesthetized dogs. Images were obtained at 3-cm intervals along the esophageal length to allow evaluation of the esophageal wall. Images were obtained with the probe in direct contact with the esophageal wall and with a water-filled balloon as a standoff.
Results—Images were obtained with (12 dogs) and without (10) the water-filled balloon. Median thickness of the esophageal wall was 2.19 mm (range, 1.03 to 5.62 mm) in the proximal third of the esophagus, 2.15 mm (range, 1.10 to 4.45 mm) in the middle third, and 2.84 mm (range, 1.35 to 5.92 mm) in the distal third. Wall thickness differed significantly between proximal and distal thirds. Results were similar when the water-filled balloon was used. Esophageal wall layers appeared as 5 alternating hyperechoic and hypoechoic bands that could not be consistently identified in all dogs. All layers could be identified in 26 of 198 (13%) images, 3 layers could be identified in 67 of 198 (34%) images, and 105 of 198 (53%) images had no layers. Visual identification of layers in images obtained with and without the balloon did not differ significantly.
Conclusions and Clinical Relevance—EUS appeared to be a useful technique for assessing esophageal wall integrity in dogs; however, complete evaluation of all layers could not be accomplished in all instances. Further studies with this technique in dogs are needed.
Objective—To investigate agreement of a feline pancreas–specific lipase assay and a colorimetric lipase assay with a 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) substrate with results of pancreatic ultrasonography in cats with suspicion of pancreatitis.
Design—Retrospective case series.
Animals—161 client-owned cats with suspicion of pancreatitis.
Procedures—Feline pancreas–specific lipase concentration and DGGR lipase activity were measured from the same blood sample in cats undergoing investigation for pancreatitis, with < 24 hours between ultrasonography and lipase determinations. Ultrasonographic variables evaluated were ultrasonographic diagnosis of pancreatitis, enlargement, margins, echogenicity, mesenteric echogenicity, peripancreatic free fluid, cysts, masses, and common bile and pancreatic duct dilation. Agreement was assessed by use of the Cohen κ coefficient.
Results—Agreement between the lipase assays was substantial (κ = 0.703). An ultrasonographic diagnosis of pancreatitis had fair agreement with feline pancreas–specific lipase concentration > 5.4 μg/L (κ = 0.264) and DGGR lipase activity > 26 U/L (κ = 0.221). The greatest agreement between feline pancreas–specific lipase concentration > 5.4 μg/L and DGGR lipase activity > 26 U/L was found for a hypoechoic and mixed-echoic (κ = 0.270 and 0.266, respectively), hypoechoic (κ = 0.261 and 0.181, respectively), and enlarged (κ = 0.218 and 0.223, respectively) pancreas.
Conclusions and Clinical Relevance—Agreement between pancreatic ultrasonography and lipase assay results was only fair. It remains unknown whether lipase results or pancreatic ultrasonography constitutes the more accurate test for diagnosing pancreatitis; therefore, results of both tests need to be interpreted with caution.
Objective—To evaluate the effects of cisapride and metoclopramide hydrochloride administered orally on the lower esophageal sphincter (LES) resting pressure in awake healthy dogs.
Animals—6 adult Beagles.
Procedures—Each dog was evaluated after administration of a single dose of cisapride (0.5 mg/kg), metoclopramide (0.5 mg/kg), or placebo (empty gelatin-free capsule) in 3 experiments performed at 3-week intervals. To measure LES pressure, a high-resolution manometry catheter equipped with 40 pressure sensors spaced 10 mm apart was used. For each experiment, LES pressure was recorded during a 20-minute period with a virtual electronic sleeve emulation before treatment (baseline) and at 1, 4, and 7 hours after drug or placebo administration. A linear mixed-effects model was used to test whether the 3 treatments affected LES pressure differently.
Results—In the cisapride, metoclopramide, and placebo experiments, median baseline LES pressures were 29.1, 30.5, and 29.0 mm Hg, respectively. For the cisapride, metoclopramide, and placebo treatments, median LES pressures at 1 hour after administration were 44.4, 37.8, and 36.6 mm Hg, respectively; median LES pressures at 4 hours after administration were 50.7, 30.6, and 31.1 mm Hg, respectively; and median LES pressures at 7 hours after administration were 44.3, 28.5, and 33.3 mm Hg, respectively. The LES pressures differed significantly only between the placebo and cisapride treatments.
Conclusions and Clinical Relevance—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.
Objective—To investigate the effects of twice-daily oral administration of hydrocortisone on the bile acids composition of gallbladder bile in dogs.
Animals—6 placebo-treated control dogs and 6 hydrocortisone-treated dogs.
Procedures—Dogs received hydrocortisone (median dose, 8.5 mg/kg) or a gelatin capsule (control group) orally every 12 hours for 84 days. Gallbladder bile samples were obtained via percutaneous ultrasound-guided cholecystocentesis from each dog before (day 0 [baseline]), during (days 28, 56, and 84), and after (days 28p, 56p, and 84p) treatment for differentiated quantification of unconjugated bile acids and taurine-conjugated and glycine-conjugated bile acids via high-performance liquid chromatography–tandem mass spectrometry.
Results—Treatment with hydrocortisone for 84 days resulted in significant and reversible increases in the concentrations of unconjugated bile acids (ie, cholic, chenodeoxycholic, and deoxycholic acids) and a significant and reversible decrease in the concentration of total taurine-conjugated bile acids, compared with baseline or control group values. Treatment with hydrocortisone had no effect on bile concentrations of glycine-conjugated bile acids.
Conclusions and Clinical Relevance—In dogs, hydrocortisone administration caused reversible shifts toward higher concentrations of the more hydrophobic unconjugated bile acids (chenodeoxycholic acid and deoxycholic acid) and toward lower concentrations of the amphipathic taurine-conjugated bile acids in gallbladder bile. These data suggest that similar bile acids changes could cause major alterations in gallbladder structure or function over time in hypercortisolemic dogs.
Objective—To determine reference ranges for serum cobalamin (Cbl), urine methylmalonic acid (uMMA), and plasma total homocysteine (tHcys) concentrations and to compare values for healthy control dogs with values for Border Collies (BCs), a breed in which hereditary cobalamin deficiency has been identified.
Animals—113 BCs, 35 healthy control dogs fed a typical diet, and 12 healthy dogs fed a bone and raw food diet exclusively.
Procedures—Urine and blood samples were obtained from each dog and Cbl, uMMA, and tHcys concentrations were determined.
Results—Reference ranges for Cbl (261 to 1,001 ng/L), uMMA (0 to 4.2 mmol/mol of creatinine), and tHcys (4.3 to 18.4 μmol/L) concentrations were determined. Four BCs had a Cbl concentration lower than the assay detection limit (150 ng/L); median uMMA and tHcys concentrations in these dogs were 4,064 mmol/mol of creatinine and 51.5 μmol/L, respectively. Clinical abnormalities included stunted growth, lethargy, anemia, and proteinuria. Abnormalities improved after administration of cobalamin. Of the 109 healthy BCs with Cbl and tHcys concentrations within reference ranges, 41 (37.6%) had a high uMMA concentration (range, 5 to 360 mmol/mol). Results for dogs fed raw food were similar to those for control dogs.
Conclusions and Clinical Relevance—Hereditary cobalamin deficiency is a rare disease with various clinical signs. The finding of methylmalonic aciduria in healthy eucobalaminemic BCs and BCs with clinical signs of Cbl deficiency was surprising and indicated these dogs may have defects in intracellular processing of Cbl or intestinal Cbl malabsorption, respectively. Studies investigating Cbl absorption and metabolic pathways are warranted.