Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia.
Domestic cats with small intestinal disease may develop cobalamin deficiency because of reduced small intestinal uptake of this vitamin. This study assessed the impact of cobalamin deficiency on biochemical and clinical findings in cats with intestinal disease. Nineteen pet cats, all with severe hypocobalaminemia (< or =100 ng/L) and histories of gastrointestinal signs, were studied. Cats received cobalamin, 250 microg SC once weekly, for 4 weeks. Biochemical indices of cobalamin availability (e.g., serum methylmalonic acid, homocysteine, and cysteine concentrations), serum feline trypsinlike immunoreactivity (fTLI) and serum folate concentrations, and clinical findings were recorded at the start of the study and after 4 weeks of cobalamin therapy. Serum methylmalonic acid (MMA) concentrations (median; range) decreased after cobalamin supplementation (5373.0; 708.5-29,329.0 versus 423.5; 214.0-7219.0 nmol/L, P < .0001). Serum homocysteine concentrations were not significantly altered (mean +/- SD 8.2 +/- 2.9 versus 10.3 +/- 4.5 micromol/L, P = .1198), whereas cysteine concentrations increased significantly (122.3 +/- 38.8 versus 191.5 +/- 29.4 micromol/L, P < .0001). Mean body weight increased significantly after cobalamin therapy (3.8 +/- 1.1 versus 4.1 +/- 1 kg, P < .01), and the average body weight gain was 8.2%. Significant linear relationships were observed between alterations in serum MMA and fTLI concentrations and the percentage body weight change (P < .05 for both, Pearson r2 = 0.26 and 0.245, respectively). Mean serum folate concentration decreased significantly (mean +/- SD 19 +/- 5 microg/L versus 15.4 +/- 6.2 microg/L, P < .001). Reduced vomiting and diarrhea were observed in 7 of 9 and 5 of 13 cats, respectively. These results suggest that cobalamin supplementation in cats with small intestinal disease and severe hypocobalaminemia is associated with normalization of biochemical test results and improvements in clinical findings in most affected cats.
Ruaux
C G
CG
Gastrointestinal Laboratory, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843-4474, USA. cruaux@cvm.tamu.edu
Steiner
J M
JM
Williams
D A
DA
D000818:Animals; D016022:Case-Control Studies; D002371:Cat Diseases / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D002415:Cats; D005260:Female; D005767:Gastrointestinal Diseases / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology / Q000662:veterinary*; D008297:Male; D014805:Vitamin B 12 / Q000097:blood / Q000627:therapeutic use*; D014806:Vitamin B 12 Deficiency / Q000097:blood / Q000503:physiopathology / Q000662:veterinary*
D014805:Vitamin B 12