Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia.
ABSTRACT 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.
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ABSTRACT: : Chronic diarrhoea is a frustrating problem in feline patients, as numerous underlying causes must be considered. In some patients, a specific diagnosis is established and targeted therapy can be provided. In many cases however, the diagnosis proves elusive or a poorly–defined disorder such as inflammatory bowel disease is established. In these cases, treatment decisions are more complicated and clinicians may select from many different therapies, either alone or in combination. This article reviews the common approaches to non-specific feline diarrhoea and discusses the applications, benefits and drawbacks of the various options available.Companion Animal. 03/2012; 17(2).
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ABSTRACT: Serum cobalamin concentration [CBL] suggests CBL deficiency in cats but serum methylmalonic acid concentration [MMA] more accurately indicates CBL deficiency. To examine the ability of [CBL] to predict CBL deficiency defined by increased [MMA], and relationships of [CBL] and [MMA] with select clinical and clinicopathological variables. One hundred sixty-three client-owned cats with [CBL] measurements, 114 cats with simultaneous [MMA] measurements; 88 cats with medical information. Prospectively collected [CBL] and [MMA] were compared using scatter plots, receiver operating characteristic and correlative analyses with historical [CBL] thresholds and those identified in the study. [CBL] and [MMA] were compared retrospectively to specific clinical and clinicopathological variables. [CBL] correlated negatively with [MMA] (τ = -0.334, P < .0001). [MMA] ≥ 1,343 nmol/L identified CBL deficiency. [CBL] = 209 pg/mL optimized sensitivity (0.51), specificity (0.96), PPV (0.89), and NPV (0.74) for detecting [MMA] ≥ 1,343 nmol/L. Prevalence of CBL deficiency was 42% (48/114) when defined by [MMA] ≥ 1,343 nmol/L versus 23% (27/114) by [CBL] ≤ 209 pg/mL. Unexpectedly, 23 and 45% of 48 cats with [MMA] ≥ 1,343 nmol/L had [CBL] > 900 pg/mL and 290 pg/mL (historical thresholds). [CBL] correlated with mean corpuscular volume (τ = -0.199, P = .013) and [MMA] with hematocrit (τ = -0.28, P = .006). Cobalamin deficiency ([MMA] ≥ 1,343 nmol/L) occurred in 42% of cats and is predicted with high specificity by [CBL] ≤ 209 pg/mL. CBL status correlates with microcytosis and anemia. Discordance between [CBL] and [MMA] cautions against relying on any single marker for determining CBL status.Journal of Veterinary Internal Medicine 07/2013; · 2.06 Impact Factor
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ABSTRACT: INTRODUCTION Diseases of the gastrointestinal tract are a common cause for dogs and cats to be presented to a veterinarian. In a recent study of new insurance claims for pets in the UK, 13.9% of new claims for dogs and 11.8% of all new claims for cats were related to gastrointestinal problems. 1 There are a wide variety of causes of clinical signs of gastrointestinal disease, such as vomiting, diarrhea, weight loss, and others. In order to arrive at the most appropriate diagnosis, veterinarians need to employ diagnostic tests. While no diagnostic test is always positive in a patient with a certain disease and no diagnostic test is always negative in a patient without the disease, the clinician needs to strive to use the tests with the highest clinical accuracy possible. In addition to a high accuracy, diagnostic tests should also be economical and as minimally invasive as possible. Folate is a water-soluble B-vitamin (vitamin B 9) that is plentiful in most commercial pet foods. However, folate in the diet is mostly supplied as folate polyglutamate, which cannot be readily absorbed. In the proximal small intestine folate polyglutamate is deconjugated by folate deconjugase and the resulting folate monoglutamate is absorbed by specific folate carriers in the proximal small intestine. In patients with proximal small intestinal disease, both folate deconjugase and folate carriers can be destroyed. If the disease process is severe enough either folate polyglutamate is no longer deconjugated or folate monoglutamate is no longer absorbed, leading to folate malabsorption. If the condition continues for a significant period of time, folate body stores are depleted and serum folate concentration decreases. The same is true in patients with diffuse small intestinal disease as long as the proximal small intestine is involved in the disease process. Many bacterial species synthesize folate and it is believed that an increased number of bacterial species (i.e., small intestinal bacterial overgrowth) can lead to significant increases in serum folate concentrations.