Prevalence and clinical relevance of hypercobalaminaemia in dogs and cats.

Hypocobalaminaemia is common in dogs and cats with exocrine pancreatic insufficiency and/or chronic enteropathy. While hypocobalaminaemia has been extensively studied, naturally-occurring serum hypercobalaminaemia (i.e. without supplementation) might be an underestimated finding in small animal medicine. Studies in human medicine have associated hypercobalaminaemia with neoplastic, hepatic and renal disease. Medical records of all dogs and cats with serum cobalamin concentration measurements (2007-2019) were retrospectively analysed; any that had received supplemental cobalamin were excluded from the analysis. Of 654 dogs, 3% (n = 21) were hypercobalaminaemic (median serum cobalamin concentration, 1307 ng/L [965 pmol/L]; range, 914-3561 ng/L [675-2628 pmol/L]). Chronic gastrointestinal signs were common in hypercobalaminaemic dogs (48%). Two of the 21 hypercobalaminaemic dogs were diagnosed with hypoadrenocorticism. Of 323 cats, 11% (n = 34) were hypercobalaminaemic (median serum cobalamin concentration, 1713 ng/L [1264 pmol/L]; range, 1370-3107 ng/L [1011-2293 pmol/L]). The following comorbidities were diagnosed in hypercobalaminaemic cats: chronic enteropathy, 65% (n = 22); acute or chronic pancreatitis, 24% (n = 8); cholangiohepatopathy, 18% (n = 6); gastric lymphoma, 6% (n = 2); and 3% hyperthyroidism (n = 1). Naturally-occurring increased serum cobalamin concentrations occurred infrequently in cats and even less often in dogs. Since hypercobalaminaemia can occur in dogs and cats with severe inflammatory, immune-mediated, and neoplastic conditions, it should not be ignored.

Acute on chronic kidney disease in cats: Etiology, clinical and clinicopathologic findings, prognostic markers, and outcome.

BACKGROUND: Chronic kidney disease (CKD) and acute decompensation of CKD (ACKD) are common in cats. OBJECTIVES: To characterize the etiology, clinical and clinicopathologic findings, and the short- and long-term prognosis of feline ACKD. ANIMALS: One hundred cats with ACKD. METHODS: Retrospective study, search of medical records for cats with ACKD. RESULTS: Common clinical signs included anorexia (85%), lethargy (60%), weight loss (39%), and vomiting (27%). Suspected etiologies included ureteral obstruction (11%), renal ischemia (9%), pyelonephritis (8%), others (6%), or unknown (66%). Hospitalization duration was longer in survivors versus nonsurvivors (median = 7 days, range = 2-26 versus median = 3 days, range = 2-20, respectively, P < .001). The survival rate to discharge was 58%. Age, serum creatinine, urea, and phosphorous concentrations were higher and venous blood pH was lower in nonsurvivors. However, only serum phosphorus remained associated with the short-term outcome in the multivariable model (P = .02; 95% confidence interval = 1.03-1.39). Survivors had a median survival time of 66 days after discharge. Serum creatinine concentrations at presentation as well as at discharge were associated with long-term survival (P < .002 for both). CONCLUSIONS: The short-term prognosis of ACKD is comparable to acute kidney injury, while the long-term prognosis is guarded.

Serum vitamin D status in sick cats with and without cholestatic liver disease.

OBJECTIVES: Vitamin D deficiency accompanies chronic cholestatic liver disease (CLD) in humans. The vitamin D status of cats with CLD is unknown. The objectives of this study were to describe serum vitamin D concentrations in cats with CLD and to determine if they correlated with indices of liver disease severity. METHODS: Thirty-six cats with CLD, defined by increases in serum bilirubin and serum alanine aminotransferase, and 23 sick cats with non-hepatobiliary diseases were prospectively enrolled. Serum 25-hydroxyvitamin D (25[OH]D), parathyroid hormone (PTH) and ionized calcium were measured. Signalment, clinical signs, comorbidities, diet history, serum bilirubin, liver enzyme activity, albumin, phosphorus, white blood cell count, prothrombin time and final hepatic cytologic/histopathologic diagnosis, when available, were recorded. RESULTS: Median serum 25(OH)D levels were similar in cats with CLD (89.5 nmol/l; range 21-112 nmol/l) and sick cats (89.0 nmol/l; range 49-115 nmol/l). Overall 12/36 (33%) cats with CLD and 4/23 (17%) sick cats had 25(OH)D levels below the lower limit of the reference interval (<65 nmol/l). Median PTH concentrations in cats with CLD were significantly higher (0.95 pmol/l; range 0-11.3 pmol/l) than in sick cats (0.70 pmol/l; range 0.5-6 pmol/l). In cats with CLD, 6/36 (17%) had high PTH levels in contrast to only 1/23 (4%) sick cats. In cats with CLD, 25(OH)D concentrations did not correlate with serum bilirubin, albumin or serum liver enzymes but were moderately negatively correlated with white blood cell count (r = - 0.402, P = 0.013). Cats with hepatic lipidosis had the highest prevalence of 25(OH)D concentrations that fell below the reference interval. CONCLUSIONS AND RELEVANCE: Many cats with CLD have serum 25(OH)D concentrations below the lower limit of the reference interval. Further study is warranted to determine the clinical relevance and whether supplementation would provide benefits.

Effects of 6 Weeks of Parenteral Cobalamin Supplementation on Clinical and Biochemical Variables in Cats with Gastrointestinal Disease.

BACKGROUND: Effects and duration of commonly used protocols for cobalamin (Cbl) supplementation on cellular Cbl deficiency have not been determined in hypocobalaminemic cats. HYPOTHESIS/OBJECTIVES: To evaluate effect of Cbl supplementation on clinical signs, serum and urine methylmalonic acid (MMA) concentrations over 16 weeks. ANIMALS: Twenty client-owned hypocobalaminemic cats with enteropathy. METHODS: Prospective 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. RESULTS: Clinical 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 IMPORTANCE: The Cbl supplementation protocol used here did not lead to complete normalization of cellular Cbl deficiency in all examined cats, and biochemical improvements were transient.

Hypocobalaminaemia as a cause of bone marrow failure and pancytopenia in a cat.

CASE REPORT: A male Domestic Short-hair cat was presented for chronic weight loss, lethargy and hyporexia. Complete haematological examination revealed non-regenerative anaemia, neutropenia and thrombocytopenia, as well as Howell-Jolly bodies, anisocytosis, polychromasia and macrocytosis on blood smear evaluation. Histopathological evaluation of bone marrow biopsy disclosed hypocellularity consistent with bone marrow failure. Concurrent hypocobalaminaemia was identified and treated with parenteral cyanocobalamin supplementation. Other differential diagnoses for pancytopenia, including infectious, toxic, immune-mediated and neoplastic causes, were ruled out. CONCLUSION: The cat's erythrocyte, leucocyte and platelet counts normalised after 2 months of cyanocobalamin supplementation, suggesting that pancytopenia may be a rare manifestation of feline cobalamin deficiency.

Double-blinded randomised placebo-controlled clinical trial of individualised homeopathic treatment of hyperthyroid cats.

Feline hyperthyroidism is a common endocrine disorder in older cats for which homeopathic treatment has been advocated. A double-blinded, placebo-controlled randomised trial was performed to look for evidence of efficacy for the use of individualised homeopathy in the treatment of this disease. Using a case definition of a concentration of the thyroid hormone T4 >66 nmol/l, cats were randomised into two treatment arms. Either a placebo or a homeopathic treatment was given to each cat blindly. After 21 days, the T4 levels, weight (Wt) and heart rate (HR) were compared with pretreatment values. There were no statistically significant differences in the changes seen between the two treatment arms following placebo or homeopathic treatment (T4 P=0.96, Wt P=0.16, HR P=0.36) or between the means of each parameter for either treatment arm before and after placebo or homeopathic treatment (all P values >0.13). In a second phase of the study, patients in both treatment arms were given methimazole treatment for 21 days and T4, Wt and HR determined again. Again there were no statistically significant differences between the groups, but there were statistically significant reductions in T4 (P<0.0001) and HR (P=0.02), and a statistically significant increase in Wt (P=0.004) in both groups compared with their pre-methimazole treatment levels. The results of this study failed to provide any evidence of the efficacy of homeopathic treatment of feline hyperthyroidism.

Oral cobalamin supplementation in cats with hypocobalaminaemia: a retrospective study.

Objectives The objective of the study was to evaluate whether oral cobalamin supplementation can restore normocobal-aminaemia in cats with hypocobalaminaemia and clinical signs of gastrointestinal disease. Methods This was a retrospective study based on a computerised database search for client-owned cats treated at Evidensia Specialist Animal Hospital, Helsingborg, Sweden, during the period December 2013 to August 2016. Inclusion criteria were cats with clinical signs of chronic enteropathy, an initial serum cobalamin concentration ⩽250 pmol/l (reference interval 214-738 pmol/l) and oral treatment with cobalamin tablets. Results Twenty-five cats met the inclusion criteria. The cats were treated with 0.25 mg cyanocobalamin tablets once daily. Serum cobalamin concentration was rechecked 27-94 days after continuous oral cobalamin supplementation. All cats had serum cobalamin concentrations above the reference interval after oral cobalamin supplementation. Median (range) serum cobalamin concentration was 128 pmol/l (111-250 pmol/l) prior to treatment and 2701 pmol/l (738-16,359 pmol/l) after supplementation. This difference was statistically significant ( P <0.0001). Conclusions and relevance Our results suggest that oral cobalamin supplementation is effective in increasing serum cobalamin to supranormal concentrations in cats with hypocobalaminaemia. Thus, oral cobalamin supplementation is a promising alternative to parenteral administration. Prospective comparative studies in cats being treated with parenteral vs oral cobalamin supplementation in a larger number of patients are warranted before oral supplementation can be recommended for routine use.

Outbreak of thiamine deficiency in cats associated with the feeding of defective dry food.

Objectives The objective of this study was to determine disease progression, association between neurological signs and magnetic resonance imaging (MRI) findings, and long-term outcome in feline thiamine deficiency associated with defective dry food. Methods The clinical records of 17 cats diagnosed with thiamine deficiency related to a defective dry food were examined and data collected. The thiamine level in the food was analysed by liquid chromatography-tandem mass spectrometry. Results The thiamine level in the food was below the recommendation of the National Research Council. Fifteen cats were fed the food exclusively. Prior to the acute development of neurological signs, most cats displayed non-specific signs such as anorexia, lethargy or vomiting. Vestibular signs of varying severity were observed in 94% of the cats, and all but one of these presented with bilateral dysfunction. Other main neurological signs included altered mentation (76%), blindness (59%) and seizures (59%). Moreover, 80% of the cats with seizures presented with cluster seizures or status epilepticus. MRI abnormalities consistent with findings reported in the previous literature were detected in five cases. MRI was unremarkable in one cat with ongoing severe neurological signs even though thiamine had been administered. Most surviving cats recovered rapidly within 2 weeks of treatment and had either returned to normal or had minimal neurological signs at the 2 month follow-up. One cat recovered slowly over 6 months. Most cats with seizures in the initial stage of the disease remained seizure free at the 24 month follow-up. Conclusions and relevance This study documented the association between feline thiamine deficiency and defective dry food. MRI examination provided valuable information in the diagnosis. However, normal MRI findings do not exclude the diagnosis of feline thiamine deficiency, especially once thiamine has been supplemented. MRI findings also may not always reflect the neurological status or severity. If treated promptly, most cats will recover rapidly with a good outcome. Occasionally, recovery may be slow and take several months.

Serum cobalamin concentrations and small intestinal ultrasound changes in 75 cats with clinical signs of gastrointestinal disease: a retrospective study.

Objectives The aim of the study was to evaluate ultrasonographic changes in the small intestine of cats with clinical signs of gastrointestinal disease and low or low-normal serum cobalamin concentrations. Methods Records for client-owned cats presenting to the small animal hospital with signs of gastrointestinal disease and in which serum cobalamin concentrations were measured from 2000-2013 were reviewed. Inclusion criteria were cobalamin concentrations <500 ng/l, abdominal ultrasound within 1 month of cobalamin testing and definitive diagnosis. Results Of 751 serum cobalamin measurements, hypocobalaminemia or low-normal cobalamin was identified in 270 cats, abdominal ultrasound was performed in 207 of those cats and a diagnosis was available for 75 of them. Small intestinal ultrasound changes were detected in 49/75 (65%) cats. Abnormalities included thickening, loss of wall layer definition, echogenicity alterations and discrete masses. Serum cobalamin concentrations <500 ng/l were observed with diagnoses of inflammatory disease, neoplasia, infectious disease and normal histopathology. Cobalamin concentration was significantly lower in cats with lymphoma or inflammatory bowel disease compared with other gastrointestinal neoplasia ( P = 0.031). No difference was found between cobalamin concentration and the presence of ultrasound abnormalities, specific ultrasound changes or albumin concentration. Conclusions and relevance One-third of symptomatic cats with hypocobalaminemia or low-normal cobalamin concentrations may have an ultrasonographically normal small intestine. For the majority of cats in this study, histopathologic abnormalities were observed in the small intestine, regardless of ultrasound changes. These findings suggest gastrointestinal disease should not be excluded based on low-normal cobalamin concentrations, even with a concurrent normal ultrasound examination. Additional studies are needed in cats with low-normal serum cobalamin concentrations, as a definitive diagnosis was not pursued consistently in those cats. However, data from this study suggest that careful monitoring, histopathologic evaluation and future cobalamin supplementation may be warranted.

Serum Cobalamin and Methylmalonic Acid Concentrations in Hyperthyroid Cats Before and After Radioiodine Treatment.

BACKGROUND: Hyperthyroidism, the most common endocrine disorder in cats, has been associated with low serum cobalamin concentrations. Whether this is a functional cobalamin deficiency of clinical importance has not been assessed. HYPOTHESIS/OBJECTIVES: Cats with hyperthyroidism experience a functional cobalamin deficiency which correlates with their clinical catabolic state and is reversible with return of the euthyroid state. ANIMALS: Thirty-nine client-owned hyperthyroid cats. METHODS: Prospective observational study. Serum cobalamin, methylmalonic acid, and clinical scores were determined in each hyperthyroid cat at enrollment and when euthyroid (60 days after radioiodine treatment). RESULTS: Five of the 39 hyperthyroid cats (13%) had a low serum cobalamin concentration ranging from <150 to 290 ng/L. Serum cobalamin concentrations normalized to >350 ng/L in 2 of the hypocobalaminemic cats once euthyroid. None of the hyperthyroid/hypocobalaminemic cats had increased serum methylmalonic acid concentrations (175-601 nmol/L). In cats with clinical and biochemical hyperthyroidism, there was no correlation between serum cobalamin concentrations with total T4 concentration (P = .12) or clinical scores including body weight (P = .11) and BCS (P = .54). CONCLUSIONS AND CLINICAL IMPORTANCE: In this population of hyperthyroid cats, the prevalence of hypocobalaminemia was low. Specifically, hyperthyroid cats, in which concurrent gastrointestinal disease is unlikely. Hypocobalaminemia is not a functional deficiency requiring supplementation in hyperthyroid cats without gastrointestinal disease.

Evaluating Sucralfate as a Phosphate Binder in Normal Cats and Cats with Chronic Kidney Disease.

Control of hyperphosphatemia is an important part of the management of chronic kidney disease (CKD). The purpose of this study was to determine the efficacy of sucralfate as a phosphate binder in normal cats and normophosphatemic CKD cats. A 500 mg sucralfate slurry was administered orally q 8 hr for 2 wk, and serum phosphorus, urine fractional excretion of phosphorus, and fecal phosphorus concentrations were measured. In normal cats treated with sucralfate, significant changes in serum phosphorus concentration or urinary excretion of phosphorus were not detected, and vomiting occurred after 14.7% of administrations. Of the five normophosphatemic cats with CKD treated with sucralfate, three experienced clinical decompensation, including vomiting, anorexia, constipation, and increased azotemia. Administration of sucralfate did not result in significant changes in fecal phosphorus concentration in these cats. The effects of sucralfate administration on serum phosphorus concentration and urinary excretion of phosphorus in CKD cats was difficult to determine because of dehydration and worsening azotemia associated with decompensation. Due to side effects and the apparent lack of efficacy of the medication, the study was discontinued. This study was unable to confirm efficacy of this sucralfate formulation as a phosphate binder, and side effects were problematic during the study.

Hypokalemia and suspected renal tubular acidosis associated with topical carbonic anhydrase inhibitor therapy in a cat.

OBJECTIVE: To describe the occurrence of hypokalemia, metabolic acidosis, and suspected renal tubular acidosis associated with the administration of topical ophthalmic carbonic anhydrase inhibitor (CAI) in a cat. CASE SUMMARY: A 2-year-old, 5.3 kg, male, castrated, domestic short-haired cat developed hyporexia 6 weeks after starting topical ophthalmic dorzolamide 2% therapy for treatment of ocular hypertension. Two weeks later, the cat was evaluated for severe weakness, cervical ventroflexion, and anorexia. Plasma electrolyte and acid-base measurement revealed hypokalemia (K+ = 2.9 mmol/L; reference interval 3.8-5.4 mmol/L) and metabolic acidosis (plasma HCO3- = 9.8 mmol/L; reference interval 15-23 mmol/L) in the presence of a urine pH of 7.5 (reference interval 6.5-7.5). The pH abnormalities were consistent with a renal tubular acidosis. Clinical and biochemical abnormalities resolved with short-term supportive care, potassium supplementation, and discontinuation of dorzolamide therapy. NEW OR UNIQUE INFORMATION PROVIDED: This is the first report of hypokalemia and metabolic acidosis associated with topical CAI therapy in a cat.

Hypercobalaminaemia is associated with hepatic and neoplastic disease in cats: a cross sectional study.

BACKGROUND: When increased serum cobalamin concentrations are encountered clinically they are usually attributed to parenteral supplementation, dietary factors, or otherwise ignored. However, recently, hypercobalaminaemia has been associated with numerous diseases in humans, most notably neoplastic and hepatic disorders. The aim of this retrospective, observational, cross-sectional study was to determine the significance of increased cobalamin in cats. RESULTS: In total, 237 records were retrieved and 174 cats, of various ages and sexes met the inclusion criteria. A total of 42 cats had increased serum cobalamin concentration, and had not received prior supplementation. Multiple logistic regression analysis revealed that increased serum cobalamin concentration was positively related to pedigree breed (pedigree breeds more likely to have increased cobalamin concentration, odds ratio [OR] 4.24, 95% CI 1.78-10.15, P = 0.001), to having liver disease (OR 9.91, 95% CI 3.54-27.68), and to having a solid neoplasm (OR 8.54, 95% CI 1.10-66.45). CONCLUSIONS: The results of the current study suggest that increased serum cobalamin concentrations should not be ignored in cats with no history of supplementation, and investigation for underlying hepatic or neoplastic disease is warranted.

Relationship among serum creatinine, serum gastrin, calcium-phosphorus product, and uremic gastropathy in cats with chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) in cats is associated with gastrointestinal signs commonly attributed to uremic gastropathy. Consequently, patients often are treated with antacids and gastrointestinal protectants. This therapeutic regimen is based on documented gastric lesions in uremic humans and dogs, but the nature and incidence of uremic gastropathy in cats are unknown. HYPOTHESIS/OBJECTIVES: Evaluate uremic gastropathy in CKD cats to facilitate refinement of medical management for gastrointestinal signs. ANIMALS: Thirty-seven CKD cats; 12 nonazotemic cats METHODS: Stomachs were evaluated for the presence of classic uremic gastropathy lesions. Histopathologic lesions were compared with serum creatinine concentrations, calcium-phosphorus product (CPP), and serum gastrin concentrations. RESULTS: Gastric ulceration, edema, and vascular fibrinoid change were not observed. The most important gastric lesions in CKD cats were fibrosis and mineralization. Sixteen CKD cats (43%) had evidence of gastric fibrosis of varying severity and 14 CKD cats (38%) had gastric mineralization. CKD cats were more likely to have gastric fibrosis and mineralization than nonazotemic controls (P = .005 and P = .021, respectively). Only cats with moderate and severe azotemia had gastric mineralization. CPP was correlated with disease severity; severely azotemic CKD cats had significantly higher CPP when compared with nonazotemic controls, and to mildly and moderately azotemic cats (P < .05). Gastrin concentrations were significantly higher in CKD cats when compared with nonazotemic controls (P = .003), but increased concentrations were not associated with gastric ulceration. CONCLUSIONS AND CLINICAL IMPORTANCE: Uremic gastropathy in CKD cats differs from that described in other species and this difference should be considered when devising medical management.

A questionnaire on survival of kittens depending on the blood groups of the parents.

Cats more than 2 months of age have alloantibodies against the blood type antigen that they do not possess. Maternal antibodies, including alloantibodies against blood groups, are transferred to the kittens' systemic circulation when they suckle colostrum during the first 12-16 h after birth. If kittens with blood group A or AB nurse from a mother with blood group B they may develop neonatal isoerythrolysis (NI). Breeders can prevent kittens at risk of NI from nursing during the first 16-24 h; after this period it is safe to let them nurse. Kittens depend, however, on the passive transfer of antibodies from the colostrum for early protection against infections. Although it is known that kittens deprived of colostrum will also be deprived of passive systemic immunity, it is not known if this will affect their health. Therefore, the aim of this study was to evaluate kitten mortality in litters with B-mothers and A-fathers compared to litters with A-mothers. In addition, the aim was to evaluate the effects of colostrum deprivation on the health of the mothers, and the breeders' opinions and experiences of these combinations of breedings. A web-based questionnaire was constructed and distributed to breeders. The results indicate that there is no difference in mortality between planned litters that have mothers with blood group A and litters with mothers that have blood group B and fathers that have blood group A. When managing blood group incompatibility in cat all factors affecting the health of the cats, including genetic variation, should be considered.

Comparison of serum fatty acid concentrations in cats with hypertrophic cardiomyopathy and healthy controls.

n-3 fatty acids have some benefits in humans and dogs with cardiac disease, and plasma n-3 fatty acid concentrations have been shown to be decreased in dogs with congestive heart failure (CHF). However, there are no published studies reporting fatty acid concentrations in cats with cardiac disease. Therefore, the goal of this study was to compare serum fatty acid concentrations in normal cats and cats with hypertrophic cardiomyopathy (HCM), and determine if fatty acid concentrations correlate with left atrial size or the presence of CHF. Serum fatty acid concentrations were measured in normal cats and cats with HCM by gas chromatography. Twenty-three cats with HCM and 20 healthy controls were enrolled. Compared with healthy controls, cats with HCM had higher concentrations of palmitic acid (P = 0.01), docosahexanoic acid (DHA; P = 0.001) and total n-3 fatty acids (P = 0.03), and lower concentrations of linoleic acid (P = 0.03). Among cats with HCM, there were no differences in plasma fatty acid concentrations, and no association between left atrial dimension and fatty acid concentrations. Cats with HCM have some alterations in plasma fatty acids compared with healthy controls. Given the higher plasma concentrations of DHA, DHA supplementation is unlikely to have benefits in terms of correcting a deficiency; however, other effects of DHA or of supplementation of EPA warrant further investigation.

Manual ventilation therapy and aggressive potassium supplementation in the management of respiratory failure secondary to severe hypokalaemia in a cat with exocrine pancreatic insufficiency.

A domestic shorthair cat was referred for progressive muscle weakness and dyspnoea. The cat had a 2-month history of severe weight loss, small intestinal diarrhoea, polyphagia and polyuria/polydipsia. Biochemical analysis and venous blood gas evaluation revealed severe hypokalaemia [1.7 mmol/l; reference interval (RI): 3.5-5.1 mmol/l] and hypoventilation (partial pressure of carbon dioxide = 68 mmHg; RI: 34-38 mmHg). Aggressive potassium supplementation was initiated. The cat was manually ventilated until serum potassium increased to 3 mmol/l. A diagnosis of exocrine pancreatic insufficiency (EPI) was made based on clinical signs and serum feline trypsin-like immunoreactivity (0.1 µg/l; RI: 12-82 µg/l). Medical management of the EPI resulted in clinical recovery.

Flow cytometric determination of allergen-specific T lymphocyte proliferation from whole blood in experimentally asthmatic cats.

The ability to quantify feline lymphocyte proliferation, especially to specific antigen or allergen, would be valuable in experimental models and naturally developing disease where activated lymphocytes drive immune responses. Traditional proliferation assays may pose radioactivity hazards, lack the ability to distinguish viable from non-viable cells, and cannot discriminate individual populations of proliferating lymphocytes (e.g., the CD4+ T cell class). We hypothesized that in an experimental model of feline allergic asthma a four-color flow cytometric assay capable of simultaneously detecting division, viability and cell surface markers (pan T cell marker CD5 or CD4) would allow characterization of lymphocytes stimulated ex vivo using the sensitizing allergen, Bermuda grass (BGA). Peripheral blood mononuclear cells were harvested from eight experimentally asthmatic cats to validate and optimize use of a cell proliferation dye or bromodeoxyuridine (BrdU) with BGA-specific stimulation in a lymphocyte proliferation flow cytometric assay. Only the latter reagent was suitable in the cat. After a 3 day incubation, antibodies with different fluorochromes were used to identify BrdU, viable cells, CD5 and CD4 for subsequent flow cytometric analysis. In asthmatic cats, the group mean ± SEM of proliferating CD5+ lymphocytes was 2.3 ± 0.5%. The group mean ± SEM of proliferating CD4+ lymphocytes was 1.2 ± 0.3%. Flow cytometry is a sensitive method for detecting simultaneous proliferation and viability of very minor populations of allergen-specific lymphocytes in experimentally asthmatic cats.

Suspected acquired hypocobalaminaemic encephalopathy in a cat: resolution of encephalopathic signs and MRI lesions subsequent to cobalamin supplementation.

UNLABELLED: PRESENTING SIGNS AND INITIAL INVESTIGATIONS: An 8-year-old female spayed British shorthair cat was presented with a history of waxing and waning neurological signs. Neuroanatomical localisation was consistent with a diffuse forebrain disease. Blood ammonia concentration was increased. Abdominal ultrasonography and a bile acid stimulation test were normal. Magnetic resonance imaging (MRI) revealed hyperintense, bilaterally symmetrical, diffuse lesions on T2-weighted sequences, predominantly, but not exclusively, affecting the grey matter. Serum cobalamin (vitamin B12) concentration was low. Hypocobalaminaemia resulting in a urea cycle abnormality was considered a likely cause of the hyperammonaemia. TREATMENT: Daily cobalamin injections resulted in a rapid clinical improvement. Eight weeks into treatment neurological examination was unremarkable and there was complete resolution of the MRI lesions. CLINICAL IMPORTANCE: This is the first reported case of acquired feline hypocobalaminaemia resulting in an encephalopathy. Additionally, this case is unique in describing reversible brain MRI abnormalities in a cobalamin-deficient companion animal.

Comparison of platelet clumping and complete blood count results with Sysmex XT-2000iV in feline blood sampled on EDTA or EDTA plus CTAD (citrate, theophylline, adenosine and dipyridamole).

False thrombocytopenia may result from platelet aggregation, especially in feline ethylenediamine tetra-acetic acid (EDTA) blood specimens. Citrate, theophylline, adenosine and dipyridamole (CTAD) was added to 46 feline EDTA specimens to test its anti-aggregation action. Platelet aggregation was estimated from blood films and a complete blood count was performed with a Sysmex XT-2000iV analyser. Platelet aggregation score was >2 in 11/46 EDTA tubes and only in one EDTA+CTAD specimen. The platelet count was higher in all CTAD-supplemented tubes except one, medians measured by cytometry being 225.5 × 10(9)/l and 249.0 × 10(9)/l in EDTA and EDTA+CTAD, respectively (P = 0.007). Adding CTAD had statistically and analytically significant but moderate effects on other blood variables, the most intense variations being observed for reticulocytes (about 3% higher in EDTA specimens) and reticulocyte indexes. Addition of CTAD to EDTA when sampling feline blood is a useful option to reduce platelet clumping.