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

Simpson, Katherine; Battersby, Ian; Lowrie, Mark

doi:10.1177/1098612x12439358

Cited by 17 publications

(22 citation statements)

References 26 publications

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“…Cobalamin is a water-soluble vitamin with important intermediary metabolic functions. The importance of hypocobalaminaemia has long been recognised: deficiency can have neurological, haematological, cardiovascular and catabolic manifestations in man and encephalopathy, myelopathy, anaemia, anorexia, cold-intolerance and failure to thrive have been reported in cats [ 1 ],[ 2 ]. Hypocobalaminaemia has been reported in cats with gastrointestinal disease [ 3 ],[ 4 ], exocrine pancreatic insufficiency [ 5 ] and hyperthyroidism [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2014

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BackgroundWhen 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.ResultsIn 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).ConclusionsThe 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.

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Section: Introductionmentioning

confidence: 99%

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

et al. 2014

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“…Cobalamin (vitamin B12) is a water‐soluble vitamin involved in neuronal function, hematopoiesis, DNA and fatty acid synthesis, and energy production . CBL absorption requires binding proteins and specific receptors along various parts of the gastrointestinal tract .…”

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confidence: 99%

The Relationship of Serum Cobalamin to Methylmalonic Acid Concentrations and Clinical Variables in Cats

Worhunsky

Toulza

Rishniw

et al. 2013

Veterinary Internal Medicne

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“…Hyperammonaemia can develop secondarily to different mechanisms: (1) acquired urea cycle amino acid deficiency; (2) cobalamin deficiency leading to accumulation of methylmalonic acid (MMA) and subsequent impaired uptake of ammonia into the urea cycle; 16 , 17 and (3) congenital deficiency in urea cycle enzymes such as ornithine transcarbamylase (OTC) deficiency. 18 The plasma amino acid profile in this case revealed several urea cycle amino acids deficiencies (citrulline, ornithine and arginine), which could be responsible for the hyperammonaemia.…”

Section: Discussionmentioning

confidence: 99%

“…The MMA status could not be assessed in this cat; however, the few feline cases reported in the literature with hyperammonaemic encephalopathy and high MMA concentration had low serum cobalamin concentrations. 16 , 17 …”

Section: Discussionmentioning

confidence: 99%

Acquired urea cycle amino acid deficiency and hyperammonaemic encephalopathy in a cat with inflammatory bowel disease and chronic kidney disease

Dor

Adamany

Kisielewicz

et al. 2018

Journal of Feline Medicine and Surgery Open Reports

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Case summaryA 5-year-old male neutered Persian cat was referred for investigation of a 4 week history of weight loss, inappetence and intermittent vomiting. Chronic kidney disease (CKD) and inflammatory bowel disease were diagnosed, and despite immunosuppressive therapy and assisted enteral nutrition, the cat experienced persistent anorexia, vomiting and severe weight loss. After 2 additional weeks of treatment, the cat developed acute-onset neurological signs associated with severe hyperammonaemia and was euthanased. Plasma amino acid assessment revealed deficiency of several amino acids involved in the urea cycle, including arginine.Relevance and novel informationTo our knowledge, this is the first reported case of an acquired urea cycle amino acid deficiency without nutritional deprivation in a cat. Several contributing factors were suspected, including intestinal malabsorption and CKD. This case demonstrates the importance of urea cycle amino acids in feline metabolism and possible necessity for parenteral supplementation, particularly in the context of persistent weight loss despite adequate enteral nutrition.

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

Abstract: 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.

Cited by 17 publications

References 26 publications

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

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

The Relationship of Serum Cobalamin to Methylmalonic Acid Concentrations and Clinical Variables in Cats

Acquired urea cycle amino acid deficiency and hyperammonaemic encephalopathy in a cat with inflammatory bowel disease and chronic kidney disease

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