Hyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile Border Collie

IA Battersby, U Giger, EJ Hall

Research output: Contribution to journalArticle (Academic Journal)peer-review

50 Citations (Scopus)

Abstract

An eight-month-old Border collie was presented with anorexia, cachexia, failure to thrive and stupor. Laboratory tests demonstrated a mild anaemia, neutropenia, proteinuria and hyperammonaemia. Serum bile acid concentrations were normal, but an ammonia tolerance test (ATT) was abnormal. The dog responded to symptomatic therapy for hepatoencephalopathy. When a low serum cobalamin (vitamin B12) concentration and methylmalonic aciduria were noted, the dog was given a supplement of parenteral cobalamin. Two weeks later, a repeat ATT was normal. Cobalamin supplementation was continued every two weeks, and clinical signs, except for proteinuria, resolved despite withdrawing all therapy for hepatoencephalopathy. A presumptive diagnosis of hereditary selective cobalamin malabsorption was made, based on the young age, Border collie breed, low serum cobalamin concentration and methylmalonic aciduria. Although hereditary selective cobalamin malabsorption in Border collies, giant schnauzers, Australian shepherd dogs and beagles has previously been reported in North America, to the authors' knowledge this the first report of the condition in the UK and the first to document an abnormal ATT in a cobalamin-deficient dog.
Translated title of the contributionHyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile Border Collie
Original languageEnglish
Pages (from-to)339 - 344
Number of pages6
JournalJournal of Small Animal Practice
Volume46 (7)
DOIs
Publication statusPublished - 2005

Bibliographical note

Publisher: Blackwell

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