Battersby I A, Giger U, Hall E J
Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 5DU.
J Small Anim Pract. 2005 Jul;46(7):339-44. doi: 10.1111/j.1748-5827.2005.tb00330.x.
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 all 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 is the first report of the condition in the UK and the first to document an abnormal ATT in a cobalamin-deficient dog.
一只八个月大的边境牧羊犬出现厌食、恶病质、发育不良和昏迷症状。实验室检查显示轻度贫血、中性粒细胞减少、蛋白尿和高氨血症。血清胆汁酸浓度正常，但氨耐受试验（ATT）异常。这只狗对肝性脑病的对症治疗有反应。当发现血清钴胺素（维生素B12）浓度低和甲基丙二酸尿症时，给这只狗补充了肠外钴胺素。两周后，重复的ATT正常。每两周继续补充钴胺素，尽管停止了所有肝性脑病治疗，但除蛋白尿外，所有临床症状均消失。基于其年轻的年龄、边境牧羊犬品种、低血清钴胺素浓度和甲基丙二酸尿症，初步诊断为遗传性选择性钴胺素吸收不良。尽管此前在北美已报道边境牧羊犬、巨型雪纳瑞犬、澳大利亚牧羊犬和比格犬存在遗传性选择性钴胺素吸收不良，但据作者所知，这是英国关于该病的首例报告，也是首例记录钴胺素缺乏犬ATT异常的报告。
