Department of Nutrition, University of Toulouse, ENVT, Toulouse, France.
Department of Internal Medicine/ Neurology, University of Toulouse, ENVT, Toulouse, France.
BMC Vet Res. 2021 Jul 22;17(1):253. doi: 10.1186/s12917-021-02959-x.
Bromide is a halide ion of the element bromine usually administered in the form of potassium salt as monotherapy or add-on treatment in epileptic dogs. It is excreted unchanged in the urine and undergoes tubular reabsorption in competition with chloride. Thus, dietary chloride content affects serum bromide concentrations. This is the first published clinical report of bromide toxicosis secondary to a dietary modification of chloride content in an epileptic dog treated with potassium bromide.
A 3-year-old 55-kg neutered male Tibetan Mastiff was evaluated because of a 1-month history of progressive signs including ataxia, lethargy and behaviour changes. The dog was successfully treated for idiopathic epilepsy since the age of 1-year-old with phenobarbital and potassium bromide. Two months prior to presentation, the owners decided to change the dog's diet without veterinary advice. Physical examination was unremarkable. A 12-kg weight gain was recorded since last follow-up (8 months). Neurological examination revealed severe symmetric 4-limbs ataxia with altered vigilance and intermittent episodes of hyperactivity and aggressive behaviour without significant abnormality of cranial nerves. Serum bromide concentration was high and increased by 103 % since last follow-up. Nutritional evaluation revealed a 53 % decrease of chloride content in the diet before and after dietary transition. Bromide toxicosis was suspected, due to bromide reduced clearance secondary to the decreased dietary chloride content. Potassium bromide treatment was lowered by 15 % without further dietary changes. Neurologic signs progressively improved over the next month, without any seizure. After two months, the serum bromide concentration lowered to the same level measured before dietary modification. After four months, neurological examination was unremarkable.
Dietary chloride content can directly influence serum bromide concentrations, therefore affecting seizure control or contributing to unexpected adverse effects. In the present case, a reduction in chloride intake markedly increased serum bromide concentrations causing bromism. Dietary changes should be avoided in dogs treated with potassium bromide to maintain stable serum bromide levels.
溴化物是溴元素的卤化物离子，通常以钾盐的形式作为单药或添加治疗在癫痫犬中使用。它以未改变的形式在尿液中排泄，并与氯离子竞争进行管状重吸收。因此，饮食中的氯化物含量会影响血清溴化物浓度。这是首例报道的由于接受溴化钾治疗的癫痫犬饮食中氯化物含量改变而导致溴化物中毒的临床病例。
一只 3 岁 55 公斤已绝育的雄性西藏獒犬，因进行性症状就诊，包括共济失调、嗜睡和行为改变，病史长达 1 个月。该犬自 1 岁起成功接受苯巴比妥和溴化钾治疗特发性癫痫。在就诊前 2 个月，主人未经兽医建议自行决定改变犬的饮食。体格检查未见明显异常。与上次就诊（8 个月前）相比，体重增加了 12 公斤。神经检查显示严重对称的四肢共济失调，警觉性降低，间歇性出现过度活跃和攻击性行为，但颅神经无明显异常。血清溴化物浓度升高，与上次就诊相比升高了 103%。营养评估显示，在饮食改变前后，饮食中的氯化物含量下降了 53%。由于饮食中氯化物减少导致溴化物清除减少，怀疑发生溴化物中毒。溴化钾治疗减少了 15%，未进行进一步的饮食改变。在接下来的一个月内，神经症状逐渐改善，无癫痫发作。两个月后，血清溴化物浓度降至饮食改变前的相同水平。四个月后，神经检查未见明显异常。
饮食中的氯化物含量可直接影响血清溴化物浓度，从而影响癫痫发作的控制或导致意外的不良反应。在本病例中，氯化物摄入减少导致血清溴化物浓度显著升高，引起溴化物中毒。在接受溴化钾治疗的犬中，应避免饮食改变，以维持稳定的血清溴化物水平。
