成人尿素循环缺陷:具有潜在脑病基因编码的肝脏代谢紊乱的临床表现、诊断和治疗

IF 3.5 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Anibh Martin Das
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引用次数: 0

摘要

高氨血症是脑病的重要病因。氨是氨基酸降解的废物,不能通过尿液排出体外。氨通过尿素循环代谢为水溶性尿素。高氨血症不仅发生在急性肝功能衰竭时,也发生在参与尿素循环的酶或转运体的罕见遗传缺陷中,导致氨浓度升高。酶缺陷包括氨甲酰磷酸合成酶、n -乙酰谷氨酸合成酶、鸟氨酸转氨基甲酰基酶、精氨酸琥珀酸裂解酶和精氨酸酶的缺乏;转运体缺陷包括柠檬素缺乏和hhh -综合征。这些尿素循环缺陷(UCD)大多在新生儿期、婴儿期或儿童期首次出现,但在成年期可能以较轻的形式出现包括脑病在内的首次临床表现。因此,治疗成人的医生应了解UCD的临床症状,及时诊断并开始治疗。在成年期,临床症状通常是非特征性的,包括头痛、避免高蛋白食物、剧烈运动或分娩引起的精神症状、自闭症、注意力缺陷、嗜睡、发育迟缓和癫痫。血液中氨浓度升高是生化标志。有些ucd可以在代谢物水平上诊断,有些则只能在遗传水平上诊断。治疗方法包括低蛋白质膳食,补充必需氨基酸和维生素/微量元素,并摄入精氨酸或瓜氨酸。氮的药理清除剂是苯甲酸盐和丁酸盐。如果保守治疗失败,应考虑血液透析。在急性危机期间及时治疗对于获得最佳结果至关重要。肝移植是考虑在代谢不稳定的患者。对于精氨酸酶缺乏症,可以使用酶替代疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Urea cycle defects in adulthood: clinical presentation, diagnosis and treatment in genetically encoded hepatic metabolic disorders with a potential for encephalopathy.

Urea cycle defects in adulthood: clinical presentation, diagnosis and treatment in genetically encoded hepatic metabolic disorders with a potential for encephalopathy.

Urea cycle defects in adulthood: clinical presentation, diagnosis and treatment in genetically encoded hepatic metabolic disorders with a potential for encephalopathy.

Hyperammonaemia is an important cause for encephalopathy. Ammonia is the waste product of amino acid degradation and cannot be excreted via urine. Ammonia is metabolized to water-soluble urea via the urea cycle. Hyperammonaemia not only occurs during acute liver failure, but also in rare genetically determined defects of enzymes or transporters involved in the urea cycle resulting in elevated ammonia concentrations. Enzyme defects include deficiency of carbamylphosphate synthase, N-acetylglutamate synthase, ornithine transcarbamylase, argininosuccinate lyase and arginase, transporter defects are citrin deficiency and HHH-syndrome. These urea cycle defects (UCD) mostly manifest for the first time during the neonatal period, infancy or childhood, however first clinical manifestations including encephalopathy may be observed in adulthood in milder forms. Therefore, physicians treating adults should be aware of clinical symptoms in UCD to make a timely diagnosis and initiate treatment. In adulthood, clinical symptoms are often uncharacteristic including headache, avoidance of high-protein food, psychiatric symptoms triggered by heavy exercise or delivery of a child, autism, attention deficit, lethargy, developmental delay and epilepsy. Elevated ammonia concentrations in blood are the biochemical hallmark. Some UCDs can be diagnosed at metabolite level, others only at genetic level. Treatment consists of eucaloric, low-protein diet supplemented with essential amino acids and vitamins/trace elements, and intake of arginine or citrulline. Pharmacological scavengers of nitrogen are benzoate and butyrate. If conservative therapy fails, hemodialysis should be considered. Prompt treatment during acute crises is essential for optimal outcome. Liver transplantation is considered in metabolically unstable patients. For arginase deficiency, enzyme replacement therapy is available.

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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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