一名同时患有吉尔伯特综合征和葡萄糖-6-磷酸脱氢酶缺乏症的患者因疟原虫疟疾而导致高胆红素血症恶化

IF 1 Q3 MEDICINE, GENERAL & INTERNAL Cureus Pub Date : 2024-11-05 eCollection Date: 2024-11-01 DOI:10.7759/cureus.73073
Hsu Y Mon, Helen Alemayehu, Keerthana Pampapathi, Samson O Oyibo
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摘要

吉尔伯特综合征和 G6PD 缺乏症是常见的遗传性疾病。它们都会通过不同的机制导致非结合性高胆红素血症。疟原虫引起的溶血是导致非结合性高胆红素血症的另一个原因。我们曾报告过一名 51 岁的亚洲男性,他在肯尼亚度假四天后出现发烧和出汗症状。他承认在度假期间没有采取疟疾预防措施。初步检查显示,他患有恶性疟原虫疟疾,并同时患有严重的 G6PD 缺乏症和吉尔伯特综合征,我们认为这都是导致未结合高胆红素血症加重(升高四倍)的原因。他接受了静脉输液、扑热息痛和口服蒿甲醚/氟苯胍联合疗法。他的临床恢复良好。一个月后,他仍表现为慢性非结合性高胆红素血症,网织红细胞计数反复升高,但没有贫血,这表明代偿性溶血进一步发作。我们还结合这个有趣的病例讨论了非结合性高胆红素血症的鉴别诊断。
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Exacerbation of Hyperbilirubinemia by Falciparum Malaria in a Patient With Coexisting Gilbert's Syndrome and Glucose-6-Phosphate Dehydrogenase Deficiency.

Gilbert's syndrome and G6PD deficiency are common genetic disorders. They both give rise to unconjugated hyperbilirubinemia through different mechanisms. Falciparum malaria-induced hemolysis is another cause of unconjugated hyperbilirubinemia. We have reported a 51-year-old Asian male who presented with a four-day history of fever and sweating just after a holiday in Kenya. He admitted to not taken malaria prophylaxis while on holiday. Initial investigations revealed that he had falciparum malaria along with co-existing severe G6PD deficiency and Gilbert's syndrome, which we believe, all contributed to an exacerbation of unconjugated hyperbilirubinemia (four-fold rise). He was treated with intravenous fluids, paracetamol and oral artemether/lumefantrine combination therapy. He made a good clinical recovery. After a month, he still exhibited chronic unconjugated hyperbilirubinemia with recurrent elevation in his reticulocyte count but no anaemia, suggesting further episodes of compensated hemolysis. We also discuss the differential diagnosis for unconjugated hyperbilirubinemia in relation to this interesting case.

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