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Neonatal-Onset Hereditary Coproporphyria: A New Variant of Hereditary Coproporphyria.新生儿期起病的遗传性粪卟啉病:遗传性粪卟啉病的一种新变体
JIMD Rep. 2017;37:99-106. doi: 10.1007/8904_2017_20. Epub 2017 Mar 28.
2
Mutations in human CPO gene predict clinical expression of either hepatic hereditary coproporphyria or erythropoietic harderoporphyria.人类CPO基因突变可预测肝性遗传性粪卟啉病或红细胞生成性原卟啉病的临床表型。
Hum Mol Genet. 2005 Oct 15;14(20):3089-98. doi: 10.1093/hmg/ddi342. Epub 2005 Sep 13.
3
The enzyme engineering of mutant homodimer and heterodimer of coproporphyinogen oxidase contributes to new insight into hereditary coproporphyria and harderoporphyria.突变同二聚体和异二聚体粪卟啉原氧化酶的酶工程有助于深入了解遗传性粪卟啉症和原卟啉症。
J Biochem. 2013 Dec;154(6):551-9. doi: 10.1093/jb/mvt086. Epub 2013 Sep 26.
4
Neonatal hemolytic anemia due to inherited harderoporphyria: clinical characteristics and molecular basis.遗传性肝性卟啉病所致新生儿溶血性贫血:临床特征及分子基础
Blood. 1998 Feb 15;91(4):1453-7.
5
Hereditary Coproporphyria遗传性粪卟啉病
6
Harderoporphyria: Case of lifelong photosensitivity associated with compound heterozygous coproporphyrinogen oxidase (CPOX) mutations.迟发性皮肤卟啉症:与复合杂合性粪卟啉原氧化酶(CPOX)突变相关的终身光敏性病例。
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7
Characterization of mutations in the CPO gene in British patients demonstrates absence of genotype-phenotype correlation and identifies relationship between hereditary coproporphyria and harderoporphyria.对英国患者中CPO基因突变的特征分析表明不存在基因型-表型相关性,并确定了遗传性粪卟啉病和硬卟啉病之间的关系。
Am J Hum Genet. 2001 May;68(5):1130-8. doi: 10.1086/320118. Epub 2001 Apr 16.
8
Harderoporphyria due to homozygosity for coproporphyrinogen oxidase missense mutation H327R.由于粪卟啉原氧化酶错义突变 H327R 导致的硬骨卟啉症。
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Harderoporphyria: a variant hereditary coproporphyria.重型血卟啉病:一种变异型遗传性粪卟啉病。
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10
Neonatal-onset hereditary coproporphyria with male pseudohermaphrodism.
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Neurodevelopmental retardation and neurological symptoms in homozygous variegate porphyria: two new cases and a literature review.纯合性杂色卟啉症中的神经发育迟缓与神经症状:两例新病例及文献综述
Orphanet J Rare Dis. 2025 Mar 20;20(1):139. doi: 10.1186/s13023-025-03606-6.

本文引用的文献

1
The enzyme engineering of mutant homodimer and heterodimer of coproporphyinogen oxidase contributes to new insight into hereditary coproporphyria and harderoporphyria.突变同二聚体和异二聚体粪卟啉原氧化酶的酶工程有助于深入了解遗传性粪卟啉症和原卟啉症。
J Biochem. 2013 Dec;154(6):551-9. doi: 10.1093/jb/mvt086. Epub 2013 Sep 26.
2
Porphyrias.卟啉症。
Lancet. 2010 Mar 13;375(9718):924-37. doi: 10.1016/S0140-6736(09)61925-5.
3
Mutations in human CPO gene predict clinical expression of either hepatic hereditary coproporphyria or erythropoietic harderoporphyria.人类CPO基因突变可预测肝性遗传性粪卟啉病或红细胞生成性原卟啉病的临床表型。
Hum Mol Genet. 2005 Oct 15;14(20):3089-98. doi: 10.1093/hmg/ddi342. Epub 2005 Sep 13.
4
Porphyrias.卟啉病
Lancet. 2005;365(9455):241-52. doi: 10.1016/S0140-6736(05)17744-7.
5
Neonatal-onset hereditary coproporphyria with male pseudohermaphrodism.
Blood. 2001 Dec 15;98(13):3871-3. doi: 10.1182/blood.v98.13.3871.
6
Hereditary coproporphyria in Germany: clinical-biochemical studies in 53 patients.德国的遗传性粪卟啉病:53例患者的临床生化研究
Clin Biochem. 2000 Aug;33(6):465-73. doi: 10.1016/s0009-9120(00)00159-4.
7
Neonatal hemolytic anemia due to inherited harderoporphyria: clinical characteristics and molecular basis.遗传性肝性卟啉病所致新生儿溶血性贫血:临床特征及分子基础
Blood. 1998 Feb 15;91(4):1453-7.
8
Homozygous hereditary coproporphyria caused by an arginine to tryptophane substitution in coproporphyrinogen oxidase and common intragenic polymorphisms.由原卟啉原氧化酶中精氨酸替换为色氨酸及常见基因内多态性引起的纯合子遗传性粪卟啉病。
Hum Mol Genet. 1994 Mar;3(3):477-80. doi: 10.1093/hmg/3.3.477.
9
Coproporphyrinogen oxidase: gene organization and description of a mutation leading to exon 6 skipping.
Hum Mol Genet. 1994 Aug;3(8):1325-30. doi: 10.1093/hmg/3.8.1325.
10
A molecular defect in coproporphyrinogen oxidase gene causing harderoporphyria, a variant form of hereditary coproporphyria.粪卟啉原氧化酶基因的分子缺陷导致硬卟啉症,这是遗传性粪卟啉症的一种变异形式。
Hum Mol Genet. 1995 Feb;4(2):275-8. doi: 10.1093/hmg/4.2.275.

新生儿期起病的遗传性粪卟啉病:遗传性粪卟啉病的一种新变体

Neonatal-Onset Hereditary Coproporphyria: A New Variant of Hereditary Coproporphyria.

作者信息

Hasegawa Kosei, Tanaka Hiroyuki, Yamashita Miho, Higuchi Yousuke, Miyai Takayuki, Yoshimoto Junko, Okada Ayumi, Suzuki Norihiro, Iwatsuki Keiji, Tsukahara Hirokazu

机构信息

Department of Pediatrics, Okayama University Hospital, Shikatacho 2-5-1, Kita-ku, Okayama, 700-8558, Japan.

Department of Pediatrics, Okayama Saiseikai General Hospital, Okayama, Japan.

出版信息

JIMD Rep. 2017;37:99-106. doi: 10.1007/8904_2017_20. Epub 2017 Mar 28.

DOI:10.1007/8904_2017_20
PMID:28349448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5740044/
Abstract

Genetic mutation of the coproporphyrinogen oxidase (CPOX) gene causes either hereditary coproporphyria (HCP) or harderoporphyria. HCP, a rare hepatic porphyria, causes acute attacks after puberty and rarely accompanies cutaneous symptoms. In contrast, harderoporphyria is an erythropoietic porphyria that represents photosensitivity and hemolytic anemia from the neonatal period. In patients with harderoporphyria, the p.Lys404Glu mutation is found in the homozygous or compound heterozygous state with another mutation, and a marked increase in harderoporphyrin is observed. This report describes a neonate with symptoms of erythropoietic harderoporphyria (photosensitivity of the skin, hemolytic anemia, and jaundice). However, the pattern of porphyrin metabolites of feces was consistent with that of typical HCP, not of harderoporphyria. We found a heterozygous, novel, four-base pair deletion in exon 7 of the CPOX gene, although other mutations including the p.Lys404Glu mutation in CPOX were not found. By unknown etiology, our patient had accompanying adrenocortical insufficiency and 46, XY disorders of sex development. Based on genetic mutation of the CPOX gene and information from a previous similar case report, we consider that neonatal-onset HCP is a variant of HCP.

摘要

粪卟啉原氧化酶(CPOX)基因突变可导致遗传性粪卟啉病(HCP)或重型卟啉病。HCP是一种罕见的肝性卟啉病,青春期后会引发急性发作,很少伴有皮肤症状。相比之下,重型卟啉病是一种红细胞生成性卟啉病,从新生儿期就表现出光敏性和溶血性贫血。在重型卟啉病患者中,p.Lys404Glu突变以纯合子或复合杂合子状态与另一种突变同时存在,且观察到重型卟啉明显增加。本报告描述了一名患有红细胞生成性重型卟啉病症状(皮肤光敏性、溶血性贫血和黄疸)的新生儿。然而,粪便中卟啉代谢物的模式与典型的HCP一致,而非重型卟啉病。我们在CPOX基因外显子7中发现了一个杂合的、新的四碱基对缺失,尽管未发现包括CPOX基因中的p.Lys404Glu突变在内的其他突变。由于病因不明,我们的患者伴有肾上腺皮质功能不全和46, XY性发育障碍。基于CPOX基因的基因突变以及之前一份类似病例报告的信息,我们认为新生儿期发病的HCP是HCP的一种变体。