| Literature DB >> 28349448 |
Kosei Hasegawa1, Hiroyuki Tanaka2,3, Miho Yamashita2, Yousuke Higuchi2, Takayuki Miyai2, Junko Yoshimoto2, Ayumi Okada2, Norihiro Suzuki4, Keiji Iwatsuki4, Hirokazu Tsukahara2.
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.Entities:
Keywords: Coproporphyrinogen oxidase; Hereditary coproporphyria; Jaundice; Neonate; Photosensitivity
Year: 2017 PMID: 28349448 PMCID: PMC5740044 DOI: 10.1007/8904_2017_20
Source DB: PubMed Journal: JIMD Rep ISSN: 2192-8304