Clinical manifestations and treatment of Menkes disease and its variants

被引:83
作者
Kodama, H [1 ]
Murata, Y [1 ]
Kobayashi, M [1 ]
机构
[1] Teikyo Univ, Sch Med, Dept Pediat, Itabashi Ku, Tokyo 1738605, Japan
关键词
clinical features; Menkes disease; occipital horn syndrome; treatment;
D O I
10.1046/j.1442-200x.1999.01095.x
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
The clinical manifestations of classical Menkes disease, mild Menkes disease and occipital horn syndrome are reviewed. Menkes disease is a neurodegenerative disease with X-linked recessive inheritance. Orally administered copper accumulates in the intestine, resulting in the failure of copper absorption. The primary metabolic defect that causes copper accumulation in the intestine is present in almost all extrahepatic tissues. The blood, liver and brain are in a state of copper deficiency, which is due to defective copper absorption. The characteristic features, including neurological disturbances, arterial degeneration and hair abnormalities, can be explained by the decrease in cuproenzyme activities. DNA-based diagnosis is now possible. Mild Menkes disease and occipital horn syndrome, which show milder forms than Menkes disease, have been identified as genetic disorders resulting from mutations in the Menkes disease gene. Because the clinical spectrum of Menkes disease is wide, males with mental retardation and connective tissue abnormalities should be evaluated for biochemical evidence of defective copper transport. The treatment accepted currently is parenteral administration of copper. When treatment is started in patients with classical Menkes disease above the age of 2 months, it does not improve the neurological degeneration. When the treatment is initiated in newborn babies affected with this disease, the neurological degeneration can be prevented in some, but not all, cases. Moreover, early treatment cannot improve non-neurological problems, such as connective tissue laxity. Therefore, alternative therapies for Menkes disease and occipital horn syndrome should be studied.
引用
收藏
页码:423 / 429
页数:7
相关论文
共 50 条
[1]   UPTAKE OF COPPER-67 COMPLEXED TO H-3 HISTIDINE BY BRAIN HYPOTHALAMIC SLICES - EVIDENCE THAT DISSOCIATION OF THE COMPLEX IS NOT THE ONLY FACTOR DETERMINING COPPER-67 UPTAKE [J].
BARNEA, A ;
KATZ, BM .
JOURNAL OF INORGANIC BIOCHEMISTRY, 1990, 40 (01) :81-93
[2]   ISOLATION OF A CANDIDATE GENE FOR MENKES DISEASE THAT ENCODES A POTENTIAL HEAVY-METAL BINDING-PROTEIN [J].
CHELLY, J ;
TUMER, Z ;
TONNESEN, T ;
PETTERSON, A ;
ISHIKAWABRUSH, Y ;
TOMMERUP, N ;
HORN, N ;
MONACO, AP .
NATURE GENETICS, 1993, 3 (01) :14-19
[3]  
Danks D.M., 1995, METABOLIC MOL BASIS, P2211
[4]  
Danks David M., 1993, P487
[5]  
DANKS DM, 1972, PEDIATRICS, V50, P188
[6]   THE MILD FORM OF MENKES DISEASE - PROGRESS REPORT ON THE ORIGINAL CASE [J].
DANKS, DM .
AMERICAN JOURNAL OF MEDICAL GENETICS, 1988, 30 (03) :859-864
[7]  
DAS S, 1994, AM J HUM GENET, V55, P883
[8]  
DAS S, 1995, AM J HUM GENET, V56, P570
[9]   MENKES DISEASE - NEUROPHYSIOLOGICAL ASPECTS [J].
FRIEDMAN, E ;
HARDEN, A ;
KOIVIKKO, M ;
PAMPIGLIONE, G .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1978, 41 (06) :505-510
[10]   EXPRESSION AND ACCUMULATION OF LYSYL OXIDASE, ELASTIN, AND TYPE-I PROCOLLAGEN IN HUMAN MENKES AND MOTTLED MOUSE FIBROBLASTS [J].
GACHERU, S ;
MCGEE, C ;
URIUHARE, JY ;
KOSONEN, T ;
PACKMAN, S ;
TINKER, D ;
KRAWETZ, SA ;
REISER, K ;
KEEN, CL ;
RUCKER, RB .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1993, 301 (02) :325-329