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      한국 정신분열병 환자에서의 혈중 Homocysteine, 엽산, Vitamin B12 농도 비교연구 = Comparison of Serum Homocysteine, Folate and Vitamin B12 Level in Korean Schizophrenics

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      https://www.riss.kr/link?id=A101640528

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      다국어 초록 (Multilingual Abstract)

      Objective:There have been a kind of transmethylation theory that high homocysteine serum concentration affects schizophrenia by neurotoxic mechanism and clinical reports that some schizophrenic patients with high homocysteine were improved by high folate ingestion. This study was done to confirm previous research results and find the clinical characteristics of schizophrenia showing high serum homocysteine and low folate. Method:We compared the serum levels of homocysteine, folate and vitamin B12 level between 234 schizophrenic patients(male 99, female 135) group and 234 normal controls(male 99, female 135) group. The subjects of two groups were age and sex matched. The evaluated clinical characteristics items were sex, age, onset of disease, hereditary loading, disease course, hallucination and subtype of schizophrenia. Results:1) Homocysteine level of the schizophrenia group was significantly higher than the normal control group and folate level of the schizophrenia group was significantly lower than the normal control group. Homocysteine level was more negatively correlated with folate level in the schizophrenia group than the normal control group. 2) The percentage of high homocysteine(above 12.46umol/L;90 percentile of normal control) was 33.8% of schizophrenia patients and 51.5% of male schizophrenia. The percentage of low folate(below 3.8nM/L;bottom tertile of normal control) was 66.2% of schizophrenia. 3) In low folate group and not-low folate group, schizophrenia showed significantly higher homocysteine level than normal control. Especially, low folate schizophrenia group showed significantly higher homocysteine level than low folate normal control group. Conclusions:Some schizophrenia patients with high serum homocysteine may be genetic defector and having low folate serum level. In that case, folate ingestion could be a good management for clinical improvement.
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      Objective:There have been a kind of transmethylation theory that high homocysteine serum concentration affects schizophrenia by neurotoxic mechanism and clinical reports that some schizophrenic patients with high homocysteine were improved by high fol...

      Objective:There have been a kind of transmethylation theory that high homocysteine serum concentration affects schizophrenia by neurotoxic mechanism and clinical reports that some schizophrenic patients with high homocysteine were improved by high folate ingestion. This study was done to confirm previous research results and find the clinical characteristics of schizophrenia showing high serum homocysteine and low folate. Method:We compared the serum levels of homocysteine, folate and vitamin B12 level between 234 schizophrenic patients(male 99, female 135) group and 234 normal controls(male 99, female 135) group. The subjects of two groups were age and sex matched. The evaluated clinical characteristics items were sex, age, onset of disease, hereditary loading, disease course, hallucination and subtype of schizophrenia. Results:1) Homocysteine level of the schizophrenia group was significantly higher than the normal control group and folate level of the schizophrenia group was significantly lower than the normal control group. Homocysteine level was more negatively correlated with folate level in the schizophrenia group than the normal control group. 2) The percentage of high homocysteine(above 12.46umol/L;90 percentile of normal control) was 33.8% of schizophrenia patients and 51.5% of male schizophrenia. The percentage of low folate(below 3.8nM/L;bottom tertile of normal control) was 66.2% of schizophrenia. 3) In low folate group and not-low folate group, schizophrenia showed significantly higher homocysteine level than normal control. Especially, low folate schizophrenia group showed significantly higher homocysteine level than low folate normal control group. Conclusions:Some schizophrenia patients with high serum homocysteine may be genetic defector and having low folate serum level. In that case, folate ingestion could be a good management for clinical improvement.

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      참고문헌 (Reference)

      1 Martorell L, "lack ofassociation with schizophrenia" 2035-2038,

      2 Olivieri O, "and folate insubjects from northern Italy with or without angiographicallydocumented severe coronary atherosclerotic disease evidence for an important genetic-environmental interaction" 4158-4163,

      3 Blom HJ, "a common mutation in methylenetetrahydrofolatereductase" 111-113,

      4 Jacques PF, "The effect of folic acid fortification on plasmafolate and total homocysteine concentrations" 1449-1454,

      5 Cohen SM, "The administrationof methionine to schizophrenic patients" 209-215, biolpsyhiatry1974;8

      6 Osmond H,, "Schizophrenia,a new approach." 309-314, jmentsci1952;98

      7 Schimke RN, "Schizophrenia in apatient with a defect in methionine metabolism" 285-290, jnervmentdis1965;141

      8 Jacques PF, "Relationship between plasma homocysteine andvitamin status in the Framingham study population" 117-145,

      9 Jacques PF, "Relation between folatestatus a common mutation in methylenetetrahydrofolatereductase" 7-9, circulation1996;1;93

      10 Lipton SA, "Neurotoxicity associated withdual actions of homocysteine at the N-methyl-D-aspartatereceptor" 94 : 5923-5928, 1997

      1 Martorell L, "lack ofassociation with schizophrenia" 2035-2038,

      2 Olivieri O, "and folate insubjects from northern Italy with or without angiographicallydocumented severe coronary atherosclerotic disease evidence for an important genetic-environmental interaction" 4158-4163,

      3 Blom HJ, "a common mutation in methylenetetrahydrofolatereductase" 111-113,

      4 Jacques PF, "The effect of folic acid fortification on plasmafolate and total homocysteine concentrations" 1449-1454,

      5 Cohen SM, "The administrationof methionine to schizophrenic patients" 209-215, biolpsyhiatry1974;8

      6 Osmond H,, "Schizophrenia,a new approach." 309-314, jmentsci1952;98

      7 Schimke RN, "Schizophrenia in apatient with a defect in methionine metabolism" 285-290, jnervmentdis1965;141

      8 Jacques PF, "Relationship between plasma homocysteine andvitamin status in the Framingham study population" 117-145,

      9 Jacques PF, "Relation between folatestatus a common mutation in methylenetetrahydrofolatereductase" 7-9, circulation1996;1;93

      10 Lipton SA, "Neurotoxicity associated withdual actions of homocysteine at the N-methyl-D-aspartatereceptor" 94 : 5923-5928, 1997

      11 Lebert F, "Methylenetetrahydrofolate reductase deficiency revealedby a neuropathy in a psychotic adult" 765-766, jneurolneurosurgpsychiatry1994;57

      12 Nygard O, "Major lifestyledeterminants of plasma total homocysteine distribution" 263-270, amjclinnutr1998;67

      13 McKeever DJ, "Links Bovine afferentlymph veiled cells differ from blood monocytes in phenotypeand accessory function" awi (awi): 3703-3709, jimmunol1991;147

      14 Kim WK, "Involvement of N-methyl-D-aspartatereceptor and free radical in homocysteine mediated toxicityon rat cerebellar granule cells" 216 : 117-120, 1996

      15 Durand P,, "Impaired homocysteinemetabolism and atherothrombosis disease" 81 : 645-672, 2001

      16 Tawakol A, "Hyperhomocysteinemiais associated with impaired endothelium dependentvasodilatation in humans" 95 : 1119-1121, 1997

      17 "Homozygous thermolabile methylenetetrahydrofolatereductase in schizophrenia-like psychosis" 931-941, jneuraltransm1997;104

      18 Johansson BV, "Homocysteinemiaand schizophrenia as a case of methylation deficiency" 143-152, jneuraltransm[gensect]1994;98

      19 Reutens S,, "Homocysteine in neuropsychiatricdisorders of the elderly" 17 : 859-864, 2002

      20 Kruman II,, "Homocysteine elicits a DNA damageresponse in neurons that promotes apoptosis and hypersensitivityto excitotoxicity" 20 : 6920-6926, 2000

      21 Fava M,, "Folate, Vitamin B12, and Homocysteinein major depressive disorder" 154 : 426-428, 1997

      22 Levine J, "Elevated homocysteine levels in youngmale patients with schizophrenia" 1790-1792, amjpsychiatry2002;159

      23 Brune CG, "Effects of methionine loadingon behavior of schizophrenic patients" 447-450, jnervmentdis1962;134

      24 Cardon PV, "Effects of amino acidfeedings in schizophrenic patients treated with iproniazid" 104-105, science1961;133

      25 American Psychiatric Association, "Diagnostic and StatisticalManual of Mental Disorders" American Psychiatric Press;1994

      26 Jacques PF, "Determinants of plasma total homocysteineconcentration in the Framingham Offspringcohort" 613-621, amjclinnutr2001;73

      27 Freeman JM, "A defect inmethylation due to deficient 5" 10 491-496,

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2026 평가예정 재인증평가 신청대상 (재인증)
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      2013-01-01 평가 등재 1차 FAIL (등재유지) KCI등재
      2010-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2007-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2006-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2004-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.19 0.19 0.19
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.14 0.15 0.475 0
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