Significance of measurements of peripheral carbonyl stress markers in a cross-sectional and longitudinal study in patients with acute-stage schizophrenia.
Altered peripheral carbonyl stress markers, high levels of serum pentosidine, which accumulates following carbonyl stress, and low levels of pyridoxal (vitamin B6), which detoxifies reactive carbonyl compounds, have been reported in a cross-sectional study of chronic schizophrenia. However, changes in the levels of these compounds in patients with schizophrenia have not been investigated in a longitudinal study. To clarify whether these markers may be biological markers that reflect the clinical course of the disease, the serum levels of these compounds were investigated in a cross-sectional and a longitudinal study. One hundred and thirty-seven acute-stage Japanese patients were enrolled. Among these, 53 patients were followed from the acute stage to remission. A portion of patients in the acute stage (14 cases, 10.2%) showed extremely high pentosidine levels. These levels were not associated with the severity of symptoms but were associated with antipsychotic dose amounts. Pyridoxal levels were lower in schizophrenia and increased according to the clinical course of the illness. Furthermore, 18 patients with decreased pyridoxal levels according to the clinical course showed that the greater the decrease in pyridoxal levels, the lesser the improvement in symptoms. Thus, extremely high pentosidine levels in a portion of patients may be caused by higher daily antipsychotic doses, whereas pyridoxal levels were lower in schizophrenia and increased according to the clinical course. Patients with decreasing pyridoxal levels during the clinical course showed less improvement in symptoms. Carbonyl stress markers may also be therapeutic biological markers in some patients with schizophrenia.
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Narimasa
N
Katsuta
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan tohru.oonuma@nifty.ne.jp.
Tohru
T
Ohnuma
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Hitoshi
H
Maeshima
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Yuto
Y
Takebayashi
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Motoyuki
M
Higa
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Mayu
M
Takeda
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Toru
T
Nakamura
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Shohei
S
Nishimon
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Takahiro
T
Sannohe
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Yuri
Y
Hotta
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Ryo
R
Hanzawa
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Ryoko
R
Higashiyama
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Nobuto
N
Shibata
Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan.
Heii
H
Arai
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D014150:Antipsychotic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008239:Lysine / Q000031:analogs & derivatives* / Q000097:blood; D008297:Male; D008875:Middle Aged; D011730:Pyridoxal / Q000097:blood*; D012559:Schizophrenia / Q000097:blood* / Q000188:drug therapy; D016896:Treatment Outcome; D055815:Young Adult
D014150:Antipsychotic Agents; D015415:Biomarkers; D011730:Pyridoxal; D001120:Arginine; C062187:pentosidine; D008239:Lysine
clinical course; pentosidine; pyridoxal; vitamin B6