Kynurenine and Tryptophan Levels in Patients With Schizophrenia and Elevated Antigliadin Immunoglobulin G Antibodies.
Kynurenine and Tryptophan Levels in Patients With Schizophrenia and Elevated Antigliadin Immunoglobulin G Antibodies.
复制标题
精神分裂症患者的犬尿氨酸和色氨酸水平以及抗麦胶蛋白免疫球蛋白 G 抗体升高。
DOI:
10.1097/psy.0000000000000352
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发表时间:
2016
影响因子:
3.3
通讯作者:
中科院分区:
文献类型:
--
作者:
Okusaga,Olaoluwa;Fuchs,Dietmar;Reeves,Gloria;Giegling,Ina;Hartmann,AnnetteM;Konte,Bettina;Friedl,Marion;Groer,Maureen;Cook,ThomasB;Stearns-Yoder,KellyA;Pandey,JanardanP;Kelly,DeannaL;Hoisington,AndrewJ;Lowry,ChristopherA;
ObjectiveSeveral studies have reported an association between nonceliac gluten sensitivity and schizophrenia. Immune and kynurenine (KYN) pathways have also been implicated in the pathophysiology of schizophrenia, and certain proinflammatory immune mediators may increase KYN and reduce tryptophan (TRP) levels.MethodsWe measured serum antigliadin immunoglobulin G (IgG), KYN, and TRP in 950 patients with schizophrenia. Patients with antibody level at the 90th percentile or higher of control participants (21.9% of all patients) were classified as having elevated antigliadin IgG. Independent t tests and linear regression models were used to compare TRP, KYN, and KYN-TRP ratio (indicator of TRP metabolism) between patients with and those without elevated antigliadin IgG. The correlation between antigliadin IgG and TRP, KYN, and the ratio was also evaluated in the patients.ResultsKYN and KYN-TRP ratio were higher in patients with elevated antigliadin IgG (geometric mean [standard deviation {SD}]= 2.65 [0.25] µmol/L versus 2.25 [0.23] µmol/L [p<. 001] and 0.05 [0.26] versus 0.04 [0.25; p=. 001] respectively), findings robust to adjustment for potential demographic and clinical confounders. Antigliadin IgG positively correlated with KYN and KYN-TRP ratio (r= 0.12, p<. 001; r= 0.11, p=. 002). TRP did not differ between the two groups and did not correlate with antigliadin IgG.ConclusionsOur results connect nonceliac gluten sensitivity with the KYN pathway of TRP metabolism in psychotic illness and hint toward potential individualized treatment targets.