Article

C-reactive protein serum level in drug-free male Egyptian patients with schizophrenia.

Psychiatry Department, Faculty of Medicine, Zagazig University, Zagazig, Sharkia, Egypt.
Psychiatry Research (Impact Factor: 2.68). 05/2011; 190(1):91-7. DOI: 10.1016/j.psychres.2011.05.010
Source: PubMed

ABSTRACT Despite the growing research interest in the role of immunological markers in schizophrenia, few studies, with conflicting results, have focused on the association between high sensitivity C-reactive protein (hs-CRP) levels and clinical characteristics in schizophrenia. In this cross-sectional case-control study, a sample of 200 antipsychotic-free male Egyptian schizophrenia patients was assessed by the Positive and Negative Syndrome Scale (PANSS) and compared with 200 healthy controls as regards serum hs-CRP level using an immunoturbidimetric method. CRP level for patients (geometric mean=3.3 mg/L) was significantly (P=0.000) higher than that for controls (geometric mean=1.4 mg/L). PANSS scores and patients' data, which significantly correlated with serum hs-CRP level, were entered into a stepwise multiple regression analysis. Results of this analysis showed that PANSS negative symptom score was second only to the waist circumference, with which they explained 54.7 % of the variation in serum hs-CRP. Comparable results were obtained when patients, controls and the relevant confounders were included in one multivariate analysis. We concluded that in Egyptian men, waist circumference and schizophrenia diagnosis are strong predictors of raised CRP level independent of a number of potentially confounding variables. In antipsychotic-free patients, CRP level is higher than in healthy controls and is positively correlated with the severity of the psychopathology as measured by PANSS. This relationship is especially notable in negative, but not positive symptoms.

0 Followers
 · 
85 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ramadan fasting is believed to be beneficial. We assessed a random sample of 100 Egyptian male schizophrenia outpatients using the Positive and Negative Syndrome Scale (PANSS) and dietary, anthropometric, clinical, and laboratory measures at baseline (T1) before Ramadan of 2014 and during the fourth week of Ramadan (T2). The metabolic syndrome was identified in 31 patients and these showed a reduction of high-density lipoprotein cholesterol (HDLc) and brain-derived neurotrophic factor (BDNF) concentrations and increase in the levels of dietary intakes, body mass index (BMI), waste circumference, systolic and diastolic blood pressure, all PANSS subscales, glucose, insulin, HOMA-IR, total cholesterol, triglycerides, low-density lipoprotein-cholesterol (LDL-c), white blood cells, granulocytes, lymphocytes, monocytes, fibrinogen and high-sensitivity C-reactive protein (hs-CRP). In a multiple regression analysis, total energy intake and body mass index (BMI) emerged as the main independent predictors of deterioration in most inflammatory and psychopathology parameters. These findings did not support our hypothesis but suggested that Ramadan fasting has a negative impact on schizophrenia patients, especially those with metabolic syndrome. This could draw attention to the need in the psycho-education management of such patients to focus more on nutrition education for safe fasting. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    Psychiatry Research 12/2014; DOI:10.1016/j.psychres.2014.11.057 · 2.68 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Inflammation and maternal or fetal infections have been suggested as risk factors for schizophrenia (SZ) and bipolar disorder (BP). It is likely that such environmental effects are contingent on genetic background. Here, in a genome-wide approach, we test the hypothesis that such exposures increase the risk for SZ and BP and that the increase is dependent on genetic variants. We use genome-wide genotype data, plasma IgG antibody measurements against Toxoplasma gondii, Herpes simplex virus type 1, Cytomegalovirus, Human Herpes Virus 6 and the food antigen gliadin as well as measurements of C-reactive protein (CRP), a peripheral marker of inflammation. The subjects are SZ cases, BP cases, parents of cases and screened controls. We look for higher levels of our immunity/infection variables and interactions between them and common genetic variation genome-wide. We find many of the antibody measurements higher in both disorders. While individual tests do not withstand correction for multiple comparisons, the number of nominally significant tests and the comparisons showing the expected direction are in significant excess (permutation p=0.019 and 0.004 respectively). We also find CRP levels highly elevated in SZ, BP and the mothers of BP cases, in agreement with existing literature, but possibly confounded by our inability to correct for smoking or body mass index. In our genome-wide interaction analysis no signal reached genome-wide significance, yet many plausible candidate genes emerged. In a hypothesis driven test, we found multiple interactions among SZ-associated SNPs in the HLA region on chromosome 6 and replicated an interaction between CMV infection and genotypes near the CTNNA3 gene reported by a recent GWAS. Our results support that inflammatory processes and infection may modify the risk for psychosis and suggest that the genotype at SZ-associated HLA loci modifies the effect of these variables on the risk to develop SZ.
    PLoS ONE 10(3):e0116696. DOI:10.1371/journal.pone.0116696 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Recent lines of research have boosted awareness of the immunological facets of schizophrenia. However, associations with protein tyrosine phosphatase regulators have never been reported. The aim of our study was to investigate the expression and promoter status methylation of phosphatase SHP-1, a key negative regulator of the inflammatory process, in Peripheral blood mononuclear cells (PBMCs) of Schizophrenic patients. We enrolled fifty-four (28 men and 26 women) unmedicated first episode subjects (SC) who met DSM-IV and thirty-eight (22 men and 16 women) healthy controls (HC). The SC psychopathological status was assessed using the Positive and Negative Syndrome Scale. We evaluated SHP-1 expression by Quantitative Real-time PCR (qPCR) and Western blotting (WB) methods and promoter status methylation through PCR bisulfate. IKK/NFkB signaling was detected by WB, and medium and plasma levels of pro-inflammatory cytokines (IL-1β, IL-2, and TNF-α) by the ELISA method. SHP-1 was silenced by treating cells with specific siRNA. We found a significantly lower level of SHP-1 gene expression in PBMCs from SC vs. HC, consistently with which the promoter region analyzed presented significant hypermethylation. Silencing of SHP-1 expression induced higher activation of IKK/NF-kB signaling and pro-inflammatory cytokine production in ex vivo PBMCs from both SC and HC. Linear regression among patients generated a model in which SHP-1 expression explained 30% of the clinical negative symptom variance (adjusted R(2)=0.30, ANOVA P<0.001). Our findings are the first to suggest that impairment of SHP-1 expression is involved in the physiopathology of schizophrenia, opening fruitful new avenues for ameliorating treatment at least of negative symptoms.
    Brain Behavior and Immunity 04/2014; 41. DOI:10.1016/j.bbi.2014.04.008 · 6.13 Impact Factor