Higher Serum C-Reactive Protein Levels in Catatonic Patients: A Comparison to Non-catatonic Patients and Healthy Controls

Abstract

Catatonia is a psychomotor syndrome defined by a constellation of predominantly motor symptoms. The aim of the present study was to determine whether recently admitted psychiatric patients with catatonia exhibited higher serum C-reactive protein (hs-CRP) levels compared to non-catatonic psychiatric patients and healthy controls (HCs). Recently admitted psychiatric patients were screened and evaluated for the catatonia syndrome using the Bush-Francis Catatonia Rating Scale and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). The study sample was formed by 150 individuals (39 male and 111 female), including 51 catatonic patients, 55 non-catatonic patients, and 44 HCs. Serum hs-CRP levels were processed with the enzyme-linked immunosorbent assay. Serum levels of creatine kinase (CK), adrenocorticotropic hormone (ACTH), immunoglobulin G (IgG), complement component 3 (C3), and complement component 4 (C4) were also determined. There was a significantly higher percentage of patients with high inflammatory levels (hs-CRP > 3000ng/ml) in the catatonic (43.1%) than in the non-catatonic (14.5%) or HCs group (9.1%) (χ 2 =18.9, P < .001). Logistic regression showed that catatonic patients had significantly higher hs-CRP levels compared to non-catatonic patients even after controlling for other clinical and laboratory variables (OR = 3.52, P = .015, 95% CI 1.28–9.79). Multiple linear regression analysis revealed that log-transformed hs-CRP was independently predicted by body mass index and log-transformed C4, ACTH, and Cortisol in catatonic patients. Findings of the present study suggest that catatonia is specifically linked to a higher level of systemic inflammation, not merely attributable to the overall psychopathology, or alterations in the stress level and complement system.

Statins in Depression: An Evidence-Based Overview of Mechanisms and Clinical Studies

“…Moreover, the prevalence of depression is higher among patients suffering from immune-mediated inflammatory disorders ( 10 ), and immunomodulation improves their depressive symptomatology irrespective of their effects on physical illness ( 11 ). Increased inflammatory markers have also been associated with specific subgroups of depressed patients, particularly those responding poorly to conventional antidepressants ( 12 , 13 ), and those with high levels of anxiety ( 14 ), sleep disturbance ( 15 ), anhedonia ( 16 ), and psychomotor retardation ( 17 , 18 ) — a cluster of symptoms that have been referred to as “depressive-inflammatory.” Therefore, targeting inflammation in depression may be a viable treatment strategy, and recent meta-analyses have described encouraging effects of anti-inflammatory agents as adjunctive treatments in depressed patients ( 19 ).…”

Complement component C4 levels in the cerebrospinal fluid and plasma of patients with schizophrenia

“…Few studies have investigated transcript and protein levels of complement molecules, particularly of C4, in patients with schizophrenia and findings have been inconsistent. Some authors have found differences between groups of ultrahigh risk or schizophrenia patients and healthy volunteers (HV) [9][10][11] whereas others did not find any differences [12,13] Unfortunately, the study designs, the C4 assays and the patients selected for the studies were quite different between studies which could explain some of the inconsistent results. In the only longitudinal study reported in the literature, Mondelli et al [14] found that baseline complement C4 serum levels predicted response to treatment in 25 FEP patients who were followed up for 1 year, with nonresponders having higher C4 levels at baseline compared to responders.…”

Cerebrospinal fluid concentration of complement component 4A is increased in first episode schizophrenia

“…Several previous studies have measured total C4 levels in plasma from patients with SCZ but with conflicting results [32][33][34][35] , and C4 levels in plasma do not significantly correlate with total C4 levels in CSF 36 . In the current study, we separate C4A and C4B levels in CSF and in line with previous experimental and genetic studies we observe that only C4A is increased in first episode patients with SCZ.…”