There is growing evidence of a link between chronic low-grade inflammation and both depression and several aging associated diseases. Moreover, major depression appears to be associated with increased plasma concentrations of cytokines and C-reactive protein, a marker used to emphasize low-grade inflammation and to predict cardiovascular events in patients with coronary heart disease.
Recently, a relationship between C-Reactive Protein and mood disorders has been proposed by some researchers.
The aim of our study was to investigate the correlation between plasma concentrations of C-Reactive Protein and both severity of symptoms and psychopathological dimensions (anhedonia, psychomotor retardation and aggression), in patients with major depression during an acute phase of illness.
67 drug-free patients (M/F = 30/37; mean age 47,41±12,68) with a Major Depressive Disorder (MDD) during a Major Depressive Episode (MDE) have been recruited at the Day Clinic of Psychiatry of the Catholic University of Sacred Heart in Rome.
A blood sample for the determination of plasma C-Reactive Protein levels was collected before starting treatment.
Severity of depressive and anxiety symptoms was measured with 21-HDRS (21 Item - Hamilton Depression Rating Scale) and HARS (Hamilton Anxiety Rating Scale). Social functioning was evaluated by SASS (Social Adaptation Self-Evaluation Scale).
Anhedonia, psychomotor retardation and aggression were evaluated by SHAPS (Snaith Hamilton Pleasure Scale), DRRS (Depression Retardation Rating Scale) and AQ (Aggression Questionnaire).
The levels of C-reactive protein were measured using a nefelometric system.
No significant correlation between C-Reactive Protein values and severity of depressive and anxious symptoms (HDRS and HARS scores) has been observed in our sample.
After controlling for age, C-Reactive Protein levels were significantly correlated to SASS scores (r = -0,64 t = 0,001).
When we considered the psychopathological dimensions of our sample, psychomotor retardation (DRRS scores; r = 0,62 t = 0,002), and anhedonic features (SHAPS scores; r = 0,46 t = 0,033) appeared to be significantly correlated to C-Reactive Protein values.
No significant correlation between aggression scores and C-Reactive Protein values has been reported.
The role of C-Reactive Protein in mood disorders is, to date, somewhat unclear. Recent evidence suggests that depressive symptoms and hostility may act together, as interacting factors, to have an effect on the circulating levels of inflammatory markers relevant to coronary artery disease. In our sample, according to previous data, a dysfunction of inflammatory response have not been related to the severity of depressive symptoms. No correlation between aggression scores and C-Reactive Protein levels has also been observed.
A psychopathological profile characterized by psychomotor retardation and anhedonia has been significantly correlated to higher C-Reactive Protein levels. Historically, psychomotor disturbances and anhedonic features continue to be regarded as essential and measurable features of major depressive disorder that also contribute to the nosology of the melancholic subtypes.
Further researches in larger samples are needed to clarify the role of C-Reactive Protein as a marker of underlying low-grade inflammation in major depression with melancholic features.