C-reactive protein, pre- and postdexamethasone cortisol levels in post-traumatic stress disorder.

BACKGROUND: Dysregulations of the hypothalamic-pituitary-adrenal axis may impact inflammatory processes in post-traumatic stress disorder (PTSD), possibly resulting in a low-grade inflammation as reflected by elevated levels of C-reactive protein (CRP). METHODS: Serum CRP levels and salivary cortisol before and after the dexamethasone suppression test (DST) were assessed in 50 inpatients with main diagnoses PTSD, major depressive disorder or borderline personality disorder. RESULTS: A strong trend for lower CRP levels was found in PTSD positive individuals compared with patients without PTSD. CONCLUSIONS: Our study does not support the hypothesis of elevated serum CRP levels in PTSD compared with other psychiatric patients. However, a dysbalanced immune system with suppressed CRP might contribute to the elevated somatic comorbidity in PTSD.

RAGE expression in the human peritoneal membrane.

BACKGROUND: Experimental animal models have demonstrated that the interaction of advanced glycation end-products (AGE) with their receptor RAGE is, at least in part, responsible for peritoneal damage. This study investigates the in vivo expression of RAGE in the peritoneal membrane of uraemic human patients. METHODS: Peritoneal biopsies of 89 subjects (48 uraemic and 41 healthy age-matched patients) were examined. The expression of CD3, IL-6, activated NFkappaBp65, VEGF, transforming growth factor (TGF)-beta1, smooth-muscle actin (SMA), methylglyoxal (MGO) and RAGE was analysed immunohistochemically. Additionally, in 4 of the 48 uraemic patients, peritoneal biopsies were repeated after 15 months at the time of catheter removal to analyse the above parameters and the extent of NFkappaB-binding activity determined by electrophoretic mobility shift assay (EMSA) in the long-term follow-up. RESULTS: In comparison to the healthy controls, uraemic patients showed a significant increase in fibrosis, angiogenesis, submesothelial thickness, MGO-derived protein adducts, RAGE, IL-6, VEGF, TGF-beta1, SMA and NFkappaBp65 in their peritonea. Four patients, followed up longitudinally from peritoneal dialysis (PD) catheter insertion to removal, demonstrated further significant increase in the above parameters, particularly in RAGE expression and NFkappaB activation. CONCLUSIONS: Along with a higher expression of several indicators for inflammation, angiogenesis, fibrosis and AGE accumulation, the peritoneal membrane of the uraemic patients showed an increased submesothelial thickness and a marked induction of RAGE expression and NFkappaB-binding activity, which both further increased after PD treatment. These findings in human peritoneum support the concept of the AGE-RAGE interaction being crucial in peritoneal damage due to uraemia and PD.