Evidence of metabolic imbalance and oxidative stress among patients suffering from pressure ulcers.

Background: Pressure ulcers (PU) are serious medical problems that involve several factors. Recent studies suggest that oxidative stress along with chronic inflammation may cause and develop PU. However, the metabolic disturbances underlying PU are not totally known. The purpose of this study is to evaluate biochemical oxidative stress markers in Tunisian patients suffering from PU. Methods: A total of 100 adult patients with PU and 213 healthy adult controls were selected for the study. Biochemical parameters related to immune profiles, and biomarkers of the liver, kidney, and inflammatory proteins were evaluated using recently developed automated measurement methods. Oxidant-antioxidant system markers (malondialdehyde (MDA), carbonyl proteins, total antioxidant potential, total oxidant status (TOS), catalase, and glutathione-S-transferase) were studied using appropriate methods. Results: Patients with PU showed, remarkably, abnormal levels of biochemical markers and relatively higher systemic oxidative stress compared to healthy subjects. This provides the first evidence that alterations in biochemical parameters and oxidative stress are features of PU. Conclusions: Understanding the signaling pathways involved in the development of PU will provide experts with additional knowledge for therapeutic strategies aimed at limiting the oxidative and inflammatory reactions in affected patients. ClinicalTrials.gov ID: NCT0257800.

Hepatic Proteins and Inflammatory Markers in Rheumatoid Arthritis Patients.

BACKGROUND: Rheumatoid arthritis is an autoimmune inflammatory rheumatic disease that causes chronic synovial inflammation eventually leading to joint destruction and disability. The aim of this study was to determine the variations of hepatic proteins, myeloperoxidase, and iron in rheumatoid arthritis Tunisian patients and their implications in inflammation and in iron metabolism. METHODS: Overall, 172 patients from the Rheumatology Department of the University Hospital "Farhat Hached", Sousse-Tunisia between 2011 and 2012, with rheumatoid arthritis (97.1% women, average age: 48±13 yr) and 147 healthy volunteers (70.1% women, average age: 46± 7 yr) were included in this study. Serum hepatic proteins (high-sensitive C-reactive protein, ceruloplasmin, albumin, transferrin, α-1-acid glycoprotein and haptoglobin) were assessed by immunoturbidimetry (COBAS INTEGRA 400, Roche) and ferritin was measured by a microparticulate immunoenzymatic technic (AxSYM, ABBOTT, Germany), Plasma myeloperoxidase was determined by Enzyme-Linked Immunosorbent Assay. Serum iron was measured according to a colorimetric method at 595 nm (CX9-BECKMANN Coulter-Fuller-Ton, CA). RESULTS: Significantly higher levels of high-sensitive C-reactive protein, α-1-acid glycoprotein, Haptoglobin and myeloperoxidase in patients compared to controls (P<10-3). Albumin and iron rates were significantly decreased in patients compared to healthy group (P=0.026 and P<10-3, respectively). There were no differences between cases and controls for levels of ceruloplasmin, transferrin and ferritin (P=0.782, P=0.808, and P=0.175, respectively). CONCLUSION: The high-sensitive C-reactive protein, α-1-acid glycoprotein, and haptoglobin increased in acute phase proteins in rheumatoid arthritis disease. The pro-inflammatory cytokines affect iron metabolism leading to the iron deficiency and rheumatoid anemia, which influenced Tf and ferritin levels.

Predictive value of interleukin-10 promoter genotypes and haplotypes in determining the susceptibility to nephropathy in type 2 diabetes patients.

BACKGROUND: The IL-10 promoter polymorphisms -1082G/A, -819C/T, and -592C/A have been consistently associated with type 2 diabetes (T2DM). We examined whether these polymorphisms variants are also associated with progression of diabetic nephropathy (DN). METHODS: These promoter variants were genotyped in 917 T2DM patients comprising 515 DN patients and 402 control patients without nephropathy (DWN), together with 748 non-diabetic control subjects. Haplotype analysis and multivariate regression analysis were employed in assessing the contribution of IL-10 haplotypes to DN risk, using genotype, clinical and biochemical profile, and their interactions as predictors of DN. RESULTS: Carriers of mutant -592A and -819T alleles, and -819T/T, -592A/A, and -819C/T genotypes were more frequent in T2DM. However, the -819C/T genotype appeared to be protective of DN, since lower frequency -819T allele and -819C/T genotype were seen in DN patients. Regression analysis identified -1082G/-819T/-592A (GTA) and -1082G/-819T/-592C (GTC) haplotypes as DN-protective haplotypes. Relative to the -1082G/-819C/-592C haplotype, GTA [P = 0.044; odds ratio (OR) = 0.54, 95% confidence interval (CI): 0.30-0.98] and GTC (P = 0.045; OR = 0.56, 95% CI: 0.31-0.99) haplotypes were associated with decreased odds ratio (OR) for DN, after controlling for a number of covariates (age, sex, body mass index (BMI), hypertension, glucose, HbA(1c), DN duration, total cholesterol). CONCLUSIONS: Our results indicate that genetic variations at the IL-10 promoter influence the risk of nephropathy in T2DM patients and thus represent a potential DN genetic-susceptibility locus worthy of replication.