ABSTRACT
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.
Subject(s)
Oxidative Stress/physiology , Pressure Ulcer/metabolism , Adult , Antioxidants/metabolism , Biomarkers/metabolism , Catalase/metabolism , Female , Humans , Inflammation/metabolism , Male , Malondialdehyde/metabolism , Middle AgedABSTRACT
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.
ABSTRACT
Hyperhomocysteinemia and hyperactivity of the angiotensin-1 converting enzyme (ACE1) are considered two unconventional coronary risk factors. The study of the variation of these two biochemical parameters in coronary patients and metabolic investigation of the relationship between these two markers has a fundamental interest. In this context, 110 patients and 80 control subjects are recruited for our study. Homocystenemia was determined by fluorescence polarization immunoassay (FPIA). ACE1 activity was measured by kinetic method. An increased of homocysteinemia and ACE1 activity was observed in patients compared with control subjects (Hcy: 23±18 µmol/L vs 9±4 µmol /L; p<0.0001); (ACEI: 81±18 UI/L vs 55±18 UI/L; p<0.0001). These two markers varied differently according to the risk factors. Homocysteinemia, was negatively correlated with ACE1 activity (r = -0.36; p<0.001). The negative correlation between these two markers reflects metabolic and physiopathological interactions.
