Fournier's gangrene is a rare but highly mortal infectious disease characterised by fulminant necrotising fasciitis involving the genital and perineal regions. The objective of this study is to analyse the demographics, clinical feature and treatment approaches as well as outcomes of Fournier's gangrene. Data were collected retrospectively from medical records and operative notes. Patient data were analysed by demographics, aetiological factors, clinical features, treatment approaches and outcomes. Twelve patients (five female and seven male) were enrolled in this study. The most common aetiology was perianal abscess (41·6%). Wound cultures showed a mixture of microorganisms in six (50%) patients. For faecal diversion, while colostomy was performed in six cases (50%), Flexi-Seal was used in two cases (16·6%). In four patients (33·4%), no faecal diversion was performed. Negative pressure wound therapy (NPWT) system was effective in the last four patients (33·4%). The mean hospitalisation period in patients who used NPWT was 18 days, while it was 20 days in the others. NPWT in Fournier's gangrene is a safe dressing method. It promotes granulation formation. Flexi-Seal faecal management is an alternative method to colostomy and provides protection from its associated complications. The combination of two devices (Flexi-Seal and NPWT) is an effective and comfortable method in the management of Fournier's gangrene in appropriate patients.
The aim of this study was to investigate the possible protective role of antioxidant treatment with syringic acid (SA) on L-arginine-induced acute pancreatitis (AP) using biochemical and histopathologic approaches. A total of 30 rats were divided into 3 groups. The control group received normal saline intraperitoneally. The AP group was induced by 3.2 g/kg body weight L-arginine intraperitoneally, administered twice with an interval of 1 hour between administrations. The AP plus SA group, after having AP induced by 3.2 g/kg body weight L-arginine, was given SA (50 mg kg À1 ) in 2 parts within 24 hours. The rats were killed, and pancreatic tissue was removed and used in biochemical and histopathologic examinations. Compared with the control group, the mean pancreatic tissue total oxidant status level, oxidative stress index, and lipid hydroperoxide levels were significantly increased in the AP group, being 30.97 6 7.13 (P , 0.05), 1.76 6 0.34 (P , 0.0001), and 19.18 6 4.91 (P , 0.01), respectively. However, mean total antioxidant status and sulfhydryl group levels were significantly decreased in the AP group compared with the control group, being 1.765 6 0.21 (P , 0.0001) and 0.21 6 ), peroxynitrite, and other nitrates, whereas carbon-centered molecules are rather complex in terms of their chemical structure and generally are produced in the xenobiotic metabolism.2 Normally, there is a delicate balance between ROS and RNS production and tissue concentrations of antioxidants in the body. This balance is related to the rate of total antioxidant status (TAS) to total oxidant status (TOS), as determined by the oxidative stress index (OSI). ROS are produced both normally through the electron transfer chain system of the mitochondria and in excessive numbers in various conditions that increase energy (ATP) demand. The latter may include, among other factors, biologic factors and exposure to heat and certain chemicals and toxins. [3][4][5] ROS plays an important role in the pathogenesis of AP, and there is also a correlation between the production of ROS and the severity of AP. The detrimental effects of ROS and RNS are mediated by their direct actions on biomolecules, such as lipids, proteins, and DNA, and the activation of proinflammatory signal cascades, which subsequently lead to the activation of immune responses. 2The dietary plant polyphenolic compounds were shown to have beneficial effects in preventing oxidative stress, inhibiting the production of free radicals and the formation of lipid peroxidation.Scientific interest in phenolic compounds has been stimulated because of their anti-inflammatory, antimutagenic, and anticarcinogenic properties. They have antioxidant activity mainly due to their redox properties, which allow them to act as reducing agents, hydrogen donors, free radical scavengers, metal chelators, and modulators of enzymatic activity, thereby preventing a lot of diseases, including diabetes mellitus, hypertension, atherosclerosis, and cancer. 6,7 Antioxidants are compounds that, even when presen...
This study aims to investigate the role of oxidants in cisplatin-induced nephrotoxicity. Cisplatin was administered intraperitoneally (i.p.) in a single dose (5 mg/kg) and guinea pigs were killed either after 24 h or 7 days. The same experiment was performed using animals treated with vitamins C and E combination and a natural antioxidant extract (SARMEX). The kidneys were then removed to be used in the analyses. Blood samples were also obtained from the animals to be used in routine biochemical assays. Twenty-four hours after treatment there was a significant decrease in the renal activities of total superoxide scavenger activity (TSSA), superoxide dismutase (SOD) and catalase (CAT) accompanied by a rise in malondialdehyde (MDA) levels. After 7 days, the fall in kidney enzymatic activities was far greater, while the increase in blood urea (BUN) and creatinine (CRE) was marked. Treatment with antioxidants causes significant increases in renal TSSA (7 day), non-enzymatic superoxide scavenger activity (NSSA) (24 h and 7 day) and SOD (7 day) activities, does not change glutathione peroxidase (GSH-Px) activity and decreases renal MDA (24 h and 7 day), blood BUN (7 day) and CRE (7 day) levels. Our results suggest that cisplatin treatment impairs both enzymatic and non-enzymatic antioxidant systems and causes peroxidation in the renal tissue, which leads to kidney failure. Antioxidant supplementation strengthens the renal antioxidant system, eliminates oxidation reactions, and prevents cisplatin-induced kidney failure.
Antioxidant defense capacity was investigated in myocardial tissue from guinea pigs treated with 5-fluorouracil (5-FU) at a dose of 400 mg/kg/d daily for 5 d administered intraperitonally. Treatment with 5-FU lowered the activities of cardiac superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) accompanied by higher catalase (CAT) activity. Further, antioxidant potential (AOP) values were lower but oxidation resistance (OR) and malondialdehyde (MDA) levels were higher in the 5-FU-treated tissue. With regard to myocardial iron (Fe) and copper (Cu) levels, no significant differences were found between the groups. Results suggest that 5-FU treatment causes impairment in the myocardial antioxidant defense system and leads to cardiac peroxidation. It has been postulated that these changes might be responsible for the 5-FU cardiotoxicity seen in some patients, and antioxidant therapy might provide a therapeutic advantage.
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