Can procalcitonin predict bone infection in people with diabetes with infected foot ulcers? A pilot study.

AIMS: The diagnosis of osteomyelitis is a key step of diabetic foot management. Previous studies showed that procalcitonin (PCT), a novel infection marker, is superior to conventional infection markers in the diagnosis of diabetic foot infection. This study aimed to investigate the serum levels of PCT and other conventional infection markers in diabetic persons with and without osteomyelitis. METHODS: Twenty-four patients (18 male, mean age: 61.9±10.8 years) with infected foot ulcers were prospectively enrolled. Clinical characteristics of the wounds were noted. Blood samples were obtained for biochemical analysis. Magnetic resonance imaging of the foot was performed in all patients to diagnose osteomyelitis. RESULTS: Osteomyelitis was found in 13 of 24 (54%) patients. PCT levels were 66.7±43.5 pg/ml in patients with osteomyelitis and 58.6±35.5 pg/ml in patients without osteomyelitis. The difference did not reach statistical significance (p=0.627). Erythrocyte sedimentation rate, but not C-reactive protein and white blood cell count, was found significantly higher in patients with osteomyelitis. CONCLUSION: In this group of patients, PCT failed to discriminate patients with bone infection. Erythrocyte sedimentation rate can be used as a marker of osteomyelitis in diabetic persons.

Covering the colon anastomoses with amniotic membrane prevents the negative effects of early intraperitoneal 5-FU administration on anastomotic healing.

PURPOSE: This study investigated whether covering the colonic anastomoses with amniotic membrane (AM) protects the anastomotic healing from the adverse effects of immediate 5-fluorouracil (5-FU) administration. METHODS: One hundred twenty wistar albino rats were randomized to one of four groups (I-IV, 30 rats in each) and underwent a standardized left colon resection and anastomoses. The anastomoses of the rats in groups II (AM) and IV (5-FU + AM) were covered with AM. Saline solution (2 ml/day; groups I (control) and II) or 5-FU (20 mg/kg/day; groups III (5-FU) and IV) was administered to the rats intraperitoneally once daily from the day of operation until sacrificed. Half of each group was sacrificed on the postoperative day 4 (IA, IIA, IIIA, and IVA) and other half on the postoperative day 8 (IB, IIB, IIIB, and IVB), and their anastomoses were evaluated when sacrificed. RESULTS: The dehiscence rate of anastomotic dehiscence and adhesion formation were significantly higher in groups IIIA and IIIB compared with groups IVA and IVB, respectively. Bursting pressure was significantly higher in the 5-FU + AM groups than in the 5-FU groups. The inflammatory cell infiltration was significantly lower in groups IIIA and IVA compared with group IA, in groups IIIB and IVB compared with group IB, and in group IVA compared with group IIIA. Neoangiogenesis, fibroblast activity, collagen deposition, and hydroxyproline levels were significantly higher in the 5FU + AM groups compared with control and 5-FU groups. Malondialdehyde levels were significantly higher in the 5-FU groups than in the 5-FU + AM groups. CONCLUSION: Covering colon anastomoses with AM protects them, preventing leakage and reversing the negative effects of 5-FU administration.

The relationship between coronary calcification and the metabolic markers of osteopontin, fetuin-A, and visfatin.

OBJECTIVES: We investigated whether coronary calcification detected by multislice computed tomography (MSCT) was correlated with plasma osteopontin, serum fetuin-A, and visfatin levels. STUDY DESIGN: The study included 64 consecutive patients (51 males, 13 females; mean age 49.5+/-10.9 years; range 33 to 78 years) who underwent MSCT for suspected coronary artery disease. Coronary artery calcification (CAC) scores of the patients were calculated using the Agatston scoring method. Plasma osteopontin, serum fetuin-A, and visfatin levels were measured from fasting blood samples and correlations were sought with calcium scores. RESULTS: Coronary calcification was detected in 32 patients (50%). The mean CAC score was 146.5+/-333.7 Agatston units (AU), indicating an intermediate risk for coronary artery disease. In 10 patients (15.6%), the CAC score exceeded 400 AU. The mean fetuin-A, visfatin, and osteopontin levels were 25.6+/-6.4 ng/ml, 19.7+/-47.2 ng/ml, and 20.4+/-16.1 ng/ml, respectively. Serum visfatin (r=0.15, p=0.37) and fetuin-A (r=0.17, p=0.22) were not correlated with the CAC score, whereas plasma osteopontin level showed a moderate correlation with the CAC score (r=0.35; p=0.008). In ROC analysis, the area under the curve for identification of CAC was greatest for osteopontin (0.741; p=0.004), followed by fetuin-A (0.574; p=0.31), and visfatin (0.580; p=0.27). The cut-off value was 18.45 ng/ml for osteopontin, with a sensitivity of 72% and specificity of 73%. CONCLUSION: Our results suggest that there might be an association between CAC and plasma osteopontin levels. Research should continue to find out a metabolic parameter that will strongly indicate coronary calcification.

Diagnostic value of serum prolidase enzyme activity to predict the liver histological lesions in non-alcoholic fatty liver disease: a surrogate marker to distinguish steatohepatitis from simple steatosis.

Determination of the liver histological lesions with noninvasive tests is an important part of the diagnostic work-up of patients with non-alcoholic fatty liver disease (NAFLD). We aimed to determine the predictive value of noninvasive biochemical markers, serum prolidase enzyme activity (SPEA), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and AST/ALT ratio for the liver histological lesions. Fifty-four liver biopsy-proven patients with NAFLD and 37 healthy controls were enrolled to the study. The diagnostic accuracies of biochemical markers were evaluated by receiver operating characteristic (ROC) curves and multiple linear regression analysis to predict the degree of fatty infiltration, lobular inflammation, NAFLD activity score, and stage of fibrosis. The SPEA of patients with steatohepatitis is significantly increased compared with the patients with simple steatosis and controls (1,338 [1,138-1,624] U/l; 974 [768-1,160] U/l; 972 [862-1,122] U/l, shown as median [25th-75th interquartile range], respectively, P < 0.0001). SPEA was positively correlated with the grade of liver fatty infiltration, lobular inflammation and NAFLD activity score, and stage of fibrosis, (r = 0.377, P < 0.005; r = 0.443, P < 0.001; r = 0.457, P < 0.001; r = 0.321, P < 0.018, respectively). SPEA was the best predictor for distinguishing steatohepatitis from simple steatosis according to the ROC analysis (area under the curve [AUC]: 0.85). Multivariate analysis revealed that the most useful single test for predicting lobular inflammation, NAFLD activity score, and fibrosis was SPEA, and for predicting the fatty infiltration, it was ALT (P < 0.00001, P < 0.001, P < 0.0001, P < 0.0001, respectively). This study demonstrated that SPEA can accurately predict the degree and stage of all histological lesions in NAFLD. It could be helpful for distinguishing steatohepatitis from simple steatosis and reducing the need for liver biopsy in the majority of patients with NAFLD.

Novel links between the long pentraxin 3, endothelial dysfunction, and albuminuria in early and advanced chronic kidney disease.

BACKGROUND AND OBJECTIVES: Albuminuria and inflammation predict cardiovascular events. Pentraxin 3, an inflammatory mediator produced by, among others, endothelial cells, may have a role in atherogenesis. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In 207 Swedish patients with stage 5 chronic kidney disease and 79 Turkish patients with type 2 diabetes and proteinuria and normal renal function, whether serum pentraxin 3 levels are associated with albuminuria and endothelial dysfunction was studied. RESULTS: Patients with stage 5 chronic kidney disease and a high degree of albuminuria more often had diabetes and higher levels of pentraxin 3, vascular cellular adhesion molecule-1, and blood pressure. Moreover, pentraxin 3 was independently associated with 24-h urinary albumin excretion. In patients with type 2 diabetes, pentraxin 3 was significantly higher than in control subjects. Patients with type 2 diabetes and more proteinuria had higher pentraxin 3, C-reactive protein, glycosylated hemoglobin, insulin, and homeostasis model assessment index as well as lower flow-mediated dilation and serum albumin. Pentraxin 3 was positively correlated with C-reactive protein, homeostasis model assessment index, and carotid intima-media thickness and negatively with flow-mediated dilation. Pentraxin 3 and glomerular filtration rate were independently associated with 24-h urinary protein excretion. Only pentraxin 3 and proteinuria were significantly and independently associated with flow-mediated dilation. CONCLUSIONS: In two different renal cohorts, one of stage 5 chronic kidney disease and one of type 2 diabetes and normal renal function, pentraxin 3 was independently associated with proteinuria. Moreover, both pentraxin 3 and proteinuria were associated with endothelial dysfunction in patients with type 2 diabetes.