Inflammatory and bone turnover markers in a cross-sectional and prospective study of acute Charcot osteoarthropathy.

AIMS: To assess markers of inflammation and bone turnover at presentation and at resolution of Charcot osteoarthropathy. METHODS: We measured serum inflammatory and bone turnover markers in a cross-sectional study of 35 people with Charcot osteoarthropathy, together with 34 people with diabetes and 12 people without diabetes. In addition, a prospective study of the subjects with Charcot osteoarthropathy was conducted until clinical resolution. RESULTS: At presentation, C-reactive protein (P = 0.007), tumour necrosis factor-α (P = 0.010) and interleukin-6 (P = 0.002), but not interleukin-1ß, (P = 0.254) were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. Serum C-terminal telopeptide (P = 0.004), bone alkaline phosphatase (P = 0.006) and osteoprotegerin (P < 0.001), but not tartrate-resistant acid phosphatase (P = 0.126) and soluble receptor activator of nuclear factor-κß ligand (P = 0.915), were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. At follow-up it was found that tumour necrosis factor-α (P = 0.012) and interleukin-6 (P = 0.003), but not C-reactive protein (P = 0.101), interleukin-1ß (P = 0.457), C-terminal telopeptide (P = 0.743), bone alkaline phosphatase (P = 0.193), tartrate-resistant acid phosphatase (P = 0.856), osteoprotegerin (P = 0.372) or soluble receptor activator of nuclear factor-kß ligand (P = 0.889), had significantly decreased between presentation and the 3 months of casting therapy time point, and all analytes remained unchanged from 3 months of casting therapy until resolution. In people with Charcot osteoarthropathy, there was a positive correlation between interleukin-6 and C-terminal telopeptide (P = 0.028) and tumour necrosis factor-α and C-terminal telopeptide (P = 0.013) only at presentation. CONCLUSIONS: At the onset of acute Charcot foot, serum concentrations of tumour necrosis factor-α and interleukin-6 were elevated; however, there was a significant reduction in these markers at resolution and these markers may be useful in the assessment of disease activity.

Analysis of adipokine concentrations in paediatric non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in children. It is important to distinguish children with more severe disease or steatohepatitis (NASH) from those with the less severe simple steatosis (SS) as prognosis differs. The importance of adipokines in the evolution of NASH is well recognized. OBJECTIVE: As adipokines are important in mediating inflammation, they may also be useful biomarkers of disease. METHODS: Plasma from 40 children (30 boys), median age 13.4 years, with liver biopsy-proven NAFLD was analysed. Liver biopsies were scored using the NAFLD activity score and compared with adipokine concentrations. RESULTS: Median body mass index z-score was 2.12 with a median homeostasis model of assessment- insulin resistance of 4.08. Resistin was lower in NASH than in SS (P = 0.03). Monocyte chemoattractant protein 1 (MCP-1) was also lower in NASH (P = 0.04). MCP-1 was higher in children with severe fibrosis (P = 0.008) with an area under the receiver operating characteristic curve (AUROC) of 0.76. Plasminogen activator inhibitor 1 (PAI-1) was also higher in this group (P = 0.011) with an AUROC of 0.78. There were no significant differences in leptin, adiponectin, adipsin, interleukin (IL) 6, IL10 or tumour necrosis factor α between groups. CONCLUSION: PAI-1 MCP-1 and resistin were differentially expressed with increasing severity of NAFLD. Though it is unlikely that this profile alone would serve as a biomarker of disease, differences found may contribute to understanding the role of these mediators in NAFLD.

Angiogenic peptides in prostatic disease.

OBJECTIVE: To determine the value of measuring serum concentrations of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in patients with benign prostatic hyperplasia (BPH), advanced and localized prostate cancer, and thus assess the role of angiogenesis factors as markers of malignancy and the formation of metastasis. PATIENTS AND METHODS: Serum was obtained from 106 suitable patients who attended a routine clinic during the study period. A histological diagnosis was confirmed for each patient and a bone scan was positive in those with metastatic disease. The level of serum prostate specific antigen (PSA) was measured and the serum concentrations of VEGF and bFGF measured using a quantitative sandwich immunoassay technique. RESULTS: There was a significant difference (1.6-fold) in the serum concentration of bFGF between patients with local and advanced prostate cancer (P=0.006), but there was no significant difference for either of the growth factors between patients with BPH and metastatic prostate cancer (Mann-Whitney test). CONCLUSION: The serum levels of VEGF and bFGF could not be used to distinguish benign from malignant prostatic disease; the serum PSA level is of more value than either, but the serum concentration of bFGF may be of some value in differentiating patients with local and advanced malignancy.

Validity of PSA, free/total PSA ratio and complexed/total PSA ratio measurements in men with acute urinary retention.

The reliability of serum prostate specific antigen (PSA) measurements in men with acute urinary retention is unclear. Total PSA, free and complexed PSA were measured, and the free/total (f/t) PSA and complexed/total (c/t) PSA ratios calculated, prior to catheterisation and at 48 and 72 h post-catheterisation in 39 men with acute retention. Subsequent histology showed 12 patients had prostate cancer and 27 benign prostatic hypertrophy. Serum free and total PSA fell following catheterisation, while complexed PSA rose during the first 48 h then subsequently fell. The f/t PSA and c/t PSA ratios provided the best discrimination at 48-72 h with 100% sensitivity and 75-82% specificity.Prostate Cancer and Prostatic Diseases (2001) 4, 167-172.