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Metacarpal morphometry represents a potentially cheap and widely available non-invasive assessment of skeletal status. In two cross-sectional studies, we compared the performance characteristics of a semiautomated technique (the Teijin Bonalyzer) with an in-house manual measurement, and with measures of skeletal strength at other sites. The metacarpal cortical index (mCI) was measured on hand radiographs of 178 osteoporotic women using both the Teijin Bonalyzer and a digitizing tablet. Measurements on the latter were consistently lower than with the Bonalyzer except for mCI (0.443+/-0.080 vs 0.364+/-0.060, p<0.001), although correlation coefficients between these two methods were highly significant (r = 0.62-0.83, p<0.001). The reproducibility errors of metacarpal bone mineral density (mBMD) were constant (1.1-1.2%) whilst those for mCI showed a marked operator-dependency (2.0-7.9%). In 379 elderly community-dwelling women, Bonalyzer mCI and mBMD showed a significant decline with age (r = -0.30 and -0.27 respectively, p<0.05). Both mCI and mBMD correlated significantly with forearm BMD (r = 0.50 and 0.57 respectively, p<0.001) and hip BMD (r = 0.48 and 0.53 respectively, p<0.001). After adjustment for age and weight, hip BMD demonstrated the best discrimination for prevalent vertebral fractures as judged by the gradient of risk for a 1 SD decrease in measurement (odds ratio (OR) 2.17, 95% CI 1.56-3.01). Similar but smaller gradients of risk were shown by Bonalyzer mCI (OR 1.32, 95% CI 1.00-1.75), mBMD (OR 1.35, 95% CI 1.02-1.78) and forearm BMD (OR 1.39, 95% CI 1.08-1.80). MCI, and in particular mBMD, may be useful assessments of bone mass and fracture risk. In our study, it is comparable to peripheral assessment of skeletal status by forearm densitometry.

Background: Atherosclerotic renal artery stenosis (ARAS) is an important cause of renal disease in the elderly, and these patients have a high morbidity and mortality. There are no data on their blood lipid profiles. Methods: The lipoprotein profiles were examined in patients with proven ARAS and compared with patients matched for age, gender, renal function and presence of diabetes. Results: The profiles did not show any significant difference for apolipoprotein B (control 1.31 ± 0.39 vs. ARAS 1.24 ± 0.28; mean ± SD), cholesterol (control 5.65 ± 1.28 vs. ARAS 6.12 ± 1.29), LDL cholesterol (control 3.72 ± 1.03 vs. ARAS 4.06 ± 1.18), fibrinogen (control 2.48 ± 1.39 vs. ARAS 3.29 ± 1.49), HDL cholesterol (control 1.16 ± 0.38 vs. ARAS 1.00 ± 0.26) and triglyceride (control 1.68 ± 0.80 vs. ARAS 2.32 ± 1.73) levels between the groups. Surprisingly lipoprotein(a) levels were higher in the control group (0.58 ± 0.45) vs. ARAS (0.31 ± 0.21). The most striking abnormality was the markedly lower apolipoprotein A1 levels in the ARAS group (control 2.09 ± 0.55 vs. ARAS 0.95 ± 0.30) and apolipoprotein A1/B ratio (control 1.74 ± 0.71 vs. ARAS 0.78 ± 0.24). Conclusion: The lipoprotein abnormality in ARAS mirrors that in other severe vascular diseases. Potential therapeutic interventions in patients with ARAS should consider treatments to modify the apolipoprotein A1 concentration rather than cholesterol alone.

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Background: The development of early renal interstitial fibrosis (IF) in renal allografts is likely to depend on multiple factors. We studied retrospectively renal biopsies from cadaveric human renal allografts, transplanted from 1996 to 1998, with the intention of detecting early fibrotic changes and determining the underlying cellular mediators. We studied 23 transplant patients whose 46 renal biopsies were analysed, including a donor biopsy taken routinely at implantation from each patient and 23 follow-up biopsies, taken as clinically indicated over a period of 3 months following transplantation. Methods: Histological evaluation of induction and progression of fibrosis relied on point count analysis of conventional (Masson’s trichrome/MT) and immunohistochemical staining for collagen III and IV, and alpha-smooth muscle actin (α-SMA) as a marker of myofibroblast differentiation. Mast cells (MC) were counted in sections stained with an anti-human mast cells tryptase monoclonal antibody. Activated macrophages as well as total, helper and cytotoxic T-lymphocytes were identified on frozen sections by direct immunofluorescence using mouse anti-CD71, CD3, CD4 and CD8 antibodies respectively. Eosinophils (E) were counted in hematoxylin and eosin (HE)-stained sections. Changes in interstitial fibrosis (IF) scores were evaluated and correlated with myofibroblasts, MC, E and lympho-monocytic cells. Results: We noted a significant increase in IF over a 3 months period following transplantation. There was also a significant increase in α-SMA⁺ cells, MC and E counts from implantation to follow-up biopsies. Similarly, there was a significant increase in interstitial infiltration by T-lymphocytes (modal category = 2 versus 0, p = 0.012) but not by macrophages. MC at implantation and follow-up were found to be predictive of IF (immunostainable collagen III) at follow-up (R² = 0.510, p = 0.023 and p = 0.030). Further, the predictive value for total T-lymphocyte infiltration at follow-up was also significant (R² = 0.617, p = 0.036). A strong correlation was found between α-SMA⁺ cells and MC counts at implantation (r = 0.7259, p < 0.001) and in follow-up biopsies (r = 0.5183, p < 0.01). However, there was no correlation between E counts and either α-SMA⁺ cells or MC either at implantation or in follow-up biopsies. Based on changes in interstitial immunostainable α-SMA, our patients were divided arbitrarily into 2 groups; group 1 (n = 12) with >100% increase in α-SMA and group 2 (n = 11) with <100% increase. Group 1 patients differed significantly from group 2 regarding the degree of MC infiltration at follow-up (t = 0.4519, p < 0.05) with the mean increase in MC count from implantation to follow-up biopsies being +5.1 cells/high power field (HPF) in group 1 and +0.8 cell/HPF in group 2 (p = 0.0237). MC counts in group 1 were associated with a higher modal category (greater than one) of cytotoxic: helper T-lymphocytes ratio compared to group 2 (2:1 versus 1:1 respectively). C...