Fibroblast growth factor 23 (FGF-23) is known to be produced by the bone and linked to metabolic risk. We aimed to explore circulating FGF-23 in association with fatness and insulin sensitivity, atherosclerosis and bone mineral density (BMD). Circulating intact FGF-23 (iFGF-23) and C-terminal (CtFGF-23) concentrations (ELISA) were measured in 133 middle aged men from the general population in association with insulin sensitivity (Cohort 1); and in association with fat mass and bone mineral density (DEXA) and atherosclerosis (intima media thickness, IMT) in 78 subjects (52 women) with a wide range of adiposity (Cohort 2). Circulating iFGF-23 was also measured before and after weight loss. In all subjects as a whole, serum intact and C-terminal concentrations were linearly and positively associated with BMI. In cohort 1, both serum iFGF-23 and CtFGF-23 concentrations increased with insulin resistance. Serum creatinine contributed to iFGF-23 variance, while serum ferritin and insulin sensitivity (but not BMI, age or serum creatinine) contributed to 17% of CtFGF-23 variance. In cohort 2, CtFGF-23 levels were higher in women vs. men, and increased with BMI, fat mass, fasting and post-load serum glucose, insulin, HOMA-IR and PTH, being negatively associated with circulating vitamin D and ferritin levels. The associations of CtFGF-23 with bone density in the radius, lumbar spine and carotid IMT were no longer significant after controlling for BMI. Weight loss led to decreased iFGF-23 concentrations. In summary, the associations of circulating FGF-23 concentration with parameters of glucose metabolism, bone density and atherosclerosis are dependent on iron and obesity status-associated insulin resistance.

The risk of developing liver cancer in hepatitis B virus (HBV) carriers differs across geographical areas, suggesting that exposure to other risk factors may contribute to HBV‐linked cancer risk. Our study estimates the mortality due to liver disease and the role of other risk factors in a Spanish HBV cohort. 2,352 hepatitis B surface antigen (HBsAg)‐positive and 15,504 HBsAg‐negative subjects were identified among blood donors during 1972–1985 and were followed until December 2000 through the Mortality Registry. Clinical examination and an epidemiological questionnaire were performed on 1,000 HBsAg‐positive survivors during 1994–1996. In subjects deceased from liver disease, medical records were revised and relatives were interviewed. A nested case‐control analysis was conducted comparing both groups. In HBsAg‐positive men, an excess mortality from liver cancer [standardized mortality ratio (SMR): 14.1; 7.7–23.6], cirrhosis (SMR: 10.5; 7.0–15.1), haematological neoplasms (SMR: 3.2; 1.2–6.9) and AIDS was detected (SMR: 5.5; 2.2–11.4). In women, an excess was found for cirrhosis (SMR: 7.2; 1.4–21.1). Progression factors to liver disease were alcohol intake [odds ratio (OR): 6.3; 3.1–12.8], diabetes (OR: 3.6; 1.3–9.6), HBV replication (OR: 50.0; 14.9–167.3) and hepatitis C virus (HCV) infection (OR: 27.4; 7.1–107.7). In conclusion, in Spain after 20 years of follow‐up, chronic HBV exposure appears as a major risk factor for liver cancer among men and for cirrhosis in both sexes. The risk of death from liver disease among HBV carriers with the presence of HBV replication, HCV, alcohol consumption and diabetes was significantly increased and suggests synergism among these exposures and HBV. Mortality from haematological neoplasms was detected and could be associated to HIV coinfection. These results support screening and adequate follow‐up among HBsAg‐positive subjects at high risk to develop liver disease, particularly when these risk cofactors are present. © 2006 Wiley‐Liss, Inc.

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Visual global wall motion and wall thickening scores obtained by gated SPECT showed good correlation between them and with the EF, but differences were observed between regional wall motion and wall thickening, especially in inferior and lateral regions of patients with infero-lateral infarctions.