Search PubMed⌕ Search

Biomedical subjects

E Taioli

Publications and source records attributed to E Taioli.

At least 37 records · Page 2Linked to original sources
PubMed2001

Increased cancer risk in a cohort of 230 patients with hereditary hemochromatosis in comparison to matched control patients with non-iron-related chronic liver disease.

It has been suggested that excess iron may facilitate the occurrence of cancer. Patients with hereditary hemochromatosis (HH) are at high risk of developing liver cancer, and studies of limited series reported a high frequency of nonhepatic cancers. To verify whether patients with HH are at higher risk of liver cancer and other malignancies as compared with patients with non-iron-related chronic liver disease (CLD), we analyzed the occurrence of neoplasms in 230 patients with HH and 230 with non-iron-related CLD. The patients were matched by sex, age, duration of follow-up (+/-5 years), and severity of liver disease. On enrollment, the following variables were considered: hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, alcohol abuse, smoking, and a family history of cancer (first-degree relatives). The diagnosis of primary cancers was confirmed by histology. During the follow-up, hepatocellular carcinoma (HCC) developed in 49 and 29 patients (all cirrhotic patients) with HH and non-iron-related CLD, respectively, with a relative risk of 1.8 (95% confidence interval [CI] 1.1-2.9); nonhepatic cancers occurred in 20 and 11 patients, respectively, with a relative risk of 1.8 (95% CI 0.8-4). Four patients with HH and 1 with non-iron-related CLD developed 2 different primary cancers during follow-up. The risk of cancer after adjustment for alcohol abuse, smoking, and family history of cancer was 1.9 (95% CI 1.1-3.1) in the patients with HH. In conclusion, patients with HH are at high risk of both liver cancer and other malignancies, which should be carefully sought during follow-up.

Adult↗
PubMed2001

International collaborative study on genetic susceptibility to environmental carcinogens (GSEC): an update.

We have created a database of published and unpublished studies on genetic susceptibility to environmental carcinogens, by bringing together many single studies that are too small to give definitive answers on the role of metabolic genes in cancer susceptibility. Possible participants were identified through a literature search of case control studies published up to June 1999 on metabolic gene polymorphisms and cancer, and invited to send their data sets without personal identifiers. Individual data from a total of over 30,000 subjects (52% cancer cases, 48% controls) have been collected. The most common type of cancer is lung, followed by bladder, head and neck, and breast. Demographic data, such as age, sex, and race were obtained for almost all the subjects. Main exposures, such as smoking, alcohol, occupational exposure were also included in a portion of the data set. The simultaneous presence of two gene polymorphisms has been assessed in 3535 controls and 3445 cases. An Advisory Committee has evaluated and approved 8 proposals to analyze the available data. This project allows the study of the main effects of genes, gene-exposure effects, ethnic and geographic differences in allele frequencies, gene-environment and gene-gene interaction as possible risk factors for cancer.

Carcinogens↗
PubMed2001

Hyperferritinemia, iron overload, and multiple metabolic alterations identify patients at risk for nonalcoholic steatohepatitis.

OBJECTIVE: The aim of this study was to define in patients with hyperferritinemia and normal transferrin saturation the relationships among hyperferritinemia, iron overload, HFE gene mutations, the presence of metabolic alterations, and nonalcoholic steatohepatitis (NASH). METHODS: Forty patients with increased serum ferritin, resistant to dietary restriction and normal transferrin saturation, 90 with ultrasonographic evidence of hepatic steatosis, and 60 obligate heterozygotes for hemochromatosis, all negative for alcohol abuse, hepatitis virus infections, and inflammation were studied. Transferrin saturation, serum ferritin, uric acid, lipids, glucose tolerance, insulin resistance, HFE gene mutations, liver histology, and hepatic iron concentration were analyzed. RESULTS: Of the 40 patients with hyperferritinemia, 29 (72%) had biochemical metabolic abnormalities, 18 of the 26 examined (69%) had insulin resistance, 26 (65%) had the presence of one of the two HFE gene mutations (normal controls, 33 of 128 [26%], p < 0.0001), and all had increased liver iron concentration. Thirty-one patients (77%) had histology compatible with NASH. At univariate analysis, NASH was significantly associated with the presence of metabolic alterations, the C282Y mutation, and severity of fibrosis. At multivariate analysis, NASH was associated with the coexistence of multiple metabolic alterations (odds ratio = 5.2, 95% CI = 0.95-28.7). The risk of having NASH augmented in the presence of higher values of ferritin and liver iron concentration. Among the 90 patients with ultrasonographic evidence of hepatic steatosis, 24 (27%) had increased serum ferritin with normal transferrin saturation, but only six remained hyperferritinemic after dietary restriction. CONCLUSION: Increased ferritin with normal transferrin saturation is frequently found in patients with hepatic steatosis, but it reflects iron overload only in those patients in whom it persists despite an appropriate diet. The simultaneous disorder of iron and glucose and/or lipid metabolism, in most of the cases associated with insulin resistance, is responsible for persistent hyperferritinemia and identifies patients at risk for NASH.

Analysis of Variance↗
PubMed2001

Homocysteine, vitamin B12, serum and erythrocyte folate in peritoneal dialysis patients.

Plasma homocysteine (tHcy) is an important risk factor for atherosclerosis in dialysis patients. Few data were reported on the prevalence and severity of hyperhomocysteinemia in peritoneal dialysis (PD) patients. In addition, little attention was paid to the search of factors possibly involved in the pathogenesis of hyperhomocysteinemia in these patients. A cross-sectional study was performed in 107 stable PD patients. None of them was given folate or vitamin B12 supplementation before or during the study. Plasma tHcy, serum vitamin B12, serum and erythrocyte folate were measured by immunoenzymatic methods. Genetic analysis of the methylentetrahydrofolate-reductase thermolabile mutation (tMTHFR) was performed in 61 patients. 97% of patients had tHcy levels higher than normal. tHcy was not different between men and women, patients with or without malnutrition, with or without clinically evident atherosclerotic vasculopathy, with or without anemia. tHcy levels were significantly higher in homozygotes for the tMTHFR mutation than in patients carrying the wild type form. Significant univariate correlation was found between hyperhomocysteinemia and time since the start of dialysis, serum and erythrocyte folate and vitamin B12. The best fitted model equation was log tHcy = 108.53 + 0.1606 (duration of dialysis) -1.1053 (s-F) -0.7980 (age) 0.0215 (vitamin B12). Our results agree with those reported by other authors in hemodialysis patients. Despite the large number of PD patients with normal serum vitamin B12 and folate status, the relation between tHcy and vitamin B12 or folate suggests that the supplementation of these vitamins could be useful irrespective of their serum levels, especially in younger patients or in those treated for a long period of time with peritoneal dialysis.

Aged↗
PubMed2001

Metabolic gene polymorphism frequencies in control populations.

Using the International Project on Genetic Susceptibility to Environmental Carcinogens (GSEC) database containing information on over 15,000 control (noncancer) subjects, the allele and genotype frequencies for many of the more commonly studied metabolic genes (CYP1A1, CYP2E1, CYP2D6, GSTM1, GSTT1, NAT2, GSTP, and EPHX) in the human population were determined. Major and significant differences in these frequencies were observed between Caucasians (n = 12,525), Asians (n = 2,136), and Africans and African Americans (n = 996), and some, but much less, heterogeneity was observed within Caucasian populations from different countries. No differences in allele frequencies were seen by age, sex, or type of controls (hospital patients versus population controls). No examples of linkage disequilibrium between the different loci were detected based on comparison of observed and expected frequencies for combinations of specific alleles.

Black People↗
PubMed2001

Current smoking, occupation, N-acetyltransferase-2 and bladder cancer: a pooled analysis of genotype-based studies.

The aim of this study was to investigate the association of NAT2 gene polymorphism with bladder cancer using the data derived from the International Project on Genetic Susceptibility to Environmental Carcinogens. Four case control studies conducted in four European countries, plus two case series, one from England and one from Germany, for a total of 1530 cases and 731 controls (all Caucasian) were included. The interaction between NAT2 and bladder cancer considering smoking habits and occupational exposure was studied. There was a significant association between NAT2 and bladder cancer (odds ratio: 1.42, 95% confidence interval: 1.14-1.77), with a slightly significant heterogeneity among studies. However, heterogeneity disappeared when smokers were divided into current and ex-smokers. The risk of cancer was elevated in smokers and occupationally exposed subjects, with the highest risk among slow acetylators. The increase in risk was limited, in fact, to current smokers (odds ratio = 1.74, 95% confidence interval: 0.96-3.15). This analysis confirms that the NAT2 genotype is a risk factor for bladder cancer by interacting with smoking or occupational exposures. Our observation suggests that NAT2 is not a risk factors per se but modulates the effect of carcinogens contained in tobacco smoke (probably arylamines) or associated with occupational exposures.

Adult↗
PubMed2001

Lack of interaction between asbestos exposure and glutathione S-transferase M1 and T1 genotypes in lung carcinogenesis.

An interaction between occupational carcinogens and genetic susceptibility factors in determining individual lung cancer risk is biologically plausible, but the interpretation of available studies are limited by the small number of exposed subjects. We selected from the international database on Genetic Susceptibility and Environmental Carcinogens the studies of lung cancer that included information on metabolic polymorphisms and occupational exposures. Adequate data were available for asbestos exposure and GSTM1 (five studies) and GSTT1 (three studies) polymorphisms. For GSTM1, the pooled analysis included 651 cases and 983 controls. The odds ratio (OR) of lung cancer was 2.0 [95% confidence interval (CI) 1.4-2.7] for asbestos exposure and 1.1 (95% CI 0.9-1.4) for GSTM1-null genotype. The OR of interaction between asbestos and GSTM1 polymorphism was 1.1 (95% CI 0.6-2.1) based on 54 cases and 53 controls who were asbestos exposed and GSTM1 null. The case-only approach, which was based on 869 lung cancer cases and had an 80% power to detect an OR of interaction of 1.56, also provided lack of evidence of interaction. The analysis of possible interaction between GSTT1 polymorphism and asbestos exposure in relation to lung cancer was based on 619 cases. The prevalence OR of GSTT1-null genotype and asbestos exposure was 1.1 (95% CI 0.6-2.0). Our results do not support the hypothesis that the risk of lung cancer after asbestos exposure differs according to GSTM1 genotype. The low statistical power of the pooled analysis for GSTT1 genotypes hampered any firm conclusion. No adequate data were available to assess other interactions between occupational exposures and metabolic polymorphisms.

Adult↗
PubMed2000

Mutations in coagulation factors in women with unexplained late fetal loss.

BACKGROUND: Factor V and prothrombin-gene mutations are independent risk factors for venous thrombosis; it is debated whether a mutation in the gene encoding methylenetetrahydrofolate reductase, an enzyme involved in homocysteine metabolism, also increases the risk of venous thrombosis. Whether any of these mutations is associated with an increased risk of late fetal death is not known. METHODS: We studied 67 women with a first episode of unexplained late fetal loss (fetal death after 20 weeks or more of gestation) and 232 women who had had one or more normal pregnancies and no late fetal losses. All the women were tested for the presence of three gene mutations. Women with other thrombophilic conditions were excluded from the study. RESULTS: Eleven of the 67 women with late fetal loss (16 percent) and 13 of the 232 control women (6 percent) had either the factor V or the prothrombin mutation. The relative risks of late fetal loss in carriers of the factor V and prothrombin mutations were 3.2 (95 percent confidence interval, 1.0 to 10.9) and 3.3 (95 percent confidence interval, 1.1 to 10.3), respectively. Thirteen percent of the women whose fetuses died and 20 percent of the control women were homozygous for the mutation in the methylenetetrahydrofolate reductase gene (relative risk, 0.8; 95 percent confidence interval, 0.5 to 1.2). CONCLUSIONS: Both the factor V and the prothrombin mutations are associated with an approximate tripling of the risk of late fetal loss.

Abortion, Spontaneous↗
PubMed2000

Diet, metabolic polymorphisms and dna adducts: the EPIC-Italy cross-sectional study.

DNA adducts in peripheral leukocytes are considered a reliable indicator of internal dose exposure to genotoxic agents and, possibly, of cancer risk. We investigated their association with diet and other individual characteristics in healthy adults. The prospective study EPIC-Italy, a section of a larger European project, enrolled 47,749 men and women, aged 35-64 years, in 5 centres: all provided individual information about dietary and life-style habits and a blood sample. In a cross-sectional study, approximately 100 volunteers were randomly selected from each of the three main geographical study areas (Northern, Central and Southern Italy). DNA adducts and four polymorphic metabolic genotypes were determined in peripheral leukocytes by using (32)P-postlabelling technique and PCR methods. Among 309 subjects (153 men), 72.8% had detectable levels of DNA adducts (mean: 8.1 +/- 0.6 per 10(9) nucleotides). Strong negative associations emerged with the reported frequency of consumption of fresh fruit and vegetables, olive oil, and the intake of antioxidants. DNA adducts were higher in subjects with GSTT1 null genotype (p = 0.05). Significant differences between study centres emerged in multivariate analyses (mean levels: 11.0, 10.0, 7.2, 6.5 and 5.2 for Florence, Naples, Turin, Varese and Ragusa, respectively). A possible opposite seasonal variation was found according to latitude: adduct levels tended to be lower in winter in Florence and the southern centres, and during summer in the two northern centres. Frequent consumption of fresh fruit and vegetables is associated with reduced levels of DNA adducts, possibly contributing to the role of diet in modulating cancer risk.

Adult↗
PubMed2000

Deletion of parental GST genes as a possible susceptibility factor in the etiology of infant leukemia.

Infant leukemia below the age of 12 months is a rare disease that exhibits a high frequency of 11q23 rearrangements. We assessed the presence of polymorphisms in several metabolic genes in 23 families of infants diagnosed with leukemia under 12 months of age in Italy. When polymorphism frequencies were calculated within families, frequencies of GST gene deletions were significantly higher than expected only among the parents of infants without the 11q23 rearrangement. These data suggest that the deletion of GST genes in parents may affect the risk of infant leukemia through a pathway independent of the MLL gene.

Chromosome Mapping↗
PubMed2000

In vitro quantification of anti-red blood cell antibody production in idiopathic autoimmune haemolytic anaemia: effect of mitogen and cytokine stimulation.

The immunopathogenic mechanisms underlying idiopathic autoimmune haemolytic anaemia (AIHA) are still unknown, although regulatory cytokines are thought to play an important role. We investigated cytokine production by mitogen-stimulated whole blood cultures from 21 patients with AIHA and from 22 age- and sex-matched controls. In parallel experiments, we studied the effect of mitogen and cytokine stimulation on anti-red blood cell (RBC) IgG antibody production, assessed as both binding on autologous RBCs and secretion in culture supernatants. To quantify anti-RBC antibody, we set up a sensitive and quantitative solid phase competitive immunoassay. The results showed that in AIHA patients production of interleukin (IL)-4, IL-6 and IL-13 was significantly increased, whereas that of interferon (IFN)-gamma was reduced. Multivariate analysis showed that IFN-gamma was the only independent factor significantly associated with the reduced T-helper-1-like cytokine profile. Patients with active haemolysis showed further reduction of IFN-gamma and IL-2 production and increased secretion of transforming growth factor (TGF)-beta. In AIHA patients, mitogen stimulation, as well as IL-6, significantly increased autologous anti-RBC-binding relative to unstimulated cultures. Mitogen stimulation and addition of IL-4, IL-6, IL-10, IL-13 and TGF-beta significantly increased both autologous anti-RBC binding and antibody secretion in AIHA patients compared with controls. The results suggest that a reduced T-helper-1- and a predominant T-helper-2-like profile and elevated TGF-beta levels might play a role in the immunopathogenesis of AIHA. Furthermore, our competitive anti-RBC antibody was able to detect anti-RBC antibody production in some direct antiglobulin test (DAT)-negative AIHA patients.

Adult↗
PubMed2000

Influence of immunogenetic background on the outcome of recurrent hepatitis C after liver transplantation.

In immunocompetent patients, specific human leukocyte antigen (HLA) class II alleles have been associated with the severity of hepatitis C virus (HCV)-related disease, in particular, HLA-DRB1*11 has been found to exert a protective effect. The authors have analyzed the role of HLA class I and II alleles in determining the frequency, timing, and progression of histologically proven recurrent hepatitis C in 89 patients who underwent a liver transplant for HCV-related cirrhosis. In addition, the influence of HLA mismatch between donor and recipient, HCV genotype, and use of steroid pulses was also evaluated. Median patient follow up was 35 months (range 4-119). HLA-DRB1 typing was performed by genomic analysis in all cases. Liver biopsies were obtained routinely and at least at yearly intervals. Histologically proven recurrent hepatitis was observed in 46 patients (52%), 10 patients progressing to stage 5-6 fibrosis in most cases within 2 years after transplant. By univariate analysis, 3 variables, HLA-B14, HLA-DRB1*04, and HLA-DRB1 donor/recipient mismatch, showed a significant effect on time to recurrent hepatitis C disease. These parameters were included in a multivariate regression model along with HCV genotype, treatment with steroid pulses and DRB1*11. HLA-B14, HLA-DRB1*04, and HLA-DRB1 donor/recipient mismatch were confirmed to provide a significant and independent contribution to the risk of hepatitic disease recurrence. As for the severity of the disease, none of the 10 patients with stage 5-6 hepatitis carried the HLA-DRB1*11 allele, in line with what was observed in nontransplant subjects. Our results suggest that in posttransplant recurrent hepatitis C, immunogenetic factors are relevant in determining HCV infection outcome.

Adult↗
PubMed2000

Glutathione S-transferase M1 polymorphism and lung cancer risk in African-Americans.

Glutathione S:-transferase M1 (GSTM1) can detoxify many carcinogens, including polycyclic aromatic hydrocarbons such as those from cigarette smoke. Though a number of studies have been published about the association between GSTM1 polymorphism and lung cancer, this association has received limited attention in the African-American population. We conducted a case-control study to investigate the role of GSTM1 polymorphism in the development of lung cancer in African-Americans. Specimens of DNA from 117 lung cancer cases and 120 controls were assayed for detection of GSTM1 genotype by polymerase chain reaction (PCR). The odds ratios (ORs) and 95% confidence intervals (CIs) for lung cancer associated with homozygous deletion of the GSTM1 gene and other risk factors were estimated by logistic regression. Thirty-seven of the 117 cases (31. 6%) and 24 of the 120 controls (20.0%) had the GSTM1 null genotype; the OR was 2.10 (95% CI 1.07-4.11) after adjustment for age, gender and smoking. The association was higher for squamous cell carcinoma (OR 2.98, 95% CI 1.09-8.19) than for adenocarcinoma (OR 1.95, 95% CI 0.81-4.66). We observed a stronger association between GSTM1 null genotype and lung cancer among heavy smokers with > or =30 pack-years (OR 4.35, 95% CI 1.16-16.23). This association was also found in squamous cell carcinoma (OR 6.26, 95% CI 1.31-29.91). In the analysis combining GSTM1 polymorphism and smoking, smokers with the null genotype had high risk (OR 8.19, 95% CI 2.35-28.62) compared with non-smokers with the wild-type genotype, and the risk increased with smoking cigarette pack-years (P: = 0.0001 for trend). Our results suggest that GSTM1 polymorphism plays a role in the development of lung cancer and modifies the risk for smoking-related lung cancer in African-Americans.

Black or African American↗
PubMed2000

Bone mineral density and body composition in patients with ulcerative colitis.

OBJECTIVE: Reduced bone mineral density (BMD) has been reported in ulcerative colitis (UC) patients, but body composition (fat and lean mass) has never been concomitantly studied. We sought to investigate BMD and body composition in a group of UC outpatients with the following characteristics: age 18-60 yr (men) and 18-45 yr (women); no intestinal resection; no immunosuppressive treatment; and regular menstruation. METHODS: Whole body and subregional BMD and body composition in 43 UC patients (21 men, 22 women; male mean age, 36.5 [21-57] yr; female mean age, 35.3 [23-45] yr) and 121 healthy volunteers were studied by means of dual X-ray photon absorptiometry. RESULTS: There were no differences in total and subregional BMD, or fat and lean mass between the patients and controls, except that the total and trunk lean mass of the UC women was lower than that in the normal controls. No correlation was found between lifetime steroid intake and BMD. CONCLUSIONS: UC outpatients do not differ from normal subjects in terms of BMD and fat mass. Mild and moderate UC does not represent a risk factor for osteopenia.

Absorptiometry, Photon↗
PubMed2000

Can large cell change and high proliferative activity predict hepatocellular carcinoma in patients with hereditary hemochromatosis?

OBJECTIVE: Patients with hereditary hemochromatosis are at high risk of developing hepatocellular carcinoma. This study was undertaken to define whether large cell change and nucleolar organizer regions proliferative index (marker of high proliferative activity) predict hepatocellular carcinoma development in hereditary hemochromatosis. METHODS: Histological staining for large cell change and high proliferative activity were done on baseline liver biopsies of 74 patients with hereditary hemochromatosis (52 with and 22 without cirrhosis), prospectively followed-up for 83 +/- 53 months (range, 1-230 months). RESULTS: Large cell change and high proliferative activity were found only in cirrhotic patients; 16 of 52 patients (31%) had either the large cell change or high proliferative activity. Large cell change was more frequent in patients with hepatitis B surface antigen than in those positive for hepatitis C virus (57% vs 14%, p = 0.04). Hepatocellular carcinoma developed in 7 of 16 (44%) and in 6 of 36 patients (16%) of the patients positive or negative for these morphological variables. The probability of developing hepatocellular carcinoma at 7 yr of follow-up was significantly higher in patients with large cell change or high proliferative activity than in those without. The length of follow-up from baseline histology to hepatocellular carcinoma occurrence was shorter in patients with large cell change or high proliferative activity than in those without these changes (46 +/- 36 and 109 +/- 34 months, p = 0.01). A multivariate analysis indicated that in patients with cirrhosis, large cell change or high proliferative activity (considered as a single variable), and age >55 yr were the only independent variables significantly associated with the risk of developing hepatocellular carcinoma, with a risk ratio of 4.8 (confidence interval 1.2-18.2) and 4.0 (confidence interval 1.1-15.6), respectively. CONCLUSIONS: In hereditary hemochromatosis, the presence of large cell change or high proliferative activity in patients older than 55 yr with cirrhosis should be considered a strong predictor of hepatocellular carcinoma development, especially if hepatitis B virus infection coexists.

Adult↗
PubMed2000

[Systemic and pulmonary vascular resistance in brain death].

BACKGROUND: Hemodynamic instability is known to affect brain dead subjects and it can be dangerous for the viability of transplantable organs. Aim of the present study was to assess the hemodynamic performance in brain dead subjects, the changes during the legal observation period and the results of therapeutic management. METHODS: The authors evaluated 28 consecutive adult brain dead subjects, all in intensive treatment, controlled ventilation, infusion therapy and/or dopamine administration and continuous direct monitoring of arterial pressure. Ten hemodynamic parameters have been registered by the thermodilution method and the Swann-Ganz catheter. The Legal Committee performed measurements at the beginning (T0) and the end (T6) of the observation period, which lasts 6 hours according to the current law on death certification (Law N. 578/93). RESULTS: Low systemic and pulmonary vascular resistances have been documented in the majority of subjects (75%), both treated only with fluids and with the additional dopamine administration (dosage lower than 10 ug/Kg/min). The above-mentioned reduction was similar at the two different monitored times (T0 and T6). CONCLUSIONS: This situation can be ascribed to the destruction of the cerebral vasoactive centers and the consequent hypotension is due to autonomic nervous system dysfunction. Hemodynamic instability must be treated by fluids and inotropic drugs, but they may cause cardiac and respiratory problems, thus it is suggested to use also low doses of vasoconstrictive drugs, provided that cardiac condition allows this therapeutic strategy.

Adolescent↗
PubMed2000

Blood donors with 'medium' or 'minor' risk factors for human immunodeficiency virus infection: are they eligible for donation?

BACKGROUND AND OBJECTIVES: We conducted a longitudinal prospective study to assess the eligibility to blood donation of donors with 'minor' risk factors (i.e. minor surgery, professional exposure, cohabitation with 'high risk' people, occasional use of light drugs) or 'medium' risk factors for human immuno-deficiency virus (HIV) infection (i.e. casual sexual relationship, multiple heterosexual exposure, sexual partnership with subjects at risk, regular use of light drugs). DESIGN AND METHODS: During a 4-year period we administered a psychosocial questionnaire to all donors attending our Center. In addition we determined anti-HIV, anti-hepatitis C virus (HCV), hepatitis B surface antigen (HBsAg) and syphilis serology (TPHA) at entry to the study and at 6-month intervals. RESULTS: Of 25,367 donors, 1,535 (6%) reported medium and 8,761 (34%) minor risk. At enrollment into the study, 4 medium risk donors were anti-HIV positive and there was a significantly higher rate of positivity for TPHA (0.33% vs 0.07%) and anti-HCV (1.17% vs 0.63%) in this group than in donors reporting no risk. No anti-HIV positivity was observed in minor or no risk donors. During a median follow-up of 18 months, none of 24,404 donors undergoing 106,503 visits seroconverted to HIV. The incidences of novel HCV and syphilis infections were almost one log greater in donors at medium risk (3 and 1x10-4/yr, respectively) than in no risk donors (0.4 and 0.1x10-4/yr, respectively). Medium risk donors were more frequently males (Odds Ratio=3.2, 95% confidence interval= 2.8-3.7), aged 26-35 yrs (1.52; 1.3-1.78), single (1.4; 1.2-1.6), divorced (2; 1.4-2.8), freelance workers (1.43; 1.1-1.9) and first-time donors (1.8; 1.6-2.1) than no risk donors. INTERPRETATION AND CONCLUSIONS: The only 4 HIV positive subjects of the cohort were medium risk donors picked up at enrollment. No HIV seroconversion was observed during the study. On the basis of this study we will continue to defer 'medium' risk donors.

Adolescent↗