Natural history of dysplasia of the uterine cervix.
(17/46662)
BACKGROUND: A historical cohort of Toronto (Ontario, Canada) women whose Pap smear histories were recorded at a major cytopathology laboratory provided the opportunity to study progression and regression of cervical dysplasia in an era (1962-1980) during which cervical squamous lesions were managed conservatively. METHODS: Actuarial and Cox's survival analyses were used to estimate the rates and relative risks of progression and regression of mild (cervical intraepithelial neoplasia 1 [CIN1]) and moderate (CIN2) dysplasias. In addition, more than 17,000 women with a history of Pap smears between 1970 and 1980 inclusive and who were diagnosed as having mild, moderate, or severe dysplasia were linked to the Ontario Cancer Registry for the outcome of any subsequent cervical cancers occurring through 1989. RESULTS: Both mild and moderate dysplasias were more likely to regress than to progress. The risk of progression from mild to severe dysplasia or worse was only 1% per year, but the risk of progression from moderate dysplasia was 16% within 2 years and 25% within 5 years. Most of the excess risk of cervical cancer for severe and moderate dysplasias occurred within 2 years of the initial dysplastic smear. After 2 years, in comparison with mild dysplasia, the relative risks for progression from severe or moderate dysplasia to cervical cancer in situ or worse was 4.2 (95% confidence interval [CI] = 3.0-5.7) and 2.5 (95% CI = 2.2-3.0), respectively. CONCLUSION: The risk of progression for moderate dysplasia was intermediate between the risks for mild and severe dysplasia; thus, the moderate category may represent a clinically useful distinction. The majority of untreated mild dysplasias were recorded as regressing to yield a normal smear within 2 years. (+info)
G20210A mutation in prothrombin gene and risk of myocardial infarction, stroke, and venous thrombosis in a large cohort of US men.
(18/46662)
BACKGROUND: A single base pair mutation in the prothrombin gene has recently been identified that is associated with increased prothrombin levels. Whether this mutation increases the risks of arterial and venous thrombosis among healthy individuals is controversial. METHODS AND RESULTS: In a prospective cohort of 14 916 men, we determined the prevalence of the G20210A prothrombin gene variant in 833 men who subsequently developed myocardial infarction, stroke, or venous thrombosis (cases) and in 1774 age- and smoking status-matched men who remained free of thrombosis during a 10-year follow-up (control subjects). Gene sequencing was used to confirm mutation status in a subgroup of participants. Overall, carrier rates for the G20210A mutation were similar among case and control subjects; the relative risk of developing any thrombotic event in association with the 20210A allele was 1.05 (95% CI, 0.7 to 1.6; P=0.8). We observed no evidence of association between mutation and myocardial infarction (RR=0.8, P=0.4) or stroke (RR=1.1, P=0.8). For venous thrombosis, a modest nonsignificant increase in risk was observed (RR=1.7, P=0.08) that was smaller in magnitude than that associated with factor V Leiden (RR=3.0, P<0. 001). Nine individuals carried both the prothrombin mutation and factor V Leiden (5 controls and 4 cases). One individual, a control subject, was homozygous for the prothrombin mutation. CONCLUSIONS: In a large cohort of US men, the G20210A prothrombin gene variant was not associated with increased risk of myocardial infarction or stroke. For venous thrombosis, risk estimates associated with the G20210A mutation were smaller in magnitude than risk estimates associated with factor V Leiden. (+info)
A historical cohort mortality study of workers exposed to asbestos in a refitting shipyard.
(19/46662)
To investigate the risks of developing asbestos-related diseases we conducted a historical cohort mortality study on 249 ship repair workers (90 laggers and 159 boiler repairers) in a single U.S. Navy shipyard in Japan. We successfully identified the vital status of 87 (96.7%) laggers and 150 (94.3%) boiler repairers, and, of these, 49 (56.3%) and 65 (43.3%) died, respectively, during the follow-up period from 1947 till the end of 1996. Our in-person interviews with some of the subjects clarified that asbestos exposure was considered to be substantially high in the 1950-60s, decreased thereafter gradually but remained till 1979 in the shipyard. The laggers, who had handled asbestos materials directly, showed a significantly elevated SMR of 2.75 (95% C.I.: 1.08-6.48) for lung cancer. The risk developing the disease was greater in the laggers after a 20-year latency (SMR = 3.42). Pancreatic cancer yielded a greater SMR than unity (7.78, 90% C.I.: 2.07-25.19) in a longer working years group. Four laggers died from asbestosis. The boiler repairers, who had many chances for secondary exposure to asbestos and a few for direct exposure, showed no elevation of the SMR of lung cancer overall, but there was a borderline statistically significant SMR of 2.41 (90% C.I.: 1.05-5.45) in a longer working years group. One boiler repairer died from mesothelioma and four from asbestosis. (+info)
A retrospective cohort study of male workers exposed to PVA fibers.
(20/46662)
In order to ascertain whether PVA fibers can produce cancer in humans or not, we have conducted a retrospective cohort study of workers exposed to PVA fibers. A total of 447 exposed and 2416 non-exposed male workers who were engaged before 1980 were followed up until the end of 1996. The SMR for all causes was 0.57 (observed 38, 95% CI: 0.41-0.78) for the exposed, and 0.66 (observed 210, 95% CI: 0.58-0.75). As for lung cancer, its SMR was 0.77 (observed 3, 95% CI: 0.15-2.24) for the exposed workers and 0.67 (12 observed, 95% CI: 0.34-1.16) for the non-exposed workers. Lung cancer SMR was 0.86 (observed 2, 95% CI: 0.10-3.11) for the workers with 20 or more years' employment. This study showed no difference in lung cancer risk between the workers exposed to PVA fibers and the non-exposed workers. (+info)
Hypertension in the haemodialysis population: any relationship to 2-years survival?
(21/46662)
BACKGROUND: Few studies have quantified the effect of hypertension on survival in the haemodialysis (HD) population. We have previously reported lack of adverse effect of hypertension on 1-year mortality in a cohort of 649 haemodialysis patients (Am J Kidney Dis 1996; 28: 737-744). We report here the effect of hypertension on 2-year survival in the same cohort of patients. METHODS: We reviewed the complete computerized files on 649 HD patients enrolled in 10 haemodialysis centres in the state of Mississippi, USA. One-month dialysis records for each patient from mid-October 1994 to mid-November 1994 were reviewed. Predialysis mean arterial pressure was calculated as immediate predialysis diastolic pressure plus one-third the difference between systolic and diastolic pressure. Patients were classified as hypertensive if their average pre-MAP was more than 114 mmHg or they were receiving antihypertensive drugs during the study period. Normotensives had a pre-MAP < 114 and were not receiving any antihypertensives. We followed these patients for 2 years to determine their survival and the effect of their BP status, as determined in October 1994, on 2-year mortality. RESULTS: In univariate analysis, hypertension was associated with improved 2-years survival (relative risk 0.64, P=0.08 compared to normotensives). Furthermore, among the hypertensives, good blood pressure control (less than 140/90) was associated with increased relative risk of death at 2 years (RR 1.86, P=0.004). In multivariate analysis, taking age, race, serum albumin, and diabetic status into consideration, there was a 27% reduction in mortality among hypertensives compared to normtensives (RR 0.73, P=0.06). Other factors of significance in multivariate analysis were age (RR 1.03/year, P=0.02), serum albumin (RR 0.36/g, P<0.0001), diabetes mellitus (RR 1.35, P=0.07), and race (RR 0.64, P=0.05). CONCLUSIONS: Our study suggests that hypertension has no adverse effect on survival at 2 years in the haemodialysis population. (+info)
A genomewide analysis provides evidence for novel linkages in inflammatory bowel disease in a large European cohort.
(22/46662)
Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation, typically starting in early adulthood. IBD is subdivided into two subtypes, on the basis of clinical and histologic features: Crohn disease and ulcerative colitis (UC). Previous genomewide searches identified regions harboring susceptibility loci on chromosomes 1, 3, 4, 7, 12, and 16. To expand our understanding of the genetic risk profile, we performed a 9-cM genomewide search for susceptibility loci in 268 families containing 353 affected sibling pairs. Previous linkages on chromosomes 12 and 16 were replicated, and the chromosome 4 linkage was extended in this sample. New suggestive evidence for autosomal linkages was observed on chromosomes 1, 6, 10, and 22, with LOD scores of 2.08, 2.07, 2.30, and 1.52, respectively. A maximum LOD score of 1.76 was observed on the X chromosome, for UC, which is consistent with the clinical association of IBD with Ullrich-Turner syndrome. The linkage finding on chromosome 6p is of interest, given the possible contribution of human leukocyte antigen and tumor necrosis-factor genes in IBD. This genomewide linkage scan, done with a large family cohort, has confirmed three previous IBD linkages and has provided evidence for five additional regions that may harbor IBD predisposition genes. (+info)
Natural history of Helicobacter pylori infection in childhood: 12-year follow-up cohort study in a biracial community.
(23/46662)
We assessed the pattern of acquisition and loss of Helicobacter pylori infection in a cohort of 212 children from a biracial community with a homogeneous socioeconomic class. The children were followed over 12 years (1973-1974 to 1985-1986) from childhood to young adulthood. H. pylori status was assessed by the presence of serum IgG antibodies to H. pylori. At ages 7-9, 19% of children had H. pylori infection (40% of blacks vs. 11% of whites; P = .0001); 12 years later, 33% were seropositive. The higher prevalence among blacks remained (P = .0001). During follow-up, 22% of children became infected; the rate of acquisition was fourfold greater among blacks than among whites (P = .001). Over the 12-year period, infection was lost in 50% of whites compared with 4% of blacks who either remained infected or became reinfected. H. pylori infection in childhood is affected by both acquisition and loss of infection in different ethnic groups. This observation is critical for understanding the epidemiology and transmission of H. pylori infection. (+info)
Platelet aggregation and incident ischaemic heart disease in the Caerphilly cohort.
(24/46662)
BACKGROUND: Platelets are involved in myocardial infarction but evidence of prediction of infarction by measures of platelet function are sparce. METHODS: Platelet aggregation to thrombin and to ADP in platelet rich plasma was recorded for 2176 men aged 49-65 years in the Caerphilly cohort study. RESULTS: Results from 364 men were excluded, 80 of whom had not fasted before venepuncture; most of the others were excluded because antiplatelet medication had been taken shortly before the platelet tests. During the five years following the platelet tests 113 ischaemic heart disease (IHD) events which fulfilled the World Health Organisation criteria were identified--42 fatal and 71 non-fatal. No measure of platelet aggregation was found to be significantly predictive of incident IHD. The possibility that platelet function is predictive for only a limited time after it is characterised, and that prediction falls off with time, was tested. When IHD events are grouped by their time of occurrence after aggregation had been measured, the test results show a gradient suggestive of prediction of early IHD events. Thus, 24% of the men who had an event within 500 days of the test had had a high secondary response to ADP while only 12% of those whose IHD event had been 1000 or more days after the test had shown a high platelet response at baseline. The trend in these proportions is not significant. CONCLUSIONS: Platelet aggregation to thrombin and ADP in platelet rich plasma was recorded in the Caerphilly cohort study. No measure of aggregation was found to be predictive of IHD. (+info)