Venous Leak Embolization in Patients with Venogenic Erectile Dysfunction via Deep Dorsal Penile Vein Access: Safety and Early Efficacy.

PURPOSE: This all-comers registry aimed to assess safety and early efficacy of venous embolization in patients with venogenic erectile dysfunction due to venous leak in an unselected cohort. METHODS: Between October 2019 and September 2022, patients with venogenic erectile dysfunction resistant to phosphodiesterase-5-inhibitors were treated with venous embolization using ultrasound-guided anterograde access via a deep dorsal penile vein in a single center. A mix of ethiodized oil and modified cyanoacrylate-based glue n-butyl 2 cyanoacrylate (NBCA) monomer plus methacryloxy-sulpholane monomer (Glubran-2, GEM, Italy) was used as liquid embolic agent. Prior to embolization, venous leak had been verified based on penile duplex sonography and computed tomography cavernosography. Procedural success was defined as technically successful and complete target vein embolization. The primary safety outcome measure was any major adverse event 6 weeks after the procedure. The primary feasibility outcome measure was IIEF-15 (International Index of Erectile Function-15) score improvement ≥ 4 points in ≥ 50% of subjects on 6 weeks follow-up post intervention. RESULTS: Fifty consecutive patients (mean age 61.8 ± 10.0 years) with severe erectile dysfunction due to venous leak underwent venous embolization. Procedural success was achieved in 49/50 (98%) of patients with no major adverse events on follow-up. The primary feasibility outcome measure at 6 weeks was reached by 34/50 (68%) of patients. CONCLUSION: Venous leak embolization via deep dorsal penile vein access using a liquid embolic agent was safe for all and efficacious in the majority of patients with severe venogenic erectile dysfunction on 6 weeks follow-up.

Insulin and glucose levels and prevalence of glucose intolerance in pedigrees with multiple diabetic siblings.

Hyperinsulinemia may be an early inherited marker for a defect in insulin action that subsequently results in glucose intolerance and non-insulin-dependent diabetes mellitus (NIDDM). To examine the role of hyperinsulinemia in individuals at high genetic risk for NIDDM and determine the prevalence of impaired glucose tolerance (IGT) and newly diagnosed diabetes in members of NIDDM pedigrees, we studied 310 members of 16 pedigrees ascertained for greater than or equal to 2 NIDDM siblings. Nondiabetic members of all pedigrees were examined by 75-g oral glucose tolerance test with fasting and 1-h insulin levels. Participants had height and weight recorded. Spouses of pedigree members (n = 88) served as control subjects. The spouse control subjects were older and slightly more obese than the undiagnosed pedigree members. The prevalence of IGT was 14.8% in spouses and 7.7% in pedigree members, and NIDDM was present in 11.3% of spouses and 2.3% of previously undiagnosed pedigree members. However, neither spouses nor pedigree members differed significantly from published age-specific prevalence rates for IGT or newly diagnosed NIDDM. Insulin and glucose levels were examined in pedigree members with normal glucose tolerance (NGT). Fasting insulin levels were not significantly different between spouses and NGT pedigree members. However, after adjustment for age, weight (body mass index), and sex, NGT pedigree members had higher 1-h insulin levels and higher fasting and 1-h glucose levels than spouses. These differences were also evident when pedigree members with at least 1 affected (NIDDM or IGT) parent were compared with spouses with no family history of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Methionine for valine substitution in exon 17 of the insulin receptor gene in a pedigree with familial NIDDM.

INSR gene mutations have been described in multiple individuals with extreme insulin resistance, but the INSR gene has not been implicated in familial NIDDM. We previously have screened members of 18 familial NIDDM pedigrees for mutations in exons encoding the tyrosine kinase domain of the INSR gene (exons 13-21) by SSCP. That analysis initially detected only patterns consistent with silent polymorphisms, but on direct sequence analysis of exon 17 we detected a Met-for-Val substitution at position 985 in 1/18 pedigrees. We confirmed the substitution by sequence analysis of subcloned, PCR-amplified DNA from two pedigree members and by hybridization to labeled primers for the normal and mutant sequences. We did not find the mutation in any other individuals. Pedigree members were typed for presence or absence of the Met985 substitution by hybridization of PCR-amplified exon 17 DNA to allele-specific oligonucleotide probes, and typing was confirmed by segregation of INSR haplotypes and by SSCP analysis. The substitution was present in 3 NIDDM individuals in 3 generations, including a lean individual with onset at age 24. The substitution was present in only 50% of NIDDM siblings in generation 2, however. To determine the clinical effect of the Met985 substitution, we compared the 5 nondiabetic pedigree members who carried the mutation with the 9 nondiabetic pedigree members without the mutation and with 266 members of other pedigrees. Fasting and 1-h postglucose insulin levels were not different between carriers and noncarriers (fasting, 71.4 pM vs. 74.5 pM; 1-h, 381 pM vs. 354 pM), even after correction for age, sex, and BMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Major gene effect for insulin levels in familial NIDDM pedigrees.

Insulin resistance and hyperinsulinemia are familial traits that may precede and predict the onset of non-insulin-dependent diabetes mellitus (NIDDM). In some populations, the distribution of fasting insulin levels and measures of in vivo insulin action suggest the effects of a single major gene. We previously noted hyperinsulinemia among unaffected members of 16 large white pedigrees ascertained through two or more NIDDM siblings. To examine the hypothesis that insulin levels are determined by a single major genetic locus, we used segregation analysis to examine fasting insulin levels in 206 family members and 65 spouses who had normal glucose tolerance tests by World Health Organization criteria. Segregation analysis supported a major locus determining fasting insulin levels and segregating as an autosomal recessive allele with a frequency of 0.25. Thus, homozygotes represented 6.25% of the population, and homozygosity for the hyperinsulinemia allele elevated the mean fasting insulin level from 70.3 to 211.1 pM (11.7-35.2 microU/ml). The analysis apportioned the variance in fasting insulin as 33.1% due to the major autosomal locus, 11.4% due to polygenic inheritance, and 55.5% due to unmeasured effects. Homozygotes for the recessive allele had higher 1-h insulin levels than all others (911.7 vs. 427.2 pM [152.0 vs. 71.2 microU/ml]). We also found evidence for a major locus determining 1-h-stimulated insulin levels, with codominant inheritance as the most likely pattern in inheritance. The causal relationship between these findings and NIDDM has not been determined, and segregation of direct measures of insulin action remains to be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Dyslipidemias among normoglycemic members of familial NIDDM pedigrees.

OBJECTIVE: To examine the hypothesis that hyperinsulinemia among relatives of NIDDM probands will increase the prevalence of DLPs, we measured insulin levels and examined the frequency of DLPs among NIDDM pedigree members. RESEARCH DESIGN AND METHODS: We performed 2-h 75-g OGTTs and measured lipid and insulin levels of 287 family members and 86 spouses from 16 large Utah pedigrees ascertained for greater than or equal to 2 siblings with NIDDM. RESULTS: One-hour insulin levels were higher among 206 family members with NGT than among 65 NGT spouses (483.3 vs. 361.7 pM, P = 0.05). Among the NGT family members, 32% had cholesterol levels at or above the age- and sex-specific 90th percentile level defined by the LRC studies, 33% had HDL levels less than or equal to 10th percentile, and 20% had triglyceride levels greater than or equal to 90th percentile. DLP (any of the three abnormalities) was found among 58% of NGT family members, which was significantly higher than the expected 27% (P less than 0.00001) and the prevalence among spouses of 45% (P less than 0.05). By NCEP criteria for hyperlipidemia, 40% of family members met criteria for diet and/or pharmacological therapy. CONCLUSIONS: Normoglycemic members of NIDDM pedigrees have a high prevalence of DLPs, which approaches the prevalence in patients with NIDDM. Our data suggest that members of NIDDM pedigrees should be screened carefully for lipid abnormalities.

Are there interactions and relations between genetic and environmental factors predisposing to high blood pressure?

An overview of published observations suggests that both genetic predisposition and environment work together to produce hypertension in most persons. High blood pressure before age 55 occurs 3.8 times more often among persons with a strong positive family history of high blood pressure. Much of the total variability in blood pressure in modern populations seems attributable to genetic factors. Estimates of the proportion of the variance attributable to all genetic factors (heritability [H2]) vary from 25% in pedigree studies to 65% in twin studies for sitting diastolic blood pressure. Several biochemical traits associated with high blood pressure are highly genetic (H2, 78-84%) and may help elucidate the pathophysiology of high blood pressure. While pertinent environmental factors such as salt intake, alcohol use, and amount of exercise also correlate significantly among relatives, only 7% of the total variance of diastolic blood pressure seems attributable to all shared environmental factors in family households. Thus most familial aggregation of high blood pressure appears to be due to genes rather than shared family environment. Practical benefit may result from identifying familial predisposition in multiple siblings with high blood pressure before age 55 and lipid abnormalities (labeled "familial dyslipidemic hypertension"). About 12% of high blood pressure patients have familial dyslipidemic hypertension and also have high risk of early coronary heart disease. Hyperinsulinemia and central obesity as well as high triglycerides and low high density lipoprotein cholesterol are prominent features of familial dyslipidemic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Food-consumption trends between adolescent and adult years and subsequent risk of prostate cancer.

A population-based, case-control study of prostate cancer in Utah was used to assess reported food-consumption patterns for the adolescent and adult years. Men reported eating eggs, whole milk, butter, white bread, cereals, and candy less frequently and red meat, fish, low-fat milk, cheese, yogurt, ice cream, margarine, fruits and vegetables, and whole-wheat bread more frequently as adults, indicating that diets changed in the hypothesized direction to correspond to national changes in food-consumption practices. Men who consumed a diet high in saturated fatty acids as adults were at a slightly increased risk of developing aggressive prostate cancer after adjusting for adolescent diet (odds ratio 1.8 comparing high with low intakes), whereas men who consumed a diet high in saturated fatty acids as adolescents were not at increased risk of developing these tumors after controlling for a diet high in saturated fatty acids as adults (odds ratio 1.1).

Diagnosing heterozygous familial hypercholesterolemia using new practical criteria validated by molecular genetics.

Heterozygous familial hypercholesterolemia (FH) is a serious disorder causing twice normal low-density lipoprotein cholesterol levels early in childhood and very early coronary disease in both men and women. Treatment with multiple medications and diet can normalize cholesterol levels in many persons with FH and prevent or delay the development of coronary atherosclerosis. Thus, there is a need for accurate and genetically validated criteria for the early diagnosis of heterozygous FH. Previously published blood cholesterol criteria greatly underdiagnosed new cases of FH among members of known families with FH in Utah and overdiagnosed FH among participants of general population screening, revealing the need for different cholesterol screening criteria in persons from these 2 different settings. The statistical concept of a priori probabilities was applied to derive 2 sets of practical screening criteria: one for persons participating in general population screening studies and another for close relatives of confirmed FH cases, showing dramatic differences. At a cholesterol level of 310 mg/dl, only 4% of persons in the general population would have FH but 95% of persons who were first-degree relatives of known cases would have FH. Detailed tables were derived to provide practical total and low-density lipoprotein blood cholesterol screening criteria for diagnosing FH in different screening settings and specific age groups. In population screening the new FH criteria require a total cholesterol > 360 mg/dl for age 40+ (or 270 mg/dl in youth). Among first-degree relatives of confirmed cases in families with FH, the new total cholesterol criteria are much lower (> 290 mg/dl for age 40+, > 220 mg/dl for youth).(ABSTRACT TRUNCATED AT 250 WORDS)

Documented need for more effective diagnosis and treatment of familial hypercholesterolemia according to data from 502 heterozygotes in Utah.

A project to help Utah residents with heterozygous familial hypercholesterolemia (FH) identified affected individuals by collecting detailed questionnaires from: (1) very high-risk persons in computer files of screening data (very high cholesterol levels, very early coronary artery disease, and strong positive family history); (2) confirmed FH index cases from a university lipid clinic; and (3) relatives of any confirmed FH cases. Questionnaires were received from 2,143 persons identifying 101 living index cases and 502 relatives meeting the criteria for the diagnosis of FH. Finding new FH heterozygotes was about one fourth as expensive by tracing relatives of confirmed FH cases by evaluating very high-risk persons. Of those meeting criteria for the diagnosis of heterozygous FH, only 31% reported being told by their physicians that they had FH, only 42% indicated that they were taking a cholesterol-lowering prescription medication, and only 23% had reasonably controlled cholesterol levels (below the 90th percentile). However, the data also suggest that good control is achievable in motivated patients. Among 106 FH heterozygotes who were early responders to a second follow-up questionnaire, 79% were taking prescription medications, of whom 49% had achieved cholesterol levels below the 90th percentile, and 17% even achieved cholesterol levels below the 50th percentile. We conclude that most patients with heterozygous FH are not diagnosed and not adequately treated. We demonstrated how many of these persons needing help could be identified efficiently by tracing relatives of known index cases.

Genetic basis of familial dyslipidemia and hypertension: 15-year results from Utah.

The genetic and environmental determinants of hypertension, lipid abnormalities, and coronary artery disease (CAD) have been studied for 15 years in Utah in population-based multigenerational pedigrees (2500 subjects among 98 pedigrees), twin pairs (74 monozygous and 78 dizygous), hypertensive siblings (131 sibships), siblings with CAD before age 55 (45 sibships), and anecdotally ascertained pedigrees with type II diabetes (271 subjects among 16 pedigrees), lipoprotein lipase deficiency (106 subjects in a single pedigree), and familial hypercholesterolemia (502 heterozygotes among 50 pedigrees). Estimates of heritability ranged from 20 to 75% for blood pressures and blood lipids. A strong positive family history predicts a future occurrence of hypertension (relative risk [RR] = 3.8) and CAD (RR = 12.7). Segregating single-gene effects were found for several 'intermediate phenotypes' associated with hypertension (erythrocyte sodium-lithium countertransport, intraerythrocytic sodium, a relative fat pattern, total urinary kallikrein excretion, and fasting insulin levels). Strong single-gene effects in segregation analysis were also found for low-density lipoprotein (LDL) cholesterol, lipoprotein (a) (Lp[a]), low high-density lipoprotein (HDL) cholesterol, and high apolipoprotein (apo) B. Deoxyribonucleic acid (DNA) markers of lipid abnormalities or hypertension have included LDL-receptor defects, lipoprotein lipase deficiency, high Lp(a), familial defective apo B, decreased quantitative levels of apo B, apo E phenotype, angiotensinogen, and 'glucocorticoid remediable aldosteronism (GRA) hypertension.' Also tested in Utah studies, but not found to be DNA markers for hypertension, were the genetic loci for the structural genes for renin and angiotensin-converting enzyme, and the sodium antiport system. In addition, important gene-gene interactions (LDL receptor with apo E2) and gene-environment interactions (kallikrein with potassium intake) were found.(ABSTRACT TRUNCATED AT 250 WORDS)

An observational study of isotretinoin recipients treated for acne in a health maintenance organization.

From September 1982 to June 1987, all members (N = 513) of the Group Health Cooperative of Puget Sound, Seattle, Wash, who were prescribed isotretinoin for acne were observed throughout the first 4- to 5-month course of therapy for effectiveness and adverse effects. The highest rates of use were among male subjects aged 15 to 24 years. Excluding 47 subjects whose prescriptions were stopped because of noncompliance or who left the care of Group Health Cooperative physicians, 39 (8.4%) of the remaining 466 discontinued taking the drug because of the following adverse effects: mucous/skin/musculoskeletal effects (17); elevated triglyceride levels (eight); headaches (five); increased liver enzyme levels (three); amenorrhea (two); and other (four). One subject, excluded from the 466 because of noncompliance, became pregnant while using medication from a previous prescription and had a therapeutic abortion; she was not under the care of a physician at the time of pregnancy. Most subjects (97%) developed a mucocutaneous symptom, and 42% developed musculoskeletal symptoms. Moderate elevations in liver enzyme levels developed in six (1.8%) of 341 subjects with normal baseline values. Of 389 subjects with normal baseline triglyceride values (less than 2.25 mmol/L), nine (2.3%) developed moderate elevations (4.5 to 9.0 mmol/L), and one (0.3%) developed a severe elevation (greater than or equal to 9.0 mmol/L). Of 24 subjects with elevated baseline triglyceride levels, three (12.5%) developed moderate elevations. Of an additional 53 subjects whose baseline serum triglyceride levels were not determined, two developed elevations during therapy, one up to 13.4 mmol/L. Subjects who were overweight or had elevated baseline serum triglyceride values had an increased risk of developing elevations in triglyceride levels during therapy (odds ratio, 6.0; 95% confidence interval, 1.6 to 22.0; and odds ratio, 4.35; 95% confidence interval, 0.9 to 20.2, respectively). Acne was improved for at least 94.0% of subjects.

Current knowledge regarding the genetics of human hypertension.

Observations over 11 years from the University of Utah Cardiovascular Genetics Research Clinic and published data from other studies are reviewed to illustrate research approaches, developing results and prospects for future studies. Strong associations with hypertension have been found for several biochemical tests that show substantial genetic determination. Suggestions of recessive major gene effects and significant polygenic background determinations have been found for several variables, including urinary kallikrein excretion, intracellular sodium concentration, sodium-lithium countertransport and sodium-potassium cotransport. Each of these variables is related in some way to sodium or potassium metabolism, or both, and may help to improve the understanding of a possibly inherited susceptibility to hypertension that is related to dietary electrolyte intake. A second major group of factors involving familial predisposition to hypertension include lipid abnormalities (increased very-low- and low-density lipoprotein cholesterol and decreased high-density lipoprotein cholesterol); increased fasting insulin levels or insulin resistance, or both; obesity (especially central or upper body obesity); and multiple environmental factors influencing these metabolic systems, including dietary fat, carbohydrate and calorie intake; physical exercise; and certain antihypertensive medications that adversely affect lipid metabolism and glucose tolerance. Some studies even suggest a possible link between these two large groups of factors (electrolyte metabolism and lipid-insulin metabolism). Hypertriglyceridaemia and hyperinsulinaemia are both significantly correlated with increased levels of several cation-flux tests. It is recommended that studies of human hypertension apply these biochemical profiles to study sibships with two or more hypertensive siblings as a cost-effective initial approach.(ABSTRACT TRUNCATED AT 250 WORDS)

Multigenic human hypertension: evidence for subtypes and hope for haplotypes.

Hypertension that occurs before the age of 60 years is strongly aggregated in families, mostly due to genetic factors with weaker contributions from a shared family environment. Hypertension is probably a heterogeneous collection of overlapping subsets of pathophysiological mechanisms, such as dyslipidemia, obesity, hyperinsulinemia and cation metabolism. Highly heritable traits such as sodium-lithium countertransport, urinary kallikrein excretion and a body fat pattern index show evidence of major gene segregation in families with hypertension. They are thought to be intermediate phenotypes in the chain of pathophysiological events leading from specific genes to the distant phenotype of hypertension. They provide evidence of measurable contributions from single gene traits to the susceptibility to hypertension. Genetic linkage studies have suggested that other specific loci (e.g. histocompatibility leukocyte antigen, blood group MN and the haptoglobin protein) contribute to the susceptibility to hypertension. DNA sequencing has shown a point mutation for lipoprotein lipase that conveys susceptibility to lipid abnormalities, and possibly also hypertension, as seen in families with dyslipidemic hypertension. Further application of these approaches, especially in families that include multiple siblings with hypertension, shows promise of a true understanding of how the combined effects of a few specific genes, the polygenic background and selected environmental factors can lead to essential hypertension. This understanding should foster better tailored and more effective approaches to the prevention, diagnosis and treatment of hypertension.

A prospective cohort of American Indian and Alaska Native people: study design, methods, and implementation.

In 2001, the National Cancer Institute funded three centers to test the feasibility of establishing a cohort of American Indian and Alaska Native people. Participating tribal organizations named the study EARTH (Education and Research Towards Health). This paper describes the study methods. A computerized data collection and tracking system was developed using audio computer-assisted survey methodology with touch screens. Data were collected on diet, physical activity, lifestyle and cultural practices, medical and reproductive history, and family history of heart disease, diabetes, and cancer. In addition, a small panel of medical measurements was obtained, including height, weight, waist and hip circumferences, blood pressure, and a lipid panel plus glucose. At the completion of the enrollment visit, data were used to provide immediate health feedback to study participants. During the initial funding period, the authors anticipate enrolling 16,000 American Indian and Alaska Native participants. The age distribution of the study population was similar to that reported in the 2000 US Census for the relevant populations. A component critical to the success of the EARTH Study has been the partnerships with tribal members. The study has focused on involvement of American Indian and Alaska Native communities in development and implementation and on provision of feedback to participants and communities.

Farming occupations and mortality from non-Hodgkin's lymphoma in Utah. A case-control study.

The association between farming occupations and the incidence of non-Hodgkin's lymphoma (NHL) was examined in a case-control study using a cancer registry to identify cases and controls and death certificates to determine the occupation and industry of employment of cancer patients. Case subjects were white males with a diagnosis of NHL who died between 1967 and 1982; control subjects were white males who died of colon cancer during the same period. Control and case subjects were frequency-matched for age and year of diagnosis; county of residence was not a matching variable. Death certificates with codable occupational information were located for 90% of the 249 case and 293 control subjects. A stratified analysis using test-based confidence intervals revealed an increased risk of NHL among farmers. The overall odds ratio, controlling for age and for year of diagnosis, was 1.3 (90% confidence limits 0.9-2.3). For diagnoses during 1952 through 1965, the odds ratio was 6.6, and for diagnoses during 1966 through 1971, the odds ratio was 3.1. The increased odds ratio was most pronounced among those aged 45 to 64 years at the time of diagnosis and those living in rural counties.

Comparison of occupation and industry information from death certificates and interviews.

Information on occupation and industry obtained via an interview prior to death was compared to occupation and industry on the death certificate of 184 colon cancer patients in Utah. The data were coded blindly using a five-digit code. Overall, agreement in the five-digit codes was found for 63 per cent. The industry codes agreed for 67 per cent of the individuals, and the occupation was identical for 68 per cent. Agreement by subjective evaluation of the two data sources, disregarding the five-digit codes, was 73 per cent. There were no differences in agreement of the five-digit codes by age, sex, and county of residence. The number of years worked at the job given by interview was related to agreement. Misclassification occurred in a random manner. It is concluded that the use of death certificates to study the association of occupation and disease is most appropriate for pilot studies.

A death-certificate case-control study of non-Hodgkin's lymphoma and occupation in men in North Carolina.

A death certificate-based case-control study was performed to investigate associations between occupation and non-Hodgkin's lymphoma (NHL) in North Carolina. Cases consisted of 501 men who died of NHL (International Classification of Diseases codes 200 and 202) during the years 1968-1970, 1975-1977, and 1980-1982. Controls were selected from other noncancer deaths, and were frequency matched for age, year of death, and race. Occupation and industry were obtained from the death certificates and coded without knowledge of case-control status. An increased risk for men in professional, technical, and managerial occupations, compared with all others, was detected among whites (OR = 2.69, 1.95-3.72). Black men classified as having "low exposures" by an occupational exposure linkage system had an odds ratio of 1.74 (0.84-3.60). Because of this finding, the occupations were ranked by social class and a statistically significant linear relationship was noted in whites, with risk increasing from lower social class to upper social class. An increased risk was also detected among whites in the rubber, plastics, and synthetics industries (p = .03), and among blacks employed in machine trades occupations (OR = 3.63, 1.32-9.97) and structural work occupations (OR = 2.38, 0.93-6.05). An increased risk was also detected for black painters (p = .02), but not for whites. There was no association found between NHL and employment in the following areas: textile industry; farming; laborers; or occupations with exposures to asbestos or benzene. The association with farming was further examined in counties with high use of pesticides and herbicides, and no increased risk of NHL was detected. Cases were more likely to live in the western part of the state than the eastern. However, NHL mortality rates provided by the North Carolina State Center for Health Statistics did not confirm the relationship.

Diabetes in Utah among adults: interaction between diabetes and other risk factors for microvascular and macrovascular complications.

From a telephone survey of the health status of a random sample of the general population of Utah, we identified 255 people with adult onset diabetes. We compared them to 622 non-diabetic controls, matched for age, sex, and urban/rural country of residence. We examined diabetes as a risk factor for heart diseases, stroke, and blindness and its interaction with other known risk factors. Diabetes interacted with smoking history so as to increase the risk of stroke, heart disease, and blindness. Diabetes also interacted with hypertension in their effect on the prevalence of blindness and, to a small extent, heart disease. Among the diabetics, duration of diabetes was associated with macrovascular and microvascular complications developing after the diagnosis of diabetes. Those with longer duration of disease showed an increase in risk for microvascular (kidney disease, blindness) and macrovascular (heart disease, stroke, amputations) complications. Although the estimates were imprecise, the effect of duration on macrovascular complications was greater among diabetics with a history of hypertension; the effect on microvascular complications was greater among smokers. The findings are compared to previous studies and the utility of diabetes prevalence data is discussed.

Occupation and bladder cancer in Utah.

The relationships between bladder cancer and occupation, industries, and occupational exposures in Utah were examined in a population-based, case-control study conducted between 1977 and 1983. Life-long occupational histories were obtained for 417 cases (332 men and 85 women) and 877 controls (685 men and 192 women). Although few positive findings emerged in this study, increased risks were detected among men for employment in the leather and textile industries which increased with duration of employment. The effects were most marked for employment beginning 45 or more years prior to interview (odds ratio [OR] for textiles = 1.92, confidence interval [CI] = 0.89-4.46; for leather OR = 2.95, CI = 0.63-13.76). Among men and women, increased risk was detected among clerical workers employed for less than 10 years (OR = 1.59, CI = 1.16-2.17) although the risk decreased with increased duration of employment (OR = 0.88, CI = 0.55-1.40 for greater than or equal to 10 years). A protective effect was seen among men and women for 10 or more years employment in professional, managerial, and technical occupations (OR = 0.68, CI = 0.50-0.92). Employment as a carpenter resulted in increased risk which increased with duration. Increased risk for bladder cancer was detected among carpenters who smoked but not among carpenters who never smoked. We used an occupation-exposure linkage system to identify workers exposed to aromatic amino compounds; such workers did not have increased risk of bladder cancer, although interaction between long-term exposure to aromatic amino compounds and smoking was detected. Interactions between smoking and other industrial or occupational exposures were not demonstrated, and for the most part, smoking did not confound the estimates of the bladder cancer-occupation relationships.