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Genetic factors play an important role in the development of many common diseases of adulthood that result in early morbidity and mortality. Prevention of these disorders and their sequelae is best established through early detection and early intervention. Although it may be feasible to screen the entire population for some disorders (e.g., hypertension), this approach would be expensive and impractical for others (e.g., colon cancer). The family history provides an inexpensive and convenient method of identifying families at risk for premature diseases of adulthood. Family screening for a disorder should be recommended if there is increased risk for the disorder among family members, if screening methods are available to detect the condition at an early age or preclinical stage, and if early intervention will alter the course of the disease. For many disorders screening and intervention can prevent the occurrence of clinical disease. The prenatal counseling session affords an ideal setting for identifying families at risk for diseases of adulthood with major genetic components. By reviewing the family history, key family members can be identified and investigated, in order to establish a specific genetic diagnosis. At-risk relatives can then be counseled and screened for the disorder preclinically and premorbidly. The screening and intervention available for a disease depends on the nature of the disorder, our understanding of its physiology and etiology, and our current technology. The disorders discussed earlier are typical of conditions of adulthood that are influenced strongly by genetic factors, especially when they appear in younger adults. Atherosclerosis, colon cancer, and diabetes are complex phenotypes. Each can be caused by single-gene defects, but commonly the genetics are more complex. Empiric data help to establish the risk to an individual in the latter cases. In all three examples, early detection should lead to treatment, which can prevent more serious sequelae: by treating the dyslipidemia, coronary artery disease can be prevented; by removing the benign polyp, malignant cancer can be avoided; and when impaired glucose tolerance is detected, diet and exercise can prevent or delay frank diabetes and its complications. The complete evaluation of individuals at risk for disorders such as those in Table 1 and their families can be a complicated task. Referral to a center experienced in the genetics of common diseases often may be necessary.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetics of common diseases of adulthood. Implications for prenatal counseling and diagnosis. 228 33

The frequency of familial dyslipidemia syndromes was determined from blood tests in 33 objectively ascertained families with early coronary heart disease (CHD) (two or more siblings with CHD by the age of 55 years). Three fourths of persons with early CHD in these families had 90th percentile lipid abnormalities (cholesterol level at or above the 90th percentile, triglyceride level at or above the 90th percentile, and/or high-density lipoprotein cholesterol (HDL-C) level at or less than the 10th percentile). The HDL-C and triglyceride abnormalities were twice as common as low-density lipoprotein-cholesterol abnormalities. The most common syndromes found were familial combined hyperlipidemia (36% to 48% of families with CHD), familial dyslipidemic hypertension (21% to 54% of families with CHD), and isolated low levels of HDL-C (15%), with overlapping familial dyslipidemic hypertension with familial combined hyperlipidemia and low-level HDL-C. Well-defined monogenic syndromes were uncommon: familial hypercholesterolemia being 3% and familial type III hyperlipidemia, 3%. Another 15% of families with CHD had no lipid abnormalities at the 90th percentile. Physicians should learn to recognize and treat these common familial syndromes before the onset of CHD by evaluating family history and all three standard blood lipid determinations. Failure to recognize and treat them leaves affected family members at high risk of premature CHD.
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PMID:Population-based frequency of dyslipidemia syndromes in coronary-prone families in Utah. 231 Feb 76

The diagnosis of intestinal ischaemia still presents numerous problems in terms of nosography, epidemiology, diagnosis and treatment with the result that it is more often excluded than diagnosed. The aim of the present study was to discover whether intestinal ischaemia was clinically identifiable by any specific early signs and symptoms and whether there were any concomitant risk factors. The medical reports on 44 patients consecutively admitted to the San Giovanni Battista Hospital, Turin in 1985-86 with suspected intestinal ischaemia were therefore examined. It was found that intestinal ischaemia was only occasionally (30% of cases) diagnosed at the onset of clinical symptoms. In the 10 patients with ischaemic colitis, the risk factor linked to the causes of the disease was systemic hypovolaemia arising in diffuse atherosclerosis. In the 8 cases of chronic ischaemia and the 26 of intestinal infarction the remote anamnesis revealed symptoms that should have aroused suspicion of intestinal ischaemia partly because the patients were suffering from widespread atherosclerosis. In fact a review of the risk factors for the onset of atherosclerosis (i.e. high blood pressure, smoking, dyslipidemia, obesity and age over 65) revealed that about 60% of the patients under study presented 3 or 4 them simultaneously. To conclude, the data emerging from the study indicate the existence of symptoms and risk factors to diffuse atherosclerosis that should permit the early diagnosis of intestinal ischaemia.
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PMID:[Intestinal ischemia: nosographic framework and risk factors]. 231 16

Essential hypertension is a heterogeneous group of disorders with different causes. This report reviews approaches taken and results found in current studies of the genetic and environmental determinants of essential hypertension. Recent observations from the University of Utah Cardiovascular Genetics Research Clinic and published data from other studies are cited. Several biochemical tests show strong associations with hypertension and substantial major gene and/or polygenic determination including: urinary kallikrein excretion, intracellular sodium concentration, sodium-lithium countertransport, plasma haptoglobin phenotypes, MN blood groups, and familial dyslipidemia.
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PMID:Definition of genetic factors in hypertension: a search for major genes, polygenes, and homogeneous subtypes. 246 8

In order to find if the metabolic disorders more frequently found in our obese population were similar to the ones reported in the literature for other countries, a study was conducted in a group of 34 obese subjects (10 men and 24 women) whose only apparent alteration was a body mass index above 30 (mean value: 36.8 +/- 4.6) to obtain the relation between anthropometric measurements (Quetelet index, skinfold measures and waist/hip ratio) and plasma levels of nine biochemical parameters (including lipids, lipoproteins and glucose and insulin levels after an oral glucose load). The results revealed a tendency to the android distribution of fat in the female population, a significantly elevated triglyceride and total lipids levels and a decreased in HDL-cholesterol in both sexes. Hypercholesterolemia was present mainly in the male population. The most frequent dyslipidemia was Type IV (23%) followed by type IIb (15%). Practically none of the subjects had abnormal glycemic values after the glucose load, however the insulin levels were highly elevated in 80% of the patients, resulting in a great insulin/glucose ratios. Correlation analysis showed no association of the BMI with any biochemical parameter; only the insulin area was positively associated with anthropometric measures (mainly waist/hip ratio) and with the most altered biochemical parameter, the triglycerides. Variance analysis showed that only low HDL-cholesterol values were significantly different in patients presenting high blood pressure and familiar history of diabetes.
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PMID:[Metabolic changes associated with obesity in adults]. 248 10

Familial dyslipidemic hypertension (FDH) is a syndrome recently described from sibships selected for early familial hypertension and found to have one or more of three fasting lipid abnormalities [high triglycerides, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-I and B, fasting plasma insulin (adjusted for body mass index), and detailed anthropometrics were different in two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglyceride and/or low HDL cholesterol levels. When compared to 20 normolipidemic hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p = 0.0001), 33% higher apolipoprotein B (p = 0.0002), smaller LDL particles (p = 0.007), and 73% higher fasting insulin (p = 0.003), but no significant differences in body mass index or skinfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p = 0.0001), with only 8% lower apolipoprotein A-I levels (p = 0.20); significantly higher subscapular skinfolds (p = 0.02), weights (p = 0.002), body mass index (p = 0.006), knee widths (p = 0.0007), and wrist circumferences (p = 0.0009); smaller, denser LDL subfractions (p = 0.001); and increased apolipoprotein B levels (p = 0.01) compared to the normolipidemic hypertensive group. Increased fasting insulin levels were similar to the normolipidemic group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and increased fasting plasma insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglyceride levels. Elevated insulin levels found in both groups, but possibly originating through different physiological mechanisms, may provide the pathophysiological connections between dyslipidemia, obesity, and hypertension.
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PMID:Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia. Study of Utah patients with familial dyslipidemic hypertension. 249 19

A study was made of the content of blood lipids in patients with associated chronic nephritis and arterial hypertension (AH). It has been established that the reduction of arterial pressure as a result of hypotensive therapy (administration of central action drugs, vasodilators of direct action, calcium antagonists, blockers of the angiotensin-transforming enzyme) was followed by a decrease in the blood of the concentration of fatty acids, glycerin, triglycerides, low density lipoproteins, total cholesterol, free cholesterol, phospholipids, characteristics of lipid peroxidation and by the rise of cholesterol concentration in high density lipoproteins. The data obtained are of clinical importance in view of the possibility of correcting dyslipidemia in patients with associated chronic nephritis and arterial hypertension during hypotensive treatment.
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PMID:[Hypotensive therapy and the level of blood lipids in patients with chronic nephritis associated with arterial hypertension]. 279 97

Atherosclerosis is a multifactorial lesion, and any attempt to prevent or reduce its development must take into account the different known factors of the disease. Each of these factors (dyslipidemia, high blood pressure, tobacco smoking, diabetes, excess weight) requires particular measures among which non-pharmacological therapy always plays an important part irrespective of the risk factors involved. Until recent years, there was widespread doubt about the need to modify life style, diet and physical activity to prevent ischemic diseases. From the evidence which now begins to accumulate, mainly due to epidemiology, a number of measures, with or without drugs, may be recommended. The criteria required to select the subjects concerned by such measures remain to be defined.
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PMID:[Role of non-pharmacological treatment in the prevention of atherosclerosis]. 294 29

The metabolic and cardiovascular complications of obesity are dependent upon the distribution of body fat excess: predominantly abdominal or "android" obesity is more pathogenic than "gynoid" obesity which predominates in the lower part of the body. Adipose tissue overloads localized to the abdomen are associated with hypermortality from vascular diseases, even in patients who are not overweight. The metabolic characteristics of abdominal adipocytes, which have increased lipolytic capacity, might account for this situation, as they would facilitate hyperinsulinism, insulin resistance and such-metabolic disturbances as arterial hypertension, diabetes mellitus and dyslipidemia. Androgens seem to play a key role in the development of obesity morphotypes. These notions have important practical applications: an excess of body fat is not necessarily pathogenic; as regards vascular and metabolic risks, body fat distribution seems to be more important than overweight.
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PMID:[Influence of the distribution of body fat on vascular risk]. 295 Apr 48

Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors--dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia--likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 +/- 10 vs 172 +/- 7 mg/dl [standard error of the mean], p less than 0.001), LDL cholesterol (140 +/- 9 vs 101 +/- 6 mg/dl, p less than 0.001), and LDL apolipoprotein-B (108 +/- 16 vs 80 +/- 16 mg/dl, p less than 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin. 305 23


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