Hereditary dyslipidemias and combined risk factors in children with a family history of premature coronary artery disease.

AIM: Schoolchildren aged 10-11 with a family history of premature coronary artery disease (CAD), were examined in order to identify children with genetically determined dyslipidemias and a combination of risk factors. METHODS: A total of 4000 questionnaires were distributed by the school; 55% of the families answered and returned the questionnaire. Blood lipids, apolipoprotein B, and Lp(a) lipoprotein were analysed in high risk children and their parents. RESULTS: A family history of premature CAD in parents or grandparents was identified in 208 families; 175 agreed to take part in a clinical examination and laboratory tests. Normal blood lipid tests were found in 89 children. Another 48 had an isolated increase of Lp(a) lipoprotein of minor clinical importance. Of the remaining 38 children, 23 had non-hereditary abnormalities of low (LDL) or high density lipoprotein (HDL) cholesterol or apolipoprotein B. Fifteen children were suspected to have genetically determined dyslipidemias or a combination of risk factors: in four, possible familial hypercholesterolaemia (FH); in five, possible familial combined hyperlipidaemia; in three, hereditary low HDL cholesterol; and in three a combination of high LDL cholesterol and Lp(a) lipoprotein concentrations. In addition, possible FH was detected in eight of the parents. CONCLUSION: It is worthwhile asking parents about the occurrence of premature CAD among their child's closest relatives.     

Lipoprotein (a) and apolipoprotein A-1 and B in schoolchildren whose grandparents had coronary and cerebrovascular events: A preliminary study of 12–13 year old Japanese children

The aim of this study was to evaluate the relationship between the serum levels of lipoprotein (a) [Lp (a)] and apolipoproteins (apo A-1 and apo B) in schoolchildren with a history of coronary and cerebrovascular events in their grandparents. We measured serum concentrations of Lp (a) and apoliproteins immunochemically in 289 schoolchildren aged 12–13 years and questioned parents about coronary and cerebrovascular events in the children's grandparents. In boys and girls, mean ± s.d. levels of apo A-1, apo B and Lp (a) were 134 ± 20.3 and 136 ± 17.4 mg/dL, 61 ± 16 and 66 ± 15 mg/dL and 12.5 ± 15.3 and 12.5 ± 15.1 mg/dL, respectively. There were no significant sex differences in the levels of apo A-1, apo B, and Lp (a). The Lp (a) levels (mean ± s.d., 12.5 ± 15.2 mg/dL; median 7.5 mg/dL, n = 289) were not affected by other variables. The Lp (a) distribution was strongly positively skewed and 75% of schoolchildren had very low levels. In the total 289 schoolchildren, thirty-two grandparents who had had coronary vascular events (21 myocardial infarction, 11 angina pectoris) and twenty-three grandparents who had had cerebrovascular events were recorded. By the boxplot statistical analysis, no difference was found in Lp (a) levels in children whose grandparents had myocardial infarction compared with those whose grandparents had no such history, or compared with those whose grandparents had suffered cerebrovascular events. Analysis also showed that the values of log Lp (a) in children whose grandparents had myocardial infarction tended to be higher than the values in children whose grandparents had no such history (P = 0.09). No significant differences in the levels of apo A-1 and apo B and in the apo B/A-1 ratio could be seen between children grouped according to the presence or absence of coronary and cerebrovascular events in their grandparents. These results suggest that high levels of Lp (a) in schoolchildren aged 12–13 years may partly reflect the existence of coronary vascular disease in older family members. Lp (a) may account for the strongest index of family history to disease risk in comparison with other apolipoproteins. Further study is needed to clarify the appropriate mass measurement method for Lp (a) in schoolchildren.     

Hereditary dyslipidemias and combined risk factors in children with a family history of premature coronary artery disease

AIM—Schoolchildren aged 10-11 with a family history of premature coronary artery disease (CAD), were examined in order to identify children with genetically determined dyslipidaemias and a combination of risk factors.METHODS—A total of 4000 questionnaires were distributed by the school; 55% of the families answered and returned the questionnaire. Blood lipids, apolipoprotein B, and Lp(a) lipoprotein were analysed in high risk children and their parents.RESULTS—A family history of premature CAD in parents or grandparents was identified in 208 families; 175 agreed to take part in a clinical examination and laboratory tests. Normal blood lipid tests were found in 89 children. Another 48 had an isolated increase of Lp(a) lipoprotein of minor clinical importance. Of the remaining 38 children, 23 had non-hereditary abnormalities of low (LDL) or high density lipoprotein (HDL) cholesterol or apolipoprotein B. Fifteen children were suspected to have genetically determined dyslipidaemias or a combination of risk factors: in four, possible familial hypercholesterolaemia (FH); in five, possible familial combined hyperlipidaemia; in three, hereditary low HDL cholesterol; and in three a combination of high LDL cholesterol and Lp(a) lipoprotein concentrations. In addition, possible FH was detected in eight of the parents.CONCLUSION—It is worthwhile asking parents about the occurrence of premature CAD among their child''s closest relatives.     

Screening programme for hyperlipidemia in children and adolescents. Prophylactic aspects of atherosclerosis

Atherosclerotic cardiovascular diseases (CVD), mainly coronary heart disease (CHD) remain the leading cause of death in adult populations of many countries. The following risk factors for atherosclerosis were identified: hypercholesterolemia, hypertension, cigarette smoking and obesity. Scientific reports and epidemiological studies have shown that atherosclerosis begins in childhood. Therefore consensus was obtained that the earlier the prevention begins the better results are achieved. But there are many controversies around early identification of hypercholesterolemia in children. Three options were considered: cholesterol mass screening, selective cholesterol screening and no screening at all. The most acceptable is selective screening performed in children of high risk families (CVD or hypercholesterolemia in the family). It is recommended by the US Expert Panel for the National Cholesterol Education Program for Children and Adolescents (NCEP-Peds). According to the NCEP-Peds, screening should include the following groups: I) children whose parents or grandparents have a history of CVD (under the age of 55 years), 2) children whose parents have a raised blood cholesterol concentration (above 240 mg/dl), 3) children with negative or unknown family history, but having other risk factors (hypertension, obesity, cigarette smoking, high-fat diet). The experts recommend that the examination should be performed in children after the age of 2 years. The NCEP-Peds guidelines set total cholesterol levels in serum for children and adolescents from families at risk, below 170 mg/dl, as acceptable. Total cholesterol level between 170 and 199 mg/dl is classified as borderline and 200mg/dl and above--as high.     

Lipoprotein(a) and cardiovascular risk factors in a cohort of 6-year-old children. The Rivas-Vaciamadrid Study

We have studied the distribution of lipoprotein(a) (Lp(a)) and its relation to lipid profiles and a family history of cardiovascular disease in grandparents in a cohort of 673 6-year-old Spanish children. Lp(a) levels were highly skewed, showed no differences between sexes and had no relevant relations with anthropometric variables. When compared with children without a family history of stroke, children with a family history of this disorder showed significantly higher levels of Lp(a) (median 13 mg/dl, range 2–110 mg/dl versus 9 mg/dl, range 2–120 mg/dl, P =0.02). Also the percentage of children with a family history of stroke was higher in the group of children with Lp(a) levels above 30 mg/dl than in the group who exhibited lower levels (20.9% versus 10.4%, P =0.002). Children with a family history of coronary heart disease had higher levels of Lp(a) than children without such history (median 14 mg/dl, range 2–120 mg/dl versus 8 mg/dl, range 2–62 mg/dl, P =0.03). Finally, when compared with children with Lp(a) levels <30 mg/dl, those with Lp(a) levels above 30 mg/dl showed significantly higher mean levels of total cholesterol (174.9 versus 169.4 mg/dl, P <0.05), low-density lipoprotein-cholesterol (109.1 versus 102.4 mg/dl, P <0.05), and apolipoprotein B (81.9 versus 74.6 mg/dl, P <0.05). Conclusion: our study shows the existence of an association between high levels of lipoprotein (a) in 6 year-old children and a family history of both cerebrovascular and coronary disease in grandparents. High levels of lipoprotein (a) were also associated with high levels of low-density lipoprotein-cholesterol and apolipoprotein B.Abbreviations Apo apolipoprotein - LDL low-density lipoprotein - Lp(a) lipoprotein(a)     

Serum lipoprotein(a) in healthy Japanese children 5 years of age

Serum lipoprotein(a) [Lp(a)] concentrations were investigated in 155 Japanese children aged 5 years. The frequency distribution of Lp(a) concentrations was highly skewed and ranged from 1 to 109 mg/dL. The mean and median values of Lp(a) were 16.5 mg/dL (s.d. 17.3 mg/dL) and 12 mg/dL. The incidence of Lp(a) concentrations ≥30 mg/dL was significantly high in children with total cholesterol ≥3200 mg/dL, not including the case of familial hypercholesterolaemia. Log Lp(a) values showed an inverse correlation with bodyweight and body mass index. No significant differences in Lp(a) levels could be seen between the groups according to the presence or absence of coronary heart disease and cerebral vascular accident in family histories. The results suggest that Lp(a) in Japanese children aged 5 years was essentially the same as that in adults. Further study may be needed to disclose the factors that influence Lp(a) concentration in childhood.     

Serum homocysteine and lipoprotein (a) concentrations in hypercholesterolemic and normocholesterolemic children

The relationship between lipids, lipoproteins, total homocysteine, and lipoprotein (a) was studied in hypercholesterolemic and normocholesterolemic children. In hypercholesterolemic children, concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein B, and triglycerides were significantly higher compared to levels in controls, whereas concentrations of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I were lower compared to those in the control group. Total serum homocysteine concentrations in children with a positive family history for cardiovascular disease CHD(+) (7.28 micromol/L) were significantly higher than those in the control group (5.45 micromol/L), and in the group of CHD(-) children (5.25 micromol/L). The median value of lipoprotein (a) in patients was 31.5 mg/dL (range, 11-209 mg/dL) and in the control group, 19 mg/dL (range, 11-95 mg/dL). Concentrations of Lp (a), exceeding 30 mg/dL, were present in 45% of CHD(+) children, in 29% of CHD(-) children, and in only 11% of the control group.     

Lipid profile with paternal history of coronary heart disease before age 40

Serum lipids were measured in children and their parents from 40 families in which the father had a myocardial infarction or coronary heart disease (CHD) before age 40 years. The relationship between physical activity and serum lipid concentrations in the children was also evaluated. Twenty six men had one or more abnormal lipid value (in mmol/l): total venous cholesterol (TVC) > 6.24, triglycerides < 2.55, low density lipoprotein cholesterol (LDL-C) > 4.42, or high density lipoprotein cholesterol (HDL-C) < 0.91. There were 15 spouses with significant hyperlipidaemia (values above). In the 107 children examined, TVC mean (SD) was 4.68 (1.17), triglycerides 1.4 (0.8), LDL-C 3.0 (1.0), and HDL-C 1.18 (0.28). Altogether 42% of the children had significant hyperlipidaemia. No significant correlation was found between the degree of physical activity of the children and their LDL-C and TVC concentrations. However, a significant positive correlation was found between the degree of physical activity and HDL-C and a significant negative one with triglyceride concentrations. It is concluded that screening the progeny of young CHD patients is highly productive in identifying young people at excessive risk for future CHD. The data also suggest that promoting high degrees of activity among these children may have a positive influence on risk factors for adult onset CHD.     

冠心病家族史儿童脂质三角的研究

目的：了解有冠心病(CHD)家族史儿童脂质三角［低密度脂蛋白-胆固醇(LDL-C),高密度脂蛋白-胆固醇(HDL-C)和甘油三脂(TG)］有无异常。方法：对83例有冠心病家族史的儿童检测血浆TG,LDL-C和HDL-C浓度,计算LDL-C/HDL-C,以无CHD家族史的健康儿童作为对照。结果：与对照组比较,有CHD家族史的儿童血TG,LDL-C浓度明显增高［(1.46±0.63) mmol/L vs (0.84±0.43) mmol/L,(2.09±1.13) mmol/L vs (0.96±0.87) mmol/L］,HDL-C水平降低［(1.48±0.48) mmol/L vs (1.72±0.53) mmol/L］,LDL-C/HDL-C升高(1.71±1.29 vs 0.96±0.68)(P1.7 mmol/L及LDL-C/HDL-C>2.5的发生率明显增高(20.5% vs 1.2%)(P均0.05)。有早发CHD家族史的儿童血TG,LDL-C水平［(1.86±0.63),(3.12±1.32) mmol/L］高于无早发CHD家族史儿童［(1.34±0.58),(1.79±0.87) mmol/L］及对照组［(0.84±0.43),(0.96±0.87) mmol/L］。有早发CHD家族史者LDL-C/HDL-C(2.85±1.21)高于无早发家族史组(1.37±1.11)和对照组(0.96±0.68)(P均<0.01),HDL-C水平［(1.11±0.26) mmol/L］低于无早发家族史者［(1.59±0.47) mmol/L］和对照组［(1.72±0.53) mmol/L］。脂质三角异常发生率(52.6%)高于无早发家族史组(10.9%)和对照组(1.2%)(P<0.01)。结论：有CHD家族史的儿童存在脂质三角异常,以有早发CHD家族史儿童明显。提示儿童期脂质三角异常与CHD家族史关系密切,有CHD家族史儿童成年后发生CHD的危险性显著增高。     

Cardiovascular risk factors in children with obesity,hypertension and diabetes: lipoprotein(a) levels and body mass index correlate with family history of cardiovascular disease

The aims of the study were to compare atherosclerosis risk factors in obese, hypertensive and diabetic children with positive and negative family history (FH) of cardiovascular disease (CVD) and to find which of the new atherosclerosis risk factors may be of clinical value in predicting future cardiovascular events. A total of 285 children and adolescents were divided into groups: obese, obese and hypertensive, hypertensive, and diabetic. Each group was further segregated into children with positive or negative FH of CVD. Positive FH groups were analysed according to FH of CVD before or after 55 years of age, and in parents and grandparents separately. We assessed lipids, body mass index (BMI) and new risk factors: lipoprotein(a) Lp(a), apolipoprotein A-I (apo A-I) and apolipoprotein B (apo B), homocysteine (Hcy), fibrinogen (FB), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1). A positive FH of CVD was found in 28% of the children and in 8.7% it was premature CVD. Children with a positive FH had higher BMI (25.4 versus 23.7 kg/m(2), P<0.05) and highest BMIs were found in those with FH of CVD <55 years (26.8 kg/m(2), P<0.05) or in parents (27.4 kg/m(2), P<0.05). Lp(a) levels were higher in children with a positive FH (0.38 versus 0.28 g/l, P<0.05) and highest in children with a FH of premature CVD (0.44 g/l, P<0.05). Differences were also found in apo B levels (0.90 versus 0.84 g/l, P<0.05). In logistic regression analysis only BMI and Lp(a) were significant in predicting future cardiovascular events. CONCLUSION: obese, hypertensive and diabetic children often originate from families with cardiovascular disease. Children with a family history of cardiovascular disease have a higher body mass index. Levels of lipoprotein(a) and apolipoprotein B may be predictive of future cardiovascular disease in predisposed children.     

有心肌梗塞家族史儿童血清脂蛋白（a）的研究

为探讨有心肌梗塞家族史的少年儿童血脂的改变，特别是脂蛋白（ａ）的改变，采用单克隆抗体酶联免疫吸附实验，对３３例有心肌梗塞家族史的少年儿童测定其脂蛋白（ａ）［Ｌｐ（ａ）］。结果：血清Ｌｐ（ａ）＞３００ｍｇ／Ｌ：心肌梗塞家族史阳性的３３例中有１６例（４８％），而对照组３３例中只有５例（１５％）（χ２＝８．５４０，Ｐ＜０．０５）；有心肌梗塞家族史儿童的血清Ｌｐ（ａ）含量明显高于对照组。提示：对有心肌梗塞家族史的后代，应适时检测Ｌｐ（ａ），及早施行干预措施，以达到预防的目的。     

Levels of lipoprotein(a) and plasma lipids in Spanish children aged from 4 to 18 years

Increased plasma lipoprotein(a)-Lp(a)-levels are linked to a high risk of cardiovascular disease unrelated to other lipoproteins. It seems that Lp(a) values in childhood remain unaltered up to adulthood. In a randomly chosen population of 1970 children, aged from 4 to 18 years and living in a Spanish community, the following serum parameters were studied: total cholesterol, total triglycerides, Lp(a), high-density lipoprotein cholesterol and low-density lipoprotein cholesterol. Mean Lp(a) serum values were 15.0 ± 14.7mg dl^-1. No differences were seen between either sex in the first years of childhood. Of the studied children, 15.1% presented Lp(a) concentrations above 30 mg dl^-1. A correlation between Lp(a) and total cholesterol concentrations, which disappeared when low-density lipoprotein cholesterol concentrations were corrected according to cholesterol present in Lp(a), was observed.     

New opportunity for vaccinating older people: Well‐child clinic visits

Background: Streptococcus pneumoniae causes considerable morbidity and mortality in the elderly. As aging of the population is making the health of the elderly a universal priority, preventive measures, such as vaccination, will become increasingly important. Methods: We designed a prospective interventional study to determine whether recommendations to vaccinate grandparents of children attending well‐child clinics would increase the pneumococcal vaccination rate in the elderly. Children younger than 5 years of age, attending a university well‐child clinic from 1 May to 31 September 2008 who had grandparents over 65 years of age were eligible. A survey including the questions about the demographic characteristics of children, their parents and grandparents over 65 was carried out by face‐to‐face interview with the parents. High‐risk medical conditions and vaccination history of grandparents was also noted and the benefits and necessity of pneumococcal vaccination (23vPPV) for the elderly was emphasized. Four months later these families were contacted to determine whether this intervention had increased the pneumococcal vaccination rates of the elderly. Results: Information was obtained from 938 grandparents of 545 children. Before the interview, among all grandparents, only 0.9% were vaccinated with 23vPPV. Four months after this intervention, immunization coverage increased to 19.1%. The sex of the grandchild (OR: 1.99) and previous hepatitis B or influenza immunization of the grandparents (OR: 2.73) were the significant parameters accounting for higher immunization rates. Conclusion: Reminding elderly grandparents about vaccines in well‐child clinics could be an opportunity in this field.     

不同家族史的少年儿童血清脂蛋白(a)的研究

目的 研究有急性脑血管病家族史的少年儿童和有心肌梗塞家族史的少年儿童血清脂蛋白(Lp)(a)的改变。方法 采用单克隆抗体酶联免疫吸附试验(ELISA)测定血清Lp(a)，有心肌梗塞家族史少年儿童33例，有急性脑血管病家族史少年儿童30例，正常儿童对照组33例。所有受检者在年龄、性别、身高、体重方面无统计学差异，心、肝、肾功能正常。结果 有心肌梗塞家族史的少年儿童，Lp(a)增高频率为48％、Lp(a)水平明显高于对照组；有急性脑血管病家族史的少年儿童，Lp(a)增高频率为33％，Lp(a)水平与正常对照组比较，差异无统计学意义。结论 对有心肌梗塞家族史的后代适时检查与继续观察Lp(a)，是实施早期干预的一项措施；对有急性脑血管病家族史的少年儿童，继续观察Lp(a)的变化，以期作为一项预报因子。     

安徽省芜湖市城区0~24月龄婴幼儿过敏性疾病的危险因素分析

目的了解安徽省芜湖城区0~24月龄婴幼儿过敏性疾病既往发病情况,探讨婴幼儿过敏性疾病的危险因素,为今后婴幼儿过敏性疾病的防治工作及发病机制的深入研究提供理论参考。方法采取整群随机抽样的方法对600名安徽省芜湖市城区0~24月龄婴幼儿母亲进行问卷调查,询问疾病史、家族史、孕期及育儿等情况,运用单因素和多因素logistic回归分析方法对资料进行分析。结果在纳入分析的597名婴幼儿中,既往被确诊为过敏性疾病者共56例(9.4%)。单因素分析显示,月龄、解热镇痛药物使用、父亲过敏史、直系祖辈亲属过敏史和孕期母亲鱼虾蟹贝类食用5项因素与既往罹患过敏性疾病相关联(P0.05)。多因素回归分析显示,月龄、父亲过敏史、直系祖辈亲属过敏史与既往罹患过敏性疾病存在正关联(OR依次为:4.0~4.9、2.7、2.4,均P0.05),而母亲孕期经常食用鱼虾蟹贝类与既往罹患过敏性疾病存在负关联(OR=0.3,P0.05)。结论过敏家族史是安徽省芜湖城区0~24月龄婴幼儿过敏性疾病发生的独立危险因素,而母亲孕期经常食用鱼虾蟹贝类是其保护因素。     

CHOLESTEROL AND THE CHILD: STUDIES OF THE CHOLESTEROL LEVELS OF BUSSELTON SCHOOL CHILDREN AND THEIR PARENTS1

In 1964 as part of a population study, the blood cholesterols of 1,292 school children in the town of Busselton in Western Australia were examined. A gradual rise in the median value throughout school life was demonstrated in both boys and girls, with a pre-adolescent rise comparable with similar studies elsewhere. In 1969 the cholesterol levels of the children with the highest, middle and lowest 5% levels in 1967 were repeated and showed a highly significant correlation, thus indicating that a single cholesterol estimation in childhood is of considerable predictive value, at least over a 2 year period. Comparison of cholesterol levels of 929 children with those of their parents revealed a significant correlation between parents and children throughout the whole cholesterol range. It has not been possible to demonstrate whether the cause is dietary or genetic, except in a few cases of genetic hyperlipidaemia, but it is likely that, at least in those children with a cholesterol higher than 250 mgm% of the cause is genetic. The mother's cholesterol is more closely related than the father's to that of the children. This might be due to both a genetic contribution to the children and her role in controlling the diet of the family, this control being greatest on the young children.     

Genetic predisposition to hypertension (as detected by Na+/Li+ countertransport) and risk of diabetic nephropathy in childhood diabetes

In order to evaluate whether insulin-dependent diabetes mellitus patients with incipient nephropathy have an overactivity of erythrocyte sodium-lithium countertransport (Na+/Li+ CT), 82 diabetic children and 38 healthy age-matched control subjects and their parents and grandparents were studied. The children were divided into two groups according to the presence of persistent microalbuminuria (MA). Diabetic children with MA had Na+/Li+ CT activity higher than normoalbuminuric diabetics and healthy controls. The parents and grandparents of microalbuminuric patients showed higher Na+/Li+ CT than parents and grandparents of normoalbuminuric diabetics and of the controls. This study demonstrates that predisposition to hypertension, as indicated by increased Na+/Li+ CT activity in erythrocytes, is more frequently detectable in patients with persistent microalbuminuria than in diabetics without persistent microalbuminuria or in healthy controls. Overactivity of Na+/Li+ CT is present also in parents and grandparents of diabetic children with MA. This study suggests that genetic predisposition to hypertension is more frequent in patients at risk of developing diabetic nephropathy, as well as in their parents and grandparents.     

Coronary risk factors in school children in relation to their family history of coronary heart disease and hyperlipidemia

A school-based study was implemented to assess the family history of coronary heart disease (CHD) and hyperlipidemia (HL) in relation to serum lipoprotein and apolipoprotein levels. One hundred and twenty-five elementary school students (aged9–10 years) and 297 junior high school students (aged12–13 years) participated. Family history was evaluated by the following scoring method: positive family history in a parent. 2 points: in a grandparent. 1 point: and onset of CHD before age 60, 1 additional point. Family history of HL was positive in 8.2% of elementary school students, and 4.2% in junior high school students. Family history of CHD was positive in 11.5% of elementary students, and 11.0% in junior students. Family history score (FHS) for HL was related to serum total cholesterol (TC), low density lipoprotein cholesterol (LDLC), high density lipoprotein cholesterol, apolipoprotein A-T, apolipoprotein B (apoB) and lipoprotein (a) in elementary students, and to TC, LDLC, triglyceride and apoB in junior students. There was no relationship between FHS for CHD and serum lipoprotein or apolipoprotein levels in any student. The children with a positive FH of HL already demonstrated an atherogenic lipid profile while those with FH of CHD did not. which was probably because lipid profiles in children are more genetically mediated by a FH of HL than of CHD.     

Reliability of family history of lifestyle-related diseases on questionnaire

Background:  Family history of lifestyle-related diseases is an important risk factor and is widely used in epidemiologic studies. To justify its use the validity of the family history needs to be assessed. The aim of the present study was therefore to examine reliability, that is, consistency in repeated measurements, of the family history obtained on questionnaire.
Methods:  A questionnaire survey on the family history of lifestyle-related diseases was conducted for 438 high school students about students' parents, grandparents, uncles and aunts, twice with a 1 year interval. The questionnaire was filled in by their parents. Discordance between the two questionnaires in age, age at death and a positive history of lifestyle-related diseases expressed by age at onset by decade age among the family members was examined. Kappa was used as a measure of agreement.
Results:  The kappas for relatives were high, mostly >0.7 for hypertension and >0.5 for myocardial infarction, angina pectoris, stroke, diabetes mellitus and hypercholesterolemia. The discordance tended to be higher among grandparents than parents, uncles and aunts. The discordance with regard to relatives was mostly <4% for angina pectoris, myocardial infarction, stroke and diabetes mellitus; for hypertension and hypercholesterolemia the discordance was <6%.
Conclusions:  The questionnaire provides a reliable and valid method of collecting family history on relatives of high school students. Thus, family history obtained through questionnaires can be used justifiably as a risk factor for lifestyle-related diseases among children and youths.     

Cholesterol screening and family history of vascular disease

Hypercholesterolaemia is a major risk factor for the development of coronary heart disease (CHD). Early detection and management of hypercholesterolaemia could retard the atherosclerotic process. Given that CHD and hypercholesterolaemia cluster within families, a screening strategy based on a family history of vascular disease has been advocated. Serum total cholesterol concentrations were measured in a random stratified sample of 1012 children aged from 12-15 years old participating in a coronary risk factor surveillance study in Northern Ireland. Information about vascular disease in close family members was obtained by means of a questionnaire. The study population was divided into two groups according to total cholesterol values: (i) normal, < 5.2 mmol/l (n = 822) and (ii) raised, > or = 5.2 mmol/l (n = 190). A family history identified 63 out of 190 individuals with hypercholesterolaemia yielding a sensitivity of 33.2% and specificity of 71.5%. Our data indicated that a strategy whereby only children from high risk families are screened for hypercholesterolaemia is ineffective. While primary prevention emphasising a healthy diet for all is essential, the role of universal screening deserves further appraisal.