Biomedical subjects

S Moorjani

Publications and source records attributed to S Moorjani.

At least 91 records · Page 5Linked to original sources

PubMed1989

Primary lipoprotein-lipase-activity deficiency: clinical investigation of a French Canadian population.

We examined 56 French Canadians, aged 1 week to 54 years, from eastern Quebec who were referred to the Laval University Lipid Research Centre and in whom coincidental finding (in 46% of the cases), abdominal pain (in 32%) or family screening (in 22%) led to the diagnosis of primary lipoprotein-lipase-activity deficiency (familial hyperchylomicronemia). Half of the patients had one or more of the following signs: lipemia retinalis, eruptive xanthomas, splenomegaly and hepatomegaly; the plasma triglyceride concentrations were significantly higher (greater than 40 mmol/L) among these patients than among those without clinical signs (mean 21.7 [standard deviation 13.5] mmol/L). The prevalence rate of this disorder was 30 times higher than the previously published rate and was highest in the counties of Charlevoix and Saguenay-Lac-St-Jean (200 and 100 cases per million respectively) because of the distinct demographic history of these areas. Because of a founder effect an autosomal recessive gene involved in lipoprotein-lipase expression or activation has probably been disseminated among this isolated French Canadian population.

Adolescent↗

PubMed1989

Familial lipoprotein lipase-activity deficiency: study of total body fatness and subcutaneous fat tissue distribution.

Total body fatness and subcutaneous fat tissue distribution were evaluated in 19 hyperchylomicronemic patients. Eleven were males, aged 10 to 57 years, and eight were females, aged 13 to 46 years. Familial lipoprotein-lipase-activity deficiency was diagnosed by the absence of lipoprotein-lipase activity in the plasma withdrawn ten and 20 minutes after intravenous injection of ten units of heparin per kilogram of body weight. The 19 patients had skin-fold measurements for evaluation of subcutaneous fat distribution. Fifteen also underwent body density measurements by underwater weighing. Percent body fat was calculated from body density. These anthropometric data were plotted against the regression curves of 1638 normal controls of both sexes (aged 10 to 54 years) for fat tissue weight, percent body fat, subcutaneous fat/total fat mass ratio and trunk/extremity skin-fold ratio. Impairments in the process of building fat tissue reserves could not be shown in the 19 hyperchylomicronemic patients, in spite of the absence of lipoprotein-lipase activity in their postheparin plasma. It is hypothesized that normal fat tissue mass in these patients could be due partly to de novo synthesis of fatty acids by adipocytes, hydrolysis of plasma triglycerides by hepatic lipase, and/or contribution of a specific fat-tissue lipase to the catabolism of plasma triglyceride-rich lipoproteins.

Adipose Tissue↗

PubMed1989

Computed tomography-measured trunk fat and plasma lipoprotein levels in nonobese women.

The associations between total adiposity, adipose tissue distribution measured by computed axial tomography (CAT), regional variation in fat cell size, and plasma lipoprotein levels were studied in a sample of 22 premenopausal healthy nonobese women aged 34.6 +/- 3.1 years (mean +/- SD) (% body fat, 27.8 +/- 5.8). In these nonobese women, no associations were found between total adiposity, adipose tissue distribution, and plasma triglyceride or very-low-density lipoprotein levels. However, total adiposity (as reflected by the body density-derived fat mass and by the adipose tissue volume measured by CAT), as well as the total trunk fat areas (measured at the abdominal and thoracic levels) were positively correlated with plasma low-density lipoprotein (LDL) cholesterol (.05 greater than P less than .01) and LDL apolipoprotein (apo) B (.05 greater than P less than .0005) levels. Because of these associations with LDL-C and LDL apo B levels, these body fatness indicators were negatively correlated with the HDL-cholesterol/LDL-cholesterol and HDL-apo A-I/LDL-apo B ratios. However, few significant associations were observed between the proportion of abdominal fat estimated by the waist/hip circumference ratio (WHR) and the lipoprotein-lipid profile (r = .45 and r = .44, P less than .05 with HDL triglyceride (TG) and LDL-apo B/LDL-cholesterol ratio, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗

PubMed1989

Hypertriglyceridemia and lower LDL cholesterol concentration in relation to apolipoprotein E phenotypes in myotonic dystrophy.

Plasma lipid, lipoprotein levels and apolipoprotein apo E phenotypes were determined in 70 patients with myotonic dystrophy (MyD) and 81 controls. Marked differences were noticed in the apo E phenotype frequencies between the two groups. Plasma triglycerides and VLDL cholesterol were higher in MyD than controls, but only the latter was related to differences in the apo E phenotypes between two groups. Accordingly, the ratio of VLDL cholesterol/plasma triglycerides was increased significantly in MyD, suggesting accumulation of intermediary density particles due to lower affinity of E2 containing lipoproteins for lipoprotein cell receptors. The LDL cholesterol concentration was lower in MyD than controls and was related to differences in the apo E phenotype frequencies between the two groups. These results indicate increased removal of LDL particles in the apo E2 phenotypes, perhaps due to upregulation of LDL (B, E) receptor activity. Plasma cholesterol and HDL cholesterol concentrations were similar in both groups. Another feature of the study was lower levels of plasma cholesterol, triglycerides, VLDL and LDL cholesterol in the homozygous E4:E4 phenotype. These results suggest increased clearance rate of both VLDL and LDL particles and support the concept that apo E4-containing lipoproteins have higher in vivo affinity for ape E and/or B, E receptors.

Adolescent↗

PubMed1989

Myotonic dystrophy: linkage with apolipoprotein E and estimation of the gene carrier status with genetic markers.

The genes for myotonic dystrophy (MD) and for apolipoprotein E (ApoE) belong to a chromosome 19 synthenic group of markers. A familial linkage analysis between MD and ApoE was performed using the J Ott LIPED program (IBM PC/XT, April 1984) to estimate the genetic distance between these 2 genes. Of a total of 136 individuals in 11 MD families, 81 were confirmed to be affected by the disease and 41 were asymptomatic. ApoE phenotypes were determined in 115 of these 122 individuals. No recombinant was observed out of 74 meioses which were informatives for both MD and the ApoE isoproteins. A global maximal lod score Z of 19.00 was obtained at the recombination fraction theta = 0. The upper theta value at the confidence interval corresponding to the peak lod score (Z max) - 1 was 0.03. This suggests that the loci for MD and ApoE are at a distance of 0 to 0.03 Morgan. Since ApoE and apolipoprotein C2 (ApoC2) have been shown by others to be about 40 kb apart, our data are therefore consistent with the distance estimate of 0.02 Morgan reported between MD and ApoC2. The D19S19 (LDR152) polymorphic DNA sequence is also tightly linked to MD on chromosome 19. The segregation of ApoE isoproteins and of ApoC2 and D19S19 DNA polymorphism was utilized for evaluating the probability for individuals at risk of inheriting the disease gene in MD families. Data are presented on 3 families to emphasize the usefulness of genetic markers to estimate the MD gene carrier status of asymptomatic individuals and also for those presenting a partial syndrome. The limitations of such approach are also discussed.

Apolipoproteins E↗

PubMed1989

Assessment of adipose tissue distribution by computed axial tomography in obese women: association with body density and anthropometric measurements.

1. Abdominal obesity is associated with numerous metabolic complications. Deep abdominal adipose tissue is critical in the association between the level of abdominal obesity and cardiovascular risk factors. 2. Adipose tissue localization was assessed by computed axial tomography (CAT), and its association with body density and anthropometric measurements was investigated in a sample of fifty-one obese women (percentage body fat 45.9 (SD 5.6)) aged 35.7 (SD 5.5) years. The CAT scans were performed at three levels: lower chest, abdomen and mid-thigh. 3. The total adipose tissue volume computed from these three scans was highly correlated with body fat mass (r 0.94, P less than 0.001). The proportion of deep abdominal fat as measured by the ratio of deep: total adipose tissue areas at the abdominal level was not significantly correlated with body fat mass, but it was moderately associated with the ratio of waist: hip circumferences (WHR) (r 0.49, P less than 0.001). The absolute amount of deep abdominal fat was, however, significantly correlated with body fat mass (r 0.72, P less than 0.001). 4. The subscapular (r 0.38) and the abdominal (r 0.38) skinfolds were the only two skinfolds that were significantly associated with the proportion of deep abdominal fat (P less than 0.01). These skinfolds were also those which showed the highest correlation with the absolute amount of deep abdominal fat (r 0.65, P less than 0.001, for both skinfolds). 5. A three-site CAT-scan procedure can be used for the estimation of body fat mass in premenopausal obese women. 6. In these obese women, there was no significant association between total adiposity and the proportion of deep adipose tissue at the abdominal level. 7. In premenopausal obese women, the absolute amount of deep abdominal fat can be predicted from anthropometric measurements with more accuracy than the relative amount of deep abdominal fat.

Adipose Tissue↗

PubMed1989

Role of deep abdominal fat in the association between regional adipose tissue distribution and glucose tolerance in obese women.

Computed tomography (CT) was used to study the association between adipose tissue localization and glucose tolerance in a sample of 52 premenopausal obese women aged 35.7 +/- 5.5 yr (mean +/- SD) and with a body fat of 45.9 +/- 5.5%. Body-fat mass and the body mass index (BMI) were significantly correlated with plasma glucose, insulin, and connecting peptide (C-peptide) areas after glucose (75 g) ingestion (.40 less than or equal to r less than or equal to .51, P less than .01). Trunk-fat accumulation and the size of fat cells in the abdomen displayed highly significant correlations with postglucose insulin levels. The C-peptide area was also positively correlated with abdominal fat cell size (r = .76, P less than .01) and was more closely associated with the sum of trunk skin folds (r = .59, P less than .001) than with the extremity skin folds (r = .29, P less than .05). Subcutaneous and deep-abdominal-fat areas measured by CT displayed comparable associations with the plasma insulin area (r = .44 and .49, respectively; P less than .001) but marked differences in the associations with glucose tolerance. Indeed, subcutaneous abdominal fat was not significantly correlated with the glucose area, whereas deep abdominal fat showed a significant correlation (r = .57, P less than .001) with the glucose area. Midthigh fat deposition measured by CT was not, however, correlated with plasma glucose, insulin, or C-peptide areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗

PubMed1989

Relation of high plasma triglyceride levels associated with obesity and regional adipose tissue distribution to plasma lipoprotein-lipid composition in premenopausal women.

Abdominal obesity is associated with high plasma triglyceride (TG) and with low plasma high density lipoprotein (HDL)-cholesterol (CHOL) levels. As plasma TG and HDL-CHOL are negatively correlated, the associations between obesity, the regional distribution of body fat, plasma TG levels, and plasma lipoprotein concentration and composition were studied in a sample of 76 premenopausal women (52 obese and 24 non-obese). Obese women had significantly higher plasma levels of VLDL-TG, low density lipoprotein (LDL)-CHOL, LDL-TG, LDL-apolipoprotein (apo) B and reduced HDL-CHOL levels compared to non-obese controls (p less than 0.01). However, plasma concentrations of HDL-apo A-I and HDL-TG were not different between obese and non-obese women. Partial correlation analyses revealed that both fat mass and abdominal fat accumulation significantly contributed to VLDL-TG and HDL-CHOL variances. After control for body fat mass, the waist-to-hip circumference ratio (WHR) remained significantly correlated with plasma LDL-apo B levels and with the LDL-apo B/LDL-CHOL ratio (0.01 greater than p less than 0.05). Body fat mass was, however, associated with TG enrichment of LDL (p less than 0.01). After control for WHR, body fat mass showed no significant association with plasma HDL-TG levels, whereas the WHR was positively correlated with HDL-TG levels (p less than 0.05). Partial correlation analyses indicated that adjustment for fat mass or for the WHR failed to eliminate the associations between plasma VLDL-TG levels and lipoprotein lipid composition. This study emphasizes the importance of plasma VLDL-TG level as a correlate of plasma LDL and HDL lipid composition in abdominal obesity.

Adipose Tissue↗

PubMed1988

Changes in plasma lipoproteins during various androgen suppression therapies in men with prostatic carcinoma: effects of orchiectomy, estrogen, and combination treatment with luteinizing hormone-releasing hormone agonist and flutamide.

Cardiovascular complications are a well recognized side-effect of antihormonal therapy in men with prostatic carcinoma. We studied changes in plasma lipoproteins in patients with prostate cancer during treatment with several androgen suppression therapies. Estrogen, orchiectomy, and a combination of LHRH agonist and antiandrogen (flutamide) reduced plasma testosterone concentrations (89-92%) and plasma estradiol decreased by 85%, 44%, and 54%, respectively. Estrogen induced hypertriglyceridemia and elevation of plasma HDL cholesterol, phospholipid, and apolipoprotein A-I and A-II concentrations. Low density lipoprotein (LDL) cholesterol decreased but LDL apolipoprotein B did not. These results suggest that the cardiovascular complications that occur during estrogen administration are not mediated through changes in lipoprotein profile, other than the hypertriglyceridemic effect. Orchiectomy caused hypercholesterolemia and an increase in both total and LDL apolipoprotein B, all of which are strong determinants of cardiovascular disease. The high density lipoprotein (HDL) concentration was not affected despite a reduction in plasma testosterone, perhaps due to a simultaneous decrease in estradiol. Combination therapy had no effect on plasma lipid and apolipoprotein B concentrations, but very low density lipoprotein (VLDL) apolipoprotein B decreased, and LDL apolipoprotein B increased. The HDL cholesterol and apolipoprotein A-I concentrations increased but A-II and phospholipids did not. These results suggest enhanced lipoprotein lipase activity, consistent with the reciprocal changes in VLDL and LDL apolipoprotein B levels, apolipoprotein B enrichment of LDL particles, and increase in HDL cholesterol. The higher apolipoprotein A-I to A-II ratio indicates an increase in HDL2 subfraction due to inhibition of endothelial hepatic lipase, increased secretion of apolipoprotein A-I, or both. These effects are attributed to estradiol, which decreased less than after orchiectomy, and to additional adrenal androgen inhibition by flutamide. We conclude that estradiol plays an important role in determining plasma lipoprotein concentrations in men, and androgens exert an antagonist effect. The lipoprotein profile resulting from the combination treatment is more beneficial than that resulting from orchiectomy or estrogen administration.

Aged↗

PubMed1988

Sensitivity to overfeeding: the Quebec experiment with identical twins.

The role of the genotype in the response to short-term overfeeding was assessed by submitted six pairs of male monozygotic twins to a 4.2 MJ (1000 kcal) per day energy intake surplus for a period of 22 consecutive days. Individual differences in fat mass and fat-free mass gains were observed in response to overfeeding but they were not randomly distributed. Indeed, the within-pair resemblance in the response was striking when compared to the heterogeneity found among the pairs in adiposity and fat-free mass gains. The intrapair resemblance in the response to overfeeding as assessed by the intraclass coefficient computed with the individual changes, reached 0.88 for total fat mass and 0.76 for fat-free mass. A similar trend for a genetically determined pattern of adaptation to overfeeding was observed for resting metabolic rate (intraclass = 0.63), thermic effect of a meal (intraclass = 0.62), and energy cost of submaximal exercise (intraclass = 0.78) when the data were analysed in terms of changes in oxygen uptake. On the other hand, no major alterations in glucose and insulin response to a glucose load or a test meal, in cardio-pulmonary adaptation to submaximal exercise and in maximal exercise tolerance were found with overfeeding. In contrast, the response of suprailiac fat cell lipolysis (intraclass of about 0.7) and heparin releasable adipose tissue lipoprotein lipase (intraclass - 0.82) varied among individuals but was highly homogeneous within genotypes. Similarly, a genotype-overfeeding interaction effect was seen for serum triglycerides (intraclass = 0.69), HDL-cholesterol (intraclass = 0.85), and the HDL-cholesterol to total cholesterol ratio (intraclass = 0.82). Multiple correlation analyses suggest that much of the variance in the response of fat mass (R = 0.65) and fat-free mass (R = 0.81) is accounted for by alterations in the energy expenditure components assessed in the study. If one takes into account the measurement errors always present in such complex studies and the fact that only a limited fraction of the energy expenditure of activity was considered by design, one can conclude that the genotype determines to a large extent the response variation to short-term overfeeding. In particular, the genotype-overfeeding interaction effect for body composition changes seems to be mediated by the various energy expenditure components, themselves characterized by significant genotype-overfeeding interaction effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗

PubMed1988

Effects of fenfluramine in hypertriglyceridemic obese subjects.

Forty-four hyperlipidemic obese subjects, selected because of their refractoriness towards diet-therapy, participated voluntarily in a 12-week double-blind study comparing the effects of a long-acting fenfluramine (Ponderal Pacaps) to those of a placebo. In spite of no dietetic intervention, a significant 3-kg weight loss (P less than 0.001) was observed in the fenfluramine-treated group, accompanied by a significant improvement of most atherogenic parameters of plasma lipoproteins. Fenfluramine-induced weight loss produced decrease in total cholesterol (P less than 0.05), total triglycerides (P less than 0.05), LDL cholesterol (P less than 0.05), total apoprotein B (P less than 0.005) and LDL apoprotein B (P less than 0.001). An apoprotein B LDL depletion seemed to occur, as suggested by the reduction of LDL cholesterol/apoprotein B ratio (P less than 0.001). Total plasma apoprotein A did not change but the total apoprotein B/total apoprotein A ratio decreased significantly (P less than 0.005). Moreover, fenfluramine increased both HDL phospholipid (P less than 0.005) and HDL cholesterol (P less than 0.05) resulting in a fall of the atherogenic LDL-cholesterol/HDL cholesterol ratio (P less than 0.001) as well as an elevation of the anti-atherogenic HDL cholesterol/LDL + VLDL cholesterol ratio (P less than 0.001). The placebo group demonstrated some improvement in lipid blood parameters without weight loss, indicating a possible qualitative amelioration of nutritional habits. Thus, fenfluramine reduces the risk for cardiovascular disease in hyperlipidemic obese individuals not responding to behavioral intervention.

Adult↗

PubMed1988

Smoking, alcohol consumption, lipid and lipoprotein levels.

The lipid profiles of 1165 French Canadian men (aged 42 to 59 years) were studied and related to drinking and smoking habits. Alcohol consumption and smoking were closely related, smokers consuming twice as much alcohol as non-smokers. When relative body weight, total cholesterol, triglyceride and alcohol consumption were controlled in a covariate analysis, plasma levels of high density lipoprotein (HDL) cholesterol, HDL2 and HDL3 differed significantly between smokers, ex-smokers and nonsmokers. Ex-smokers had higher levels of HDL cholesterol than nonsmokers who had higher levels than smokers. The higher levels of HDL in ex-smokers could be explained by the confounding effects of alcohol intake. Alcohol users had significantly higher levels of HDL cholesterol, HDL2 and HDL3 than nondrinkers. Men who drank the equivalent of more than 3 ounces of absolute alcohol per week had significantly higher levels of HDL cholesterol and HDL3 than those who drank less than 3 ounces or did not drink at all. HDL2 levels were only significantly different between nondrinkers and those who consumed more than 3 ounces per week. These results show that smoking and alcohol have strong but opposing effects on HDL and its subfractions in middle-aged French Canadian men.

Adult↗

PubMed1987

Increase in plasma high-density lipoprotein concentration following complete androgen blockage in men with prostatic carcinoma.

There is evidence that endogenous estrogens have a positive effect on plasma high density lipoprotein (HDL) concentration, whereas the relation between HDL and male sex hormones is unclear, since both positive and negative effects have been reported. This study examined the effects of LHRH agonist in combination with an antiandrogen on plasma lipids and lipoproteins in 17 elderly men with prostatic carcinoma. Subjects were examined prior to and after therapy at 4-week intervals up to 16 weeks. Prior to therapy, their lipid and lipoprotein profiles were not significantly different from a control group composed of individuals of similar age and living in the same community area. Following therapy plasma levels of testosterone and dihydrotestosterone were markedly decreased (above 90%) and their residual activity neutralized through effective use of an antiandrogen. Plasma estradiol decreased between 65% and 85% and the concentration of cortisol was unaffected. The very low density lipoprotein (VLDL) apo-B decreased and low density lipoprotein (LDL) apo-B increased; thus, no change was observed in the total plasma apo-B levels. Total plasma cholesterol increased by 6% (baseline v peak values, mg/dL, mean +/- SEM; 219 +/- 9 v 233 +/- 9, P less than 0.05) due to a significant rise in HDL cholesterol concentration (45.5 +/- 2.8 v 56.5 +/- 3.6, P less than 0.01). Both VLDL and LDL cholesterol levels remained unchanged. The mean elevation of 21% in HDL cholesterol was accompanied by a significant rise in HDL apo-A concentration (161 +/- 6 v 193 +/- 10, P less than 0.01), thus suggesting an increase in HDL mass and/or particle number.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

PubMed1987

Genotype-influenced changes in serum HDL cholesterol after short-term overfeeding in man: association with plasma insulin and triglyceride levels.

Six pairs of male monozygotic (MZ) twins were submitted to a 22-day overfeeding period during which they ingested a daily surplus of 1,000 kcal above their individual daily energy needs in the form of a mixed diet. Serum lipids, lipoproteins, and apoprotein A and B concentrations were measured before and after the overfeeding period. Percentage of body fat, fasting plasma glucose, and insulin levels as well as plasma glucose and insulin concentrations after a glucose challenge were also measured before and after overfeeding. Results showed that before overfeeding, MZ twins exhibited a significant intrapair resemblance for total serum cholesterol (CHOL), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), and for the high density lipoprotein-cholesterol/total cholesterol ratio (HDL-C/CHOL) (8.2 less than or equal to F ratios less than or equal to 32.7, P less than .01). The overfeeding experiment induced significant increases only in serum CHOL (P less than .01) and in serum LDL-C (P less than .05). However, although mean group values of serum TG, HDL-C, and HDL-C/CHOL ratio were not significantly modified by overfeeding, there were large interindividual variations in the response of these variables to the experiment. Results suggest that changes in serum TG, HDL-C, and in the HDL-C/CHOL ratio were significantly associated with the genotype of the subjects as a significant intrapair resemblance in the response to overfeeding was observed for these variables (0.69 less than or equal to r less than or equal to .85, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins A↗

PubMed1986

Severe lipemia induced by tamoxifen.

A 61-year-old woman was treated with tamoxifen for breast cancer and had marked hyperlipoproteinemia: high plasma triglyceride levels (2790 mg/dl); increased very low density lipoprotein (VLDL) cholesterol levels (241 mg/dl); and high VLDL apoprotein B levels (126 mg/dl). Low density lipoprotein (LDL) cholesterol was decreased (104 mg/dl) and LDL apoprotein B was at 107 mg/dl. A low activity of both postheparin plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (h-TGL) was also noted. All these observations were reversed following tamoxifen withdrawal. Plasma triglyceride levels fell to 361 mg/dl. VLDL cholesterol and VLDL apoprotein B decreased to 41 mg/dl (83%) and 21 mg/dl (83%), respectively. Meanwhile, LDL cholesterol rose to 194 mg/dl (86%) and LDL apoprotein B increased to 138 mg/dl (29%). LPL and h-TGL activities did increase following tamoxifen withdrawal. Our observations show that, in some patients, the previously described weak hypertriglyceridemic effect of tamoxifen is amplified. That observation supports the concept and helps to explain that, in such severe induced lipemia, reduction of the activities of LPL and h-TGL might impede the conversion of VLDL to LDL, thus causing an amplification of the effect.

Breast Neoplasms↗

PubMed1986

Plasma triglycerides related decrease in high-density lipoprotein cholesterol and its association with myocardial infarction in heterozygous familial hypercholesterolemia.

Recent studies suggest that decreased levels of high-density lipoprotein (HDL) may contribute to the risk of premature occlusive atherosclerosis in familial hypercholesterolemia (FH). To investigate further, we have analyzed the concentration as well as distribution of HDL cholesterol in relation to plasma triglycerides and their influence on ischaemic heart disease in FH subjects. The study was carried out in 71 men with heterozygous FH and 46 matched controls. FH subjects were relatively young with a mean age of 38 +/- 11 years. Tendon xanthomatas were observed in 57% of the subjects, whereas ischemic heart disease was identified in 33%. Compared to normals, the mean value of HDL cholesterol is significantly reduced by 21% in FH heterozygotes (42 +/- 12 v 33 +/- 9 mg/dL, P less than 0.001). The decrease in HDL cholesterol is highly correlated to the levels of plasma triglycerides (r = -0.50, P less than 0.001) and VLDL cholesterol (r = -0.53, P less than 0.001). Moreover, HDL cholesterol decrease is not associated with elevated levels of LDL cholesterol (r = -0.20, NS), which is the primary characteristic feature of FH subjects. However, HDL cholesterol decrease is weakly related to total plasma cholesterol concentration (r = -0.24, P less than 0.05). The body weight is also contributory to the reduction of HDL cholesterol (r = -0.42, P less than 0.01), probably due to its strong positive correlation to plasma triglycerides (r = +0.54, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Lipid profile of a French-Canadian population: 1. Association of plasma lipid and lipoprotein levels with age, relative body weight and education.

Plasma lipid and lipoprotein levels were determined in a randomly selected population of 1169 French-Canadian men in the Quebec City area. The mean levels of total plasma cholesterol and triglycerides were 224.0 and 166.5 mg/dL respectively. The mean level of low-density lipoprotein cholesterol was higher and the mean level of high-density lipoprotein (HDL) cholesterol lower than those reported in a recent study in English-Canadian men. The mean HDL2 and HDL3 levels were lower than those reported in American men. Stratification of plasma triglyceride levels for all age groups showed that mean HDL2 levels decreased rapidly with moderate rises in triglyceride levels. Less than 9% of the variation in lipid or lipoprotein levels was related to age or relative body weight. Education had no significant effect on the levels.

Adult↗

PubMed1985

Articular manifestations of familial hypercholesterolaemia.

Familial hypercholesterolaemia is characterised by a decreased removal of low density lipoproteins and premature coronary artery disease. Tendinous xanthomata are a hallmark of the disease. The affected joints may also be the sites of inflammation and pain. Arthropathy has been associated mainly with the homozygous form of familial hypercholesterolaemia, but it is also known to occur in the heterozygous form. We report on the articular manifestations in 73 patients with heterozygous familial hypercholesterolaemia. About 40% of these patients had at least one episode of articular symptoms. The observed articular manifestations may be classified into four types: Achilles pain (18%), Achilles tendinitis (11%), oligoarticular arthritis (7%), polyarticular or rheumatic fever-like arthritis (4%). It is concluded that in heterozygous familial hypercholesterolaemia articular manifestations are frequent, diverse, and may be the first symptom of this metabolic disorder.

Achilles Tendon↗