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PubMed1993

Rheumatic manifestations of hyperlipidemia and antihyperlipidemia drug therapy.

Conflicting data exist with respect to the existence and clinical manifestations of a hyperlipidemic arthropathy. Reasonable evidence supports the existence of a migratory polyarthritis similar to rheumatic fever in patients homozygous for type II hyperlipidemia. Although similar complaints have been described in patients heterozygous for this condition, findings have been inconsistent among various reports. It is possible that high lipid levels are required to induce rheumatic complaints, and these are found predominantly in homozygous patients. Even so, rheumatic syndromes appear to be more attributable to periarthritis because evidence of inflammatory arthritis is largely lacking. In contrast, Achilles tendinitis appears to be associated with heterozygous type II hyperlipidemia and presumably is based on lipid deposits within the tendon. Gout is an accepted association of type IV hyperlipidemia. In addition, oligoarticular symptoms have been described with type IV hyperlipidemia. However, no consistent clinical entity has emerged. Drugs used in the treatment of hyperlipidemia are associated with a variety of rheumatic problems, including proximal myopathy and lupus-like syndromes. The most commonly implicated drugs are the hydroxymethylglutaryl-coenzyme A reductase inhibitors and the fibric acid derivatives.

Diagnosis, Differential↗
PubMed1993

Effect of early hyperlipidemia on graft and patient survival in cyclosporine-treated renal transplant patients.

Hyperlipidemia commonly occurs following renal transplantation. As hyperlipidemia has been postulated to contribute to renal dysfunction in animal models, the effect of early hyperlipidemia was studied in a cohort of 43 cyclosporine-treated renal transplant recipients over a 4-year follow-up period. Hypercholesterolemia occurred in 25 patients, with 18 patients remaining normolipidemic during the initial 3 months following transplantation. Prospective follow-up over a 4-year period was available for 16 of the 18 normolipidemic patients and 25 patients who developed hyperlipidemia, as well as 11 other hyperlipidemic patients who were not included in the initial analysis. Graft function was maintained in 11 (69%) of the patients with early normolipidemia and there has been one patient death (7%). Of the hypercholesterolemic group, two patients were lost to follow-up and 23 of the remaining 34 (68%) had persistent graft function. There have been two patient deaths (6%). No deaths from cardiovascular deaths have occurred in either group, all deaths resulting from infection/sepsis. Mean cholesterol values at 4-year follow-up were 202.0 +/- 11.2 mg/dL for the patients with early normolipidemia 282.9 +/- 14.3 mg/dL for the patients with early hyperlipidemia (p < 0.00001). The most recent cholesterol value was not associated with pretransplant cholesterol value, creatinine, or cyclosporine dose, but was associated with cholesterol value at 3 months both by regression analysis (P < 0.0001) and by Pearson R (r = 0.71, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Cyclosporine↗
PubMed2001

Relation between sodium-lithium countertransport and hypertriglyceridemia in type V hyperlipidemia.

Sodium-lithium countertransport (SLC) kinetics were measured in 30 patients with type V hyperlipidemia, 30 patients with type IIB hyperlipidemia on similar treatment, and 30 age- and sex-matched healthy controls. Clinical and laboratory data including basic anthropometry and blood pressure were obtained and blood was taken for detailed lipid biochemistry, glucose, insulin, and leptin measurements. Patients with type V hyperlipidemia were normotensive but more obese than controls, had elevated triglycerides, very low-density lipoprotein, glucose, and insulin; and reduced HDL cholesterol compared with type IIb controls. The median SLC activity (0.23 v 0.21 mmol Li+/L RBC/h) and median maximal velocity (0.33 v 0.31 mmol Li+/L RBC/h) were increased, but not significantly, compared to controls. In patients with type V hyperlipidemia SLC maximal velocity correlated with log triglycerides (r2 = 0.853; P < .001) and log very low-density lipoprotein (VLDL) triglycerides (r2 = 0.947; P < .001). Sodium-lithium countertransport maximal velocity correlated weakly with the homeostasis model assessment index of insulin resistance (r2 = 0.224; P = .06). The sodium affinity of the transporter did not differ between the groups and was independent of any of clinical or biochemical parameter studied. We conclude that VLDL triglyceride is strongly correlated with SLC maximal velocity and activity in patients with type V hyperlipidemia.

Adult↗
PubMed2001

The pressor response to acute hyperlipidemia is enhanced in lean normotensive offspring of hypertensive parents.

Family history is an important predictor of the cardiovascular risk factor cluster associated with insulin resistance. The dyslipidemia associated with insulin resistance may contribute to elevated blood pressure (BP). This study was undertaken to further explore the link between family history, dyslipidemia, and BP regulation. Twenty-three lean normal volunteers with a negative family history (FH-, n = 11) or positive family history (FH+, n = 12) of hypertension were evaluated under baseline conditions and during a 4-h infusion of intralipid and heparin (acute hyperlipidemia). Fasting blood was drawn for lipids including nonesterified fatty acids (NEFA). After 2 and 4 h of intralipid and heparin, blood was drawn for NEFA. The BP was measured at baseline and every 30 min after starting the intralipid and heparin infusion. Baseline triglycerides and very low density lipoprotein cholesterol concentrations were higher in FH+ than FH- subjects (P < .05). However, NEFA increased similarly in both groups during the infusion of intralipid and heparin. The BP and heart rate increased with acute hyperlipidemia in all subjects combined (P < .05). Despite the similar increase of NEFA, mean BP, pulse pressure, and pressure-rate product increased significantly in FH+ subjects but not in FH- volunteers with acute hyperlipidemia. Although systolic BP increased in both groups, the increase was greater in FH+ than in FH- volunteers during acute hyperlipidemia (14 +/- 2 v 10 +/- 2 mm Hg, P < .05). These results suggest that higher plasma lipids combined with a greater pressor response to hyperlipidemia may contribute to the development of high BP in subjects with a family history of hypertension.

Acute Disease↗
PubMed2003

Acute hyperlipidemia increases oxidative stress more in African Americans than in white Americans.

Oxidative stress emerges as a potential factor in the pathogenesis of hypertension and a common signal transduction mechanism by which various risk factors mediate cardiovascular and renal disease. A greater level of oxidative stress could contribute to higher rates of hypertension and related cardiovascular and renal complications in African Americans than in white Americans. The objective of this study was to compare oxidative stress induced by a standardized episode of acute hyperlipidemia in the two groups. Fifteen African Americans (37 +/- 1 years, 9 women/6 men, body mass index 30 +/- 2 kg/m(2)) and 15 whites (38 +/- 2 years, 9 women/6 men, body mass index 27 +/- 1 kg/m(2)) were evaluated. Acute hyperlipidemia was induced by a 4-h long infusion of Intralipid and heparin. Blood samples were drawn at baseline and after 2 and 4 h of acute hyperlipidemia for nonesterified fatty acids, triglycerides, and F2-isoprostanes, a biomarker of oxidative stress. Plasma nonesterified fatty acids and triglycerides increased significantly and similarly in African Americans and whites after 2 and 4 h of the Intralipid and heparin infusion. Although baseline plasma F2-isoprostanes did not differ between groups, F2-isoprostanes increased more in African Americans than in whites at 2 h (12.2 +/- 2.6 v 5.0 +/- 2.9 pg/mL, P <.05) and 4 h (13.9 +/- 3.1 v 3.0 +/- 3.0 pg/mL, P <.05) of acute hyperlipidemia. The results indicate that acute hyperlipidemia increases F2-isoprostanes more in African Americans than in whites. The findings may have important implications for ethnic differences in the prevalence of hypertension and cardiovascular and renal disease.

Acute Disease↗
PubMed2004

Prevalence of diabetes, obesity, hypertension and hyperlipidemia in the central area of Argentina.

OBJECTIVES: There is little information available about the prevalence of chronic metabolic diseases in many Latin American countries. Between 1995 and 1998, studies on the prevalence of obesity, hypertension, hyperlipidemia and diabetes were carried out in four cities located in central Argentina: Dean Funes, Oncativo, Pehuajo and Venado Tuerto. The data provided by these surveys are reanalysed here in order to determine prevalence of obesity, hypertension, hyperlipidemia and diabetes using new epidemiological criteria. METHODS: Representative samples of the population, based on a multistage probabilistic sampling design, were taken from each of the four cities. The sample size was calculated to obtain a precision of 4% for the prevalence assessment. The subjects included were aged 20 years and over. Standardization of the prevalence rates used the entire study sample as the reference population. RESULTS: Age-standardised prevalence rates for the cities ranged between 22.4% and 30.8% for obesity, 27.9% and 43.6% for hypertension, 24.2% and 36.4% for hyperlipidemia, and 6.5% and 7.7% for diabetes mellitus. All these prevalences increased with age. 58.1% of the obese subjects and 51.2% of the diabetic subjects had hypertension, while 43.2% of the obese subjects and 52.8% of the diabetic subjects had hyperlipidemia. CONCLUSIONS: While the prevalence of diabetes mellitus was between 6% and 8%, the prevalence of obesity was close to 26% and hypertension and hyperlipidemia affected one third of the population. These data can be considered as indicative of the prevalences of these four diseases in the population aged 20 years and over, in the central region of Argentina.

Adult↗
PubMed1995

Metabolism of low density lipoproteins in nephrotic dyslipidemia: comparison of hypercholesterolemia alone and combined hyperlipidemia.

High levels of low-density lipoprotein cholesterol (LDL) (hypercholesterolemia) are commonly present in the nephrotic syndrome. Another pattern of dyslipidemia in nephrotic patients is an elevation of both cholesterol and triglyceride levels (combined hyperlipidemia). It has been postulated that the underlying cause of nephrotic dyslipidemia is an hepatic overproduction of apolipoprotein B (apo B)-containing lipoproteins. To examine this hypothesis, the metabolism of LDL-apo B was compared between nephrotic patients with hypercholesterolemia and with combined hyperlipidemia. Thirteen patients (7 with hypercholesterolemia, and 6 with combined hyperlipidemia) underwent measurements of turnover rates of autologous LDL apo B. The results were compared to normolipidemic controls and to patients with primary combined hyperlipidemia previously studied in our laboratory. Nephrotic patients with hypercholesterolemia generally had: (a) lower fractional catabolic rates of LDL apo B than normolipidemic healthy individuals; (b) LDL particles enriched in cholesterol; but (c) no overproduction of LDL apo B. In contrast, patients with combined hyperlipidemia were found to have: (a) high fractional catabolic rates for LDL apo B compared to normolipidemic controls; (b) cholesterol-poor LDL particles; and (c) markedly elevated production rates for LDL. Also, for the group as a whole, there was a positive correlation between plasma triglyceride levels and fractional catabolic rates. These data indicate that the metabolism of LDL is strikingly different between the two forms of nephrotic dyslipidemia. Although there may be common mechanisms contributing to LDL levels in nephrotic patients, there also appears to be a divergence of mechanisms depending on whether hypertriglyceridemia is associated with hypercholesterolemia.

Adolescent↗
PubMed2006

Pivotal role of xanthine oxidase in the initiation of tubulointerstitial renal injury in rats with hyperlipidemia.

Hyperlipidemia can induce or aggravate renal tubulointerstitial injury. Experiments in a complex rat model with chronic glomerulonephritis and long-standing, coexisting hyperlipidemia suggested that induction of xanthine oxidase (XO), with increased oxygen radical generation, is involved in aggravation of tubulointerstitial injury. To separate the role of XO in the initial events of lipid-mediated tubulointerstitial injury, short-term experiments with diet-induced hyperlipidemia over 21 and 35 days were performed in otherwise healthy rats. XO expression in relation to the antioxidant enzymes was examined in the cortical tubulointerstitium (TIS) and proximal tubules (PT). Subsequent experiments with XO inhibition were performed, examining tubulointerstitial infiltration with ED1-positive cells and expression of adhesion molecules and monocyte chemoattractant protein-1 (MCP-1) as indicators of early injurious events. Hyperlipidemia increased XO activity in TIS by 40 and 86%, and in PT by 28 and 90% at days 21 and 35, compared with controls on regular diet. This increased activity was associated with increased reactive oxygen species. Among the antioxidant enzymes, glutathione peroxidase activity increased in TIS by 40% and in PT by 90%. Histological evaluation showed a three-fold increase in ED1-positive cells and increased MCP-1 and vascular cell adhesion molecule-1 (VCAM-1) expression at day 35 in the TIS. Inhibition of XO prevented tubulointerstitial ED1 cell infiltration, together with a decreased expression of MCP-1 and VCAM-1. These results point to an important role for XO in the early stage of hyperlipidemia-associated renal injury, mediating macrophage infiltration by a putatively redox-dependent upregulation of MCP-1 and VCAM-1.

Animals↗
PubMed2006

Hyperlipidemia guideline adherence and association with patient gender.

BACKGROUND: Gender disparities in cardiovascular disease (CVD) management have become increasingly apparent in recent years. Previous research has focused on inpatient disparities, but little is known about how patient gender affects assessment, treatment, and management of patients for hyperlipidemia and cardiovascular risk in primary care settings. Patients with coronary artery disease (CAD) and hyperlipidemia are at high risk for cardiovascular and cerebrovascular morbidity. We sought to examine the effect of patient gender on assessment, treatment, and target maintenance of hyperlipidemia among patients with CAD in a primary care setting. METHODS: Chart abstraction was done for 715 patients with CAD in 55 family practices in New Jersey and eastern Pennsylvania as part of the Using Learning Teams for Reflective Adaptation (ULTRA) project. Hyperlipidemia assessment, treatment, and target adherence scores were determined for those at-risk patients based on National Heart, Lung, and Blood Institute (NHLBI) recommended National Cholesterol Education Program (NCEP) ATP III guidelines. Generalized linear models were used to determine the association of hyperlipidemia guideline adherence with patient gender, using comorbidities and age as confounders. RESULTS: After controlling for comorbidities and age, women were less likely to be assessed for lipids (p = 0.0462). There was no difference in treatment (p = 0.1074) or target laboratory values (p = 0.3949). CONCLUSIONS: Women with CAD are less often assessed for lipids than men in primary care practices. More intensive efforts may be necessary to educate physicians and patients about cardiovascular risk for women.

Adult↗
PubMed1988

Retinal arteriolar changes in patients with hyperlipidemias.

Hyperlipidemia is a known risk factor for atherosclerosis systemically. To determine whether it causes changes in retinal arterioles, a group of 26 patients with hyperlipidemia (serum cholesterol or triglycerides greater than 95th percentile for age) were compared with 22 "normal" patients (comparison group) and 35 patients with contralateral branch retinal vein occlusion to determine the presence or absence of changes in the retinal arterioles. The arterioles of all groups were evaluated in a masked fashion to determine the presence of arteriovenous nicking, "sclerosis," narrowing, and tortuosity. No differences in the retinal arterioles between the patients with hyperlipidemia and the comparison group were found. Patients with branch retinal vein occlusion in the contralateral eye had significantly more arteriovenous nicking and "sclerosis" than the other groups. These data suggest that hyperlipidemia by itself is not a risk factor for the development of retinal arteriolar changes. Thus examining the retinal arterioles would not be helpful in detecting hyperlipidemia.

Arterioles↗
PubMed2006

Genetics of familial combined hyperlipidemia.

PURPOSE OF REVIEW: To provide an overview of recent advances that have defined the first putative genes behind familial combined hyperlipidemia, the most common genetic dyslipidemia and a major risk factor for early coronary heart disease. RECENT FINDINGS: The first locus for familial combined hyperlipidemia on 1q21-23 revealed a gene encoding a transcription factor critical in lipid and glucose metabolism, USF1. All the associated variants represent noncoding single nucleotide polymorphisms, one of which affects the binding site of nuclear proteins with a putative effect on transcript levels of USF1. Transcript analyses of fat biopsies have exposed risk-allele related changes in the downstream genes. Another recent clue to the molecular pathogenesis of familial combined hyperlipidemia is the association of the high triglyceride trait with the APOA5 gene, located on 11q. More familial combined hyperlipidemia genes are expected to be found, since linkage evidence exists for additional loci on 16q24 and 20q12-q13.1. SUMMARY: Genetic research of familial combined hyperlipidemia families has revealed several linked loci guiding to susceptibility genes. The USF1 transcription factor is the major gene underlying the 1q21-23 linkage. Modifying genes, especially influencing the high triglyceride trait, include APOC3 and APOA5, the latter representing a downstream target of USF1 and implying a USF1-dependent pathway in the molecular pathogenesis of dyslipidemias.

Apolipoproteins↗
PubMed1994

Effect of insulin resistance, apoE2 allele, and smoking on combined hyperlipidemia.

Combined hyperlipidemia may result from the interaction of several metabolic and environmental factors. We explored to what extent fasting insulin concentration, apolipoprotein (apo) E2 frequency, and cigarette smoking explained the serum levels of triglyceride and high-density lipoprotein cholesterol (HDL-C) in patients with combined hyperlipidemia. Forty-nine untreated patients with combined hyperlipidemia were compared with 49 hypercholesterolemic patients who were matched for gender, age, and body mass index. All laboratory values were obtained after 9 weeks of standardized dietary intake and after an overnight fast. The patients with combined hyperlipidemia had a significantly higher (33 pmol/L, 50%) mean insulin concentration than matched hypercholesterolemic control subjects, indicating that the combined hyperlipidemic patients were more insulin resistant. However, the differences in the fasting insulin and triglyceride concentrations within the pairs were only slightly correlated (adjusted r = .29). The combined hyperlipidemic patients were also characterized by a higher frequency of apoE2 alleles (25% versus 6%) and smokers (41% versus 16%). In a matched multiple linear regression model, the differences in insulin concentration, apoE2 allele frequency, and smoking explained 12%, 8%, and 9%, respectively, of the mean paired difference in triglyceride concentration. The differences in insulin concentration or apoE2 allele frequency did not significantly explain the mean paired difference in HDL-C concentration, whereas smoking explained 17% of the difference. In conclusion, fasting insulin concentration, the presence of the apoE2 allele, and smoking may explain 30% of the hypertriglyceridemia and the low levels of HDL-C in nonobese patients with combined hyperlipidemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1973

Hyperlipidemia in coronary heart disease. 3. Evaluation of lipoprotein phenotypes of 156 genetically defined survivors of myocardial infarction.

Although analysis of lipoprotein phenotypes is widely used to diagnose and classify the familial hyperlipidemias, an evaluation of this system as a method for genetic classification has hitherto not been published. The present study of 156 genetically defined survivors of myocardial infarction was therefore designed to examine the relationship between lipoprotein phenotypes and genetic lipid disorders. The lipoprotein phenotypes of each survivor was determined primarily by measurement of his plasma triglyceride and low density lipoprotein (LDL)-cholesterol concentrations; his genetic disorder was identified by analysis of whole plasma cholesterol and triglyceride levels in relatives. The mean levels of LDL-cholesterol discriminated statistically among the three monogenic lipid disorders; it was highest in survivors with familial hypercholesterolemia (261+/-61 mg/100 ml [mean +/-SD]); intermediate in those with familial combined hyperlipidemia (197+/-50); and lowest in those with familial hypertriglyceridemia (155+/-36) (P < 0.005 among the three groups). However, on an individual basis no lipoprotein pattern proved to be specific for any particular genetic lipid disorder; conversely, no genetic disorder was specified by a single lipoprotein pattern. This lack of correlation occurred for the following reasons: (a) individual LDL-cholesterol levels frequently overlapped between disorders; (b) in many instances a small quantitative change in the level of either LDL-cholesterol or whole plasma triglyceride caused qualitative differences in lipoprotein phenotypes, especially in individuals with familial combined hyperlipidemia, who showed variable expression (types IIa, IIb, IV, or V); (c) lipoprotein phenotypes failed to distinguish among monogenic, polygenic, and sporadic forms of hyperlipidemia; (d) clofibrate treatment of some survivors with genetic forms of hyperlipidemia caused their levels of triglyceride and LDL-cholesterol to fall below the 95th percentile, thus resulting in a normal phenotype; and (e) beta-migrating very low density lipoproteins (beta-VLDL), previously considered a specific marker for the type III hyperlipidemic disorder, was identified in several survivors with different lipoprotein characteristics and familial lipid distributions. These studies indicate that lipoprotein phenotypes are not qualitative markers in the genetic sense but instead are quantitative parameters which may vary among different individuals with the same genetic lipid disorder. It would therefore seem likely that a genetic classification of the individual hyperlipidemic patient with coronary heart disease made from a quantitative analysis of lipid levels in his relatives may provide a more meaningful approach than determination of lipoprotein phenotypes.

Adult↗
PubMed2005

ApoC-III deficiency prevents hyperlipidemia induced by apoE overexpression.

Adenovirus-mediated overexpression of human apolipoprotein E (apoE) induces hyperlipidemia by stimulating the VLDL-triglyceride (TG) production rate and inhibiting the LPL-mediated VLDL-TG hydrolysis rate. Because apoC-III is a strong inhibitor of TG hydrolysis, we questioned whether Apoc3 deficiency might prevent the hyperlipidemia induced by apoE overexpression in vivo. Injection of 2 x 10(9) plaque-forming units of AdAPOE4 caused severe combined hyperlipidemia in Apoe-/- mice [TG from 0.7 +/- 0.2 to 57.2 +/- 6.7 mM; total cholesterol (TC) from 17.4 +/- 3.7 to 29.0 +/- 4.1 mM] that was confined to VLDL/intermediate density lipoprotein-sized lipoproteins. In contrast, Apoc3 deficiency resulted in a gene dose-dependent reduction of the apoE4-associated hyperlipidemia (TG from 57.2 +/- 6.7 mM to 21.2 +/- 18.5 and 1.5 +/- 1.4 mM; TC from 29.0 +/- 4.1 to 16.4 +/- 9.8 and 2.3 +/- 1.8 mM in Apoe-/-, Apoe-/-.Apoc3+/-, and Apoe-/-.Apoc3-/- mice, respectively). In both Apoe-/- mice and Apoe-/-.Apoc3-/- mice, injection of increasing doses of AdAPOE4 resulted in up to a 10-fold increased VLDL-TG production rate. However, Apoc3 deficiency resulted in a significant increase in the uptake of TG-derived fatty acids from VLDL-like emulsion particles by white adipose tissue, indicating enhanced LPL activity. In vitro experiments showed that apoC-III is a more specific inhibitor of LPL activity than is apoE. Thus, Apoc3 deficiency can prevent apoE-induced hyperlipidemia associated with a 10-fold increased hepatic VLDL-TG production rate, most likely by alleviating the apoE-induced inhibition of VLDL-TG hydrolysis.

Animals↗
PubMed1999

Acceleration of development of diabetic cataract by hyperlipidemia and low high-density lipoprotein in rats.

Diabetic cataracts are thought to be caused by hyperglycemia associated with disturbed glucose metabolism. Diabetes mellitus often involves abnormal lipid metabolism in addition to abnormal glucose metabolism. To date, however, very few studies have counted hyperlipidemia as a risk factor for diabetic cataracts. The present study was undertaken to determine whether this abnormal lipid metabolism is a risk factor for diabetic cataracts in rats. Cataracts were caused by streptozotocin (STZ) administration in the ordinary diet or cholesterol rich diet fed rats. When rats with STZ (65 mg/kg)-induced diabetes mellitus were fed an ordinary diet, cataracts became evident at 9 weeks in 26.7% of animals, and increased to an incidence of 53.3% after 10 weeks of STZ treatment. However, in rats with STZ-induced diabetes mellitus that were fed a cholesterol rich diet to induce severe hyperlipidemia and low high density lipoprotein (HDL) cholesterol, cataracts were observed one week earlier, after 8 weeks of treatment, in 40.0% of animals, with an increase to a 53.3% incidence and an 86.7% incidence after 9 and 10 weeks of STZ treatment, respectively. Plasma glucose levels did not differ between the groups. These results suggest that hyperlipidemia and low HDL cholesterol are associated with an earlier onset and an elevated incidence of diabetic cataracts. We then investigated the relationship between plasma lipids and cataracts by STZ (45-85 mg/kg) administration. The results showed that the onset of cataracts correlated positively with plasma total cholesterol, triglyceride, non-HDL cholesterol and glucose levels, and negatively with HDL cholesterol levels. The results of this study suggest that hyperlipidemia and low HDL cholesterol levels may be risk factors for the onset of diabetic cataracts and that diabetic cataracts may be accelerated by hyperlipidemia and low HDL cholesterol in rats.

Albumins↗
PubMedDate not supplied

[Hyperlipidemia and glucose intolerance in patients with HIV infection receiving antiretroviral therapy].

OBJECTIVE: To determine the prevalence of secondary effects on lipid metabolism as a result of highly active antiretroviral therapy (HAART), as well as the impact of different types of antiretroviral regimens on lipids and glucose in a group of patients in Yucatan, Mexico. MATERIAL AND METHODS: A cross-sectional study was conducted. A questionnaire created for this study was administered to each patient and total cholesterol, triglycerides and fasting glucose values were determined. The presence of hyperlipidemia and alterations in glucose were determined as well as their relation to the epidemiological variables obtained from the questionnaire. RESULTS: A total of 211 subjects were studied [36 (17%) of which were women and 175 (83%) men]. Ninety-two patients (44%) were found to have hyperlipidemia. Of these, 43 (20%) had hypercholesterolemia (HC) and 82 (39%) hypertriglyceridaemia (HT). The presence of combined HC and HT was observed in 30 (14%) patients. Nineteen (9%) patients had alterations in glucose, six (3%) diabetes mellitus and 13 (6%) impaired glucose tolerance. The variables associated with the presence of hyperlipidemia were: levels of lymphocytes CD4 >350 cells/microl (OR = 2.79 1.08-7.27, p = 0.03), male gender (OR = 3.6 1.4-9.12, p = 0.006) and the use of nucleoside-reverse transcriptase inhibitors (NRTI) (OR = 3.1 1.2-8.1, p = 0.01). CONCLUSIONS: Patients with HIV infection who receive HAART have an increased risk of presenting hyperlipidemia. In this group of patients the presence of hyperlipidemia and impaired glucose tolerance was significant. Unlike what has been indicated in most published reports, the alterations of lipids were associated more frequently with INTR use, for which it is concluded that the pathogeny of these alterations is not unique, that it is probable that concurrent effects exist between different antiretroviral drug families and that other host factors are involved in the pathogenic mechanism of these alterations.

Adult↗
PubMed1992

A case of glomerular lipidosis accompanied by familial combined hyperlipidemia and panhypopituitarism.

This is a report of a case of glomerular lipidosis with familial combined hyperlipidemia and panhypopituitarism. A 60-yr-old woman was admitted for evaluation of hyponatremia. Administration of hydrocortisone normalized the level of serum Na. A pituitary hormone-stimulating test and brain computed tomography revealed panhypopituitarism with an empty sella. Glucocorticoid deficiency due to secondary hypoaldosteronism was thought to have caused the Na loss. She had been treated for thyroid dysfunction and hyperlipidemia with replacement of thyroid hormone and a lipid-lowering drug. Hyperlipidemia changed from type V into IIa in 4 yr. Furthermore, one of her brothers and one of her sons were suspected to have type IV hyperlipidemia. Familial combined hyperlipidemia accompanied by secondary hypothyroidism was thought to have increased the levels of both total cholesterol and triglyceride. Two renal biopsies in 3 yr showed lipid deposits in the mesangial cells and indicated a positive correlation between the levels of serum lipids and lipid deposits in glomeruli, which suggested an important role of abnormal lipid metabolism in the progression of glomerular lipidosis.

Empty Sella Syndrome↗
PubMed2000

MR imaging of the salivary glands in sicca syndrome: comparison of lipid profiles and imaging in patients with hyperlipidemia and patients with Sjögren's syndrome.

OBJECTIVE: We correlated abnormalities on MR imaging with the plasma lipid profiles of patients with hyperlipidemia and symptoms of sicca syndrome. SUBJECTS AND METHODS: MR imaging features of the salivary glands, salivary function, immunologic abnormalities, and plasma lipid profiles were analyzed in 24 patients with hyperlipidemia and symptoms of sicca syndrome and compared with those of 50 patients with Sjögren's syndrome. RESULTS: Swelling of the parotid gland, impaired salivary flow, or both were observed in 20 (83%) of 24 patients with hyperlipidemia and symptoms of sicca syndrome. MR imaging findings included an enlarged parotid gland replaced with extensive lipid infiltration, whereas sialography of the parotid gland revealed normal findings. Immunologic studies and analyses of the labial glands of the mouth revealed distinctive features in patients with Sjögren's syndrome. Importantly, elevated levels of plasma triglyceride correlated with parotid gland swelling, and increased cholesterol levels significantly affected salivary flow. CONCLUSION: Our findings suggest a distinct entity of sicca syndrome in patients with hyperlipidemia compared with patients with Sjögren's syndrome. Characteristic MR imaging findings of salivary glands in patients with hyperlipidemia included extensive lipid infiltration and gland enlargement.

Adolescent↗