Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPERLIPEMIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1996

Survival analysis approach to risk factors associated with hyperlipemia in donkeys.

OBJECTIVE: To investigate the effect of gender, body condition, and age as risk factors for the development of hyperlipemia in a population of donkeys. DESIGN: Retrospective survival analysis. ANIMALS: 130 donkeys with hyperlipemia from a source population of 4,126 donkeys. PROCEDURE: A Kaplan-Meier product limit survival method was used to evaluate the effect of gender and body condition on the probability of diagnosis of clinical hyperlipemia. Cox's proportional hazard model was used to evaluate the risk of being diagnosed with hyperlipemia controlling for gender, body condition, and age at entry into the population. RESULTS: Female donkeys and donkeys of obese body condition were more at risk for developing hyperlipemia than males or those of moderate or poor body condition, respectively. None of the females in the study was pregnant. Donkeys were more likely to become hyperlipemic soon after entering the source population. Investigation of the effect of age at entry into the population indicated that older animals were at higher risk than younger animals and, controlling for age, the hazard ratios associated with being female and being overweight were 2 and 1.5, respectively. CLINICAL IMPLICATIONS: Although pregnancy and lactation are widely acknowledged as risk factors for hyperlipemia, in this population, females and obese donkeys were at highest risk, regardless of pregnancy status. Risk was greatest around the time donkeys first entered the source population. Control of body condition, reduction of stress, and close monitoring of high-risk donkeys might reduce incidences of, or allow more timely intervention for, this potentially fatal condition.

Age Factors↗
PubMed1983

Adriamycin causes hyperlipemia as a consequence of nephrotoxicity.

Adriamycin induced hyperlipemia: its features and mechanism(s) in rats were investigated. Massive hyperlipemia occurred 14-21 days after a single dose of adriamycin (7.5 mg/kg i.v.). All lipoprotein fractions were affected. Mild but significant changes in tissues were observed (liver and intestine triglycerides and kidney phospholipids were reduced). Lipid synthesis and secretion was decreased, as shown by the Triton WR1339 test 7 days after treatment, but subsequently returned to normal. Mitochondrial oxidation of long-chain fatty acids was markedly reduced in kidney, and a slight reduction was also observed in heart. Lipoprotein lipase activity was reduced in adipose tissue. These results suggest that adriamycin hyperlipemia is due to reduced lipid storage and utilization. Carnitine did not counteract hyperlipemia and proteinuria after adriamycin. Analogies to hyperlipemia following puromycin aminonucleoside-induced nephrotoxicity are discussed.

Animals↗
PubMedDate not supplied

Hyperlipemia in 9 miniature horses and miniature donkeys.

The medical records from 9 consecutive miniature horses (n = 5) and miniature donkeys (n = 4) with hyperlipemia (serum triglyceride concentration > 500 mg/dL) were reviewed. In all cases, hyperlipemia was a secondary complication of a primary systemic disease including septicemia, colitis, parasitism, esophageal obstruction, gastric impaction and rupture, fecalith, and pituitary adenoma. Therapy consisted of specific treatment for the primary disease, supportive care, and nutritional support. The mean time for resolution of hyperlipemia in cases requiring nutritional support (n = 6) was 7 days, and the duration of nutritional support in surviving patients was 11.7 days. Seven of 9 patients survived. The primary disease resulted in death in 2 patients. Enteral feeding with commercially prepared low residue diets and treatment of the primary disease was successful in reversing hyperlipemia in 5 of 6 surviving patients that required nutritional support. Parenteral administration of a glucose-based (non-lipid) solution was successful in resolving hyperlipemia in 1 patient.

Animals↗
PubMed2005

[Interleukin-8 protein and gene expression in atherosclerotic lesions of hyperlipemia rabbits].

Interleukin-8 is CXC chemokine that is initially discovered using chemotaxis and the activation of neutrophils and induces the migration and proliferation of smooth muscle cells. Interleukin-8 is a potent angiogenic factor that may play a role in atherosclerosis. To establish the temporal correlation between IL-8 expression and plaque development, we examined the expression during atherosclerosis of hyperlipemia rabbits using immunohistochemistry, ELISA, in situ hybridization. By location of immunohistochemistry, the expression of IL-8 protein increased obviously in intima of hyperlipemia rabbits at 8 and 12 week. Quantitative analysis of the expression of IL-8 Immunohistochemistry indicated that positive area of AS model was 4.48 times and 8.76 times that of control group at 8 and 12 week. The valuation of IOD of AS model was 4.16 times and 4.36 times that of control group at 8 and 12 week. By specific ELISA, the ratio of the IL-8 protein to total protein of AS model was 1.84 times and 2.06 times that of control group at 8 and 12 week. By location of in situ hybridization, positive location was strong in intima of hyperlipemia rabbits at 8 week. We observed the dynamic alteration of interleukin-8 protein and gene expression in atherosclerotic lesions of hyperlipemia rabbits with establishing model. Interleukin-8 protein and gene expression was up-regulation in the development of fatty streaks in hyperlipemia rabbit.

Animals↗
PubMed1979

[Type V hyperlipemia. 54 cases (author's transl)].

Type V hyperlipemia is not very common. The series of 54 cases descrubed here is the largest reported to date. Our observations were recorded when lipidograms showed the presence of chylomicrons and a large pre-beta-lipoprotein spot in the serum of fasting subjects. Type V hyperlipemia was often combined with other metabolic syndromes such as diabetes, hyperuricemia or gout, or obesity. Chronic alcoholism was also noted in half our subjects, in whom hyperlipemia quickly regressed after alcohol consumption ceased. Ischemic arterial complications, chiefly coronary, were found in one third of our cases, and the vascular risks accompanying this type of hyperlipemia rose considerably in patients with high blood pressure. Various type of treatment were administered, but all subjects were put on a special diet, comprising either the elimination of alcoholic drinks only, or, in addition to this, reduced carbohydrate or calorie intake. As a rule, these measures resulted in a distinct regression of lipid anomalies. Clofibrate or derivatives proved effective in cases where hyperlipemia failed to respond to dietary measures.

Adolescent↗
PubMed1986

[Pathologic decrease in lipoprotein lipase activity in relation to the development of hyperlipemias and their significance for coronary heart disease].

There is much evidence that altered lipid metabolism contributes to the development of coronary artery disease (CAD). It is generally accepted that there is a direct association between the extent of CAD and total plasma cholesterol, as well as an inverse association between the extent of CAD and plasma HDL-cholesterol. No general agreement exists about the atherogenetic potential of plasma triglycerides and of triglyceride-rich lipoproteins. Since lipoprotein lipase (LPL) is the key-enzyme in the catabolism of triglyceride-rich lipoproteins (chylomicrons and very low-density lipoproteins), we examine the relationship between triglyceride-rich lipoproteins and LPL in vitro and in vivo. The concentrations of the main lipoprotein density classes, namely very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3, are measured by rate zonal ultracentrifugation. The preparation of VLDL, IDL, LDL, HDL2, and HDL3 is performed by sequential ultracentrifugation. The activity of LPL is measured radioenzymatically in a glycerol-based triolein emulsion. It can be demonstrated in vitro that VLDL, IDL, and HDL2 from normal plasma are able to increase LPL-activity in contrast to VLDL, IDL, and HDL2 from hyperlipemic plasma. This difference seems to be caused by an altered composition of apolipoproteins in hyperlipemic lipoproteins. An artificial acidosis in three healthy subjects shows in contrast to alkalotic and neutral blood-pH a significant decrease of LPL-activity. This result seems to be of some interest, since diseases associated with acidotic blood-pH, such as chronic renal disease, diabetes mellitus or chronic alcoholism, show secondary hyperlipemias caused by a deficit of LPL-activity. It can be shown in 15 male patients who produce a secondary type-V hyperlipemia during severe abuse of alcohol, that LPL-activity is decreased significantly as compared to 15 healthy controls. During sober phases, this alcohol-induced hyperlipemia and the impairment of LPL-activity disappears completely. In an other group of 8 male patients, who are not producing severe secondary hyperlipemia during approximately the identical alcohol intake, LPL-activity is also significantly decreased, but the activity of hepatic lipase is significantly increased. This increase of the activity of hepatic lipase seems to protect these patients from the development of secondary type-V hyperlipemia. In 89 male patients with angiographically assessed CAD a very strong inverse association between the activity of LPL and the extent of CAD is found.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1970

Metabolism of lysolecithin in vivo: effects of hyperlipemia and atherosclerosis in squirrel monkeys.

We have studied the effect of long-term hyperlipemia and atherosclerosis in squirrel monkeys on the metabolism of lysolecithin-(14)C (1-palmitoyl-1'-(14)C sn-glycerol 3-phosphorylcholine) in order to explain elevated plasma and arterial concentrations of lysolecithin. The die-away curves of lysolecithin-(14)C from plasma and the timing of appearances of other (14)C-labeled moieties in plasma and other tissues demonstrated a complex pattern of metabolic reactions. There was a rapid equilibration of specific activities of lysolecithin of plasma, liver, and aortic intima plus inner media. The specific activities of lecithin peaked first in liver, then in plasma, and rose slowly in aortic intima plus inner media. The appearance of lecithin-(14)C in heart and skeletal muscle was also slower than in the liver and some other tissues. Triglycerides, and to a lesser extent, cholesteryl esters contained radioactivity. The concentrations of aortic lysolecithin in the atherosclerotic aortas were several times greater than comparable values for control aortas, and the time of equilibration of plasma and aorta lysolecithin-(14)C was much greater for the atherosclerotic group. The quantities of lysolecithin in plasma and in the pool of which the plasma was a part, were increased with hyperlipemia and atherosclerosis, as was the rate of lysolecithin production in the fast pool. Hyperlipemia was also associated with an early increase in plasma lecithin:cholesterol acyltransferase (LCAT) activity in vitro. Furthermore, nutritional hyperlipemia influenced the distribution of lysolecithin-(14)C and lecithin-(14)C between different plasma lipoproteins. The increase in concentrations of lysolecithin in the aorta occurred more slowly than that in plasma after we had induced hyperlipemia in the monkeys.

Acyltransferases↗
PubMed1980

[Effects of 5-methyl-7-diethylamino-s-triazolo-(1, 5-a) pyrimidine (trapidil) on various experimental hyperlipemias (author's transl)].

Effects of 5-methyl-7-diethylamino-s-triazolo-1, 5-a) pyrimidine (trapidil, Rocornal), a therapeutic agent for ischemic heart disease, on various types of experimental hyperlipemias were studied. With administration of trapidil, elevation of serum high density lipoprotein cholesterol (HDL-C) levels and reduction in serum total cholesterol (TC), low density lipoprotein and very low density lipoprotein cholesterol (LDL-C) and the ratio of HDL-C to LDL-C (LDL-C/HDL-c) were observed in most disease models. Changes in HDL-C levels and LDL-C/HDL-C in the hyperlipemia induced by lipid-enriched diet in mice and in the hyperlipemia induced by high cholesterol diet in Japanese quails were of statistical significance. Also, amelioration of reduction in HDL-C induced by high fat emulsion plus 6-n-propyl-2-thiouracil in rats was observed to be significant. Moreover, trapidil significantly reduced TC, LDL-C levels and LDL-C/HDL-C in the hyperlipemia in hamsters. To investigate possible mechanisms of therapeutic effects of trapidil, blood enzyme activities in Japanese quails with hyperlipemia were assayed. Trapidil showed increases in plasma lipoprotein lipase and serum lecithin-cholesterol acyltransferase activities. These results suggest that trapidil may be an effective chemotherapeutic agent for treating ischemic heart disease.

Animals↗
PubMed1984

Hyperlipemia and arteriosclerotic cardiovascular disease in the Polynesian population of Rarotonga.

Total cholesterol, total triglyceride and high density lipoprotein (HDL) cholesterol and their relation to arteriosclerotic cardiovascular disease (ASCVD) were investigated in a population of Polynesian Maoris in Rarotonga who are becoming increasingly westernized. 8.5% of the population had plasma triglyceride elevations (triglyceride greater than or equal to 200 mg/dl), and the occurrence of hypertriglyceridemia was significantly higher in males than females. 5.8% of the population had elevations of total cholesterol (cholesterol greater than or equal to 250 mg/dl), and the proportion with elevation of total cholesterol was similar for males and females. 3.2% of the population had elevations of both triglyceride and cholesterol. HDL cholesterol concentrations were relatively low, and no sex differences were observed at any age. Analysis of lipoprotein cholesterol and triglyceride in a subset of those who had hyperlipemia indicated that the elevations of total cholesterol and triglyceride were mainly due to elevations of low density lipoprotein (LDL) cholesterol and very low density lipoprotein (VLDL) triglyceride, respectively; furthermore, elevations of VLDL triglyceride and LDL cholesterol were significantly correlated with increase in VLDL apolipoprotein B (apo B) and LDL apo B, respectively. Although an appreciable prevalence of diabetes was observed in this population (male: 6.7%, female: 8.4%), the diabetes could not account for the hyperlipemia. Among 693 subjects between the ages of 30 and 59 years, approx. 3% of males and 1% of females had Q-wave changes, and 16% of females and 4% of males had ST-T changes. Among males with Q-wave abnormalities, hyperlipemia was more frequent. There was also increased frequency of hypertension in those with elevated lipids. The data indicate the occurrence of some hyperlipemia in this population which could be of the familial-combined type; the elevated plasma lipids may contribute to the increased frequency of coronary heart disease.

Adult↗
PubMed1988

Hyperlipemia, fibrinolysis and arteriosclerosis.

In this work we investigated the influence of hyperlipemia on the fibrinolytic system and also attempted to determine whether vascular lesions may modify the response of plasminogen activators to hyperlipemia. The study was made on rats. Three different diets were administered to the animals, two of the diets only increased the levels of plasmatic lipids in the animals (hyperlipemic groups), but the third induced hyperlipemia and lipid infiltration in aorta (arteriosclerotic group). Fibrinolytic activity was evaluated in the plasma, on the aorta endothelial surface and in aorta wall. In the plasma, plasminogen activator (PA) activity was increased in the hyperlipemic and arteriosclerotic groups compared to control group, however, the activity of fibrinolysis inhibitors was also increased. On the endothelial surface and in the aorta wall, fibrinolytic activity was increased in the groups which received hyperlipidic diets but in the arteriosclerotic group only the endothelial surface showed a clear increase of fibrinolytic activity. A positive correlation was observed between PA activity and levels of hyperlipemia. However, no correlation has been shown between fibrinolytic activity in the aorta with cholesterol and triglyceride levels in this vascular wall.

Animals↗
PubMed2005

Hyperlipemia and oxidation of LDL induce vascular smooth muscle cell growth: an effect mediated by the HLH factor Id3.

Hyperlipemia and oxidized LDL (ox-LDL) are important independent cardiovascular risk factors. Ox-LDL has been shown to stimulate vascular smooth muscle cell (VSMC) proliferation. However, the effects of hyperlipemia and the molecular mechanisms mediating hyperlipemia and ox-LDL effects on VSMC growth are poorly understood. The helix-loop-helix (HLH) transcription factor, Id3, is a redox-sensitive gene expressed in VSMC in response to mitogen stimulation and vascular injury. Accordingly, we hypothesize that Id3 is an important mediator of ox-LDL and hyperlipemia-induced VSMC growth. Aortas harvested from hyperlipemic pigs demonstrated significantly more Id3 than normolipemic controls. Primary VSMC were stimulated with ox-LDL, native LDL, sera from hyperlipemic pigs, or normolipemic pigs. VSMC exposed to hyperlipemic sera demonstrated increased Id3 expression, VSMC growth and S-phase entry and decreased p21cip1 expression and transcription. Cells stimulated with ox-LDL demonstrated similar findings of increased growth and Id3 expression and decreased p21cip1 expression. Moreover, the effects of ox-LDL on growth were abolished in cells devoid of the Id3 gene. Results provide evidence that the HLH factor Id3 mediates the mitogenic effect of hyperlipemic sera and ox-LDL in VSMC via inhibition of p21cip1 expression, subsequently increasing DNA synthesis and proliferation.

Animals↗
PubMed1973

Pathogenesis of postprandial hyperlipemia in rats fed ethanol-containing diets.

To study the mechanism of the increase in serum lipoproteins which occurs in rats fed alcohol chronically, and especially to assess the role of the intestine, the effects of acute and chronic ethanol administration on lymph and plasma lipids were compared in rats with and without intestinal lymph fistulae. In rats not previously given alcohol, the administration of one dose of a diet containing ethanol (3 g/kg) produced a significant increase in lymph flow, lipid output, and incorporation of dietary fat into lymph lipids when compared with the effects of a control diet containing isocaloric carbohydrate. However, no hyperlipemia developed after ethanol. By contrast, previous feeding of ethanol for several weeks modified the acute effects of ethanol on both lymph and serum lipids. Compared with control animals pair-fed with isocaloric carbohydrate-containing diets, rats which had been fed a diet with 36% of total calories as ethanol for 3-4 wk developed postprandial hyperlipemia when given a single dose of the ethanol-containing or even the ethanol-free diet. This was associated with an increased incorporation of labeled dietary fat and of intravenously injected [(3)H]lysine into plasma lipoproteins of d < 1.006. However, postprandial lymph flow and lipid output were not higher in rats fed alcohol chronically than in their pair-fed controls. Moreover, when rats with lymph fistulae were given intravenous (i.v.) infusions of lymph lipids (to substitute for the diverted intestinal lymph), the ethanol-fed animals still developed hyperlipemia. Incorporation of i.v. lysine into d < 1.006 plasma lipoproteins also remained significantly increased. Thus, under these conditions, alcoholic hyperlipemia does not result from changes in intestinal lymph lipids. Two main factors appear to be involved; the acute effects of ethanol on hepatic lipid metabolism and the development of an increased capacity for lipoprotein synthesis during chronic ethanol feeding. The latter most likely occurs in the liver and it is postulated that it is linked to the associated changes in the hepatic endoplasmic reticulum.

Animals↗
PubMed2000

Hyperlipemia and early pancreatic injury induced by ethanol intake in rats.

The pathogenesis of alcoholic pancreatitis is unknown, and even though hyperlipemia has been hypothesized to be a risk factor for alcoholic pancreatitis, no studies directly investigating whether there is a relationship between the two have ever been reported. Therefore, to determine if a relationship exists between hyperlipemia and alcoholic pancreatitis, especially the early stage of alcoholic pancreatic injury, we administered a regular liquid Lieber-DeCarli diet, with and without ethanol as 35% of total calories, to rats for 2 wk. Thereafter we measured their plasma lipid concentrations, pancreatic zymogen granule fragility, and plasma lipase activity and subsequently investigated the correlations between these parameters. Significant increases in plasma triglyceride, total cholesterol, phospholipid, nonesterified fatty acid, pancreatic zymogen granule fragility, and plasma lipase activity were observed in the ethanol liquid diet group, compared with the values of the control liquid diet group, and pancreatic zymogen granule fragility was correlated with plasma triglyceride (r=0.62), total cholesterol (r=0.77), phospholipid (r=0.76), nonesterified fatty acid concentrations (r=0.62), and lipase activity (r=0.63). These results show a possible relationship between hyperlipemia and the early stage of alcoholic pancreatic injury, and they may support the hypothesis that hyperlipemia contributes to the etiology of alcoholic pancreatitis.

Amylases↗
PubMed2004

[Determination of trace copper and zinc in hypertension complicated with hyperlipemia by atomic absorption spectrophotometry].

The serum levels of Zn, Cu, cholesterol (Ch) and triglyceride (TG) were determined in 44 patients with hypertension complicated with hyperlipemia, 42 patients with hypertension (HP) and 30 healthy controls by atomic absorption spectrophotometry and automatic biochemical analytical instrument of reagent kit. It was found that the contents of Zn, Ch, TG and Zn/Cu ratio in hypertension complicated with hyperlipemia were significantly higher than in HP and control, while Cu in hypertension complicated with hyperlipemia was significantly lower than in HP and control. The contents of Zn, Ch, TG and Zn/Cu ratio in hypertension were significantly increased. It is suggested that hypertension complicated with hyperlipemia is closely related with Zn and Cu.

Aged↗
PubMed2005

[Study of the effect of crocin on rat experimental hyperlipemia and the underlying mechanisms].

OBJECTIVE: To study the effect of crocin on rat experimental hyperlipemia and its mechanisms. METHOD: Hyperlipemia model was established by feeding heavy cholesterol for 2 months and the effect of crocin on blood lipid in experimental hyperlipemia rats was observed. Aortic smooth muscle cells were cultured in different culture media and proliferation was measured by MTT assay. Western blotting was used to detect the effect of crocin on phosphorylation of p38 MAPK. RESULT: Crocin not only decreased greatly the content of cholesterol, triglyceride and density lipoprotein in blood, but also increased the content of high density lipoprotein. In addition, the proliferation of smooth muscle cells and the activation of p38MAPK were inhibited by Crocin. CONCLUSION: Crocin prevents atherosclerosis in hyperlipemia, which may be mediated by the inhibition of both proliferation of smooth muscle cells and activation of p38MAPK.

Animals↗
PubMed2005

[The assessment of arteriolosclerosis by serum lipids data, and carotid ultrasonography and pulse wave velocity, and its evaluation as a tool for preventive medicine: II. Carotid ultrasonography and pulse wave velocity for hyperlipemia and diabetes mellitus].

We studied the test results of carotid ultrasonography and pulse wave velocity against a sample of hyperlipemia and diabetes mellitus. Sixty four hyperlipemia samples (HL), 85 diabetes mellitus samples (DS), and 27 complicated samples (CS) were compared with 56 healthy samples (HS). Hyperlipemia samples were selected from cholesterol under 300 mg/dl, and neutral fat under 300 mg/dl. Diabetes mellitus samples were selected from fasting plasma glucose (FBS) under 200 mg/dl. Samples from severe conditions with various disease were excluded. Ratio over 1.1 mm intima-media thickness (IMT) was 0% in HS, 48% in HL, 40% in DS and 33% in CS. PWV value was max 1896cm/s in CS. There was no significant correlation within IMT, serum lipid(Total Cholesterol, Neutral Fat, HDL-Cholesterol, LDL-Cholesterol) and FBS. For early treatment or accurate diagnosis of arteriosclerosis in hyperlipemia or diabetes mellitus patients, who are at high risk of developing arteriosclerosis, to vital function tests (carotid ultrasonography and pulse wave velocity) should be performed, in addition to normal blood tests.

Adult↗
PubMed1995

Hyperlipidemia, hyperlipemia, and hepatic lipidosis in American miniature horses: 23 cases (1990-1994).

The medical records of 23 American Miniature Horses with hyperlipidemia, hyperlipemia, or hepatic lipidosis were reviewed. The most common clinical signs were anorexia and lethargy. The mean duration of clinical signs was 2.4 days. A primary disease was identified in 19 cases. Enterocolitis was the most common primary disease (n = 10). Intentional feed restriction, as part of treatment for colic, resulted in hyperlipemia in 2 horses and hyperlipidemia in 1. Four horses had primary hyperlipemia, 3 of which had signs of hepatoencephalopathy secondary to hepatic lipidosis. Dextrose, heparin, and insulin were the most common treatments. The overall survival was 61% (14/23). All horses with peak serum triglyceride concentrations > 1,200 mg/dl died or were euthanatized, whereas all but 1 with peak serum triglyceride concentrations < 1,200 mg/dl survived. These findings suggest that when American Miniature Horses, like other ponies and donkeys, are in a negative energy balance, they can rapidly develop hyperlipidemia or hyperlipemia. Early detection and treatment may improve survival.

Animal Feed↗
PubMed1996

[Treatment of hyperlipemia: opinions of primary care physicians of the La Rioja region].

BACKGROUND: Primary health care physicians (PHCP) play a fundamental role in the detection and treatment of hyperlipemias in a general population. The aim of this study was to estimate the opinion of the PHCP in the Autonomic Community of La Rioja, Spain, regarding desirable lipemic values and treatment of hyperlipemias. METHODS: A survey with personal interview was carried out to all the PHCP in the Spanish National Health Care (INSALUD) in La Rioja in May and June 1994. RESULTS: Of the 177 PHCP included 97% completed the questionnaire. The main coronary risk factor for 46% of physicians was high blood pressure followed by serum cholesterol (30%). Fifty-six percent of the physicians believed that the desired populational cholesterolemia should be less than 200 mg/dl and this percentage rose if the physician worked in an urban environment (p < 0.01). Sixty-six percent considered 200 mg/dl as the desired triglyceridemia. For treatment and follow-up of hyperlipemia, 78% of physicians use cholesterol linked to low density lipoproteins (cLDL). This use of cLDL increased among those who were familiar with the recommendations of the Spanish Society of Arteriosclerosis (p < 0.002) or who worked in health care centers (p < 0.02). Regarding initiation of dietetic treatment most chose cholesterolemia between 200-250 mg/dl, a cLDL value between 150-185 mg/dl and triglyceridemia between 200-250 mg/dl. For the use of pharmacologic treatment these levels were 250-300 mg/dl, 150-185 mg/dl and 250-300 mg/dl, respectively. Ninety-nine percent of physicians indicated diet as the first therapeutic measure. In isolated hypercholesterolemia the resins were most used by the Family Medicine specialists (p < 0.002) and fibrates (p < 0.03) and statins (p < 0.02) the least used. The use of statins was lower in the physicians working in health care centers (p < 0.03). CONCLUSIONS: Knowledge of theshold values of serum cholesterol and triglicerides levels and the use of drugs among the primary health care physicians from La Rioja, Spain, are generally correct. The physicians with good knowledge of the National Consensus Guides on hyperlipemias had the most adequate opinion.

Cholesterol↗