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PubMedDate not supplied

Characterization of hypertriglyceridemia induced by L-asparaginase therapy for acute lymphoblastic leukemia and malignant lymphoma.

Plasma lipids and apolipoproteins were determined in 19 children with acute lymphoblastic leukemia (ALL) or malignant lymphoma (ML) who were treated by L-asparaginase with prednisolone and vincristine. Extreme hypertriglyceridemia, i.e., over 10,000 mg/l of the maximum serum triglyceride concentration, was induced in 8 patients; these concentrations were not over 10,000 mg/l in the remaining 11 patients. The possibility was raised that the apolipoprotein E (apoE) isoform apoE4 (epsilon 4) participated in the induction of extreme hypertriglyceridemia, since the frequency of the apoE4/E3 phenotype in the patients with extreme hypertriglyceridemia was higher compared to those in the patients without extreme hypertriglyceridemia and control subjects (n = 248). The acute and severe hypertriglyceridemia was induced at 8 to 14 days after the end of the L-asparaginase therapy, with an earlier remarkable increase in the apoCIII/apoCII ratio and an extreme decrease of fibrinogen concentrations (a marker of the protein productivity of the liver). It is well known that apoCII and apoCIII have possible functions as an activator and an inhibitor of lipoprotein lipase (LPL), respectively. The extreme increase in the apoCIII/apoCII ratio could be one of the reasons for the accumulation of triglyceride-rich lipoproteins in plasma.

Adolescent↗
PubMed1988

Further resolution and comparison of the heterogeneity of plasma low-density lipoproteins in human hyperlipoproteinemias: type III hyperlipoproteinemia, hypertriglyceridemia and familial hypercholesterolemia.

The heterogeneity of the plasma low-density lipoproteins (LDL) in subjects with type III hyperlipoproteinemia (3 cases), with hypertriglyceridemia (4 cases) and with the heterozygous form of familial hypercholesterolemia (FH, 4 cases) has been evaluated using a new, high resolution equilibrium density gradient ultracentrifugation procedure. The mass distribution profile, physicochemical properties, particle heterogeneity and apoprotein B content of a series of 13 LDL subfractions was examined in the 3 hyperlipidemic groups and the data were compared with those reported earlier in normolipidemic subjects. In FH, LDL mass was distributed as a narrow peak of d approximately 1.031-1.034 g/ml, whereas the distribution in hypertriglyceridemia was markedly asymmetric with a single peak of elevated density (d approximately 1.037-1.043 g/ml); the distribution in type III subjects was distinguished by its bi- or trimodal nature and broad profile. The chemical composition of LDL gradient subfractions in FH and in hypertriglyceridemia markedly resembled that of the respective parent LDL of d = 1.019-1.063 g/ml, displaying elevated proportions of cholesteryl ester in FH and of protein in hypertriglyceridemia. LDL subfractions in type III disease were enriched in free cholesterol. The Stokes diameters of LDL particles in corresponding subfractions from the 3 hyperlipidemic states were similar; however, whereas a single particle species was characteristic of each LDL subfraction in both FH and in our normolipidemic group, 2 species were frequently present in each subfraction in both type III and type IV diseases; in addition, subfractions from type III subjects occasionally exhibited 3 size species. Apolipoprotein B-100 was the predominant protein component in LDL subfractions from all 3 hyperlipidemic groups. Plasma LDL consist then of multiple particle species which constitute a particularly complex spectrum in type III hyperlipoproteinemia and in hypertriglyceridemia. The origin(s) of such particle subspecies is indeterminate at present; moreover, they may differ in their intravascular metabolism, in their degradation in tissues and in their relative atherogenicities.

Adolescent↗
PubMed1978

Impaired very low density lipoprotein and triglyceride removal in broad beta disease: comparison with endogenous hypertriglyceridemia.

The removal rate of apoprotein-B (apo B) in very low density lipoprotein (VLDL) was decreased in individuals with broad beta disease when compared with endogenous hypertriglyceridemia. Following the injection of 125I-VLDL isolated from individuals with endogenous hypertriglyceridemia, both VLDL apo B fractional catabolic rate (0.058 +/- 0.029 hr-1) and VLDL apo-B turnover rate (0.300 +/- 0.070 mg/kg/hr) were lower in broad beta disease than in endogenous hypertriglyceridemia (fractional catabolic rate 0.112 +/- 0.046, p less than .05; turnover rate 0.640 +/- 0.199, p less than .005) despite equivalent plasma concentrations of VLDL-apo-B. Furthermore, conversion of VLDL apo-B to LDL was impaired in broad beta disease relative to endogenous hypertriglyceridemia. Differences in the kinetics of lipoprotein lipase-related triglyceride removal during a maximal heparin infusion were also demonstrated between these two disorders. These differences suggest an abnormality in the interaction of lipoprotein lipase with the lipoproteins of unusual composition in broad beta disease. This is further supported by the normalization of lipoprotein composition in broad beta disease by estrogen therapy, with a simultaneous change in the kinetics of lipoprotein lipase-related triglyceride removal towards those seen in endogenous hypertriglyceridemia.

Adult↗
PubMed1982

Studies of the mechanism of fructose-induced hypertriglyceridemia in the rat.

Carbohydrate-induced hypertriglyceridemia is easily produced in the rat, and fructose has been shown to be particularly potent in this regard. In this study we have compared the effects of feeding rats diets high (66% of total calories) in fructose or glucose on various aspects of carbohydrate and lipid metabolism. The results confirmed previous observations that fructose (456 +/- 276 mg/dl) was more potent (p less than 0.001) in raising plasma TG concentration than was glucose (242 +/- 13 mg/dl), and indicated that the difference in magnitude of hypertriglyceridemia produced by the two carbohydrates was closely related to the ability of the test diets to increase VLDL-TG secretion (r = 0.85, p less than 0.001). Both glucose and fructose feeding led to comparable degrees of hyperinsulinemia, and plasma TG concentrations increased before hyperinsulinemia evolved in fructose-fed rats. Therefore, it was concluded that fructose can act directly on the liver to increase VLDL-TG secretion, and that fructose-induced hypertriglyceridemia can occur in the absence of hyperinsulinemia. On the other hand, the rise in plasma TG concentration produced by fructose was reduced dramatically in exercise-trained rats, and this was associated with a decrease in plasma insulin concentration. Based upon these observations, we suggest that fructose feeding produces hypertriglyceridemia by directly stimulating hepatic VLDL-TG secretion, as well as by producing insulin resistance and hyperinsulinemia, and that it is the combined effect of these two separate actions which accounts for the magnitude of fructose-induced hypertriglyceridemia.

Animals↗
PubMed1983

Severe hypertriglyceridemia: role of familial and acquired disorders.

To evaluate the role of familial and secondary factors in the etiology of severe hypertriglyceridemia, family studies were performed and potential secondary causes of hypertriglyceridemia were evaluated in 54 patients with plasma triglyceride levels above 2000 mg/dl. Every subject had hypertriglyceridemic relatives, compatible with a familial form of hyperlipidemia, although plasma triglyceride levels in the relatives were substantially lower than in the index patients. In 5 index patients, both parents had hyperlipidemia. Four of these 5 had no coexisting secondary cause for hypertriglyceridemia. Forty-six of the remaining 49 (94%) also had potential secondary causes of hypertriglyceridemia, most commonly untreated diabetes mellitus. These findings suggest that severe hypertriglyceridemia frequently results from the coexistence of familial and secondary forms of hyperlipidemia.

Adolescent↗
PubMed1982

Chylomicronemia syndrome. Interaction of genetic and acquired hypertriglyceridemia.

Chylomicrons accumulating in plasma obtained after an overnight fast are always abnormal and can be detected in association with triglyceride levels above 1000 mg per dl. The chylomicronemia syndrome is associated with marked hypertriglyceridemia (plasma triglyceride level above 2000 mg per dl), abdominal pain or pancreatitis, eruptive xanthomata, lipemia retinalis, dyspnea, mental aberrations, and other minor findings. The marked hypertriglyceridemia is usually due to the interaction of a common familial form of hypertriglyceridemia and a common acquired form of hypertriglyceridemia secondary to another disease, drug, or alcohol. Rarely, genetic abnormalities in lipoprotein lipase are the cause of the marked hypertriglyceridemia. Therapy that successfully lowers plasma triglyceride levels is associated with clearing of the symptoms and signs of the chylomicronemia syndrome and prevention of its recurrence.

Abdomen↗
PubMedDate not supplied

Diabetic hypertriglyceridemia.

The conference opened with the clinical presentation of a 50-year-old male with fasting hyperglycemia (296 mg per cent) and hypertriglyceridemia (2736 mg per cent). The discussion began with a summary of current concepts regarding the manner in which chylomicra (intestine) and very low density lipoproteins (intestine and liver) are formed, transported into the plasma, and removed from the circulation. This was followed by a consideration of diabetic hypertriglyceridemia in which this syndrome was subdivided into two categories. The first form is seen in patients with severe fasting hyperglycemia, and is characterized by marked insulin deficiency, decreased very low density lipoprotein production, a fall in the activity of lipoprotein lipase, and hypertriglyceridemia secondary to a defect in removal of lipoproteins from the plasma. In contrast the other form of diabetic hypertriglyceridemia is seen in patients with minimal abnormalities of carbohydrate tolerance, and in this instance insulin resistance, not insulin lack, seems to play the pivotal role. In these patients, the rise in plasma triglyceride levels seems to be secondary to increased production of very low density lipoproteins, presumably as a result of the hyperinsulinemia associated with the insulin resistance. The conference ended with an attempt to relate the patient presented to the models of diabetic hypertriglyceridemia that had been defined.

Animals↗
PubMed1988

Association of apolipoprotein epsilon 4 allele with hypertriglyceridemia in obesity.

Hypertriglyceridemia is the most frequent lipid abnormality associated with obesity. Genetic polymorphism of apolipoprotein E (apoE) has been demonstrated to influence lipid levels. We wanted to assess the role of apoE alleles in the hypertriglyceridemias of the obese population. The apoE phenotypes and lipid status were investigated in a population of 172 obese French subjects. The frequencies of phenotypes E4/3, E4/4 and E4/2 were 29.7%, 8.1% and 2.1%, respectively, in a subgroup with triglycerides greater than or equal to 200 mg/dl (n = 37) versus 14.2%, 2.7% and 0.9% in the normolipidemic subgroup (p less than 0.005). The odds ratio of hypertriglyceridemia was 3.15 for obese subjects with epsilon 4; 27.7% of hypertriglyceridemias could be attributed to epsilon 4 allele. It is concluded that the genetic polymorphism of apoE modulates the effects of obesity on lipids and lipoproteins and that allele epsilon 4 increases the risk of obesity-induced hypertriglyceridemia.

Adult↗
PubMed2004

Inherited apolipoprotein A-V deficiency in severe hypertriglyceridemia.

OBJECTIVE: Mutations in LPL or APOC2 genes are recognized causes of inherited forms of severe hypertriglyceridemia. However, some hypertrigliceridemic patients do not have mutations in either of these genes. Because inactivation or hyperexpression of APOA5 gene, encoding apolipoprotein A-V (apoA-V), causes a marked increase or decrease of plasma triglycerides in mice, and because some common polymorphisms of this gene affect plasma triglycerides in humans, we have hypothesized that loss of function mutations in APOA5 gene might cause hypertriglyceridemia. METHODS AND RESULTS: We sequenced APOA5 gene in 10 hypertriglyceridemic patients in whom mutations in LPL and APOC2 genes had been excluded. One of them was found to be homozygous for a mutation in APOA5 gene (c.433 C>T, Q145X), predicted to generate a truncated apoA-V devoid of key functional domains. The plasma of this patient was found to activate LPL in vitro less efficiently than control plasma, thus suggesting that apoA-V might be an activator of LPL. Ten carriers of Q145X mutation were found in the patient's family; 5 of them had mild hypertriglyceridemia. CONCLUSIONS: As predicted from animal studies, apoA-V deficiency is associated with severe hypertriglyceridemia in humans. This observation suggests that apoA-V regulates the secretion and/or catabolism of triglyceride-rich lipoproteins. Mutations in APOA5 gene might be the cause of severe hypertriglyceridemia in subjects in whom mutations in LPL or APOC2 genes have been excluded. We detected a nonsense mutation in APOA5 gene (Q145X) in a boy with hyperchylomicronemia syndrome. This is the first observation of a complete apoA-V deficiency in humans.

Amino Acid Substitution↗
PubMedDate not supplied

Triglyceride and cholesterol metabolism in primary hypertriglyceridemia.

To determine mechanisms of elevated plasma triglycerides (TG) in patients with primary hypertriglyceridemias, simultaneous studies were carried out on kinetics of very low density lipoprotein-triglycerides (VLDL-TG) and synthesis of cholesterol and bile acids. Sixteen hypertriglyceridemic patients with familial combined hyperlipidemia (FCHL) and 12 patients with poorly classified, primary hypertriglyceridemia were studied, and their results were compared to a series of normal and obese subjects previously studied in our laboratory. The mean value for transport (synthesis) of VLDL-TG in patients with FCHL was about twice normal. Although the upper normal synthesis rates overlapped with transport rates of some patients with FCHL, it appeared that the major cause of hypertriglyceridemia in FCHL was an elevated production of VLDL-TG. However, the height of the plasma TG in FCHL patients also was influenced by individual clearance capacities for VLDL-TG, and fractional clearance rates in several seemed particularly low. Synthesis rates for cholesterol and/or bile acids were high in several patients with FCHL, suggesting simultaneous overproduction of VLDL-TG and sterols; however, increased synthesis of both was not observed in all the patients. Most patients with poorly classified hypertriglyceridemia had over-production of VLDL-TG, but an apparent reduction in clearance was common. In these patients, increased synthesis of cholesterol and bile acids was infrequent. Our results indicate that abnormally high production of VLDL-TG seemed to be the major factor in causing primary hypertriglyceridemia, but that clearance capacity can play an important role in determining the the severity of the TG elevation.

Adult↗
PubMedDate not supplied

Kinetic heterogeneity of low density lipoproteins in primary hypertriglyceridemia.

The kinetics of two subfractions of low density lipoproteins (LDL) were examined in nine patients with primary hypertriglyceridemia. LDL was subjected to equilibrium ultracentrifugation, and three patterns of LDL subfractions were noted. The LDL of five patients with moderate hypertriglyceridemia (plasma triglycerides (TG) ranging from 333 to 580 mg/dl) appeared to contain two distinct subfractions. One was less dense and had a high TG content; the other was more dense and had a reduced content of all lipids, particularly cholesterol. Each subfraction was labeled separately and was reinjected into the patient. Of the two subfractions, the more dense LDL usually had a higher fractional catabolic rate (FCR), although the turnover rates of both subfractions for these hypertriglyceridemic patients were higher than normal. Two other patients with mild hypertriglyceridemia had only a single LDL after gradient equilibrium ultracentrifugation. This fraction was divided into less dense and more dense subfractions, and their FCR was determined. In both patients, turnover rates of the two subfractions were similar and both were in the normal range. Finally, two more patients with mildly elevated TG had a very dense LDL, besides having a single, less dense band. For both patients, the FCR for the less dense and very dense subfractions were similar, although the denser LDL had a greater fraction in the extravascular compartment. Thus, patients with primary moderate hypertriglyceridemia often have distinct subfractions that have different turnover rates. For patients with mild hypertriglyceridemia, the LDL is more homogeneous, and its subfractions are kinetically similar.

Humans↗
PubMed1976

Evidence for a familial form of hypertriglyceridemia as disorders coupled with insulin resistance.

To evaluate the role of insulin in familial hypertriglyceridemia, 34 relatives of the pedigrees of 3 index cases of endogenous hypertriglyceridemia and hepatic steatosis as well as 9 spouses were examined for plasma lipids and responses of blood glucose and plasma insulin during oral glucose tolerance tests. The combined disorders of hypertriglyceridemia and hyperinsulinemia plus glucose intolerance--insulin resistance--were most commonly found among the relatives, which were often accompanied by an impaired liver function. Some relatives showed hyperinsulinemia without hypertriglyceridemia. Obesity was frequent, but its incidence was similar to the controls. Thus, the observed form of familial hypertriglyceridemia was apparently coupled with insulin resistance; and hyperinsulinemia, or insulin resistance by itself, might be a basic genetical trait in this form of lipid disorder.

Adolescent↗
PubMed1981

Diabetic hypertriglyceridemia: evidence for three clinical syndromes.

Based on studies of both man and rat, it is proposed that at least three distinct syndromes of hypertriglyceridemia occur as the result of abnormalities of carbohydrate metabolism. We believe that these syndromes are the predictable results of the changes in plasma insulin and/or free fatty acid (FFA) concentration that occur in patients with impaired glucose tolerance (IGT), non-insulin-dependent diabetes mellitus (NIDDM), and insulin-dependent diabetes mellitus (IDDM). In patients with IGT the basic defect is postulated to be loss of normal insulin sensitivity, leading to compensatory hyperinsulinism, increased very low density lipoprotein (VLDL)-triglyceride (TG) secretion, and hypertriglyceridemia. In contrast, patients with NIDDM have ambient insulin concentrations that are "normal" in absolute terms, and in these subjects we believe that the elevated circulating FFA concentrations increase hepatic VLDL-TG secretion, which, in turn, is responsible for the hypertriglyceridemia. However, elevated FFA levels do not stimulate hepatic VLDL-TG secretion in insulin-deficient patients with IDDM, presumably because the livers of such individuals are not capable of responding to the increased FFA flux. In these subjects, the development of hypertriglyceridemia, when it does occur, is secondary to the existence of a profound defect in the removal of VLDL-TG from plasma. These generalizations are consistent with results in both man and rat, and provide models that account for the development of hypertriglyceridemia in the three major clinical categories of abnormal carbohydrate metabolism.

Animals↗
PubMedDate not supplied

Parenteral feeding in a patient with hypertriglyceridemia and increased liver enzyme levels.

OBJECTIVE: To discuss nutritional support in a patient with hypertriglyceridemia and liver dysfunction. METHODS: We describe the hospital course of a critically ill patient with hepatic dysfunction and hypertriglyceridemia who required nutritional support, and we provide an overview of lipid metabolism. RESULTS: A 27-year-old man with hepatic dysfunction and hypertriglyceridemia, who had undergone kidney transplantation 4 months previously, was admitted to the intensive-care unit with upper gastrointestinal bleeding. He was unable to tolerate enteral feeding, and central parenteral nutrition was initiated. Calories from dextrose and fat were limited because of the presence of increased liver enzyme levels and hypertriglyceridemia. A modified regimen of parenteral nutrition was developed for the patient. The short-term reduction of total calories to 75% of the predicted need is safe. CONCLUSION: Nutritional support in patients with liver dysfunction and hypertriglyceridemia is complicated and may require temporary underfeeding because of the need to limit fat and dextrose intake.

Journal Article↗
PubMed1995

Abnormal bile acid absorption in familial hypertriglyceridemia.

To better define the abnormality of bile acid metabolism associated with hypertriglyceridemia, we measured bile acid kinetics and absorption as well as preferential use of newly synthesized cholesterol for bile acid synthesis in eleven controls and ten subjects with hypertriglyceridemia, six of whom could be classified as having familial hypertriglyceridemia (FHT). Fractional turnover rates of cholic acid and chenodeoxycholic acid were both significantly elevated in hypertriglyceridemic subjects to nearly twice the rates in controls. Bile acid synthesis was also significantly higher in hypertriglyceridemic subjects while bile acid pools were either unchanged or somewhat reduced. Consistent with these kinetics, bile acid absorption was significantly lower in hypertriglyceridemic subjects than in controls. Overall only 10-12% of bile acid was derived from newly synthesized cholesterol, and hypertriglyceridemic subjects did not differ from controls. Because hypertriglyceridemia should not alter bile acid absorption, these results are consistent with the previously suggested possibility (B. Angelin, K. S. Hershon, and J. D. Brunzell, 1987. Proc. Natl. Acad. Sci. USA. 84: 5434-5438) that impaired bile acid absorption may be a primary defect in some patients with hypertriglyceridemia.

Absorption↗
PubMed1993

The use of gemfibrozil in a patient with chronic myelogenous leukemia to successfully manage retinoid-induced hypertriglyceridemia.

Systemic retinoids are used in the management of chronic cutaneous conditions and life-threatening dermatoses. Unfortunately, drug-induced hypertriglyceridemia may necessitate either dose reduction or discontinuation of therapy. The purpose of this article is to describe the successful management of isotretinoin-induced hypertriglyceridemia with gemfibrozil in a leukemia patient. Sequential serum chemistries were performed prior to, during, and following treatment with a systemic retinoid and a lipid-regulating agent. A prompt and sustained normalization of fasting triglycerides occurred following the initiation of gemfibrozil in a patient with isotretinoin-induced hypertriglyceridemia. When retinoids are being used in the management of serious conditions, the initiation of therapy with gemfibrozil to reduce the elevated triglycerides may be appropriate in those patients with retinoid-induced hypertriglyceridemia.

Acne Vulgaris↗
PubMed2000

Dietary fiber prevents carbohydrate-induced hypertriglyceridemia.

Plant foods rich in carbohydrate and dietary fiber have many health benefits. One concern often expressed about higher carbohydrate, lower fat diets is that they may increase fasting serum triglycerides. Recently the importance of hypertriglyceridemia as an independent risk factor for coronary heart disease has been reaffirmed. For 40 years, clinicians have noted "carbohydrate-induced hypertriglyceridemia" when persons were fed high-carbohydrate, low-fiber diets. The role of fiber in protecting from carbohydrate-induced hypertriglyceridemia has not been discussed by many reviewers. Systematic review of the literature documents that high fiber intakes clearly protect from carbohydrate-induced hypertriglyceridemia. These are reviewed. Thus, recent and earlier research indicates that use of a higher carbohydrate, higher fiber diet compared with a lower carbohydrate, higher fat diet is associated with a small reduction in fasting serum triglyceride values.

Coronary Disease↗
PubMed1989

Hypertriglyceridemia in the acquired immunodeficiency syndrome.

PURPOSE: A relationship between the induction of hypertriglyceridemia by cytokines and the cachexia seen in chronic infection has been proposed by other investigators. Since patients with the acquired immunodeficiency syndrome (AIDS) often experience progressive tissue wasting, we decided to examine serum lipid levels and body cell mass in patients with AIDS. PATIENTS AND METHODS: Serum lipid levels and body cell mass were measured in 32 patients with the acquired immunodeficiency syndrome (AIDS), eight asymptomatic subjects who were anti-human immunodeficiency virus (HIV) antibody positive, and 17 heterosexual and homosexual control subjects who did not have antibodies to HIV. RESULTS: Mean triglyceride concentrations and the prevalence of hypertriglyceridemia (50 percent) were significantly increased in patients with AIDS compared with control subjects (p less than 0.002 and p less than 0.005, respectively), whereas the mean triglyceride levels of HIV-positive subjects were intermediate. There were no differences in cholesterol levels among the three groups. Using total body potassium adjusted for height and age (KHT) as a measure of body cell mass, 16 of 32 patients with AIDS but none of the HIV-positive or control subjects had significant depletion of body cell mass. There was no direct relationship between triglyceride levels and KHT among AIDS or HIV-positive subjects. In patients with AIDS, mean triglyceride levels and the prevalence of hypertriglyceridemia were similar in the presence and absence of wasting. CONCLUSION: Hypertriglyceridemia is a common finding in AIDS and is independent of the degree of wasting.

Acquired Immunodeficiency Syndrome↗