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PubMed1989

[Acute pancreatitis and hypertriglyceridemia].

The etiology and pathogenesis of acute pancreatitis are unknown in the majority of patients. However, it is well known that there are several relevant clinical conditions associated to acute pancreatitis such as, gallstone disease, alcoholism and hypertriglyceridemia. The possible pathogenic relationships between acute pancreatitis and hypertriglyceridemia are discussed in this article. It has recently been shown that a significant proportion of patients with a history of acute pancreatitis have an abnormal clearance of exogenous triglycerides, indicating the presence of a preexistent metabolic abnormality in this population. This observation supports the hypothesis of a possible genetic heterogeneity related to either an abnormal apoprotein profile of chylomicrons, or hepatic receptor mechanism of chylomicron remnants uptake in the liver. If this hypothesis proves to be correct, then a genetic marker may be available to identify the subjects at high risk for acute pancreatitis.

Acute Disease↗
PubMed1989

[Acute pancreatitis and hypertriglyceridemia].

An association between acute pancreatitis and hypertriglyceridemia has long been recognized. The frequency of this association may be as high as 25 per cent. Whether the lipid abnormalities are secondary to acute pancreatitis and therefore temporary or whether they are primary and possibly etiologically involved is unsettled. Most experimental and clinical evidences suggest that hypertriglyceridemia precedes and apparently cause the development of pancreatitis. The mechanism of injury may be mediated through free fatty acids released from the triglycerides. It has recently been identified a group of normotriglyceridemic patients with a previous attack of acute pancreatitis, at least 6 months earlier, who had an impaired clearance of serum triglycerides after an oral fat tolerance test. The clearance of ingested triglycerides was significantly impaired as compared with a control group, irrespective of the presence of diabetes, alcohol consumption or biliary lithiasis. The authors suggested that a triglyceride tolerance test is the only way to detect those patients in whom future attacks of pancreatitis may be precipitated by a diet rich in fat or an alcoholic debauch. In a further study the authors suggested that the abnormal oral fat tolerance test in these patients with previous acute pancreatitis and normotriglyceridemia is secondary to an impaired chylomicron remnants clearance. These findings strongly suggest a relatively common and preexistent defect in lipid metabolism which may be important in the pathogenesis of the disease.

Acute Disease↗
PubMed1995

Lipoprotein lipase gene polymorphisms: associations with hypertriglyceridemia and body mass index in obese people.

OBJECTIVE: To compare body mass index (BMI), lipid, lipoprotein and apolipoprotein concentrations according to the Hind III and Pvu II restriction polymorphisms of the LPL gene in obese subjects. DESIGN: Cross sectional study of anthropometric and lipid variables in relation to genetic factors. SETTING: Nutrition Outpatient Clinic of Bichat Hospital in Paris, France. SUBJECTS: 236 unrelated patients (162 women and 74 men) were selected on the basis of 120% of ideal body weight. MAIN OUTCOME MEASURES: Anthropometry (body mass index, waist to hip ratio), blood lipids and lipoproteins, determination of LPL Hind III and Pvu II genotypes. RESULTS: Digestion with Hind III generated two alleles, H1 (absence of cutting site) and H2 (presence of cutting site), with frequencies of 0.30 and 0.70 respectively. Digestion with Pvu II generated two alleles P1 and P2 with frequencies of 0.49 and 0.51 respectively. The Hind III polymorphism was significantly associated with body mass index (BMI) (P < 0.05). The H2H2 genotype was associated with hypertriglyceridemia: 68% of the hypertriglyceridemic subjects have the H2H2 genotype vs 43% of the normotriglyceridemic group (P < 0.05). Plasma triglyceride levels varied significantly among the Hind III genotypes, H2H2 genotype having the highest total and VLDL-triglyceride levels; the Hind III polymorphism also showed a significant association with HDL2-cholesterol. These associations were only seen in women and were not explained by the variations in BMI and age. No significant associations were found between lipid traits and Pvu II genotype. CONCLUSION: These results suggest that genetic variation in the LPL gene in obese subjects is associated with hypertriglyceridemia and possibly with a predisposition to obesity.

Alleles↗
PubMed1994

[Comparative study of the influence of fish oil and gemfibrozil on levels of serum lipoprotein in endogenous hypertriglyceridemia].

Hypolipemic action of fish oil and gemfibrozil was compared. The study was performed in 12 men with endogenous hypertriglyceridemia. Subjects received fish oil 12 grams daily (3.6 g of eicosapentaenoic and docosahexaenoic fatty acids) for 3 weeks, and then, after an interval of at least 6 weeks, gemfibrozil in the dose of 900 mg daily. Results after gemfibrozil were compared with those after fish oil. Fish oil was shown to be less effective than gemfibrozil in decreasing concentrations of serum triglycerides and triglycerides and cholesterol in VLDL. However, the difference did not reach the level of statistical significance. The agents differed significantly in their influence on the LDL fraction. Fish oil slightly increased and gemfibrozil significantly decreased LDL-chol level. LDL-apoB increased after fish oil, but did not change after gemfibrozil. It may be concluded that fish oils, although effective in decreasing concentrations of serum triglycerides and lipid components of the VLDL fraction, are not alternative for gemfibrozil in monotherapy of endogenous hypertriglyceridemia.

Adult↗
PubMed1993

Endotoxin-induced hypertriglyceridemia is mediated by suppression of lipoprotein lipase at a post-transcriptional level.

Previous studies have demonstrated that endotoxin/lipopolysaccharide treatment causes a decrease in adipose tissue and heart lipoprotein lipase (LPL) activities in rats, producing hypertriglyceridemia in these animals. To examine the mechanisms for this effect of endotoxin, we studied the effects of endotoxin administration on LPL mRNA, and LPL synthetic rates and activity in rat adipose tissue and heart. Endotoxin treatment (i.p., 3 mg/100 g body weight or higher doses) produced a pronounced increase in serum triglycerides associated with a 65% decrease in adipose tissue and heart LPL activities within 7 h. Fast protein liquid chromatography (FPLC), used to separate lipoproteins in rat serum, showed that the increase in triglyceride was all in the very low density lipoprotein fraction which was accompanied by a concomitant decrease in high density lipoprotein. In contrast, there was no change in adipose tissue or heart LPL mRNA up to 24 h after treatment and no change in adipose tissue LPL synthetic rate, as measured by L-[35S]methionine incorporation and immunoprecipitation. Plasma insulin levels remained unchanged. The results indicate that endotoxin-induced hypertriglyceridemia in rats can be attributed to an impaired triglyceride clearance associated with a decrease of LPL activity mediated at a post-transcriptional level.

Adipose Tissue↗
PubMed1996

Reversible parotid enlargement and pseudo-Sjögren's syndrome secondary to hypertriglyceridemia.

We describe 2 patients with a Sjögren-like syndrome apparently secondary to hypertriglyceridemia. Both had bilateral parotitis in addition to musculoskeletal and sicca symptoms. Parotid gland histology revealed fatty infiltration with no inflammation. Therapy with dietary modification and triglyceride lowering drugs resulted in resolution of symptoms and parotid swelling in one patient. In the 2nd patient, hypertriglyceridemia was resistant to triglyceride lowering drugs, and parotid symptoms and swelling continued unabated. Our findings suggest aggressive treatment of hyperlipidemia in pseudo-Sjögren's syndrome may result in amelioration of musculoskeletal and parotid symptoms.

Adult↗
PubMed1996

[Hypertriglyceridemia following treatment with interferon alpha in essential thrombocythemia].

A case of essential thrombocytemia treated with alpha interferon is reported, with hematological remission, but as a side effect hypertriglyceridemia is relevant. It was normalized when alpha interferon was stopped. This is the first case of essential thrombocythemia in Venezuela treated with biological modifiers, with hematological remission, but with hypertriglyceridemia as side effect.

Adult↗
PubMed1996

[Severe hypertriglyceridemia in pregnancy. A clinical case report].

Cholesterol (TC) and triglyceride (TG) plasma levels physiologically increase during pregnancy. The lipid increment is respectively 23%-53% above pregravidic level for TC and two-three fold the pre-pregnancy level for TG. If the TC and TG are higher than normal values in pregnancy the patient must be carefully monitored. Acute pancreatitis is the main consequence of hyperlipidemia and it can occur either during pregnancy, in the third trimester, or in the puerperium. Mortality is high both for the mother (21%) and the fetus (20%). The authors report a case of 37-year-old pregnant woman at 35 week gestation with hypercholesterolemia (TC = 425 mg/dl) and severe hypertriglyceridemia (TG = 3315 mg/dl). The patient was admitted to the hospital for treatment with an appropriate diet and drug lowering lipid levels (gemfibrozil). The baby was delivered by cesarean section at week 36. The neonatal weight at birth was 2670 g and the Apgar score was 9 at the first minute. After delivery the maternal triglyceride levels showed a remarkable reduction. According to a review of the literature, severe hypertriglyceridemia in pregnancy should be treated with a careful restriction of calories and fat; for preventing acute pancreatitis hospitalization for intravenous fluid therapy and plasma exchange must be required.

Acute Disease↗
PubMedDate not supplied

Safety and efficacy of Omacor in severe hypertriglyceridemia.

BACKGROUND: Severe hypertriglyceridemia is a risk factor for acute pancreatitis, therefore decreasing serum triglyceride concentrations is an important component of risk management. Omega-3 fatty acids are well known hypotriglyceridemic agents, but their efficacy in severe forms of the disorder is not well documented. Our objective was to examine the effects of Omacor, a drug composed of 85% omega-3 fatty acid ethyl esters. METHODS: Forty-two patients with triglyceride concentrations between 5.65 and 22.60 mmol/l (500 and 2000 mg/dl) were studied in a prospective, double-blind, placebo-controlled trial of Omacor (4 g/day for 4 months). RESULTS: Compared with baseline values, Omacor significantly reduced mean triglyceride concentrations by 45% (P<0.00001), cholesterol by 15% (P< 0.001), very-low-density lipoprotein cholesterol by 32% (P< 0.0001) and cholesterol:high density lipoprotein (HDL) cholesterol ratio by 20% (P=0.0013), and increased HDL cholesterol by 13% (P=0.014) and low-density lipoprotein cholesterol by 31% (P=0.0014). The placebo had no effect on these parameters. Omacor was well tolerated and no patient discontinued medication because of side effects. CONCLUSIONS: Four capsules of Omacor per day markedly decreased triglyceride concentrations in patients with severe hypertriglyceridemia. The availability of a potent and safe omega-3 fatty acid preparation for this patient population should diminish the risk for acute pancreatitis, and may also reduce the long-term risk for cardiovascular disease.

Cholesterol↗
PubMed1983

Primary hypertriglyceridemia in childhood.

Five of six children with severe familial primary hypertriglyceridemia in the first three to five years of life had what we believe is a new clinical feature, intermittent swelling of the limbs and scrotum. This was associated with higher levels of plasma triglyceride (greater than 2,000 mg/dL) and, in some instances, venous stasis of the affected part. All children had severe elevation of plasma chylomicron levels and mild elevation of very low-density lipoprotein levels. Four of the subjects were siblings who demonstrated heterogeneity in plasma lipase activities after heparin sodium administration. The clinical features and the lipase heterogeneities suggest that these patients possibly have an unusual variant of primary hypertriglyceridemia.

Child, Preschool↗
PubMed1981

Chenodeoxycholic acid and ursodeoxycholic acid effects in endogenous hypertriglyceridemias. A controlled double-blind trial.

A double-blind controlled trial was carried out to compare the effects of chenodeoxycholic acid (CDCA), ursodeoxycholic acid (UDCA), and placebo on cholesterol and triglyceride levels in patients with endogenous hypertriglyceridemias. The dose of both bile acids was four 150-mg capsules day. Total serum cholesterol levels did not show appreciable changes with any of the treatments. HDL cholesterol was significantly increased after CDCA but not after UDCA or placebo. CDCA feeding was associated with a significant decrease in serum triglyceride levels, whereas the other treatments failed to show an effect. It is concluded that UDCA does not affect serum lipid levels, whereas CDCA lowers serum triglycerides and may be useful in the treatment of endogenous hypertriglyceridemia.

Adult↗
PubMed1993

Effect of gemfibrozil on fatty acids in lipid fractions of plasma from patients with hypertriglyceridemia.

The fatty acid composition of plasma triglycerides, phospholipids, and cholesterol esters have been studied during gemfibrozil (G)-induced lipid-lowering treatment in six patients with hypertriglyceridemia. Gemfibrozil caused significant plasma triglyceride reductions from 776 +/- 573 to 226 +/- 82 mg/dL (P < .001). Gemfibrozil therapy also caused significant changes in the plasma lipid fatty acid composition, mainly by increasing palmitoleic acid (16:1) in triglycerides (2.1-5.6%) and cholesterol esters (2.2-3.7%), concomitant with the significant decrease in the content of the linoleic acid (18:2) in phospholipids (20.1-16.0%) and triglycerides (18.0-15.2%). The ratio of unsaturated fatty acids (20:3 + 20:4/18:2) was increased in the phospholipid fraction. These findings support a G effect on the desaturation of fatty acids in patients with hypertriglyceridemia. Because fatty acid composition was significantly altered by G, those biologic systems dependent on the pattern of fatty acids may be modified in clinical important ways.

Fatty Acids↗
PubMed1991

HDL metabolism in HDL deficiency associated with familial hypertriglyceridemia: effect of treatment with gemfibrozil.

Plasma high density lipoproteins (HDL) and their major proteins--apolipoprotein (apo) AI and apo AII--are subnormal in most patients with familial hypertriglyceridemia. However, the pathophysiology of low plasma apo AI and apo AII is unclear. The kinetic parameters (turnover) of HDL apo AI and apo AII were studied in six lean patients with primary HDL deficiency associated with familial hypertriglyceridemia and normolipidemic healthy controls. The radioactivity decay curve of 125I labelled HDL was used for assessment of kinetics. Mean plasma apo AI and apo AII were significantly lower (p less than 0.001) in patients than normals (70.4 +/- 2.7 v 106.9 +/- 7.0; 24.2 +/- 1.6 v 39.2 +/- 0.9 mg/dl, respectively). The mean fractional catabolic rates (FCR) obtained from plasma 125I-HDL, apo AI, apo AII radioactivity decay curves and by Berson and Yalow's method (urine/plasma radioactivity ratios) were significantly greater (p less than 0.05) in patients than in controls (0.387 v 0.299; 0.391 v 0.309; 0.361 v 0.275; 0.272 v 0.207/d; respectively). The synthetic rates (SR of apo AI and apo AII were significantly lower in patients than in controls (11.12 v 14.17 mg/kg body weight/d. p less than 0.05; 3.53 v 4.68 mg/kg body weight/d, p less than 0.05, respectively). Each patient was also investigated for HDL and triglyceride metabolism immediately before and after 8 wk of gemfibrozil (1200 mg/d) treatment. Gemfibrozil significantly increased plasma HDL cholesterol, apolipoprotein (apo) AI, and apo AII by 36%, 29%, and 38% from baseline, respectively. Plasma TG decreased by 54%. Gemfibrozil increased synthetic rates of apo AI and apo AII by 27% and 34%, respectively, without changing the FCR.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗
PubMed1991

C-13 NMR spectroscopy of plasma reduces interference of hypertriglyceridemia in the H-1 NMR detection of malignancy. Application in patients with breast lesions.

We have previously described the application of water-suppressed proton nuclear magnetic resonance (H-1 NMR) spectroscopy of plasma for detection of malignancy. Subsequently, hypertriglyceridemia has been identified as a source of false positive results. We now describe a confirmatory, adjunctive technique--analysis of the carbon-13 (C-13) NMR spectrum of plasma--which also identifies the presence of malignancy but is not sensitive to the plasma triglyceride level. Blinded plasma samples from 480 normal donors and 208 patients scheduled for breast biopsy were analyzed by water-suppressed H-1 and C-13 NMR spectroscopy. Triglyceride levels were also measured. Among the normal donors, there were 38 individuals with hypertriglyceridemia of whom 18 had results consistent with malignancy by H-1 NMR spectroscopy. However, the C-13 technique reduced the apparent H-1 false positive rate from 7.0% to 0.6%. Similarly, in the breast biopsy cohort, C-13 reduced the false positive rate from 2.8% to 0.9%. Furthermore, the accuracy of the combined H-1/C-13 test in this blinded study was greater than 96% in 208 patients studied.

Adult↗
PubMed1978

The role of dietary fat and hepatic triglyceride secretion in cancer-induced hypertriglyceridemia.

Growth of Ehrlich ascites carcinoma induces hyperlipemia in mice. In the present study using male Swiss-Webster mice, we examined whether the usual elevations of plasma triglyceride levels in cancerous mice would occur in the absence of dietary fat. Hypertiglyceridemia developed at a similar rate and to a comparable degree in tumerous mice eating a fat-free (58% glucose) diet and in those fed Purina chow. Maximal hyperlipidemia was observed on day 6 or day 8 in tumorous mice fed either diet. To determine whether the endogenous cancer-induced hyperlipidemia was due to hypersecretion of triglycerides by the liver, triglyceride secretion rates were studied 0, 2, 4, 6, 8, 10, and 12 days after tumor inoculation using Triton WR-1339. The secretory rates did not increase prior to or during the development of hypertriglyceridemia in tumorous mice and were not significantly different from those of control mice. On days 10 and 12, triglyceride secretion actually decreased in tumorous mice. Other possible causes for hypertriglyceridemia are discussed in light of the present findings of undetectable differences in triglyceride secretion rates accompanying growth of Ehrlich ascites carcinoma in mice.

Animals↗
PubMedDate not supplied

Glycosylated hemoglobin in endogenous hypertriglyceridemia.

Fifty out-patients with endogenous hypertriglyceridemia were submitted to glycosylated hemoglobin (GHb) and glucose tolerance assessment. Fifteen had normal glucose tolerance (NGT), 15 had impaired glucose tolerance (IGT) and 20 had non-insulin-dependent diabetes mellitus (NIDDM). GHb was 6.3% in NGT, 7.3% in IGT and 8.11% in NIDDM and was significantly correlated to fasting and post-prandial plasma glucose (p less than 0.001) in NIDDM group and to peak, area (p less than 0.001) and 2-h plasma glucose levels (p less than 0.05) of OGTT in the NGT and IGT groups. Out of the 15 IGT subjects only 6 had GHb levels above the control range, while 9 had normal GHb values. These data show that also in hyperlipemic subjects GHb values are related to glucose tolerance, and suggest that GHb evaluation alone is not sufficient for the diagnosis of impaired glucose tolerance. In order to evaluate whether plasma turbidity can affect GHb dosage, GHb was evaluated in 10 hyperlipemic subjects with various degrees of hypertriglyceridemia both in the presence (whole blood hemolysate) and absence (isotonic saline hemolysate) of plasma triglycerides. The results show that, with our method, plasma turbidity does not affect GHb evaluation.

Adult↗
PubMedDate not supplied

Metabolic effects of glucagon in endogenous hypertriglyceridemia.

The metabolic effects of glucagon, administered i.v. in doses of 1 microgram/kg, were evaluated in two groups of patients with endogenous hypertriglyceridemia (Types IV and V according to Fredrickson) with normal and reduced glucose tolerance and in a control group. Glucagon had a lipolytic effect, evaluated as the plasma increase of free fatty acids (FFA) during the first 20 min in normal subjects, but not in the two hyperlipemic groups. A negative correlation was observed between fasting IRI level and FFA mobilization. The ketogenic and hypotriglyceridemic effects of glucagon were demonstrated in normal and hyperlipemic groups. It would seem, therefore, that at the pharmacological doses injected, there is no resistance to the hypotriglyceridemic effect of glucagon in endogenous hypertriglyceridemia.

Adult↗
PubMed1991

Insulin resistance, hyperinsulinemia, and hypertriglyceridemia in the etiology and clinical course of hypertension.

Patients with untreated hypertension have been shown to be resistant to insulin-stimulated glucose uptake and are more hyperinsulinemic and hypertriglyceridemic than matched groups of patients with normal blood pressure. In addition, insulin resistance, hyperinsulinemia, and hypertriglyceridemia have been demonstrated in spontaneous hypertensive rats and in Sprague-Dawley rats fed a fructose-enriched diet. The defect in insulin-stimulated glucose uptake in these experimental models can also be shown at the cellular level. Experimental interventions that prevent insulin resistance or hyperinsulinemia from developing in fructose-fed rats also greatly attenuate the increase in blood pressure. Since endogenous hyperinsulinemia and hypertriglyceridemia have been identified as factors that increase the risk of coronary artery disease (CAD), it is likely that they contribute to the increased prevalence of CAD in hypertensive patients. Antihypertensive treatment may have exacerbated these metabolic abnormalities, which could help explain why it has been difficult to show that lowering blood pressure decreases the risk of CAD. These observations raise the possibility that abnormalities of carbohydrate and lipoprotein metabolism may play a role in both the etiology and clinical course of hypertension.

Animals↗