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PubMed2005

Beneficial effects of fenofibrate to improve endothelial dysfunction and raise adiponectin levels in patients with primary hypertriglyceridemia.

OBJECTIVE: Improvement in endothelial function is predicted to improve insulin sensitivity, and this may be one mechanism by which fenofibrate decreases the incidence of coronary heart disease. We hypothesize fenofibrate improves endothelial function by enhancing insulin sensitivity. RESEARCH DESIGN AND METHODS: We administered placebo or fenofibrate 200 mg daily for 8 weeks to 46 patients with primary hypertriglyceridemia (24 had metabolic syndrome). This study was randomized, double blind, placebo controlled, and crossover in design. RESULTS: Compared with placebo, fenofibrate decreased total cholesterol, non-HDL cholesterol, apolipoprotein B, and triglycerides and increased HDL cholesterol and apolipoprotein A-I (all P < 0.001) while tending to decrease LDL cholesterol (P = 0.069). Fenofibrate significantly improved percent flow-mediated dilator response to hyperemia by 48 +/- 5% (P < 0.001) and lowered plasma levels of high-sensitivity C-reactive protein (hsCRP) relative to baseline measurements from 0.80 to 0.70 mg/l (P = 0.001) and fibrinogen levels by 16 +/- 3% (P < 0.001). Compared with placebo, fenofibrate therapy significantly increased plasma levels of adiponectin by 14 +/- 5% (P = 0.008) and increased insulin sensitivity (assessed by quantitative insulin sensitivity check index [QUICKI]) by 6 +/- 2% (P = 0.048). There were significant correlations between percent changes in adiponectin levels and percent changes in flow-mediated dilation (r = 0.401, P = 0.006), hsCRP (r = -0.443, P = 0.002), or QUICKI (r = 0.292, P = 0.049). Multivariate regression analysis showed that only changes in adiponectin levels persisted as an independent predictor of changes in flow-mediated dilation (r = 0.504, P = 0.013). Overall, we observed similar results in 24 patients with metabolic syndrome. CONCLUSIONS: Fenofibrate therapy significantly improved percent flow-mediated dilator response to hyperemia, reduced inflammation marker levels, increased adiponectin levels, and improved insulin sensitivity in hypertriglyceridemic or metabolic syndrome patients.

Adiponectin↗
PubMed2003

Hypertriglyceridemia associated with decreased post-heparin plasma hepatic triglyceride lipase activity in hypoxic rats.

Exposure of sated rats to 45% N2 in air for 5h increased serum triglyceride levels by 212% over the levels in normoxic rats. This increase in triglyceride levels was accompanied by a decrease in plasma triglyceride hydrolase activity after intravenous injection of heparin. Further fractionation of the activity by inhibition of lipoprotein lipase indicated that the low triglyceride hydrolase activity is mainly due to a reduction in hepatic triglyceride lipase, which is inversely correlated with the serum triglyceride level. The hypoxic exposure decreased the arterial blood [acetoacetate]/[beta-hydroxybutyrate] ratio in the sated rats, which is believed to reflect the oxidation-reduction state in hepatic mitochondria, but did not affect the level of serum enzymes indicative of tissue damage. On the other hand, triglyceride levels did not change during hypoxic exposure in fasted rats. Thus, hypertriglyceridemia in sated rats following exposure to hypoxia may result from impaired removal of circulating triglycerides by hepatic triglyceride lipase located in the sinusoidal surface of the liver.

Animals↗
PubMed1996

Hypertriglyceridemia and fatty liver of fasting rats after administration of emeriamine.

The effect of emeriamine, a potent inhibitor of the entry of fatty acids into mitochondria on lipid metabolism, was examined. Emeriamine (10 mg/kg body weight) was orally administered to rats under the two different physiological conditions of a 2-day fast or refeeding with a high-carbohydrate diet after a 2-day fast. When rats were refed with a high-carbohydrate diet, serum and hepatic ketone bodies and the levels of free fatty acids decreased, and triglycerides significantly increased compared with fasting rats. However, no significant effect of emeriamine on serum and hepatic lipids was observed between two refeeding groups with or without emeriamine. Conversely, when emeriamine was administered to fasting rats, the levels of serum and hepatic triglycerides increased about 11- and 5-fold, respectively. However, the increased level of hepatic triglycerides was not accompanied by the activities of fatty acid synthetase and NADPH-generating enzymes. The analysis of serum lipoprotein revealed that very low-density lipoprotein consisted of triglyceride-rich particles and there were less apolipoproteins in the fasting rat given emeriamine. We also determined the 120-kDA protein content, which was probably dependent on lipogenesis. The level of 120-kDa protein was greatly increased with or without the administration of emeriamine after refeeding with a high-carbohydrate diet, but the concentration of 120-kDa protein was slight in the fasting rat with emeriamine. These results suggest that specific inhibition of fatty acid oxidation by emeriamine diverted the exogenous fatty acid to the esterification pathway, and induced fatty liver and hypertriglyceridemia under fasting conditions.

Animals↗
PubMedDate not supplied

Tuberous xanthomas associated with olanzapine therapy and hypertriglyceridemia in the setting of a rare apolipoprotein E mutation.

OBJECTIVE: To describe a patient with tuberous xanthomas and high levels of cholesterol and triglycerides, who was found to have type III hyperlipoproteinemia (HLP) and a rare apolipoprotein E (apoE) mutation. METHODS: We present a case report with extensive clinical, laboratory, and genetic documentation. RESULTS: A 33-year-old African American man presented for evaluation of hypertriglyceridemia. His medical history was remarkable for schizophrenia necessitating ongoing olanzapine therapy for the past 6 years. A few months after olanzapine treatment was begun, he noted the development of nontender, firm, papular skin lesions on his elbows and knees. His family history was negative for lipid disorders or premature vascular disease. Physical examination revealed the presence of prominent tuberous xanthomas on both elbows and knees. Results of a lipid panel demonstrated a total cholesterol level of 374 mg/dL (9.7 mmol/L) and triglycerides of 828 mg/dL (9.3 mmol/L). A work-up for causes of secondary hyper-triglyceridemia was negative. Results of apoE genotyping by a commercial laboratory showed the E3/E3 genotype, based on gene sequencing at codons 112 and 158. Because the skin lesions were typical for type III HLP, his entire apoE gene was sequenced. This analysis revealed an apoE2/E2 (arginine 145 to cysteine) mutation, previously reported to be a rare cause of type III HLP in 5 patients of African descent. Triglyceride-lowering therapy with gem-fibrozil was initiated, in addition to lifestyle modification. At follow-up several months later, total cholesterol was 276 mg/dL (7.14 mmol/L) and triglycerides were 479 mg/dL (5.41 mmol/L). CONCLUSION: We speculate that olanzapine therapy, with its known metabolic side effects, exacerbated this patient's underlying lipoprotein metabolic abnormality. To our knowledge, this is the first report of an association between olanzapine therapy and tuberous xanthomas and the sixth report of this rare apoE2/E2 (arginine 145 to cysteine) mutation in the literature.

Adult↗
PubMed1999

Postprandial hypertriglyceridemia and insulin resistance in normoglycemic first-degree relatives of patients with type 2 diabetes.

BACKGROUND: Impaired ability to eliminate lipids in the postprandial state is an atherogenic trait associated with insulin resistance. OBJECTIVE: To assess insulin sensitivity and postprandial triglyceride metabolism in prediabetic persons. DESIGN: Cross-sectional study. SETTING: Sahlgrenska University Hospital, Göteborg, Sweden. PARTICIPANTS: 13 healthy, normotriglyceridemic men with two first-degree relatives with type 2 diabetes and 13 carefully matched controls without known diabetes heredity. MEASUREMENTS: Oral glucose tolerance test, insulin sensitivity (euglycemic clamp technique), and fasting and postprandial triglyceride levels after a mixed meal. RESULTS: Relatives of persons with type 2 diabetes were insulin resistant but had normal glucose tolerance. They exhibited postprandial hypertriglyceridemia; the 6-hour triglyceride incremental area under the curve was 50% higher than that of the control group (P = 0.037). CONCLUSIONS: These healthy male first-degree relatives of patients with type 2 diabetes are insulin resistant and exhibit postprandial lipid intolerance despite having normal fasting triglyceride levels. These characteristics, which occur in the absence of glucose intolerance, are associated with an increased risk for macroangiopathy.

Adult↗
PubMedDate not supplied

[Hypertriglyceridemia during active intercurrent infections in HIV-infected patients].

BACKGROUND: Many reports have confirmed that hypertriglyceridemia (HTG) is more common in HIV-infected patients than in the general population, but the relationship between HTG and clinical conditions have not been well established. This work analyzes the relationships between CD4+ cell count, HTG and the presence of active intercurrent infections in patients hospitalized for HIV infection. METHODS: Blood specimens from hospitalized HIV-infected patients and healthy controls without HIV infection were analyzed. Clinical conditions when the specimens were collected were recorded. RESULTS: The average level of serum triglycerides from 89 HIV-infected patients was significantly higher than the 29 healthy controls (1.57 +/- 0.09 vs 0.78 +/- 0.08 mmol/l respectively) (p < 0.001). In the study group, HTG was detected in 25 patients (27%). Twenty-six patients had intercurrent infections and 50 were asymptomatic. Clinical conditions of the remaining 13 were not available. HTG was detected in 18 out of 26 patients having intercurrent infections (68%), and in 4 out of the 50 patients without active infections (8%) (p < 0.000000417). CONCLUSIONS: HTG was more frequent in HIV-infected patients than in healthy controls, and it was significantly associated with the presence of intercurrent infections. This has important diagnostic implications, because the presence of HTG might be considered an unspecific marker for intercurrent infections in HIV patients.

AIDS-Related Opportunistic Infections↗
PubMed1999

[Hypertriglyceridemias].

Triglyceride atherogenicity is still a matter of controversy for reasons related to their biological and epidemiological characteristics. The authors discuss and review several of these problems, as well as the metabolic relationship of triglycerides and HDL-cholesterol, data indicating a strong influence of triglycerides on cardiovascular risk, mechanisms mediating the pathogenicity of triglycerides, and some questions of drug treatment of hypertriglyceridemias.

Arteriosclerosis↗
PubMed1999

Post-prandial effects of gemfibrozil vs simvastatin in hypercholesterolemic subjects with borderline hypertriglyceridemia.

BACKGROUND AND AIM: Impaired triglyceride-rich lipoprotein metabolism is most probably related to an enhanced cardiovascular risk, and may be associated with a pro-coagulant state. A double-blind, randomized study was undertaken to evaluate two widely utilized hypolipidemic drugs in the post-prandial phase and their impact on lipid, coagulation and fibrinolytic parameters. METHODS AND RESULTS: Thirty middle-aged men selected according to their low density lipoprotein-cholesterol (LDL-C) > or = 160 and < or = 240 mg/dl and borderline hypertriglyceridemia (110-220 mg/dl) after at least one month of a lipid-lowering diet received gemfibrozil (600 mg bid) or simvastatin (20 mg qd) and the corresponding placebo. On enrollment and after 2 months of drug treatment, they were tested with a standard oral fat load (OFL) (35 g fat/m2 body surface). On both occasions plasma total-cholesterol, LDL-C, HDL-C, triglycerides, lipoprotein[a] (Lp[a]), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), antithrombin-III (AT-III), plasminogen and fibrinogen were determined just before the meal (t0) and at times 2 hours, 4 h, 6 h, 8 h after it (t2-t8). A two-factor (time and visit) multivariate analysis for repeated measurements was performed to evaluate the data. Total cholesterol, and LDL-C were significantly diminished 2 months after both gemfibrozil and simvastatin, the latter being more active. Plasma triglycerides showed a marked reduction with gemfibrozil at all times, while simvastatin regimen yielded only minor modifications. HDL-C was only slightly increased by simvastatin; Lp[a] plasma levels were almost unaffected. Small fibrinogen (t0, t2, t6, t8), PAI-1 (t6) and AT III (t0-t8) increases were observed after gemfibrozil, while simvastatin did not significantly modify these parameters. CONCLUSIONS: In the post-prandial phase, gemfibrozil and simvastatin induce different metabolic effects that beneficially influence the lipid pattern, whereas fibrinolytic and coagulative parameters display minor variations of undetermined significance.

Adult↗
PubMed1999

Tumor necrosis factor alpha as a uremic toxin: correlation with neuropathy, left ventricular hypertrophy, anemia, and hypertriglyceridemia in peritoneal dialysis patients.

Tumor necrosis factor alpha (TNF alpha) is usually excreted by the kidney. In dialysis patients, it accumulates. TNF alpha has been implicated in the pathogenesis of malnutrition, diabetic neuropathy, and erythropoietin resistance. We studied TNF alpha plasma levels in 49 stable peritoneal dialysis (PD) patients, with the aim of correlating those levels with the presence and severity of peripheral neuropathy, hypertrophic cardiomyopathy, and anemia. Kt/Vurea' residual renal creatinine clearance (CrC), nutritional markers, and general biochemistry were also determined. The average plasma level of TNF alpha was 67 +/- 32 pg/mL (range: 18.1-156.3 pg/mL; normal value 3-20 pg/mL). No correlation was observed between TNF alpha and KT/Vurea' but a negative correlation with CrC was seen (r: -0.37, p < 0.05). TNF alpha levels were higher in patients with neuropathy as compared to patients with normal results (72.5 +/- 32 pg/mL vs 44 +/- 22 pg/mL, p < 0.05). Patients with neuropathy also showed a lower CrC value (1.5 +/- 1.7 mL/min vs 3.9 +/- 2.6 mL/min, p < 0.01). TNF alpha levels were higher in patients with left ventricular hypertrophy (LVH) with respect to normal individuals (70.4 +/- 32 pg/mL vs 38.5 +/- 20.8 pg/mL, p < 0.05). Patients with severe LVH showed the lowest CrC value. A direct, significant relationship was found between TNF alpha levels and weekly erythropoietin dose (r: 0.41, p < 0.05). Patients with hypertriglyceridemia or taking lipid-lowering agents showed a positive linear correlation between TNF alpha and triglycerides (r = 0.7, n = 14, p < 0.05). These data suggest that accumulation of TNF alpha may contribute to the development or maintenance of some neurologic, hematologic, and cardiac complications of uremic syndrome. Loss of residual renal function conditions an increment in TNF alpha levels. These data continue to add support to the idea that TNF alpha may be considered a uremic toxin.

Adult↗
PubMed2001

[Study on apoE gene polymorphism in Chinese endogenous hypertriglyceridemia].

OBJECTIVE: To investigate apolipoprotein(apo) E polymorphism and its relationship with serum lipids and apolipoproteins in Chinese patients with endogenous hypertriglyceridemia(HTG). METHODS: apoE genotype was assayed by polymerase chain reaction- restriction fragment length polymorphism(PCR-RFLP), serum lipids were determined by enzyme method, and apolipoproteins were measured by radial immunodiffusion assay in 225 endogenous HTG patients whose fasting serum TG levels were > or = 2.26 mmol/L and in 230 healthy subjects whose fasting serum lipids levels were TG<1.82 mmol/L, TC<6.21 mmol/L from a population of Chinese Han nationality in Chengdu area. RESULTS: Compared with the controls, the values of BMI, TG, TC, nHDLC, apoB100, CII, CIII, E and TG/HDLC in HTG patients were significantly increased and the values of HDLC, apoAI and apoE/apoCIII were significantly decreased(P<0.001). apoE3/3 genotype and allele epsilon(3) frequency in HTG group and the control group were both the highest, and allele epsilon( 2) frequency in HTG group tended to increase than that in the control group(P>0.05). Both in HTG group and control group, the genotype of apoE2 had higher serum TG and apoE levels, lower LDLC level and decreased apoE/apoCIII ratio as compared with the genotype of apoE3 or apoE4(P<0.001). CONCLUSION: Allele epsilon(2) of apoE gene was associated with higher serum TG and apoE levels and lower serum LDLC level, and the lower ratio of apoE/apoCIII was associated with the higher serum level of TG in endogenous HTG.

Adult↗
PubMedDate not supplied

Association of hypertriglyceridemia and insulin resistance in uremic patients undergoing CAPD.

OBJECTIVE: Hyperlipidemia is frequently encountered in uremic patients and may be worsened by continuous ambulatory peritoneal dialysis (CAPD) treatment. The lipid abnormalities in these patients may be multifactorial. Insulin resistance (or its compensatory hyperinsulinemia) is commonly observed in uremic patients, but its association with hyperlipidemia in these patients has not been studied. PATIENTS AND METHODS: Lipid profiles of 35 nondiabetic nonobese patients undergoing CAPD for more than 1 year (mean 52.3 months) were studied. Current laboratory data and parameters related to peritoneal dialysis (PD) within the previous 3 months were recorded. After overnight fasting and interruption of PD, an oral 75-g glucose tolerance test (OGTT) was examined. RESULTS: After CAPD treatment for more than 12 months, these patients had higher serum triglyceride (TG) (p = 0.001) and total cholesterol (p = 0.0058) levels than their values before commencing CAPD. Twelve of 14 patients with serum TG higher than 200 mg/dL (high-TG) were diagnosed de novo, in contrast with only 1 patient diagnosed of de novo hypercholesterolemia (total cholesterol > 240 mg/dL). There was no difference in age, gender, body mass index (BMI), duration of PD treatment, serum albumin, hematocrit, intact serum parathyroid hormone (iPTH), peritoneal glucose load, solute transport, or weekly Kt/V urea between normal-TG and high-TG patients. After adjusting for age, gender, BMI, weekly Kt/V urea, and iPTH, the high-TG patients had higher levels of area under the curve for glucose (AUC(Glu)), area under the curve for insulin (AUC(Ins)), and AUC(Ins)/AUC(Glu) ratios (F = 10.63, 10.14, and 8.65; p = 0.0029, 0.0035, and 0.0065, respectively), indicating that the high-TG patients were more insulin resistant. There were 24 patients with normal glucose tolerance (NGT), and 11 patients with impaired glucose tolerance (IGT). The IGT group had higher serum TG (F = 10.43, p = 0.003) and total cholesterol (F = 8.05, p = 0.009) than the NGT group, after adjusting for BMI, duration of CAPD treatment, peritoneal glucose load, solute transport, serum albumin, and lipid levels before PD treatment. TheTG levels after CAPD treatment were positively correlated with AUC(Glu), AUC(Ins), and AUC(Ins)/AUC(Glu) ratio (r = 0.48, 0.53, and 0.49; p = 0.0037, 0.001, and 0.0028, respectively). CONCLUSIONS: These results indicate that insulin resistance is an important factor in the development of hypertriglyceridemia in CAPD patients.

Adult↗
PubMed2001

Distinct patterns of lipoproteins with apoB defined by presence of apoE or apoC-III in hypercholesterolemia and hypertriglyceridemia.

Apolipoprotein (apo) E and apoC-III concentrations in VLDL and LDL are associated with coronary heart disease. We studied the relationship between apoE and apoC-III and the abnormal concentrations and distribution of apoB lipoproteins in 10 hypercholesterolemic and 13 hypertriglyceridemic patients compared with 12 normolipidemic subjects (mean age, 45 years). Sixteen distinct types of apoB lipoprotein particles were separated by first using anti-apoE and anti-apoC-III immunoaffinity chromatography in sequence and then ultracentrifugation [light VLDL, dense VLDL, IDL, and LDL, with apoE with or without apoC-III (E(+)C-III(+), E(+)C-III(-)) or without apoE with or without apoC-III (E(-)C-III(+), E(-)C-III(-))]. The concentrations of VLDL particles with apoC-III (E(+)C-III(+), E(-)C-III(+)) were increased in the hypertriglyceridemic group compared with the hypercholesterolemic and normolipidemic groups. These particles were the most triglyceride rich of the particle types, and their triglyceride content was twice as high in hypertriglyceridemics compared with the other two groups. Hypertriglyceridemics had a similar concentration of total E(-)C-III(-) particles compared with normolipidemics, but the E(-)C-III(-) particles were distributed more to VLDL and IDL than to LDL. Hypercholesterolemics, in contrast, were distinguished from the normolipidemic group by 2-fold higher concentrations of apoB lipoproteins without apoE or apoC-III (E(-)C-III(-)), mainly LDL, which had high cholesterol content. Nonetheless, both normolipidemics and hypercholesterolemics had apoC-III-containing VLDL, which comprised 68% and 43% of their total VLDL particles. E(+)C-III(-) particles were a minor type, comprising <10% of particles in all lipoproteins and patient groups. Therefore, VLDL particles with apoC-III may play a central role in identifying the high risk of coronary heart disease in hypertriglyceridemia, but their substantial prevalence in normolipidemics may be of clinical significance as well.

Apolipoprotein C-III↗
PubMed2002

[The paraoxonase Gln-Arg 192 polymorphism in patients with endogenous hypertriglyceridemia in Chinese population].

OBJECTIVE: To investigate the 192 Gln-Arg polymorphism of paraoxonase (PON) gene and its relationship with serum lipids and apolipoproteins (apo) levels in patients with endogenous hypertriglyceridemia in Chinese population in Chengdu area. METHODS: The genotype and allele frequencies of paraoxonase gene 192 Gln-Arg polymorphism were assayed by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP). Serum lipids were measured by enzymatic kits and apolipoproteins AI, A II, B100, C I, C II and E were measured by the RID kits developed by the Apolipoprotein Research Unit of this university in 128 HTG patients whose fasting serum TG levels were > or = 2.26 mmol/L and 129 healthy subjects whose fasting serum TG levels were < 1.82 mmol/L and TC levels < 6.2 mmol/L from a population of Chinese Han nationality in Chengdu area. RESULTS: Both in HTG group and control group, the QR genotype of PON gene was the major one, and the frequencies were 0.515 and 0.581 respectively. No differences were found in PON gene Gln-Arg polymorphism between the HTG group and the control group. In the control group, the QQ genotype of PON gene was found to have higher serum apoA I levels, compared with the RR genotype (P < 0.05). But in the HTG group, when compared with the RR genotype, the QQ genotype was found to have lower serum apoA I and A II levels and higher serum apoE levels. CONCLUSION: These may be an association of the QQ genotype of the paraoxonase 192 Gln-Arg polymorphism with the decrease of serum apoA I level and the increase of serum apoE level in endogenous hypertriglyceridemica.

Aged↗
PubMedDate not supplied

Hypertriglyceridemia-induced acute pancreatitis--treatment with heparin and insulin.

Heparin and insulin stimulate lipoprotein lipase and are known to decrease serum triglyceride levels. However, their efficacy in hypertriglyceridemia-induced acute pancreatitis is not well documented. We report a 51-year-old man in whom treatment with heparin and insulin was accompanied by reduction in serum triglyceride levels and resolution of pancreatitis.

Acute Disease↗
PubMedDate not supplied

[Interaction between hypertriglyceridemia and noise in human hearing].

We carry out a cross-sectional study on 1205 workers exposed to industrial noise. After the clinical, analytical and audiological examination, we can't demonstrate any influence of hypertriglyceridemia on noise induced hearing loss. We get a statistically significant relationship between noise and hearing loss only in the group of workers with normotriglyceridemia.

Adult↗
PubMed2004

[Effects of hypertriglyceridemia on platelet activities in endogenous hypertriglyceridemic patients].

OBJECTIVE: To explore the effects of hypertriglyceridemia on platelet activities. METHODS: The plasma prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (Fg), blood platelet count (BPC) and platelet alpha granule membrane protein-140 (GMP-140) levels in endogenous hypertriglyceridemic patients were determined, and the relationship between platelet activities and fasting plasma lipids was assessed. RESULTS: It was found that PT, Fg levels, BPC and plasma GMP-140 concentration showed no statistically significant difference between the control and hypertriglyceridemic subjects (P > 0.05). PT was correlated with the levels of plasma BG and apo E (r = 0.500, P = 0.012), the levels of Fg was positively correlated with BG (r = 0.598, P = 0.000), and BPC of HTG subjects was negatively correlated with TG (r = -0.489, P < 0.05). GMP-140 content was positively correlated with the levels of plasma TC and LDL-C (r = 0.647, 0.833, P < 0.01); in HTG patients it was inversely correlated with age and PT (r = -0.480, -0.490, P < 0.05). CONCLUSION: All of these indicated that increasing of coagulation activity in hypertriglyceridemic patients was correlated with dysfunction of plasma lipids and change of apolipoproteins levels. Plasma GMP-140 was not obviously correlated with plasma TG content, but was positively correlated with plasma TC and LDL-C contents.

Aged↗
PubMed2004

[Hypertriglyceridemia--diagnostics, risk and treatment].

BACKGROUND: Hypertriglyceridemia and low HDL cholesterol values are associated with adiposity, type 2 diabetes and metabolic syndrome. METHODS: This review article is based on literature studies, data from Rikshospitalet and Furst Medical Laboratory, sales figures for fibrates and clinical experience. RESULTS AND INTERPRETATION: Insulin resistance is a common contributory cause to hypertriglyceridaemia. In hypertriglyceridaemia, fasting glucose, HbA1c, TSH, creatinine, ALAT, ASAT, gamma GT, ALP and urine strips should be measured. The patient must be evaluated with regard to adiposity, use of alcohol, eating disorders and pregnancy. Direct measurement of LDL cholesterol gives a correct measure independent of the triglyceride level up to 13.0 mmol/L. LDL cholesterol levels may be low despite high total cholesterol levels and high triglyceride levels. Diet and lifestyle intervention is important. Blood sugar control is crucial. Statins are the first choice of drugs in combined hyperlipidaemia. Isolated hypertriglyceridaemia >10 mmol/L represents a large risk for pancreatitis. Purified omega-3 fatty acids, fibrates and eventually niacin are the drugs of choice in this condition. If LDL cholesterol levels are elevated, statins should also be considered. Combination of statin/fibrate or statin/niacin increase the risk of myopathy.

Anticholesteremic Agents↗
PubMed2005

Acute pancreatitis due to hypertriglyceridemia: report of 2 cases.

Hypertriglyceridemia (HTG) is a rare but well known cause of acute pancreatitis (AP), which can be a life- threatening complication if the degree of HTG is severe enough. It might be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy, or drugs. A serum triglyceride (TG) level of more than 1,000 to 2,000 mg/dL in patients with type I, IV, or V hyperlipidemia (Fredrickson's classification) is the identifiable risk factor. HTG-induced AP typically presents as an episode of AP or recurrent AP. The clinical course of HTG-induced AP is not different from other causes. Routine management of HTG-induced AP should be similar to other causes. A thorough family history of lipid abnormalities should be obtained, and an attempt to identify secondary causes should be made. The mainstay of treatment includes dietary restriction of fatty meal and lipid-lowering medications (mainly fibric acid derivatives). Although there are limited experiences with plasmapheresis, lipid apheresis, heparinization and insulin application, these can support the treatment of HTG- induced AP. We report two cases of HTG-induced AP which were successfully treated by plasmapheresis.

Acute Disease↗