[Treatment of hypertriglyceridemia. Current aspects]. / Trattamento dell'ipertrigliceridemia. Aspetti attuali.

The hypertriglyceridemia attends the physiopathology of the atherosclerosis by various mechanisms: association of low levels of high density lipoprotein-cholesterol (HDL-c), modification of quality of low density lipoprotein-cholesterol (LDL-c), influence on hemostatic processes, association with other hazard's factors (obesity, hypertension, etc.). The hypertriglyceridemia distinguishes in primary and secondary. In primary forms the origin is essentially genetic, while the secondary ones are metabolic consequence of various pathologies (renal, thyroid, diabetes mellitus etc.). The hypertriglyceridemia's treatment is founded on a correct feeding and/or on eventual use of drugs. Apart from the secondary forms, in which is obligatory to treat at first the basal disease, the pharmacological therapy of the hypertriglyceridemia is suggested only in resistant cases to alone dietetic therapy and overall in presence of other factors of atherothrombotic hazard. The most utilized drugs are: omega-3 fatty acids, the nicotinic acid and its derivatives, the fibrates and the statins. The stronghold of alpha-glucosidases inhibitors is the acarbose. It reduces the biosynthesis of very low density lipoproteins (VLDL) by the reduction of substrata with an improvement of glucidic metabolism. Atorvastatin and cerivastatin develop a greater action to reduce serum levels of triglycerides as to the foregoing ones because of the better selectivity of receptor binding, the greater halflife and inhibition of the apolipoprotein's B100 synthesis.

Fish oil treatment of interferon-alpha-induced dyslipidaemia: study in patients with chronic hepatitis C.

OBJECTIVE: Our study was designed to evaluate the role of omega-3 fatty acids (OFAs) in reducing serum triglyceride levels in patients with chronic hepatitis C receiving treatment with interferon-alpha (IFNalpha). DESIGN: 52 patients (23 males, 29 females) with chronic hepatitis C were randomly assigned to nonblind treatment with IFNalpha 3 million units (MU) three times weekly alone (group A) or in combination with OFAs 3 g/day for 6 months (group B). RESULTS: Hepatitis C virus (HCV) RNA serum levels decreased significantly in both groups compared with baseline, but there was no significant difference in HCV RNA levels between the 2 groups. At the end of treatment there was a statistically significant difference in ALT levels between patients in group A and in group B (72.15 vs 50.05 IU/L; p = 0.01). A statistically significant increase in triglyceride levels occurred in group A during treatment (p = 0.03 vs baseline). In contrast, a statistically significant decrease in triglyceride serum levels occurred in group B (p = 0.001 vs baseline). CONCLUSION: Concurrent administration of OFAs reversed IFNalpha-induced hypertriglyceridaemia in patients with chronic hepatitis C.

Beneficial effects of acarbose on familiar hypertriglyceridemias.

Elevated serum triglyceride levels may be related to the following clinical features: increased blood coagulation and viscosity, increased serum fibrinogen levels, decreased fibrinolysis, and for serum levels over 1000 mg/dl, a strong increase of acute pancreatitis rate. Pharmacological choice among the numerous drugs to treat hypertriglyceridemias is currently debated. Our study was aimed to assess the therapeutic efficacy of acarbose in the treatment of non-diabetic subjects, affected by familiar hypertriglyceridemia (FH). We studied 18 non-diabetic patients (10 males, 8 females; mean age 57.61+/-6.85 years) without family history of diabetes mellitus affected by familiar hypertriglyceridemia. The study protocol planned a treatment period of 20 weeks, divided into five 4-week courses and made up as follows: diet plus acarbose therapy (4 weeks); diet therapy alone (4 weeks) alternatively. In the second and fourth 4-week courses diet plus acarbose were administered, while diet therapy alone was administered in the first, third, and fifth 4-week courses. Acarbose doses consisted of 50 mg (1/2 pill) twice daily. Mean serum triglyceride levels, after first month of dietary treatment, underwent a significant reduction from 481.5 +/- 67.1 mg/dl to 389.5 +/- 62.7 mg/dl, even if they did not reach the optimal levels to keep on the dietary therapy alone. After the first month of treatment with acarbose associated to diet, we observed a further reduction of serum triglycerides levels (p = 0.02). When diet alone was administered, mean triglyceride serum levels underwent a significant enhancement (p = 0.003). Restarting for the second time the association treatment, we observed a noteworthy reduction of mean serum triglyceride levels (p = 0.0001). Acarbose acts on the pathogenesis of FH, lowering the production of endogenous triglycerides. Our data suggested that acarbose can be considered a valid therapeutic tool in the treatment of familiar hypertriglyceridemias, also in non-diabetic patients.

Lipid profile variations in a group of healthy elderly and centenarians.

Epidemiological and clinical studies have clearly shown a close relationship between plasma cholesterol concentrations and vascular risk. We focused our attention on the phenotypic-biohumoral conditions capable of influencing longevity in relation to different age classes. We evaluated the lipid profile in an elderly institutionalized population of 80 subjects (20 males and 60 females divided into age classes) in the town of Catania. Our results revealed a statistically significant reduction in total cholesterol, triglycerides and LDL-cholesterol concentrations as well as Apolipoprotein B100/Apolipoprotein A1, total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol ratios, and a significant increase in HDL-cholesterol, Apolipoprotein A1, Apolipoprotein B100 and Lipoprotein (a) values. This changes are progressive with age. We believe that low total cholesterol, LDL-cholesterol and triglyceride concentrations, elevated HDL-cholesterol values, and low ratios protect subjects from ischemic and thrombotic events, thus favouring longevity. These changes are most evident and statistically significant in the most advanced decades of life, especially in centenarians, and may depend on diverse determinants, such as body composition, environmental factors, physical activity, diet and drugs.

Eosinophilic gastroenteritis.

Eosinophilic gastroenteritis is a rare disease of unknown aetiology characterized by eosinophilic infiltration of the gastrointestinal wall and increased peripheral blood eosinophilia. The frequent finding of concomitant extradigestive involvement calls for differential diagnosis to distinguish some multisystemic pathologies, such as connective tissue disease. We recently treated a young woman affected by eosinophilic infiltration of the small and large intestine which spread to other organs. Tests ruled out allergic or parasitic aetiopathogenesis of the disease. The clinical, biological and evolutive findings suggest that eosinophilic gastroenteritis may evolve into idiopathic hypereosinophilic syndrome.

Lipoprotein(a) in cirrhosis. A new index of liver functions?

Over the last few years, lipoprotein(a) [Lp(a)] levels have been investigated because clinical studies have related it to increased cardiovascular and cerebrovascular risk. Although it is known that serum Lp(a) concentrations are controlled genetically, little is known about its metabolism. We studied changes in the lipid profile and Lp(a) values in 57 patients (34 males and 23 females) affected by cirrhosis of the liver subdivided into Child's classes in order to assess whether this lipoprotein is sensitive to reduced liver protein synthesis. The patients presented with low total cholesterol, normal HDL-cholesterol (HDL-c), LDL-cholesterol (LDL-c), triglycerides, apoprotein A1 (Apo-A1) and apoprotein B100 (Apo-B100) concentrations, while Lp(a) concentrations seemed elevated. Grouping the patients into Child's classes revealed that all the lipid parameters investigated reduced as the disease progressed. Lp(a) reduced significantly between Child's Classes I and II and seems to be correlated with the severity of cirrhosis and the clinical worsening of the patients' conditions. These findings suggest that Lp(a) is not only an index of atherosclerosis risk, but also plays a role in monitoring liver functions.

Lipoprotein(a) concentration in patients with chronic active hepatitis C before and after interferon treatment.

Patients with chronic active hepatitis C show low lipoprotein(a) (Lp[a]) values. We studied the changes in Lp(a) levels caused by treatment with interferon in 24 patients (9 men and 15 women; mean age, 56.8 +/- 7.3 years) affected by chronic active hepatitis C. Fifteen healthy subjects (6 men and 9 women; mean age, 57.4 +/- 10.3 years) were used as controls. All of the patients with chronic hepatitis C were treated with intramuscular interferon, 3 million units 3 times per week for 6 months. These patients had lower baseline serum Lp(a) concentrations than the controls (4.8 +/- 3.8 mg/dL vs 13.4 +/- 10.3 mg/dL, respectively; P = 0.0007). A significant increase in Lp(a) levels (6.6 +/- 7.2 mg/dL; P = 0.05) occurred after 6 months of treatment in patients with chronic active hepatitis C. Only complete responders presented a significant increase in Lp(a) values (P = 0.01). We believe that increased Lp(a) levels represent an expression of improved liver functions.