Hyperlipidemias: Tsimihodimos V

Tsimihodimos V, Dounousi E, Siamopoulos KC. · Department of Nephrology, Medical School, University of Ioannina, Ioannina, Greece. · Am J Nephrol. · Pubmed #18612199 No free full text.

Abstract: BACKGROUND/AIMS: Cardiovascular disease (CVD) is a major cause of mortality in patients with mild to moderate chronic kidney disease (CKD) and end-stage renal disease (ESRD). Dyslipidemia has been established as a well-known traditional risk factor for CVD in the general population and it is well known that patients with CKD exhibit significant alterations in lipoprotein metabolism. In this review the pathogenesis and treatment of renal dyslipidemia are discussed. METHODS: Studies on lipid abnormalities in CKD stages 1-4, in nephrotic syndrome, and in hemodialysis and peritoneal dialysis patients are analyzed, as well as the lipid profile of kidney graft recipients. Also, the results of the effects of epoietin treatment and hypolipidemic drugs in CKD patients are reported. RESULTS: Disturbances in lipoprotein metabolism are evident even at the early stages of CKD and usually follow a downhill course that parallels the decline of renal function. However, several intrinsic or exogenous factors can influence the phenotypic expression of these alterations. According to the literature, current evidence suggests that unlike dialysis patients, mild to moderate CKD patients could be benefit from the use of statins. CONCLUSION: The use of statins is indicated in patients with mild to moderate CKD, while in subjects with ESRD lipid-lowering therapy should be individualized.

Tsimihodimos V, Karabina SA, Tambaki A, Bairaktari E, Achimastos A, Tselepis A, Elisaf M. · Department of Internal Medicine, Medical School, University of Ioannina, 45110 Ioannina, Greece. · J Cardiovasc Pharmacol. · Pubmed #12883336 No free full text.

Abstract: The authors investigated the effect of atorvastatin (40 mg qd) on low-density lipoprotein (LDL) particle distribution in patients with dyslipidemias of type IIA (n = 55) and IIB (n = 21). Atorvastatin therapy induced a significant decrease in total and LDL cholesterol in both patient groups. A significant reduction in triglyceride values, which was more profound in type IIB patients, was also observed. In type IIA patients, LDL-3 was the predominant subfraction. Atorvastatin therapy induced a significant reduction in total LDL mass in this group of patients that was mainly due to the reduction in large and intermediate subspecies (LDL-1 to LDL-3), whereas the mass of dense LDL particles (LDL-4 and LDL-5) remained unchanged. As a consequence, the percentage contribution of dense subfractions to the total LDL mass increased significantly after atorvastatin therapy. The dense LDL-4 subfraction was the predominant one in type IIB patients. In this group, atorvastatin therapy resulted in a significant reduction in the total LDL mass, which was due to the reduction in all LDL subfractions. Thus, the percentage mass distribution of LDL particles remained unaffected. These results suggest that the effect of atorvastatin on LDL subfractions is affected by the underlying genetic defect.

Tsimihodimos V, Kostoula A, Kakafika A, Bairaktari E, Tselepis AD, Mikhailidis DP, Elisaf M. · Department of Internal Medicine, Medical School, University of Ioannina, 45110 Ioannina, Greece. · J Cardiovasc Pharmacol Ther. · Pubmed #15094966 No free full text.

Abstract: BACKGROUND: Atherosclerosis is the leading cause of death in developed countries. Although the mechanisms that underlie this process are not well defined, it has been proposed that atherosclerosis is mainly an inflammatory disease. In this context, a number of inflammatory markers have been studied for their ability to predict future cardiovascular events in asymptomatic individuals or patients with established atherosclerotic disease. METHODS AND RESULTS: The aim of our study was to evaluate the effect of micronized fenofibrate on serum inflammatory markers, such as C-reactive protein, fibrinogen, and plasma platelet-activating factor acetylhydrolase (PAF-AH) in patients with high triglyceride values. An analysis of baseline values revealed that hypertriglyceridemic patients (n = 58) exhibit an atherogenic phenotype, characterized not only by elevated lipid values but also by high concentrations of serum inflammatory markers. Along with the improvement in serum lipid profile (reduction in triglycerides and total cholesterol, low-density lipoprotein, and non-high-density lipoprotein-cholesterol, with a concomitant increase in high-density lipoprotein-cholesterol levels), fenofibrate administration significantly reduced the values of serum inflammatory markers by 34%, 9.5%, and 24.8% for C-reactive protein, fibrinogen, and plasma PAF-AH, respectively. However, with the exception of PAF-AH, these reductions in inflammatory markers were not correlated with the changes in lipid values. CONCLUSIONS: In addition to its well-known hypolipidemic effects, fenofibrate may also possess significant anti-inflammatory properties that can contribute its antiatherogenic effect.

Tsimihodimos V, Kakafika A, Tambaki AP, Bairaktari E, Chapman MJ, Elisaf M, Tselepis AD. · Department of Internal Medicine, University of Ioannina, 45110 Ioannina, Greece. · J Lipid Res. · Pubmed #12611907 links to  free full text

Abstract: Human plasma platelet-activating factor acetylhydrolase (PAF-AH) is an enzyme associated mainly with the apolipoprotein B (apoB)-containing lipoproteins and primarily with LDL. A small proportion of enzymatic activity is also associated with HDL. Plasma paraoxonase 1 (PON1) is an esterase exclusively associated with HDL. The effect of fenofibrate on PAF-AH and PON1 activities in patients with dyslipidemias of Types IIA, IIB, and IV were studied. Fenofibrate reduced plasma PAF-AH activity in all patient groups. In Type IIA patients, this reduction was mainly due to a fall in enzyme activity associated with the dense LDL subspecies, whereas in Type IIB and Type IV patients, it was due to the decrease in PAF-AH activity associated with both the VLDL+IDL and dense LDL subspecies. Drug therapy in Type IIB and Type IV patients significantly increased the HDL-associated PAF-AH activity due to the increase in enzyme activity associated with the HDL-3c subfraction. Fenofibrate did not affect serum PON1 activities toward paraoxon and phenylacetate in either patient group. The fenofibrate-induced elevation of HDL-associated PAF-AH activity in dyslipidemic patients of Type IIB and Type IV, as well as the reduction in enzyme activity associated with atherogenic apoB-containing lipoproteins in all patient groups, may represent a new and important antiatherogenic effect of this potent lipid-modulating agent.

Rizos E, Bairaktari E, Ganotakis E, Tsimihodimos V, Mikhailidis DP, Elisaf M. · Department of Internal Medicine, Medical School, University of Ioannina, Greece. · J Cardiovasc Pharmacol Ther. · Pubmed #12490967 No free full text.

Abstract: AIM: The action of ciprofibrate in hypertriglyceridemic patients is well established. Not only is ciprofibrate able to alter the lipid profile, but it can also change the values of fibrinogen, C-reactive protein, creatinine, transaminases, gamma-glutamyl transpeptidase and serum alkaline phosphatase. However, previous studies focused on the effect of ciprofibrate in hypertriglyceridemic patients, leaving unanswered the question of whether ciprofibrate exerts the same effect on hyperlipidemic patients with normal triglyceride values. The aim of this study is to answer this question. METHODS: In this randomized clinical trial, 64 men and women with elevated cholesterol or triglyceride levels were included. Two subgroups were formed according to triglyceride levels: one (36 patients) with elevated triglyceride levels (> 200 mg/dL [2.26 mmol/L]) and another (28 patients) with normal triglyceride levels (< 200 mg/dL [2.26 mmol/l]). After a 6-week period of step 1 diet according to the National Cholesterol Education Program, ciprofibrate (100 mg once daily) was administered for 16 weeks. Primary efficacy points were the changes of lipid parameters (total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, triglycerides, apoproteins A1, B, E and lipoprotein [a], high sensitivity C reactive protein, fibrinogen, glucose, insulin, aspartate transaminase, alanine transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase, urea and creatinine levels in a fasting blood sample before and after treatment with ciprofibrate. RESULTS: The subgroup with triglyceride < 200 mg/dL (2.26 mmol/L): After the administration of ciprofibrate total cholesterol and low-density lipoprotein cholesterol were reduced by 15% (P < 0.001), and 19% (P < 0.001), respectively, while high-density lipoprotein cholesterol increased by 9% (P = 0.02). Apoproteins B and E levels were reduced by 21% (P < 0.001) and 11% (P = 0.002), respectively. Subgroup with triglyceride > 200 mg/dL (2.26 mmol/L): After the administration of ciprofibrate, no significant change in LDL cholesterol levels was observed. Total cholesterol levels were reduced by 15% (P < 0.001) and high-density lipoprotein cholesterol levels were increased by 13% (P = 0.004). Apoprotein B and apoprotein E levels were reduced by 16% (P < 0.001) and 30% (P < 0.001), respectively. Apoprotein-A1 levels were increased by 5% (P = 0.024). In the whole group of patients, the fibrinogen levels fell by 7% (P = 0.043), and the serum creatinine level increased by 10% (P < 0.001). This rise in serum creatinine was more pronounced in patients with low triglyceride levels (15% vs 5%, P = 0.009). Ciprofibrate decreased C-reactive protein levels by 26% in 44 patients who had C-reactive protein measurements (P < 0.001). gamma-glutamyl transpeptidase activity was similarly decreased (by approximately 40%) in both groups of patients. Alkaline phosphatase activity decreased in both groups, a reduction which was greater in hypertriglyceridemics (20% vs 10%, P = 0.004). CONCLUSIONS: Ciprofibrate improved some of the vascular risk factors, such as total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apoproteins A1, B, and E, and fibrinogen levels in both hypertriglyceridemics and normotriglyceridemics. In addition, ciprofibrate raised the serum creatinine and improved the activity of the hepatic enzymes in the plasma in both patient subgroups.

Liamis G, Kakafika A, Bairaktari E, Miltiadous G, Tsimihodimos V, Goudevenos J, Achimastos A, Elisaf M. · Department of Internal Medicine, University of Ioannina, Greece. · Curr Med Res Opin. · Pubmed #12094821 No free full text.

Abstract: Combined statin and fibrate therapy is often imperative for the improvement of the serum lipid profile in patients with mixed hyperlipidemia. However, the potential risk of myopathy has limited the widespread use of such therapy. Preferably this treatment should involve low optimally tolerable doses of hypolipidemic drugs. Thus, we undertook a study to determine the safety and efficacy of combination therapy with fibrates and small doses of atorvastatin. Twenty-two patients with mixed hyperlipidemia were started on a fibrate regimen (micronised fenofibrate 200mg/day or ciprofibrate 100 mg/day). Because after 12 weeks of therapy the fibrate failed to normalise the serum lipid profile, small doses of atorvastatin (5 mg/day) were added for a further 12 weeks. The administration of the fibrates resulted in a significant decrease in total and LDL-cholesterol levels, as well as in triglycerides, and an increase in HDL-cholesterol levels. The addition of atorvastatin (5 mg/day) resulted in a further decrease in total and LDL-cholesterol levels. Consequently, the hypolipidemic therapy target was achieved in most of the patents. Combination therapy was well tolerated and no significant increases in serum liver and muscle enzymes were noticed. We conclude that the careful administration of small doses of atorvastatin in patients with mixed dyslipidemia receiving fibrates is associated with a significant amelioration of lipid abnormalities.

Tsimihodimos V, Karabina SA, Tambaki AP, Bairaktari E, Goudevenos JA, Chapman MJ, Elisaf M, Tselepis AD. · Department of Internal Medicine, University of Ioannina, Ioannina, Greece. · Arterioscler Thromb Vasc Biol. · Pubmed #11834533 links to  free full text

Abstract: Human plasma platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A(2) that is primarily associated with low density lipoprotein (LDL). PAF-AH activity has also been found in high density lipoprotein (HDL), although it has recently been indicated that there is no PAF-AH protein in HDL. Plasma paraoxonase 1 (PON1) is an HDL-associated esterase, which also exhibits PAF-AH-like activity. The effect of atorvastatin (20 mg per day for 4 months) on PAF-AH and PON1 activities in patients with dyslipidemia of type IIA (n=55) or type IIB (n=21) was studied. In both patient groups, atorvastatin significantly reduced plasma PAF-AH activity because of the decrease in LDL plasma levels and the preferential decrease in PAF-AH activity on dense LDL subfractions (LDL-4 and LDL-5). Drug therapy did not affect HDL-associated PAF-AH activity or serum PON1 activities toward paraoxon and phenylacetate in either patient group. However, because of the reduction in LDL cholesterol levels, the ratios of HDL-associated PAF-AH and serum PON1 activities to LDL cholesterol levels were significantly increased after drug administration. The reduction of the LDL-associated PAF-AH activity and the elevation in the ratios of HDL-associated PAF-AH and PON1 activities to LDL plasma levels may represent a new dimension in the antiatherogenic effect of atorvastatin.

Gazi IF, Milionis HJ, Filippatos TD, Tsimihodimos V, Kostapanos MS, Doumas M, Tselepis AD, Elisaf M. · Department of Internal Medicine, Medical School, University of Ioannina, Ioannina, Greece. · Diabetes Metab Res Rev. · Pubmed #17966968 No free full text.

Abstract: BACKGROUND: To assess the metabolic profile and the prevalence of the metabolic triad (i.e. hyperinsulinaemia, hyperapobetalipoproteinaemia, and decreased low-density lipoprotein particle size) in women characterized by the hypertriglyceridaemic waist (HTGW) phenotype and to identify cut-off values for triglycerides and waist circumference, effectively discriminating women with the metabolic triad. METHODS: Two hundred and twenty-eight female subjects without any history of vascular disease or diabetes mellitus attending an Outpatient Lipid Clinic setting at the University Hospital of Ioannina, Greece were studied. RESULTS: Currently available HTGW criteria for women were unable to detect any significant differences in the metabolic profile either in the pre- or post-menopausal women, and proved similar in terms of sensitivity and specificity in identifying women with the metabolic triad. A cut-off value of 1.26 mmol/L for triglycerides and 84.5 cm for waist circumference were determined by Receiver-operating Curve evaluation. Women with both triglycerides and waist circumference above these thresholds had four-fold higher odds of presenting with the metabolic triad compared with women with non-HTGW phenotype. CONCLUSIONS: A HTGW phenotype definition of 1.26 mmol/L for triglycerides and 84.5 cm for waist circumference may effectively identify Mediterranean women with the atherogenic metabolic triad. Whether these criteria are also associated with a higher incidence of vascular disease and/or new-onset diabetes in women remains to be investigated.

Gazi IF, Filippatos TD, Tsimihodimos V, Saougos VG, Liberopoulos EN, Mikhailidis DP, Tselepis AD, Elisaf M. · Department of Internal Medicine, Medical School, University of Ioannina, Ioannina, Greece. · Lipids. · Pubmed #17069348 No free full text.

Abstract: The hypertriglyceridemic waist (HTGW) phenotype (hypertriglyceridemia and increased waist circumference) has been proposed as an inexpensive tool to monitor individuals with the atherogenic metabolic triad, hyperinsulinemia, hyperapobetalipoproteinemia, and increased levels of small, dense LDL (sdLDL) particles. We assessed the association of the HTGW phenotype with the metabolic syndrome (MetSyn) and the atherogenic metabolic triad in inhabitants (n = 260) of northwestern Greece attending the Outpatient Lipid Clinic of the University Hospital of Ioannina. The LDL subfractions were assessed using the Lipoprint LDL System. HTGW (+) individuals had a more adverse lipid and lipoprotein profile compared with HTGW (-) individuals. Moreover, HTGW (+) subjects had elevated levels of sdLDL-C, as well as decreased mean and peak LDL particle size compared with HTGW (-) subjects. To our knowledge, this is the first report documenting the sdLDL-C abnormality in HTGW (+) subjects. Among men (n = 105), 52.3% of the MetSyn (+) individuals and 66.7% of the HTGW (+) individuals had the metabolic triad. Among women (n = 155), the corresponding percentages were 42.3% and 50.0%. Only 22.2% and 10.6% of the MetSyn (-) subjects (men and women, respectively) and 19.6% and 15.2% of the HTGW (-) subjects (men and women, respectively) had the atherogenic metabolic triad. In conclusion, the HTGW (+) phenotype is associated with a hostile lipid profile that includes higher levels of sdLDL-C and decreased LDL particle size. The HTGW phenotype, compared with the MetSyn criteria, can provide an easy and inexpensive tool to monitor patients characterized by an adverse lipid and lipoprotein profile.

Kakafika AI, Xenofontos S, Tsimihodimos V, Tambaki AP, Lourida ES, Kalaitzidis R, Cariolou MA, Elisaf M, Tselepis AD. · Department of Internal Medicine, Department of Chemistry, University of Ioannina, 45110 Ioannina, Greece. · J Lipid Res. · Pubmed #12867538 links to  free full text

Abstract: The platelet-activating factor acetylhydrolase activity associated with high density lipoprotein (HDL-PAF-AH) may substantially contribute to the antioxidant, anti-inflammatory, and overall antiatherogenic effects of HDL. Two enzymes associated with HDL express PAF-AH catalytic activity, PAF-AH itself and paraoxonase-1 (PON1). The relative contribution of these enzymes in the expression of PAF-AH activity on HDL remains to be established. We investigated whether the PON1 polymorphisms (M55L and Q192R) or the PAF-AH polymorphism V379A could affect the PAF-AH activity associated with HDL in both normolipidemic and dyslipidemic (type IIA and IIB) populations. We show for the first time that the PON1 M55L polymorphism significantly affects the HDL-PAF-AH activity in all studied groups, the PON1 L55L individuals having lower enzyme activity compared to those having 1 M and 2 M alleles. No differences in the HDL content concerning the major apolipoprotein and lipid constituents were observed between individuals carrying the PON1 L55L and those with the M55M polymorphism. Our results provide evidence that PON1 significantly contributes to the pool of HDL-PAF-AH activity in human plasma, and suggest that the low PAF-AH activity in HDL carrying the PON1 L alloenzyme may be an important factor contributing to the low efficiency of this HDL in protecting LDL against lipid peroxidation.

Ganotakis E, Tsimihodimos V, Bairaktari E, Rizos E, Athyros V, Seferiades C, Elisaf M. · No affiliation provided · Atherosclerosis. · Pubmed #12208487 No free full text.

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Achimastos A, Liberopoulos E, Nikas S, Bairaktari E, Miltiadous G, Tsimihodimos V, Elisaf M. · Department of Internal Medicine, Medical School, University of Athens, Greece. · Curr Med Res Opin. · Pubmed #12017210 No free full text.

Abstract: OBJECTIVE: Hyperuricaemia is associated with indapamide administration. In contrast, micronised fenofibrate can significantly decrease serum uric acid levels. However, there are no data on the effect of combination therapy of indapamide with micronised fenofibrate on uric acid metabolism. METHODS:We studied 20 non-diabetic hypertensive patients with mixed dyslipidaemia in whom serum metabolic parameters, including uric acid levels in serum and urine, were measured before and after eight weeks of indapamide administration (2.5 mg once daily). This study was continued for a further eight weeks, when the indapamide was combined with micronised fenofibrate (200 mg once daily). RESULTS: Indapamide significantly decreased mean systolic and diastolic blood pressure (BP) from 153 +/- 9/97 +/- 8 mmHg to 138 +/- 8/93 +/- 4 mmHg (p< 0.05 for both comparisons). A significant increase in serum uric acid levels occurred after indapamide administration (from a mean value of 5.6 +/- 1.3 mg/dl (0.33 +/- 0.07 mmol/l) to 6.4 +/- 1.1 mg/dl (0.38 +/- 0.06 mmol/l), p < 0.01]. This effect was associated with a decrease in the fractional excretion of uric acid (from a mean value of 9.5 +/- 5% to 7 +/- 5.5%, p < 0.05). The addition of micronised fenofibrate significantly decreased plasma fibrinogen levels as well as total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B (ApoB) and triglycerides, and increased high-density lipoprotein cholesterol and ApoA, levels. Fenofibrate administration was followed by a significant decrease in serum uric acid levels to 4.7 +/- 1.2 mg/dl (0.28 +/- 0.07 mmol/l), p < 0.01, owing to a substantial increase in fractional urate excretion to 11 +/- 3%, p < 0.01. CONCLUSION:The addition of micronised fenofibrate can correct the hyperuricaemic effect of indapamide administration.

Tsimihodimos V, Karabina SA, Tambaki AP, Bairaktari E, Miltiadous G, Goudevenos JA, Cariolou MA, Chapman MJ, Tselepis AD, Elisaf M. · Department of Internal Medicine, University of Ioannina, 45110 Ioannina, Greece. · J Lipid Res. · Pubmed #11861667 links to  free full text

Abstract: Platelet-activating factor-acetylhydrolase (PAF-AH) is a lipoprotein-associated phospholipase A2 capable of hydrolyzing platelet-activating factor (PAF) and oxidatively modified phospholipids. We studied the plasma- and lipoprotein-associated PAF-AH activity in patients with primary hypercholesterolemia. Thirty-eight unrelated patients with heterozygous familial hypercholesterolemia (HeteroFH), five patients with homozygous FH (HomoFH), and 33 patients with primary non-FH hypercholesterolemia (NonFH) participated in the study. In all patient groups the plasma PAF-AH activity was significantly elevated compared with 33 normolipidemic controls, the HomoFH having the highest and the NonFH patients showing the lowest enzyme activity. Gradient ultracentrifugation studies showed that this increase is not only due to the elevation in the plasma LDL but also to the increase in the PAF-AH activity associated with each LDL subfraction, being more profound in the small-dense LDL-5. Unlike LDL, no difference in the HDL-associated PAF-AH activity was observed among all groups. Consequently, an altered distribution of enzyme activity among apolipoprotein B (apoB)- and apolipoprotein A-I (apoA-I)-containing lipoproteins is observed in hypercholesterolemic patients, resulting in a significant decrease in the ratio of the HDL-associated PAF-AH to the total plasma enzyme activity compared with controls. This reduction is proportional to the increase of the plasma LDL-cholesterol (LDL-C) levels and consequently to the severity of the hypercholesterolemia. Thus, the ratio of HDL-associated PAF-AH-total plasma enzyme activity may be useful as a potential marker of atherogenicity in subjects with primary hypercholesterolemia.

Bairaktari E, Elisaf M, Katsaraki A, Tsimihodimos V, Tselepis AD, Siamopoulos KC, Tsolas O. · Laboratory of Biochemistry, University Hospital, Medical School, Ioannina, Greece. · Clin Biochem. · Pubmed #10480448 No free full text.

Abstract: OBJECTIVES: To evaluate the analytical performance of a new homogeneous HDL-cholesterol assay (Olympus Diagnostica). To investigate possibly discrepant results in chronic hemodialysis patients who commonly exhibit quantitative and qualitative lipoprotein abnormalities, responsible for atherogenic complications in these patients. DESIGN AND METHODS: Serum samples were collected from 50 healthy subjects and 65 chronic hemodialysis patients. HDL-C levels measured by the homogeneous assay were compared with the routine dextran sulfate-Mg2+ precipitation method and the ultracentrifugation/dextran sulfate-Mg2+ precipitation as reference method. RESULTS: The homogeneous assay was linear up to at least 220 mg/dL. The analytical precision was estimated with three different sets of commercial controls and one set of human pooled serum control. The within-day CV ranged between 1.7% and 3.8% and the between-day CV ranged between 1.0% and 2.3%. HDL-C values in both populations correlated highly with the dextran sulfate-Mg2+ precipitation method and the ultracentrifugation/dextran sulfate-Mg2+ precipitation method (r > or = 0.96, bias between -0.9 and 2.3 mg/dL). Lipemia up to triglyceride concentration of 600 mg/dL did not alter the HDL-C value. CONCLUSIONS: The homogeneous assay for HDL-C (Olympus) uses much less sample, is accurate and convenient to handle, and allows full automation. The test should considerably facilitate the screening of individuals at an increased risk of cardiovascular disease, including hemodialysis patients.

Tsimihodimos V, Bairaktari E, Tzallas C, Miltiadus G, Liberopoulos E, Elisaf M. · Department of Internal Medicine, Medical School, University of Ioannina, Greece. · Thyroid. · Pubmed #10319942 No free full text.

Abstract: Thyroid disorders are known to influence lipoprotein metabolism. In the current study we examined the incidence of thyroid function abnormalities in patients attending our outpatient lipid clinic. During the last 2 years, 248 patients were admitted to our lipid clinic for the diagnosis and management of dyslipidemia. In all cases, a detailed medical history was obtained and a thorough physical examination was performed with emphasis on the presence of symptoms/signs indicative of underlying thyroid diseases. In addition to lipid parameters, thyrotropin (TSH) and free thyroxine (FT4) levels were measured in a fasting blood sample. Seven female asymptomatic patients (2.8%) had frank biochemical hypothyroidism, and 11 patients (9 female, 2 male) (4.4%) had subclinical hypothyroidism with TSH levels between 5.8-19 mU/L. After restoration of a euthyroid state with levothyroxine therapy, no significant changes in serum lipid parameters were observed in the whole group of patients with subclinical hypothyroidism. However, in 4 patients with TSH levels >12 mU/L relatively small doses of levothyroxine (75 microg/day) were followed by a significant improvement of serum lipid profile. Interestingly, 3 patients exhibited clinical or subclinical hyperthyroidism that influenced serum lipid parameters as well as the effectiveness of hypolipidemic treatment. It is concluded that thyroid function abnormalities are relatively common in dyslipidemic patients attending a lipid clinic and could significantly affect the patients' lipid profile as well as the patients' management.

Miltiadous G, Tsimihodimos V, Bairaktari E, Elisaf M. · No affiliation provided · Atherosclerosis. · Pubmed #11463004 No free full text.

This publication has no abstract.

Tsimihodimos V, Miltiadous G, Elisaf M. · No affiliation provided · Atherosclerosis. · Pubmed #11187858 No free full text.

This publication has no abstract.