HORMONES 2002, 1(4):218-223
DOI: 10.14310/horm.2002.1170
Dyslipidemia in patients with thyroid disorders
Evagelos N Liberopoulos, Moses S Elisaf

Department of Internal Medicine, University of Ioannina Medical School, Ioannina, Greece


Thyroid disorders are known to influence lipid metabolism and are common in dyslipidemic patients. Overt and subclinical hypothyroidism have an adverse effect on the serum lipid profile that may predispose to the development of atherosclerotic disease. Although thyroid substitution therapy is beneficial for patients with overt hypothyroidism, the question of whether subclinical hypothyroidism must be treated remains unanswered. The association between thyroid autoimmunity and lipoprotein (a) levels is controversial. Hyperthyroidism may be the underlying cause for acquired hypocholesterolemia or unexpected improvement of the lipid profile of a previously hyperlipidemic patient.


Hypothyroidism, hyperthyroidism, dyslipidemia, thyroid autoimmunity, thyroid disorders, lipoprotein (a)

Read PDF

It is well known that alterations in thyroid function result in changes in the composition and transport of lipoproteins1-3. In general, overt and subclinical hypothyroidism is associated with hypercholesterolemia mainly due to elevation of low density lipoprotein (LDL) cholesterol levels, whereas high density lipoprotein (HDL) cholesterol concentration is usually normal or even elevated3-5. On the other hand, hyperthyroidism (both overt and subclinical) is accompanied by a decrease in serum levels of total, LDL and HDL cholesterol6. These changes in the lipid profile are explained by the regulatory effect of thyroid hormones on the activity of some key enzymes of lipoprotein metabolism. Specifically, the thyroid hormone stimulates the hepatic de novo cholesterol synthesis by inducing the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase that catalyzes the conversion of HMG-CoA to mevalonate, the first step in the biosynthesis of cholesterol7. This results in an enhanced intracellular cholesterol concentration in hyperthyroidism and a decreased one in hypothyroidism. Additionally, thyroid hormones activate the LDL receptors (figure); the promoter of the LDL receptor gene contains a thyroid hormone responsive element (TRE) which allows the triiodothyronine (T3) to upregulate the gene expression of the LDL receptor8. Moreover, thyroid hormones stimulate the cholesteryl ester transfer protein (CETP), an enzyme which transports cholesteryl esters from HDL2 to the very low density lipoproteins (VLDL) and triglycerides in the opposite direction9 (figure). Finally, thyroid hormones stimulate the lipoprotein lipase (LPL), which catabolizes the triglyceride-rich lipoproteins, and the hepatic lipase (HL), which hydrolyzes HDL2 to HDL310 (figure). The alterations in the lipid profile observed in different thyroid abnormalities, the effect of treatment of these disturbances on the restoration of lipid metabolism, as well as the potential clinical implications and therapeutic guidelines are briefly discussed.

Figure. Thyroid hormones modulate lipid metabolism by a variety of ways: 1) upregulation of the low density lipoprotein (LDL) receptors, which results in enhanced catabolism of the LDL particles, 2) stimulation of the cholesteryl ester transfer protein (CETP), an enzyme which transports cholesteryl esters from high density lipoproteins 2 (HDL2) to the very low density lipoproteins (VLDL) and the intermediate density lipoproteins (IDL), and triglycerides to the opposite direction, 3) activation of the lipoprotein lipase (LPL), which hydrolyses the triglyceride-rich lipoproteins, 4) stimulation of hepatic lipase (HL), which catabolizes HDL2 to HDL3 and IDL to LDL, and 5) inhibition of LDL oxidation. FC; free cholesterol, LCAT; lecithin cholesterol acyltransferase.


Hypothyroidism is a common metabolic disorder in the general population, especially in older women; 9.5% of the participants of the Colorado prevalence study had elevated levels of thyroid stimulating hormone3. Levels of total and LDL cholesterol tend to increase as the thyroid function declines3. Therefore, hypothyroidism constitutes a significant cause of secondary dyslipidemia11,12.


In hypothyroid patients, despite the reduced activity of HMG-CoA reductase, there is often an increase in the serum total cholesterol concentration, mainly due to raised levels of serum LDL cholesterol and intermediate density lipoprotein (IDL) cholesterol4,12. Decreased activity of LDL-receptors' resulting in decreased receptor-mediated catabolism of LDL and IDL is the main cause of the hypercholesterolemia observed in hypothyroidism13-15. Hypertriglyceridemia associated with increased levels of VLDL and occasionally fasting chylomicronemia are found less commonly in this population15. These changes are attributable to the decreased activity of LPL, which results in a decreased clearance of triglyceride-rich lipoproteins16. The VLDL and IDL particles in hypothyroidism are rich in cholesterol and apolipoprotein E, thus resembling β-VLDL particles of type III hyperlipoproteinemia17. It is not surprising that patients homozygous for the apolipoprotein E2 allele may develop the full-blown clinical syndrome of type III hyperlipoproteinemia if they become hypothyroid18.

Hypothyroid patients usually exhibit elevated levels of high density lipoprotein (HDL) cholesterol mainly due to increased concentration of HDL2 particles19. Decreased activity of the CETP results in reduced transfer of cholesteryl esters from HDL to VLDL, thus increasing HDL cholesterol levels20. Furthermore, decreased activity of the HL leads to decreased catabolism of HDL2 particles21. Lipoprotein (a) [Lp(a)] levels, which are an independent risk factor for cardiovascular events, are also elevated in hypothyroid patients22,23.

The above described abnormalities of lipid metabolism associated with overt hypothyroidism may predispose to the development of atherosclerotic coronary artery disease (CAD)24,25. Furthermore, hypothyroidism may contribute to the development of atherosclerosis by other mechanisms as outlined below: a) Decreased thyroid function not only increases the number of LDL particles but also promotes LDL oxidability26,27 (figure); an obvious reason being that T4 has three specific binding sites on apolipoprotein (apo) B and inhibits LDL oxidation in vitro26 b) Thyroid failure is accompanied by an increase in plasma homocysteine levels28,29 with its known adverse effect on the cardiovascular system c) Hypothyroidism is strongly associated with arterial hypertension (especially diastolic)30,31 via sympathetic and adrenal activation30, and increased aortic stiffness31 d) The insufficient concentration of thyroid hormones induces a hypercoagulable state32. A precise relationship between overt hypothyroidism and CAD has not been confirmed although data linking these two conditions have been demonstrated in autopsy studies24,25.

Substitution therapy with L-thyroxine significantly improves the above described abnormalities of lipid metabolism and increases the previously low biliary cholesterol excretion33. In a recent meta-analysis, the mean decrease of serum total and LDL cholesterol levels after T4 substitution was -7.9 mg/dl and -10 mg/dl, respectively34. The reduction was larger in individuals with higher pre-treatment cholesterol levels and in hypothyroid individuals previously taking suboptimal T4 doses34. Serum HDL cholesterol levels tend to decrease with thyroid replacement, but this is a less consistent finding35. Serum Lp(a) levels also tend to decrease with restoration of euthyroidism11,23. In general, changes in serum lipoproteins in hypothyroid patients are correlated with changes in free thyroxin (FT4)36. Normally, it takes 4-6 weeks of replacement therapy with thyroxin to correct dyslipidemia in overt hypothyroidism. Superimposed dyslipidemia should be taken into account in cases of failure of substitution therapy to normalize the lipid profile, despite the restoration of euthyroidism1.

Prevalence of overt hypothyroidism in patients with dyslipidemia is not low; in one of our studies, 2.8 % of the patients who were examined in our outpatient lipid clinic had elevated levels of TSH and reduced levels of FT411. After restoration of euthyroidism with levothyroxine therapy, a significant decrease of serum levels of total and LDL cholesterol, apolipoprotein B and Lp(a) was observed while levels of HDL cholesterol, triglycerides and apolipoprotein AI were not changed significantly11.


Subclinical hypothyroidism (SH), defined as the clinical status of mildly elevated serum TSH levels (up to 10 mU/L) with normal levels of FT4 and FT3, is a far more common disorder than overt hypothyroidism with a higher prevalence among women and older subjects34,37. Patients with SH tend to have higher levels of serum total and LDL cholesterol34,38,39. Even subjects with high normal TSH levels (2-4 mU/L) but with positive antithyroid antibodies may present with elevated cholesterol levels40. Among 248 patients who were followed in our outpatient lipid clinic for a period of 2 years, 11 patients (4.4%, 9 female, 2 male) had SH11. In a cross-sectional study we evaluated the serum lipid parameters of 66 patients with SH and 75 age- and sex-matched euthyroid controls41. Patients with SH had significantly higher levels of total cholesterol, LDL cholesterol, apolipoprotein B and Lp(a), whereas levels of triglycerides, HDL cholesterol and apolipoprotein AI did not differ significantly compared to euthyroid controls41.

Certain studies have indicated that subclinical hypothyroidism has been associated with increased risk of CAD, especially in women with antibodies to thyroid peroxidase as well as in smokers, the SH-induced lipid abnormalities offering the most obvious explanation for this association42,43. Moreover, SH impairs ventricular function as well as cardiovascular and respiratory adaptation to effort and, decreases heart rate variability impairs flow-mediated vasodilation, which is a marker of endothelial function43. Smoking may deteriorate the lipid profile in women with SH and aggravate the degree of thyroid failure, thus contributing to the development of atherosclerosis44,45.

Several studies have shown conflicting results concerning the effect of levothyroxine substitution therapy on lipid parameters in patients with SH23,25,34,39,40,46,47. In a reanalysis, total cholesterol was decreased by 15 mg/dl irrespective of the initial level39. In another follow-up study, restoration of euthyroidism in 37 patients with SH resulted in no significant changes in serum lipid parameters except for a significant decrease in HDL cholesterol concentration by 6.8%41. However, patients with high pre-treatment total cholesterol levels (TC > 240 mg/dl) as well as high pre-treatment levels of serum TSH (> 10 mU/L) exhibited a significant reduction in both total and LDL cholesterol levels following thyroid substitution therapy41. On the other hand, levothyroxine replacement did not produce any significant changes in Lp(a) concentrations in any of the studied groups23,41.

Although it is clear that thyroid replacement therapy has beneficial effects on the serum lipid profile and on the risk of CAD in patients with overt hypothyroidism, the question of whether SH should be treated or not is still pending. It seems that thyroid substitution, if used, would be most beneficial in patients with prominent thyroid dysfunction (TSH levels > 10 mU/L), higher initial cholesterol levels and in smokers44. On the other hand, a possible thyroid substitution-induced decrease of HDL cholesterol concentration could undermine the beneficial effect of total and LDL cholesterol reduction in these patients. When treating people with angina pectoris or heart disease, one should be very cautious since thyroxin therapy may exacerbate angina or promote cardiac arrhythmia.

In conclusion, subclinical hypothyroidism is relatively common among hypercholesterolemic patients. Thus, the measurement of serum TSH levels should be included in the screening of patients with dyslipidemia1,46,47. Hypercholesterolemic patients with SH may be treated with thyroxin substitution therapy since the restoration of euthyroidism can effectively lower the lipid levels, relieve certain symptoms and may prevent progression to overt hypothyroidism48.


It has recently been reported that euthyroid males and postmenopausal females with evidence of thyroid autoimmunity (increased titers of thyroperoxidase and/or thyroglobulin autoantibodies) have increased Lp(a) levels49. In one study, the levels of Lp(a) in 22 euthyroid subjects (9 males and 13 postmenopausal females) with thyroid autoimmunity were compared with those of 64 age- and sex-matched controls without thyroid autoimmunity50. There were no significant differences in the values of lipid parameters, including Lp(a), between the two groups even when apo(a) phenotypes, which are known to influence Lp(a) levels, were taken into account50. Moreover, no significant difference in the Lp(a) levels was found in euthyroid patients with chronic renal failure regardless of the presence of thyroid autoimmunity, the apo(a) phenotype, the stage of renal failure and the mode of dialysis in end stage patients51. Finally, the presence of thyroid autoimmunity does not influence the serum lipid parameters even in patients with SH41.


Despite the increased activity of the HMG-CoA reductase, levels of total cholesterol, LDL cholesterol, apolipoprotein B and Lp(a) tend to decrease in patients with clinical or subclinical hyperthyroidism due to increased bile excretion of cholesterol and mainly to increased LDL receptor gene expression resulting in enhanced LDL receptor-mediated catabolism of LDL particles6,52. Furthermore, HDL cholesterol levels are also decreased in hyperthyroidism due to increased CETP-mediated transfer of cholesteryl esters from HDL to VLDL and increased HL-mediated catabolism of HDL26,52. Triglyceride levels remain unchanged. Therapy of hyperthyroidism results in restoration of the above mentioned alterations of lipid metabolism6,52. Furthermore, hyperthyroidism results in enhanced LDL oxidability, which is strictly related to FT4 levels27.

The incidence of hyperthyroidism is lower than that of hypothyroidism in the general population (2.2 vs 9.5%)3, as well as in patients attending a lipid clinic, since only 3 out of the 248 patients of our study had thyrotoxicosis11. However, hyperthyroidism constitutes not only a significant cause of acquired hypobetalipoproteinemia but can also be the underlying cause of unexpected improvement of the lipid profile of hyperlipidemic patients53. In the latter case, therapy of thyrotoxicosis restores the lipid parameters to the previously elevated levels53.


Biochemical screening for thyroid dysfunction is of paramount importance in all dyslipidemic patients, as well as in all patients with unexpected improvement or worsening of their lipid profile. Underlying thyroid disorders should be recognized and treated in this setting. On the other hand, there is an absolute need for large studies designed to answer the question as to whether thyroid abnormalities (and especially SH) are associated with increased risk for CAD and whether therapy of these disorders might influence cardiovascular mortality.

1. Duntas LH, 2002 Thyroid disease and lipids. Thyroid 12: 287-293.
2. Friis T, Pedersen LR, 1987 Serum lipids in hyper- and hypothyroidism before and after treatment. Clin Chim Acta 162: 155-163.
3. Canaris GJ, Manowitz NR, Mayor G, Ridgway C, 2000 The Colorado thyroid disease prevalence study. Arch Intern Med 160: 526-534.
4. O'Brien T, Dinneen SF, O'Brien PC, Palumbo PJ, 1990 Hyperlipidemia in patients with primary and secondary hypothyroidism. Mayo Clin Endocrinol 68: 860-866.
5. Muls E, Rossenen M, Blaton V, Lesaffre E, Lamberigts G, De Moor P, 1984 Serum lipids and apolipoproteins AI, AII and B in primary hypothyroidism before and during treatment. Eur J Clin Invest 14: 12-15.
6. Kung A, Pang R, Lander I, Lam K, Janus E, 1995 Changes in serum lipoprotein (a) and lipids during treatment of hyperthyroidism. Clin Chem 41: 226-231.
7. Ness GC, Dugan RE, Lakshmanan MR, Nepokroeff CM, Porter JW, 1973 Stimulation of hepatic ™-hydroxy-methyl-glutaryl Coenzyme A reductase in hypophysectomized rats by L-triiodothyronine. Proc Natl Acad Sci USA 70: 3839-3842.
8. Bakker O, Hudig F, Meijssen S, Wiersinga WM, 1998 Effects of triiodothyronine and amiodarone on the promoter of the human LDL receptor gene. Biochem Biophys Res Commun 240: 517-521.
9. Lagrost L, 1994 Regulation of cholesteryl ester transfer protein (CETP) activity: Review of in vitro and in vivo studies. Biochem Biophys Acta 1215: 209-236.
10. Kussi T, Sacrinen P, Nikkila EA, 1980 Evidence for the role of hepatic endothelial lipase in the metabolism of plasma high density lipoprotein 2 in man. Atherosclerosis 36: 589-593.
11. ’simihodimos V, Bairaktari E, Tzallas C, Miltiadus G, Liberopoulos E, Elisaf M, 1999 The incidence of thyroid function abnormalities in patients attending an outpatient lipid clinic. Thyroid 9: 365-358.
12. Stone NJ, 1994 Secondary causes of hyperlipidemia. Med Clin North Am 78: 117-141.
13. Walton KW, Scott PJ, Dykes PW, Davies JWL, 1965 The significance of alterations in serum lipids in thyroid dysfunction. II. Alterations of the metabolism and the turnover of 131I-low density lipoproteins in hypothyroidism and thyrotoxicosis. Clin Sci 29: 984-994.
14. Thompson GR, Soutar AK, Spengel FA, Jadhav A, Gavigan S, Myant NB, 1981 Defects of the receptor-mediated low density lipoprotein metabolism in homozygous familiar hypercholesterolaemia and hypothyroidism in vivo. Proc Natl Acad Sci USA 78: 2591-2595.
15. Abrams JJ, Grundy SM, 1981 Cholesterol metabolism in hypothyroidism and hyperthyroidism in man. J Lipid Res 22: 323-338.
16. Nikkilia EA, Kekki M, 1972 Plasma triglyceride metabolism in thyroid disease. J Clin Invest 51: 2103-2114.
17. Clifford C, Salel AF, Shore B, Shore V, Mason DT, 1975 Mechanisms of lipoprotein alterations in patients with idiopathic hypothyroidism. Circulation 18: 51-52.
18. Hazzard WR, Biemman EL, 1972 Aggravation of broad-beta disease (Type III hyperlipoproteinaemia) by hypothyroidism. Arch Intern Med 130: 822-828.
19. Heimberg M, Olubadewo JO, Wilcox HG, 1985 Plasma lipoproteins and regulation of hepatic metabolism of fatty acids in altered thyroid states. Endocrine Rev 6: 590-607.
20. Dullaart RPF, Hoogenberg K, Groener JEM, Dikkeschei LD, Erkelens DW, Doorenbus H, 1990 The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high-density lipoproteins. Eur J Clin Invest 20: 581-587.
21. Lam KSL, Chan MK, Yeung RTT, 1986 High-density lipoprotein cholesterol, hepatic lipase and lipoprotein lipase activities in thyroid dysfunction - effects of treatment. Quarterly J Med 229: 513-521.
22. De Bruin TWA, van Barlingen H, van Linde-Sibenius Trip M, van Vuurst de Vries AR, Akveld MJ, Erkelens DW, 1993 Lipoprotein (a) and apolipoprotein B plasma concentrations in hypothyroid, euthyroid and hyperthyroid states. J Clin Endocrinol Metab 76: 121-126.
23. Tzotzas T, Krassas GE, Konstadinidis T, Bougoulia M, 2000 Changes in lipoprotein (a) levels in overt and subclinical hypothyroidism before and during treatment. Thyroid 10: 803-808.
24. Tunbridge WMG, Evered DC, Hall R, et al, 1977 Lipid profiles and cardiovascular disease in the Wickham areas with particular reference to thyroid failure. Clin Endocrinol 7: 495-508.
25. Pucci E, Chiovato L, Pinchera A, 2000 Thyroid and lipid metabolism. Int J Obesity 24: 109-112.
26. Dieckman T, Demacker PN, Kasyelein JJ, Stanenhoef AF, Wiersinga WM, 1998 Increased oxidability of low-density lipoproteins in hypothyroidism. J Clin Endocrinol Metab 83: 1752-1755.
27. Costantini F, Pierdomenico SD, de Cesare D, de Remigis P, Bucciarelli T, Bittolo-Bon G, Cazzolato G, Nubile G, Guagnano MT, Sensi S, Cuccurulo F, Mazzeti A, 1998 Effect of thyroid function on LDL oxidation. Arterioscler Thromb Vasc Biol 18: 732-737.
28. Morris MS, Bostom AG, Jacques PF, Selhub S, Rosenberg IH, 2001 Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third US National Health and Nutrition Examination Survey. Atherosclerosis 155: 195-200.
29. Bicikova M, Tallova J, Hill M, Vanuga A, Putz Z, Tomandl J, 2001 Effect of treatment of hypothyroidism on the plasma concentrations of neuroactive steroids and homocysteine. Clin Chem Lab Med 39: 753-757.
30. Fommei E, Iervasi G, 2002 The role of thyroid hormone in blood pressure homeostasis: evidence from short-term hypothyroidism in humans. J Clin Endocrinol Metab 87: 1996-2000.
31. Dernellis J, Panaretou M, 2002 Effects of thyroid replacement therapy on arterial blood pressure in patients with hypertension and hypothyroidism. Am Heart J 143: 718-724.
32. Muller B, Tsakiris DA, Roth CB, Guglielmetti M, Staub JJ, Marbet GA, 2001 Haemostatic profile in hypothyroidism as potential risk factor for vascular or thrombotic disease. Eur J Clin Invest 31: 131-137.
33. Miettinen T, 1968 Mechanism of serum cholesterol reduction by thyroid hormones in hypothyroidism. J Lab Clin Med 71: 537-547.
34. Danese MD, Ladenson PW, Meinert CL, Powe NR, 2000 Clinical review 115: effect of thyroxine therapy on serum lipoproteins in patients with mild thyroid failure: a quantitative review of the literature. J Clin Endocrinol Metab 85: 2993-3001.
35. Verdugo C, Perrot L, Ponsin G, Valentin C, Berthezene F, 1987 Time-course of alterations of high density lipoproteins (HDL) during thyroxine administration to hypothyroid women. Eur J Clin Invest 17: 313-316.
36. Wiseman SA, Powell JT, Humphiries SE, Press M, 1993 The magnitude of the hypercholesterolemia of hypothyroidism is associated with variation in the low density lipoprotein receptor gene. J Clin Endocrinol Metab 77: 108-112.
37. Samuels MH, 1998 Subclinical thyroid disease in the elderly. Thyroid 9: 803-813.
38. Luboshitzky R, Aviv A, Herer P, Lavie L, 2002 Risk factors for cardiovascular disease in women with subclinical hypothyroidism. Thyroid 12: 421-425.
39. Tanis BC, Westendorp RGJ, Smelt AHM, 1996 Effect of thyroid substitution on hypercholesterolemia in patients with subclinical hypothyroidism: a reanalysis of intervention studies. Clin Endocrinol 44: 643-649.
40. Michalopoulou G, Alevizaki M, Piperingos G, Mitsibounas D, Mantzos E, Adamopoulos P, Koutras D, 1998 High serum cholesterol levels in persons with 'high-normal' TSH levels: should one extend the definition of subclinical hypothyroidism?. Eur J Endocrinol 138: 141-145.
41. Efstathiadou Z, Bitsis S, Milionis HJ, Kukuvitis A, Bairaktari E, Elisaf M, Tsatsoulis A, 2001 Lipid profile in subclinical hypothyroidism: is L-thyroxine substitution beneficial?. Eur J Endocrinol 145: 705-710.
42. Hak AE, Pols HAP, Visser TJ, Drexhage HA, Hoffman A, Witteman JCM, 2000 Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: the Rotterdam Study. Ann Intern Med 132: 270-278.
43. Kahaly GJ, 2000 Cardiovascular and atherogenic aspects of subclinical hypothyroidism. Thyroid 10: 665-679.
44. Muller B, Zulewski H, Huber P, Ratcliffe JG, Staub JJ, 1995 Impaired action of thyroid hormone associated with smoking in women with hypothyroidism. N Engl J Med 333: 964-969.
45. Pontikides N, Krassas GE, 2002 Influence of cigarette smoking on thyroid function, goiter formation and autoimmune thyroid disorders. Hormones 1: 91-98.
46. Cooper DS, 1998 Subclinical thyroid disease: a clinician's perspective. Ann Intern Med 129: 135-138.
47. Helfand M, Redfern CC, 1998 Screening for thyroid disease: an update. Ann Intern Med 129: 144-158.
48. Ayala AR, Danese MD, Ladenson PW, 2000 When to treat mild hypothyroidism. Endocrinol Metab Clin North Am 29: 399-415.
49. Lotz H, Salabe GB, 1997 Lipoprotein (a) increase associated with thyroid autoimmunity. Eur J Endocrinol 136: 87-91.
50. Bairaktari ET, Tselepis AD, Milionis HJ, Elisaf MS, 1999 Lipoprotein (a) levels, apolipoprotein (a) phenotypes and thyroid autoimmunity. Eur J Endocrinol 140: 474-476.
51. Bairaktari ET, Milionis HJ, Katopodis K, Tzallas C, Tselepis AD, Tsolas O, Siamopoulos KC, Elisaf MS, 2000 Lipoprotein (a), apolipoprotein (a) phenotypes, and thyroid autoimmunity in uremic patients. The Endocrinologist 10: 383-388.
52. Aviram M, Luboshitzky R, Brook JG, 1982 Lipid and lipoprotein pattern in thyroid dysfunction and the effect of therapy. Clin Biochem 15: 62-66.
53. Liberopoulos E, Miltiadous G, Elisaf M, 2001 Impressive lipid changes following hypolipidaemic drug administration can unveil subclinical hyperthyroidism. Diabet Obes Metab 3: 97-98.

Address correspondence and requests for reprints to:
Moses S Elisaf, MD, FACA, FRSH, Department of Internal Medicine,
University of Ioannina, 451 10 Ioannina, Greece,
Tel. +306510-97509, Fax +306510-97016,
e-mail: egepi@cc.uoi.gr

Received 10-06-02, Revised 08-07-02, Accepted 20-08-02