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www.kardiologiapolska.pl

Kardiologia Polska 2012; 70, 12: 1320 ISSN 0022–9032

LIST DO REDAKCJI / LETTER TO THE EDITOR

Address for correspondence:

Address for correspondence:

Address for correspondence:

Address for correspondence:

Address for correspondence:

Dr Sait Demirkol, Department of Cardiology, Gulhane School of Medicine, Tevfik Saglam St., 06018 Etlik-Ankara, Turkey, tel: +90-312-3044281, fax: +90-312-3044250, e-mail: saitdemirkol@yahoo.com

Copyright © Polskie Towarzystwo Kardiologiczne

Insulin like growth factor−1 and lipoprotein metabolism in stable angina patients

Sait Demirkol

l

, Ömer Kurt

2

, Seref Demirbas

2

, Muharrem Akhan

2

, Sevket Balta

1

, Mustafa Cakar

2

1Department of Cardiology, Gulhane Medical Academy, Ankara, Turkey

2Department of Internal Medicine, Gulhane Medical Academy, Ankara, Turkey

We read the article: ”Association between insulin like growth factor-1 and lipoprotein metabolism in stable angina patients on statin therapy: a pilot study” by Burchardt et al.

[1] with interest. The authors concluded that owing to asso- ciation with products of lipid oxidation, oxidised proteins, and high values of Lp(a); IGF-1 and IGFBP3 levels could be useful indicators of atherosclerosis progression. We believe that these findings should act as a guide for further studies.

IGF-1 plays an important role in the cell protection of mul- tiple systems, where its signal transduction helps to preserve tis- sues from hypoxia, ischaemia and oxidative stress. IGF-1 and its binding proteins (IGFBP) have association with hypertensive pa- tients with left ventricular hypertrophy and arteriosclerosis, espe- cially coronary artery sclerosis [2, 3]. IGF is produced mostly by the liver and transported by their own binding proteins (IGBP) in the circulation. Seven different IGFBPs have been reported to date, with IGFBP-3 being the most abundant. The effects of the-

se proteins not only bind IGFs, but also have receptors in tissues.

An increase in IGFBP-3 levels in patient with a chronic kidney disease (CKD) is shown [4]. IGF levels have been affected in dif- ferent ways in CKD. It would be better if it could be clearly sta- ted that CKD and liver diseases are excluded from the study.

Conflict of interests: none declared References

1. Burchardt P, Tabaczewski P, Goździcka Józefiak A et al. Asso- ciation between insulin like growth factor-1 and lipoprotein me- tabolism in stable angina patients on statin therapy: a pilot study.

Kardiol Pol, 2012; 70: 1017–1022.

2. Burchardt P, Goździcka-Józefiak A, Siminiak T. IGF-1: a new risk factor for coronary atherosclerosis. Kardiol Pol, 2006; 64:

1297–1302.

3. Wilk BK, Skrzypek KS, Śliwa A et al. Peripheral blood concen- trations of TGFb1, IGF-1 and bFGF and remodelling of the left ventricle and blood vessels in hypertensive patients. Kardiol Pol, 2010; 68: 996–1002.

Author’s response

I would like to thank Demirkol et al. for their interest and their comments on our article [1]. As to their remarks, of co- urse we agree on the impact of both — kidney and liver — on IGFBP3 and IGF-1 plasma levels. However, the exclusion criteria from the study were provided in the quoted article [2]. For the sake of thoroughness, we would like to emphasi- se that patients with documented liver disease or its dysfunc- tion (ALT, AST > ULN) were excluded from the study. Also excluded were patients with chronic kidney disease or their dysfunction qualified when GFR was < 60 mL/min. We must admit that the method of assessing GFR by the MDRD rule used by us has its own limitations. Secondly, GFR 60 mL/min was a priori assumed as the cut-off point for kidney disease.

Thus, patients with kidney disease in stage I by Kidney Dise- ases Outcome Quality Initiative (without GFR limitation) or

in stage II (90 < GFR > 60 mL/min) could be included in the study, which is another limitation of our protocol.

Conflict of interest: none declared References

1. Burchardt P, Tabaczewski P, Goździcka-Józefiak et al. Associa- tion between insulin like growth factor-1 and lipoprotein me- tabolism in stable angina patients on statin therapy: a pilot study.

Kardiol Pol, 2012; 70: 1017–1022.

2. Burchardt P, Goździcka-Józefiak A, Żurawski J et al. Are eleva- ted levels of IGF-1 caused by coronary arteriesoclerosis? Mole- cular and clinical analysis. Protein J, 2010; 29: 538–544.

Paweł Burchardt, PhD, MD, MSc Division of Cardiology-Intensive Therapy, Poznan University of Medical Sciences, Poland

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