View More View Less
  • 1 NAGY GÉN Diagnosztikai és Kutatási Kft. Budapest
  • | 2 Semmelweis Egyetem, Általános Orvostudományi Kar I. Szülészeti és Nőgyógyászati Klinika Budapest
  • | 3 Zirc Városi Erzsébet Kórház Rendelőintézet Zirc
  • | 4 Pécsi Tudományegyetem Pécs
  • | 5 Genetikával az Egészségért Egyesület Budapest
Open access

A szív-ér rendszeri megbetegedések világszerte a leggyakoribb halálozási okok közé tartoznak. Az utóbbi évek tudományos eredményei arra utalnak, hogy a hyperhomocystinaemia a szív-ér rendszeri betegségek egyik jelentős kockázati tényezője. A homocisztein és a folsav metabolizmusát befolyásoló gének közül a metilén-tetrahidrofolát-reduktáz (MTHFR) polimorfizmusai – az MTHFR C677T és az MTHFR A1298C – összefüggésbe hozhatóak a cardiovascularis betegségekkel. A magas vérnyomás kialakulásában az MTHFR C677T polimorfizmusa is hajlamosító tényező lehet. Nem egyértelmű ugyanakkor az összefüggés a hyperhomocystinaemia és az MTHFR említett génvariánsai között. A legújabb kutatási eredmények szerint az 5-metil-tetrahidrofolát (5-MTHF) is befolyásolja az endothelfunkciókat. Így valószínűsíthető, hogy az MTHFR polimorfizmusai a homociszteintől függetlenül is hajlamosítanak a magas vérnyomásra és a szív-ér rendszeri megbetegedések kialakulására. Ennek tükrében kiemelkedő fontosságú lehet a folsavanyagcserében részt vevő génpolimorfizmusok és a cardiovascularis kockázati tényezők közötti kapcsolat vizsgálata és a molekuláris patomechanizmusok feltárása. Orv. Hetil., 2012, 153, 445–453.

  • Clarke, R., Daly, L., Robinson, K., et al.: Hyperhomocysteinemia: an independent risk factor for vascular disease. N. Engl. J. Med., 1991, 324, 1149–1455.

    Robinson K. , 'Hyperhomocysteinemia: an independent risk factor for vascular disease ' (1991 ) 324 N. Engl. J. Med. : 1149 -1455.

    • Search Google Scholar
  • Wang, W., Lee, E. T., Fabsitz, R. R., et al.: A longitudinal study of hypertension risk factors and their relation to cardiovascular disease: the Strong Heart Study. Hypertension, 2006, 47, 403–409.

    Fabsitz R. R. , 'A longitudinal study of hypertension risk factors and their relation to cardiovascular disease: the Strong Heart Study ' (2006 ) 47 Hypertension : 403 -409.

    • Search Google Scholar
  • Ando, K., Fujita, T.: Control of morning blood pressure: the best preventive strategy against stroke. Hypertens. Res., 2006, 29, 555–556.

    Fujita T. , 'Control of morning blood pressure: the best preventive strategy against stroke ' (2006 ) 29 Hypertens. Res. : 555 -556.

    • Search Google Scholar
  • Selhub, J., Jacques, P. F., Wilson, P. W., et al.: Vitamin status and intake as primary determinants of homocysteinemia in an elderly population. JAMA, 1993, 270, 2693–2698.

    Wilson P. W. , 'Vitamin status and intake as primary determinants of homocysteinemia in an elderly population ' (1993 ) 270 JAMA : 2693 -2698.

    • Search Google Scholar
  • Refsum, H., Ueland, P. M., Nygård, O., et al.: Homocysteine and cardiovascular disease. Review. Annu. Rev. Med., 1998, 49, 31–62.

    Nygård O. , 'Homocysteine and cardiovascular disease ' (1998 ) 49 Review. Annu. Rev. Med. : 31 -62.

    • Search Google Scholar
  • Nygård, O., Refsum, H., Ueland, P. M., et al.: Major lifestyle determinants of plasma total homocysteine distribution: the Hordaland Homocysteine Study. Am. J. Clin. Nutr., 1998, 67, 263–270.

    Ueland P. M. , 'Major lifestyle determinants of plasma total homocysteine distribution: the Hordaland Homocysteine Study ' (1998 ) 67 Am. J. Clin. Nutr. : 263 -270.

    • Search Google Scholar
  • Ueland, P. M., Nygård, O., Vollset, S. E., et al.: The Hordaland Homocysteine Studies. Lipids, 2001, 36 (Suppl.), S33–S39.

    Vollset S. E. , 'The Hordaland Homocysteine Studies ' (2001 ) 36 Lipids : S33 -S39.

  • Van der Gaag, M. S., Ubbink, J. B., Sillanaukee, P., et al.: Effect of consumption of red wine, spirits, and beer on serum homocysteine. Lancet, 2000, 355, 1522.

    Sillanaukee P. , 'Effect of consumption of red wine, spirits, and beer on serum homocysteine ' (2000 ) 355 Lancet : 1522 -.

    • Search Google Scholar
  • Ubbink, J. B., Vermaak, W. J., van der Merwe, A., et al.: Vitamin requirements for the treatment of hyperhomocysteinemia in humans. J. Nutr., 1994, 124, 1927–1933.

    Merwe A. , 'Vitamin requirements for the treatment of hyperhomocysteinemia in humans ' (1994 ) 124 J. Nutr. : 1927 -1933.

    • Search Google Scholar
  • Kanani, P. M., Sinkey, C. A., Browning, R. L., et al.: Role of oxidant stress in endothelial dysfunction produced by experimental hyperhomocyst(e)inemia in humans. Circulation, 1999, 100, 1161–1168.

    Browning R. L. , 'Role of oxidant stress in endothelial dysfunction produced by experimental hyperhomocyst(e)inemia in humans ' (1999 ) 100 Circulation : 1161 -1168.

    • Search Google Scholar
  • Upchurch, G. R., Jr., Welch, G. N., Fabian, A. J., et al.: Homocyst(e)ine decreases bioavailable nitric oxide by a mechanism involving glutathione peroxidase. J. Biol. Chem., 1997, 272, 17012–17017.

    Fabian A. J. , 'Homocyst(e)ine decreases bioavailable nitric oxide by a mechanism involving glutathione peroxidase ' (1997 ) 272 J. Biol. Chem. : 17012 -17017.

    • Search Google Scholar
  • Sainani, G. S., Sainani, R.: Homocysteine and its role in the pathogenesis of atherosclerotic vascular disease. J. Assoc. Physicians India, 2002, 50 (Suppl.), 16–23.

    Sainani R. , 'Homocysteine and its role in the pathogenesis of atherosclerotic vascular disease ' (2002 ) 50 J. Assoc. Physicians India : 16 -23.

    • Search Google Scholar
  • Perna, A. F., Ingrosso, D., De Santo, N. G.: Homocysteine and oxidative stress. Amino Acids, 2003, 25, 409–417.

    Santo N. G. , 'Homocysteine and oxidative stress ' (2003 ) 25 Amino Acids : 409 -417.

  • Tsai, J. C., Perrella, M. A., Yoshizumi, M., et al.: Promotion of vascular smooth muscle cell growth by homocysteine: a link to atherosclerosis. Proc. Natl. Acad. Sci. USA, 1994, 91, 6369–6373.

    Yoshizumi M. , 'Promotion of vascular smooth muscle cell growth by homocysteine: a link to atherosclerosis ' (1994 ) 91 Proc. Natl. Acad. Sci. USA : 6369 -6373.

    • Search Google Scholar
  • Majors, A. K., Sengupta, S., Jacobsen, D. W., et al.: Upregulation of smooth muscle cell collagen production by homocysteine-insight into the pathogenesis of homocystinuria. Mol. Genet. Metab., 2002, 76, 92–99.

    Jacobsen D. W. , 'Upregulation of smooth muscle cell collagen production by homocysteine-insight into the pathogenesis of homocystinuria ' (2002 ) 76 Mol. Genet. Metab. : 92 -99.

    • Search Google Scholar
  • Durand, P., Lussier-Cacan, S., Blache, D.: Acute methionine load-induced hyperhomocysteinemia enhances platelet aggregation, thromboxane biosynthesis, and macrophage-derived tissue factor activity in rats. FASEB J., 1997, 11, 1157–1168.

    Blache D. , 'Acute methionine load-induced hyperhomocysteinemia enhances platelet aggregation, thromboxane biosynthesis, and macrophage-derived tissue factor activity in rats ' (1997 ) 11 FASEB J. : 1157 -1168.

    • Search Google Scholar
  • Poddar, R., Sivasubramanian, N., DiBello, P. M., et al.: Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells: implications for vascular disease. Circulation, 2001, 103, 2717–2723.

    DiBello P. M. , 'Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells: implications for vascular disease ' (2001 ) 103 Circulation : 2717 -2723.

    • Search Google Scholar
  • Boushey, C. J., Beresford, S. A., Omenn, G. S., et al.: A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA, 1995, 274, 1049–1057.

    Omenn G. S. , 'A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes ' (1995 ) 274 JAMA : 1049 -1057.

    • Search Google Scholar
  • Homocysteine Studies Collaboration: Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA, 2002, 288, 2015–2022.

    'Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis ' (2002 ) 288 JAMA : 2015 -2022.

    • Search Google Scholar
  • Wald, D. S., Law, M., Morris, J. K.: Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis. BMJ, 2002, 325, 1202.

    Morris J. K. , 'Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis ' (2002 ) 325 BMJ : 1202 -.

    • Search Google Scholar
  • Wang, X., Qin, X., Demirtas, H., et al.: Efficacy of folic acid supplementation in stroke prevention: a meta-analysis. Lancet, 2007, 369, 1876–1882.

    Demirtas H. , 'Efficacy of folic acid supplementation in stroke prevention: a meta-analysis ' (2007 ) 369 Lancet : 1876 -1882.

    • Search Google Scholar
  • Yang, Q., Botto, L. D., Erickson, J. D., et al.: Improvement in stroke mortality in Canada and the United States, 1990 to 2002. Circulation, 2006, 113, 1335–1343.

    Erickson J. D. , 'Improvement in stroke mortality in Canada and the United States, 1990 to 2002 ' (2006 ) 113 Circulation : 1335 -1343.

    • Search Google Scholar
  • Bønaa, K. H., Njølstad, I., Ueland, P. M., et al.: NORVIT Trial Investigators: Homocysteine lowering and cardiovascular events after acute myocardial infarction. N. Engl. J. Med., 2006, 354, 1578–1588.

    Ueland P. M. , 'NORVIT Trial Investigators: Homocysteine lowering and cardiovascular events after acute myocardial infarction ' (2006 ) 354 N. Engl. J. Med. : 1578 -1588.

    • Search Google Scholar
  • Lonn, E., Yusuf, S., Arnold, M. J., et al.: The Heart Outcomes Prevention Evaluation (HOPE) 2 Investigators: Homocysteine lowering with folic acid and B vitamins in vascular disease. N. Engl. J. Med., 2006, 354, 1567–1577.

    Arnold M. J. , 'The Heart Outcomes Prevention Evaluation (HOPE) 2 Investigators: Homocysteine lowering with folic acid and B vitamins in vascular disease ' (2006 ) 354 N. Engl. J. Med. : 1567 -1577.

    • Search Google Scholar
  • Nygård, O., Vollset, S. E., Refsum, H., et al.: Total plasma homocysteine and cardiovascular risk profile. The Hordaland Homocysteine Study. JAMA, 1995, 274, 1526–1533.

    Refsum H. , 'Total plasma homocysteine and cardiovascular risk profile. The Hordaland Homocysteine Study ' (1995 ) 274 JAMA : 1526 -1533.

    • Search Google Scholar
  • Lim, U., Cassano, P. A.: Homocysteine and blood pressure in the Third National Health and Nutrition Examination Survey, 1988–1994. Am. J. Epidemiol., 2002, 156, 1105–1113.

    Cassano P. A. , 'Homocysteine and blood pressure in the Third National Health and Nutrition Examination Survey, 1988–1994 ' (2002 ) 156 Am. J. Epidemiol. : 1105 -1113.

    • Search Google Scholar
  • Sundström, J., Sullivan, L., D’Agostino, R. B., et al.: Plasma homocysteine, hypertension incidence, and blood pressure tracking: the Framingham Heart Study. Hypertension, 2003, 42, 1100–1105.

    D’Agostino R. B. , 'Plasma homocysteine, hypertension incidence, and blood pressure tracking: the Framingham Heart Study ' (2003 ) 42 Hypertension : 1100 -1105.

    • Search Google Scholar
  • Jacques, P. F., Bostom, A. G., Wilson, P. W., et al.: Determinants of plasma total homocysteine concentration in the Framingham Offspring cohort. Am. J. Clin. Nutr., 2001, 73, 613–621.

    Wilson P. W. , 'Determinants of plasma total homocysteine concentration in the Framingham Offspring cohort ' (2001 ) 73 Am. J. Clin. Nutr. : 613 -621.

    • Search Google Scholar
  • Goyette, P., Pai, A., Milos, R., et al.: Gene structure of human and mouse methylenetetrahydrofolate reductase (MTHFR). Mamm. Genome, 1998, 9, 652–656.

    Milos R. , 'Gene structure of human and mouse methylenetetrahydrofolate reductase (MTHFR) ' (1998 ) 9 Mamm. Genome : 652 -656.

    • Search Google Scholar
  • Kang, S. S., Zhou, J., Wong, P. W., et al.: Intermediate homocysteinemia: a thermolabile variant of methylenetetrahydrofolate reductase. Am. J. Hum. Genet., 1988, 43, 414–421.

    Wong P. W. , 'Intermediate homocysteinemia: a thermolabile variant of methylenetetrahydrofolate reductase ' (1988 ) 43 Am. J. Hum. Genet. : 414 -421.

    • Search Google Scholar
  • Kang, S. S., Wong, P. W., Susmano, A., et al.: Thermolabile methylenetetrahydrofolate reductase: an inherited risk factor for coronary artery disease. Am. J. Hum. Genet., 1991, 48, 536–545.

    Susmano A. , 'Thermolabile methylenetetrahydrofolate reductase: an inherited risk factor for coronary artery disease ' (1991 ) 48 Am. J. Hum. Genet. : 536 -545.

    • Search Google Scholar
  • Guenther, B. D., Sheppard, C. A., Tran, P., et al.: The structure and properties of methylenetetrahydrofolate reductase from Escherichia coli suggest how folate ameliorates human hyperhomocysteinemia. Nat. Struct. Biol., 1999, 6, 359–365.

    Tran P. , 'The structure and properties of methylenetetrahydrofolate reductase from Escherichia coli suggest how folate ameliorates human hyperhomocysteinemia ' (1999 ) 6 Nat. Struct. Biol. : 359 -365.

    • Search Google Scholar
  • Czeizel, E., Tímár, L., Botto, L.: Prevalence of methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) in the Hungarian population. [A metiléntetrahidrofolát-reduktáz (MTHFR) gén polimorfizmusának (C677T) magyarországi gyakorisága.]. Orv. Hetil., 2001, 142, 1227–1229. [Hungarian]

    Botto L. , 'Prevalence of methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) in the Hungarian population. [A metiléntetrahidrofolát-reduktáz (MTHFR) gén polimorfizmusának (C677T) magyarországi gyakorisága.] ' (2001 ) 142 Orv. Hetil. : 1227 -1229.

    • Search Google Scholar
  • Brattström, L., Wilcken, D. E., Ohrvik, J., et al.: Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis. Circulation, 1998, 98, 2520–2526.

    Ohrvik J. , 'Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis ' (1998 ) 98 Circulation : 2520 -2526.

    • Search Google Scholar
  • Li, Y. Y.: Methylenetetrahydrofolate reductase C677T gene polymorphism and coronary artery disease in a Chinese Han population: a meta-analysis. Metabolism, 2011. [Epub ahead of print.]

  • Girelli, D., Martinelli, N., Pizzolo, F., et al.: The interaction between MTHFR 677 C–>T genotype and folate status is a determinant of coronary atherosclerosis risk. J. Nutr., 2003, 133, 1281–1285.

    Pizzolo F. , 'The interaction between MTHFR 677 C–>T genotype and folate status is a determinant of coronary atherosclerosis risk ' (2003 ) 133 J. Nutr. : 1281 -1285.

    • Search Google Scholar
  • Cattaneo, M., Chantarangkul, V., Taioli, E., et al.: The G20210A mutation of the prothrombin gene in patients with previous first episodes of deep-vein thrombosis: prevalence and association with factor V G1691A, methylenetetrahydrofolate reductase C677T and plasma prothrombin levels. Thromb. Res., 1999, 93, 1–8.

    Taioli E. , 'The G20210A mutation of the prothrombin gene in patients with previous first episodes of deep-vein thrombosis: prevalence and association with factor V G1691A, methylenetetrahydrofolate reductase C677T and plasma prothrombin levels ' (1999 ) 93 Thromb. Res. : 1 -8.

    • Search Google Scholar
  • Inbal, A., Freimark, D., Modan, B., et al.: Synergistic effects of prothrombotic polymorphisms and atherogenic factors on the risk of myocardial infarction in young males. Blood, 1999, 93, 2186–2190.

    Modan B. , 'Synergistic effects of prothrombotic polymorphisms and atherogenic factors on the risk of myocardial infarction in young males ' (1999 ) 93 Blood : 2186 -2190.

    • Search Google Scholar
  • Brattström, L., Wilcken, D. E., Ohrvik, J., et al.: Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis. Circulation, 1998, 98, 2520–2526.

    Ohrvik J. , 'Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis ' (1998 ) 98 Circulation : 2520 -2526.

    • Search Google Scholar
  • Schneider, J. A., Rees, D. C., Liu, Y. T., et al.: Worldwide distribution of a common methylenetetrahydrofolate reductase mutation. Am. J. Hum. Genet., 1998, 62, 1258–1260.

    Liu Y. T. , 'Worldwide distribution of a common methylenetetrahydrofolate reductase mutation ' (1998 ) 62 Am. J. Hum. Genet. : 1258 -1260.

    • Search Google Scholar
  • Trabetti, E.: Homocysteine, MTHFR gene polymorphisms, and cardio-cerebrovascular risk. Review. J. Appl. Genet., 2008, 49, 267–822.

    Trabetti E. , 'Homocysteine, MTHFR gene polymorphisms, and cardio-cerebrovascular risk ' (2008 ) 49 Review. J. Appl. Genet. : 267 -822.

    • Search Google Scholar
  • Poduri, A., Kumari, S., Jain, S., et al.: A case-control study of the association between the MTHFR gene and essential hypertension in Asian Indians. J. Hum. Hypertens., 2009, 23, 140–142.

    Jain S. , 'A case-control study of the association between the MTHFR gene and essential hypertension in Asian Indians ' (2009 ) 23 J. Hum. Hypertens. : 140 -142.

    • Search Google Scholar
  • Heux, S., Morin, F., Lea, R. A., et al.: The methylentetrahydrofolate reductase gene variant (C677T) as a risk factor for essential hypertension in Caucasians. Hypertens. Res., 2004, 27, 663–667.

    Lea R. A. , 'The methylentetrahydrofolate reductase gene variant (C677T) as a risk factor for essential hypertension in Caucasians ' (2004 ) 27 Hypertens. Res. : 663 -667.

    • Search Google Scholar
  • Jiang, S., Hsu, Y. H., Niu, T., et al.: A common haplotype on methylenetetrahydrofolate reductase gene modifies the effect of angiotensin-converting enzyme inhibitor on blood pressure in essential hypertension patients – a family-based association study. Clin. Exp. Hypertens., 2005, 27, 509–521.

    Niu T. , 'A common haplotype on methylenetetrahydrofolate reductase gene modifies the effect of angiotensin-converting enzyme inhibitor on blood pressure in essential hypertension patients – a family-based association study ' (2005 ) 27 Clin. Exp. Hypertens. : 509 -521.

    • Search Google Scholar
  • Qian, X., Lu, Z., Tan, M., et al.: A meta-analysis of association between C677T polymorphism in the methylenetetrahydrofolate reductase gene and hypertension. Eur. J. Hum. Genet., 2007, 15, 1239–1245.

    Tan M. , 'A meta-analysis of association between C677T polymorphism in the methylenetetrahydrofolate reductase gene and hypertension ' (2007 ) 15 Eur. J. Hum. Genet. : 1239 -1245.

    • Search Google Scholar
  • Newton-Cheh, C., Johnson, T., Gateva, V., et al.: Genome-wide association study identifies eight loci associated with blood pressure. Nat. Genet., 2009, 41, 666–676.

    Gateva V. , 'Genome-wide association study identifies eight loci associated with blood pressure ' (2009 ) 41 Nat. Genet. : 666 -676.

    • Search Google Scholar
  • Guillén, M., Corella, D., Portolés, O., et al.: Prevalence of the methylenetetrahydrofolate reductase 677C >T mutation in the Mediterranean Spanish population. Association with cardiovascular risk factors. Eur. J. Epidemiol., 2001, 17, 255–261.

    Portolés O. , 'Prevalence of the methylenetetrahydrofolate reductase 677C >T mutation in the Mediterranean Spanish population. Association with cardiovascular risk factors ' (2001 ) 17 Eur. J. Epidemiol. : 255 -261.

    • Search Google Scholar
  • Benes, P., Kanková, K., Muzík, J., et al.: Methylenetetrahydrofolate reductase polymorphism, type II diabetes mellitus, coronary artery disease, and essential hypertension in the Czech population. Mol. Genet. Metab., 2001, 73, 188–195.

    Muzík J. , 'Methylenetetrahydrofolate reductase polymorphism, type II diabetes mellitus, coronary artery disease, and essential hypertension in the Czech population ' (2001 ) 73 Mol. Genet. Metab. : 188 -195.

    • Search Google Scholar
  • Fridman, O., Porcile, R., Vanasco, V., et al.: Study on homocysteine levels and methylenetetrahydrofolate reductase gene variant (C677T) in a population of Buenos Aires City. Clin. Exp. Hypertens., 2008, 30, 574–584.

    Vanasco V. , 'Study on homocysteine levels and methylenetetrahydrofolate reductase gene variant (C677T) in a population of Buenos Aires City ' (2008 ) 30 Clin. Exp. Hypertens. : 574 -584.

    • Search Google Scholar
  • Wilson, C. P., McNulty, H., Scott, J. M., et al.: Postgraduate symposium: The MTHFR C677T polymorphism, B-vitamins and blood pressure. Proc. Nutr. Soc., 2010, 69, 156–165.

    Scott J. M. , 'Postgraduate symposium: The MTHFR C677T polymorphism, B-vitamins and blood pressure ' (2010 ) 69 Proc. Nutr. Soc. : 156 -165.

    • Search Google Scholar
  • Van der Put, N. M., Gabreëls, F., Stevens, E. M., et al.: A second common mutation in the methylenetetrahydrofolate reductase gene: an additional risk factor for neural-tube defects? Am. J. Hum. Genet., 1998, 62, 1044–1051.

    Stevens E. M. , 'A second common mutation in the methylenetetrahydrofolate reductase gene: an additional risk factor for neural-tube defects? ' (1998 ) 62 Am. J. Hum. Genet. : 1044 -1051.

    • Search Google Scholar
  • Weisberg, I., Tran, P., Christensen, B., et al.: A second genetic polymorphism in methylenetetrahydrofolate reductase (MTHFR) associated with decreased enzyme activity. Mol. Genet. Metab., 1998, 64, 169–172.

    Christensen B. , 'A second genetic polymorphism in methylenetetrahydrofolate reductase (MTHFR) associated with decreased enzyme activity ' (1998 ) 64 Mol. Genet. Metab. : 169 -172.

    • Search Google Scholar
  • Friso, S., Girelli, D., Trabetti, E., et al.: A1298C methylenetetrahydrofolate reductase mutation and coronary artery disease: relationships with C677T polymorphism and homocysteine/folate metabolism. Clin. Exp. Med., 2002, 2, 7–12.

    Trabetti E. , 'A1298C methylenetetrahydrofolate reductase mutation and coronary artery disease: relationships with C677T polymorphism and homocysteine/folate metabolism ' (2002 ) 2 Clin. Exp. Med. : 7 -12.

    • Search Google Scholar
  • Zetterberg, H., Coppola, A., D’Angelo, A., et al.: No association between the MTHFR A1298C and transcobalamin C776G genetic polymorphisms and hyperhomocysteinemia in thrombotic disease. Thromb. Res., 2002, 108, 127–131.

    D’Angelo A. , 'No association between the MTHFR A1298C and transcobalamin C776G genetic polymorphisms and hyperhomocysteinemia in thrombotic disease ' (2002 ) 108 Thromb. Res. : 127 -131.

    • Search Google Scholar
  • Szczeklik, A., Sanak, M., Jankowski, M., et al.: Mutation A1298C of methylenetetrahydrofolate reductase: risk for early coronary disease not associated with hyperhomocysteinemia. Am. J. Med. Genet., 2001, 101, 36–39.

    Jankowski M. , 'Mutation A1298C of methylenetetrahydrofolate reductase: risk for early coronary disease not associated with hyperhomocysteinemia ' (2001 ) 101 Am. J. Med. Genet. : 36 -39.

    • Search Google Scholar
  • Szolnoki, Z., Somogyvári, F., Szabó, M., et al.: Interactions between the MTHFR C677T and MTHFR A1298C mutations in ischaemic stroke. [A metiléntetrahidrofolsav-reduktáz gén C677T- és A1298C-mutációinak interakciója ischaemiás stroke-ban.]. Clin. Neurosci./Ideggy. Szle, 2006, 59, 107–112. [Hungarian]

    Szabó M. , 'Interactions between the MTHFR C677T and MTHFR A1298C mutations in ischaemic stroke. [A metiléntetrahidrofolsav-reduktáz gén C677T- és A1298C-mutációinak interakciója ischaemiás stroke-ban.] ' (2006 ) 59 Clin. Neurosci./Ideggy. Szle : 107 -112.

    • Search Google Scholar
  • Antoniades, C., Shirodaria, C., Warrick, N., et al.: 5-methyltetrahydrofolate rapidly improves endothelial function and decreases superoxide production in human vessels: effects on vascular tetrahydrobiopterin availability and endothelial nitric oxide synthase coupling. Circulation, 2006, 114, 1193–1201.

    Warrick N. , '5-methyltetrahydrofolate rapidly improves endothelial function and decreases superoxide production in human vessels: effects on vascular tetrahydrobiopterin availability and endothelial nitric oxide synthase coupling ' (2006 ) 114 Circulation : 1193 -1201.

    • Search Google Scholar
  • Baragetti, I., Raselli, S., Stucchi, A., et al.: Improvement of endothelial function in uraemic patients on peritoneal dialysis: a possible role for 5-MTHF administration. Nephrol. Dial. Transplant., 2007, 22, 3292–3297.

    Stucchi A. , 'Improvement of endothelial function in uraemic patients on peritoneal dialysis: a possible role for 5-MTHF administration ' (2007 ) 22 Nephrol. Dial. Transplant. : 3292 -3297.

    • Search Google Scholar
  • Antoniades, C., Tousoulis, D., Stefanadis, C., et al.: Effects of endothelial nitric oxide synthase gene polymorphisms on oxidative stress, inflammatory status, and coronary atherosclerosis: an example of a transient phenotype. J. Am. Coll. Cardiol., 2007, 49, 1226.

    Stefanadis C. , 'Effects of endothelial nitric oxide synthase gene polymorphisms on oxidative stress, inflammatory status, and coronary atherosclerosis: an example of a transient phenotype ' (2007 ) 49 J. Am. Coll. Cardiol. : 1226 -.

    • Search Google Scholar
  • Verhaar, M. C., Stroes, E., Rabelink, T. J.: Folates and cardiovascular disease. Arterioscler. Thromb. Vasc. Biol., 2002, 22, 6–13.

    Rabelink T. J. , 'Folates and cardiovascular disease ' (2002 ) 22 Arterioscler. Thromb. Vasc. Biol. : 6 -13.

    • Search Google Scholar
  • Leclerc, D., Campeau, E., Goyette, P., et al.: Human methionine synthase: cDNA cloning and identification of mutations in patients of the cblG complementation group of folate/cobalamin disorders. Hum. Mol. Genet., 1996, 5, 1867–1874.

    Goyette P. , 'Human methionine synthase: cDNA cloning and identification of mutations in patients of the cblG complementation group of folate/cobalamin disorders ' (1996 ) 5 Hum. Mol. Genet. : 1867 -1874.

    • Search Google Scholar
  • Brandalize, A. P., Bandinelli, E., Dos Santos, P. A., et al.: Maternal gene polymorphisms involved in folate metabolism as risk factors for Down syndrome offspring in Southern Brazil. Dis. Markers, 2010, 29, 95–101.

    Santos P. A. , 'Maternal gene polymorphisms involved in folate metabolism as risk factors for Down syndrome offspring in Southern Brazil ' (2010 ) 29 Dis. Markers : 95 -101.

    • Search Google Scholar
  • Galbiatti, A. L., Ruiz, M. T., Biselli-Chicote, P. M., et al.: 5-methyltetrahydrofolate-homocysteine methyltransferase gene polymorphism (MTR) and risk of head and neck cancer. Braz. J. Med. Biol. Res., 2010, 43, 445–450.

    Biselli-Chicote P. M. , '5-methyltetrahydrofolate-homocysteine methyltransferase gene polymorphism (MTR) and risk of head and neck cancer ' (2010 ) 43 Braz. J. Med. Biol. Res. : 445 -450.

    • Search Google Scholar
  • Harmon, D. L., Shields, D. C., Woodside, J. V., et al.: Methionine synthase D919G polymorphism is a significant but modest determinant of circulating homocysteine concentrations. Genet. Epidemiol., 1999, 17, 298–309.

    Woodside J. V. , 'Methionine synthase D919G polymorphism is a significant but modest determinant of circulating homocysteine concentrations ' (1999 ) 17 Genet. Epidemiol. : 298 -309.

    • Search Google Scholar
  • Hyndman, M. E., Bridge, P. J., Warnica, J. W., et al.: Effect of heterozygosity for the methionine synthase 2756 A–>G mutation on the risk for recurrent cardiovascular events. Am. J. Cardiol., 2000, 86, 1144–1146, A9.

    Warnica J. W. , 'Effect of heterozygosity for the methionine synthase 2756 A–>G mutation on the risk for recurrent cardiovascular events ' (2000 ) 86 Am. J. Cardiol. : 1144 -1146, A9.

    • Search Google Scholar
  • Laraqui, A., Allami, A., Carrié, A., et al.: Influence of methionine synthase (A2756G) and methionine synthase reductase (A66G) polymorphisms on plasma homocysteine levels and relation to risk of coronary artery disease. Acta Cardiol., 2006, 61, 51–61.

    Carrié A. , 'Influence of methionine synthase (A2756G) and methionine synthase reductase (A66G) polymorphisms on plasma homocysteine levels and relation to risk of coronary artery disease ' (2006 ) 61 Acta Cardiol. : 51 -61.

    • Search Google Scholar
  • Gaughan, D. J., Kluijtmans, L. A., Barbaux, S., et al.: The methionine synthase reductase (MTRR) A66G polymorphism is a novel genetic determinant of plasma homocysteine concentrations. Atherosclerosis, 2001, 157, 451–456.

    Barbaux S. , 'The methionine synthase reductase (MTRR) A66G polymorphism is a novel genetic determinant of plasma homocysteine concentrations ' (2001 ) 157 Atherosclerosis : 451 -456.

    • Search Google Scholar
  • Barbosa, P. R., Stabler, S. P., Machado, A. L., et al.: Association between decreased vitamin levels and MTHFR, MTR and MTRR gene polymorphisms as determinants for elevated total homocysteine concentrations in pregnant women. Eur. J. Clin. Nutr., 2008, 62, 1010–1021.

    Machado A. L. , 'Association between decreased vitamin levels and MTHFR, MTR and MTRR gene polymorphisms as determinants for elevated total homocysteine concentrations in pregnant women ' (2008 ) 62 Eur. J. Clin. Nutr. : 1010 -1021.

    • Search Google Scholar
  • Vinukonda, G., Shaik Mohammad, N., Md Nurul Jain, J., et al.: Genetic and environmental influences on total plasma homocysteine and coronary artery disease (CAD) risk among South Indians. Clin. Chim. Acta, 2009, 405, 127–131.

    Nurul Jain J. , 'Genetic and environmental influences on total plasma homocysteine and coronary artery disease (CAD) risk among South Indians ' (2009 ) 405 Clin. Chim. Acta : 127 -131.

    • Search Google Scholar
  • Scazzone, C., Acuto, S., Guglielmini, E., et al.: Methionine Synthase Reductase (MTRR) A66G polymorphism is not related with plasma homocysteine concentration and risk for vascular disease.; Exp. Mol. Pathol., 2009. [Epub ahead of print.]

  • Lievers, K. J., Kluijtmans, L. A., Heil, S. G., et al.: A 31 bp VNTR in the cystathionine beta-synthase (CBS) gene is associated with reduced CBS activity and elevated post-load homocysteine levels. Eur. J. Hum. Genet., 2001, 9, 583–589.

    Heil S. G. , 'A 31 bp VNTR in the cystathionine beta-synthase (CBS) gene is associated with reduced CBS activity and elevated post-load homocysteine levels ' (2001 ) 9 Eur. J. Hum. Genet. : 583 -589.

    • Search Google Scholar
  • Heil, S. G., Lievers, K. J., Boers, G. H., et al.: Betaine-homocysteine methyltransferase (BHMT): genomic sequencing and relevance to hyperhomocysteinemia and vascular disease in humans. Mol. Genet. Metab., 2000, 71, 511–519.

    Boers G. H. , 'Betaine-homocysteine methyltransferase (BHMT): genomic sequencing and relevance to hyperhomocysteinemia and vascular disease in humans ' (2000 ) 71 Mol. Genet. Metab. : 511 -519.

    • Search Google Scholar
  • Wang, L., Ke, Q., Chen, W., et al.: Polymorphisms of MTHFD, plasma homocysteine levels, and risk of gastric cancer in a high-risk Chinese population. Clin. Cancer Res., 2007, 13, 2526–2532.

    Chen W. , 'Polymorphisms of MTHFD, plasma homocysteine levels, and risk of gastric cancer in a high-risk Chinese population ' (2007 ) 13 Clin. Cancer Res. : 2526 -2532.

    • Search Google Scholar
  • Jacques, P. F., Bostom, A. G., Williams, R. R., et al.: Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation, 1996, 93, 7–9.

    Williams R. R. , 'Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations ' (1996 ) 93 Circulation : 7 -9.

    • Search Google Scholar
  • Girelli, D., Friso, S., Trabetti, E., et al.: Methylenetetrahydrofolate reductase C677T mutation, plasma homocysteine, and folate in subjects from northern Italy with or without angiographically documented severe coronary atherosclerotic disease: evidence for an important genetic-environmental interaction. Blood, 1998, 91, 4158–4163.

    Trabetti E. , 'Methylenetetrahydrofolate reductase C677T mutation, plasma homocysteine, and folate in subjects from northern Italy with or without angiographically documented severe coronary atherosclerotic disease: evidence for an important genetic-environmental interaction ' (1998 ) 91 Blood : 4158 -4163.

    • Search Google Scholar
  • Salomon, O., Steinberg, D. M., Zivelin, A., et al.: Single and combined prothrombotic factors in patients with idiopathic venous thromboembolism: prevalence and risk assessment. Arterioscler. Thromb. Vasc. Biol., 1999, 19, 511–518.

    Zivelin A. , 'Single and combined prothrombotic factors in patients with idiopathic venous thromboembolism: prevalence and risk assessment ' (1999 ) 19 Arterioscler. Thromb. Vasc. Biol. : 511 -518.

    • Search Google Scholar
  • Pezzini, A., Grassi, M., Del Zotto, E., et al.: Cumulative effect of predisposing genotypes and their interaction with modifiable factors on the risk of ischemic stroke in young adults. Stroke, 2005, 36, 533–539.

    Zotto E. , 'Cumulative effect of predisposing genotypes and their interaction with modifiable factors on the risk of ischemic stroke in young adults ' (2005 ) 36 Stroke : 533 -539.

    • Search Google Scholar
  • Franco, R. F., Morelli, V., Lourenço, D., et al.: A second mutation in the methylenetetrahydrofolate reductase gene and the risk of venous thrombotic disease. Br. J. Haematol., 1999, 105, 556–559.

    Lourenço D. , 'A second mutation in the methylenetetrahydrofolate reductase gene and the risk of venous thrombotic disease ' (1999 ) 105 Br. J. Haematol. : 556 -559.

    • Search Google Scholar
  • Zetterberg, H., Rymo, L., Coppola, A., et al.: Reply to ‘MTHFR C677T and A1298C polymorphisms and mutated sequences occurring in cis’. Eur. J. Hum. Genet., 2002, 10, 579–582.

    Coppola A. , 'Reply to ‘MTHFR C677T and A1298C polymorphisms and mutated sequences occurring in cis’ ' (2002 ) 10 Eur. J. Hum. Genet. : 579 -582.

    • Search Google Scholar
  • Laraqui, A., Allami, A., Carrié, A., et al.: Relation between plasma homocysteine, gene polymorphisms 278 E. Trabetti of homocysteine metabolism-related enzymes, and angiographically proven coronary artery disease. Eur. J. Int. Med., 2007, 18, 474–483.

    Carrié A. , 'Relation between plasma homocysteine, gene polymorphisms 278 E. Trabetti of homocysteine metabolism-related enzymes, and angiographically proven coronary artery disease ' (2007 ) 18 Eur. J. Int. Med. : 474 -483.

    • Search Google Scholar
  • Chen, J., Stampfer, M. J., Ma, J., et al.: Influence of a methionine synthase (D919G) polymorphism on plasma homocysteine and folate levels and relation to risk of myocardial infarction. Atherosclerosis, 2001, 154, 667–672.

    Ma J. , 'Influence of a methionine synthase (D919G) polymorphism on plasma homocysteine and folate levels and relation to risk of myocardial infarction ' (2001 ) 154 Atherosclerosis : 667 -672.

    • Search Google Scholar
  • Chen, L., Liu, L., Hong, K., et al.: Three genetic polymorphisms of homocysteine-metabolizing enzymes and risk of coronary heart disease: A meta-analysis based on 23 case-control studies. DNA Cell Biol., 2011. [Epub ahead of print.]

The author instructions are available in PDF.
Instructions for Authors in Hungarian HERE.
Mendeley citation style is available HERE.

Főszerkesztő - Editor-in-Chief:
 
Zoltán PAPP (professor emeritus, Semmelweis Egyetem, Szülészeti és Nőgyógyászati Klinika, Budapest)

Read the professional career of Zoltán PAPP HERE.

All scientific publications of Zoltán PAPP are collected in the Hungarian Scientific Bibliography.

Főszerkesztő-helyettesek - Assistant Editors-in-Chief: 

  • Erzsébet FEHÉR (professor emeritus, Semmelweis Egyetem, Anatómiai, Szövet- és Fejlődéstani Intézet)
  • Krisztina HAGYMÁSI (egyetemi docens, Semmelweis Egyetem, I. Sebészeti és Intervenciós Gasztroenterológiai Klinika, Budapest)

Főmunkatársak - Senior Editorial Specialists:

  • László KISS (a Debreceni Egyetem habilitált doktora)
  • Gabriella LENGYEL (ny. egyetemi docens, Semmelweis Egyetem, I. Sebészeti és Intervenciós Gasztroenterológiai Klinika, Budapest)
  • Alajos PÁR (professor emeritus, Pécsi Tudományegyetem, I. Belgyógyászati Klinika)

 A Szerkesztőbizottság tagjai – Members of the Editorial Board:

  • Péter ANDRÉKA (főigazgató, Gottsegen György Országos Kardiovaszkuláris Intézet, Nemzeti Szívinfartkus Regiszter, Budapest)
  • Géza ÁCS Jr. (egyetemi tanár Floridában)
  • Csaba BALÁZS (egyetemi tanár, Budai Endokrinközpont, Budapest)
  • Péter BENCSIK (volt folyóirat-kiadás vezető, Akadémiai Kiadó, Budapest)
  • Zoltán BENYÓ (egyetemi tanár, Semmelweis Egyetem, Transzlációs Medicina Intézet, Budapest)
  • Dániel BERECZKI (egyetemi tanár, Semmelweis Egyetem, Neurológiai Klinika, Budapest)
  • Anna BLÁZOVICS (professor emeritus, Semmelweis Egyetem, Farmakognóziai Intézet, Budapest)
  • Elek DINYA (professor emeritus, biostatisztikus, Semmelweis Egyetem, Budapest)
  • Attila DOBOZY (professor emeritus, Szegedi Tudományegyetem, Bőrgyógyászati Klinika, Szeged)
  • András FALUS (professor emeritus, Semmelweis Egyetem, Genetikai, Sejt- és Immunbiológiai Intézet, Budapest)
  • Csaba FARSANG (egyetemi tanár, Szent Imre Oktató Kórház, Belgyógyászati Osztály, Budapest)
  • János FAZAKAS (egyetemi docens, Semmelweis Egyetem, Transzplantációs és Sebészeti Klinika, Budapest)
  • Béla FÜLESDI (egyetemi tanár, Debreceni Egyetem, Aneszteziológiai és Intenzív Terápiás Klinika, Debrecen)
  • Beáta GASZTONYI (egyetemi magántanár, kórházi főorvos, Zala Megyei Kórház, Belgyógyászat, Zalaegerszeg)
  • István GERGELY (egyetemi docens, Marosvásárhelyi Orvosi és Gyógyszerészeti Egyetem, Románia)
  • Judit GERVAIN (osztályvezető főorvos, Fejér Megyei Szent György Kórház, Belgyógyászat, Székesfehérvár)
  • Béla GÖMÖR (professor emeritus, Budai Irgalmasrendi Kórház, Reumatológiai Osztály, Budapest)
  • László GULÁCSI (egyetemi tanár, Óbudai Egyetem, Egészségügyi Közgazdaságtan Tanszék, Budapest)
  • János HANKISS (professor emeritus, Markusovszky Lajos Oktató Kórház, Belgyógyászati Osztály, Szombathely)
  • Örs Péter HORVÁTH (professor emeritus, Pécsi Tudományegyetem, Sebészeti Klinika, Pécs)
  • Béla HUNYADY (egyetemi tanár, Somogy Megyei Kaposi Mór Kórház, Belgyógyászat, Kaposvár)
  • Péter IGAZ (egyetemi tanár, Semmelweis Egyetem, Belgyógyászati és Onkológiai Klinika, Budapest)
  • Ferenc JAKAB (c. egyetemi tanár, Uzsoki Utcai Kórház, Sebészet, Budapest)
  • András JÁNOSI (c. egyetemi tanár, Gottsegen György Országos Kardiovaszkuláris Intézet, Nemzeti Szívinfartkus Regiszter, Budapest)
  • György JERMENDY (egyetemi tanár, Bajcsy-Zsilinszky Kórház, Belgyógyászat, Budapest)
  • László KALABAY (egyetemi tanár, Semmelweis Egyetem, Családorvosi Tanszék, Budapest)
  • János KAPPELMAYER (egyetemi tanár, Debreceni Egyetem, Laboratóriumi Medicina Intézet, Debrecen)
  • Éva KELLER (ny. egyetemi tanár, Semmelweis Egyetem, Igazságügyi és Biztosítás-orvostani Intézet, Budapest)
  • Mátyás KELTAI (ny. egyetemi docens, Gottsegen György Országos Kardiovaszkuláris Intézet, Nemzeti Szívinfartkus Regiszter, Budapest)
  • András KISS (egyetemi tanár, Semmelweis Egyetem, II. Patológiai Intézet, Budapest)
  • László KÓBORI (egyetemi tanár, Semmelweis Egyetem, Transzplantációs és Sebészeti Klinika, Budapest)
  • Lajos KULLMANN (ny. egyetemi tanár, Országos Rehabilitációs Intézet, Budapest)
  • Emese MEZŐSI (egyetemi tanár, Pécsi Tudományegyetem, I. Belgyógyászati Klinika, Pécs)
  • József MOLNÁR (professor emeritus, Szegedi Tudományegyetem, Mikrobiológiai és Immunológiai Intézet, Szeged)
  • Péter MOLNÁR (professor emeritus, Debreceni Egyetem, Magatartástudományi Intézet, Debrecen)
  • Györgyi MŰZES (egyetemi docens, Semmelweis Egyetem, Belgyógyászati és Hematológiai Klinika, Budapest)
  • Bálint NAGY (egyetemi tanár, Debreceni Egyetem, Humángenetikai Tanszék, Debrecen)
  • Endre NAGY (egyetemi tanár, Debreceni Egyetem, Belgyógyászati Intézet, Debrecen) 
  • Péter NAGY (egyetemi tanár, Semmelweis Egyetem, I. Patológiai és Kísérleti Rákkutató Intézet, Budapest)
  • Viktor NAGY (főorvos, Semmelweis Egyetem, Belgyógyászati és Hematológiai Klinika, Budapest)
  • Zoltán Zsolt NAGY (egyetemi tanár, Semmelweis Egyetem, Szemészeti Klinika, Budapest)
  • Balázs NEMES (egyetemi docens, Debreceni Egyetem, Transzplantációs Tanszék, Debrecen)
  • Attila PATÓCS (tudományos főmunkatárs, Semmelweis Egyetem, Belgyógyászati és Hematológiai Klinika, Budapest)
  • Gabriella PÁR (egyetemi docens, Pécsi Tudományegyetem, I. Belgyógyászati Klinika)
  • György PFLIEGLER (egyetemi tanár, Debreceni Egyetem, Ritka Betegségek Tanszéke, Debrecen)
  • István RÁCZ (egyetemi tanár, főorvos, Petz Aladár Megyei Oktató Kórház, Belgyógyászat, Győr)
  • Imre ROMICS (professor emeritus, Semmelweis Egyetem, Urológiai Klinika, Budapest)
  • László Jr. ROMICS (Angliában dolgozik) 
  • Imre RURIK (egyetemi tanár, Debreceni Egyetem, Családorvosi és Foglalkozás-egészségügyi Tanszék, Debrecen)
  • Zsuzsa SCHAFF (professor emeritus, Semmelweis Egyetem, II. Patológiai Intézet, Budapest)
  • Péter SCHMIDT (házi gyermekorvos, Győr)
  • Kornél SIMON (ny. osztályvezető főorvos, Siófoki Kórház, Belgyógyászat, Siófok)
  • Gábor SIMONYI (vezető főorvos, Szent Imre Kórház, Anyagcsere Központ, Budapest)
  • Gábor Márk SOMFAI (egyetemi docens, Semmelweis Egyetem, Szemészeti Klinika, Budapest)
  • Anikó SOMOGYI (ny. egyetemi tanár, Semmelweis Egyetem, Belgyógyászati és Hematológiai Klinika, Budapest)
  • Péter SÓTONYI (professor emeritus, Semmelweis Egyetem, Igazságügyi és Biztosítás-orvostani Intézet, Budapest)
  • Péter Jr. SÓTONYI (egyetemi tanár, Semmelweis Egyetem, Városmajori Szív- és Érsebészeti Klinika, Budapest)
  • Ildikó SÜVEGES (professor emeritus, Semmelweis Egyetem, Szemészeti Klinika, Budapest)
  • György SZABÓ (professor emeritus, Semmelweis Egyetem, Arc-Állcsont-Szájsebészeti és Fogászati Klinika, Budapest)
  • Ferenc SZALAY (professor emeritus, Semmelweis Egyetem, Belgyógyászati és Onkológiai Klinika, Budapest)
  • Miklós SZENDRŐI (professor emeritus, Semmelweis Egyetem, Ortopédiai Klinika, Budapest)
  • István SZILVÁSI (egyetemi tanár, Semmelweis Egyetem, Belgyógyászati és Hematológiai Klinika, Budapest)
  • Miklós TÓTH (egyetemi tanár, Semmelweis Egyetem, Belgyógyászati és Onkológiai Klinika, Budapest)
  • László TRINGER (professor emeritus, Semmelweis Egyetem, Pszichiátriai és Pszichoterápiás Klinika, Budapest)
  • Tivadar TULASSAY (professor emeritus, Semmelweis Egyetem, I. Gyermekgyógyászati Klinika, Budapest)
  • Zsolt TULASSAY (professor emeritus, Semmelweis Egyetem, Belgyógyászati és Hematológiai Klinika, Budapest)
  • Lívia VASAS (ny. könyvtárigazgató, Semmelweis Egyetem, Központi Könyvtár, Budapest)
  • Barna VÁSÁRHELYI (egyetemi tanár, Semmelweis Egyetem, Laboratóriumi Medicina Intézet, Budapest)
  • László VÉCSEI (professor emeritus, Szegedi Tudományegyetem, Neurológiai Klinika, Szeged)
  • Gábor WINKLER (egyetemi tanár, Szent János Kórház, Belgyógyászati Osztály, Budapest)

Nemzetközi szerkesztőbizottság - International Editorial Board:

  • Elnök/President Péter SÓTONYI (Budapest)
  • Ernest ADEGHATE (Al Ain)
  • Ferenc ANTONI (Edinburgh)
  • Maciej BANACH (Łódź)
  • Klára BERENCSI (Rosemont)
  • Angelo BIGNAMINI (Milano)
  • Anupam BISHAYEE (Signal Hill)
  • Hubert E. BLUM (Freiburg)
  • G. László BOROS (Los Angeles)
  • Frank A. CHERVENAK (New York)
  • Meinhard CLASSEN (München)
  • József DÉZSY (Wien)
  • Peter ECKL (Salzburg)
  • Péter FERENCI (Wien)
  • Madelaine HAHN (Erlangen)
  • S. Tamás ILLÉS (Bruxelles)
  • Michael KIDD (Toronto)
  • Andrzej KOKOSZKA (Warsaw)
  • Márta KORBONITS (London)
  • Asim KURJAK (Zagreb)
  • Manfred MAIER (Wien)
  • Neil MCINTYRE (London)
  • Lajos OKOLICSÁNYI (Padova)
  • Amado Salvador PENA (Amsterdam)
  • Guliano RAMADORI (Goettingen)
  • Olivér RÁCZ (Košice)
  • Roberto ROMERO (Detroit)
  • Rainer SCHÖFL (Linz)
  • Zvi VERED (Tel Aviv)
  • Josef VESELY (Olomouc)
  • Ákos ZAHÁR (Hamburg)

Akadémiai Kiadó Zrt. 1117 Budapest
Budafoki út 187-189.
A épület, III. emelet
Phone: (+36 1) 464 8235
Email: orvosihetilap@akademiai.hu

2020  
Total Cites 1277
WoS
Journal
Impact Factor
0,540
Rank by Medicine, General & Internal 155/169 (Q4)
Impact Factor  
Impact Factor 0,310
without
Journal Self Cites
5 Year 0,461
Impact Factor
Journal  0,17
Citation Indicator  
Rank by Journal  Medicine, General & Internal 203/313 (Q4)
Citation Indicator   
Citable 261
Items
Total 229
Articles
Total 32
Reviews
Scimago 21
H-index
Scimago 0,176
Journal Rank
Scimago Medicine (miscellaneous) Q4
Quartile Score  
Scopus 921/1187=0,8
Scite Score  
Scopus General Medicine 494/793 (Q3)
Scite Score Rank  
Scopus 0,283
SNIP  
Days from  28
sumbission  
to acceptance  
Days from  114
acceptance  
to publication  
Acceptance 72%
Rate

2019  
Total Cites
WoS
1 085
Impact Factor 0,497
Impact Factor
without
Journal Self Cites
0,212
5 Year
Impact Factor
0,396
Immediacy
Index
0,126
Citable
Items
247
Total
Articles
176
Total
Reviews
71
Cited
Half-Life
6,1
Citing
Half-Life
7,3
Eigenfactor
Score
0,00071
Article Influence
Score
0,045
% Articles
in
Citable Items
71,26
Normalized
Eigenfactor
0,08759
Average
IF
Percentile
10,606
Scimago
H-index
20
Scimago
Journal Rank
0,176
Scopus
Scite Score
864/1178=0,4
Scopus
Scite Score Rank
General Medicine 267/529 (Q3)
Scopus
SNIP
0,254
Acceptance
Rate
73%

 

Orvosi Hetilap
Publication Model Hybrid
Submission Fee none
Article Processing Charge 900 EUR/article
Printed Color Illustrations 20 EUR (or 5000 HUF) + VAT / piece
Regional discounts on country of the funding agency World Bank Lower-middle-income economies: 50%
World Bank Low-income economies: 100%
Further Discounts Editorial Board / Advisory Board members: 50%
Corresponding authors, affiliated to an EISZ member institution subscribing to the journal package of Akadémiai Kiadó: 100%
Subscription fee 2021 Online subsscription: 844 EUR / 1124 USD
Print + online subscription: 956 EUR / 1326 USD
Subscription fee 2022 Online subsscription: 858 EUR / 1157 USD
Print + online subscription: 975 EUR / 1352 USD
Subscription Information Online subscribers are entitled access to all back issues published by Akadémiai Kiadó for each title for the duration of the subscription, as well as Online First content for the subscribed content.
Purchase per Title Individual articles are sold on the displayed price.

Orvosi Hetilap
Language Hungarian
Size A4
Year of
Foundation
1857
Publication
Programme
2021 Volume 162
Volumes
per Year
1
Issues
per Year
52
Founder Markusovszky Lajos Alapítvány -- Lajos Markusovszky Foundation
Founder's
Address
H-1088 Budapest, Szentkriályi u. 46.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 0030-6002 (Print)
ISSN 1788-6120 (Online)

Monthly Content Usage

Abstract Views Full Text Views PDF Downloads
May 2021 0 8 74
Jun 2021 0 8 22
Jul 2021 0 5 23
Aug 2021 0 2 25
Sep 2021 0 6 47
Oct 2021 0 8 24
Nov 2021 0 0 0