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Year 2014, Volume: 36 Issue: 4, 459 - 465, 30.12.2014
https://doi.org/10.7197/cmj.v36i4.1008001689

Abstract

Aim. It is observed in studies that hypertension is a feature of familial and a variety of gene polymorphism is associated with hypertension. Method. This study was planned in two stages.At the first stage; to evaluate gene mutation, in population under the age of 45 CVD (CardiovascularDisease) case group of 50 persons with essential hypertension and at the same age group and sex, within normal blood pressure limits in a control group of 50 people was selected.In the second stage, cases of first-degree relatives of patients with homozygous polimorfizm DD ACE gene group (parents and siblings) family group of 50 people, were evaluated for genetic polymorphism. Results. Those with cases of allele ApoE3/E4 group, 88.9% had a family history of hypertension. In the same way, in all of those with the E3/E2 genotype, family history was positive. In the case group, 5 people (10%) E3/E2 ApoE gene polymorphism, 9 patients (18%) had APOE E3/E4 gene polymorphism. In the control group, these numbers was about respectively, 7, and 3 (14% and 6%).In the control group, ApoE3/E2 gene polymorphism, higher than control group (p>0.05). Case group E3/E4 genotype, higher than the control group; but this difference was not statistically significant. Total cholesterol 200 mg/dL and above those 62.5% of people were in the case group and this ratio compared to control group (37.5%) were significantly higher (p<0.05). In the family group, this rate was 66%. The mean values of HDL was lower in the 3 groups (case group, 41.9 ± 11.2, family group, 40.4 ± 13.4 and control group 44.9 ± 15.24 mg/dL).Mean LDL values were determined as 133.6 ± 32.2 mg /dL in case group, 137.8 ± 30.8 mg/dL in family group, and 123.4 ± 32.9 mg /dL in control group. Total cholesterol/HDL cholesterol ratios were 4978 ± 1.41 in case group, 5.7 ± 2.3 in family group and 4670 ± 1.83 in control group. The prevalence of hypertension was 56% in family group, (37% in individuals 45 years and under). 42.9% of those diagnosed before the age of 40 had hypertension. Conclusion. Both the case and the family group, cholesterol, LDL levels and total cholesterol/HDL ratio is high, low HDL levels, lipid values should be within normal limits suggests that lifestyle changes are necessary to bring. As a result, while the etiology of hypertension is querying, also genetic factors should be considered in, and studies on genes and hypertension should be held responsible.In addition, hypertensive patients should be monitorized for hypertension and other cardiovascular diseases by screening of all family members while they are being evaluated. Especially patients with hypertension was diagnosed before the age of 40 and their families should be monitored for both genetic and other risk factors (BMI, lipid profile, smoking, alcohol). Lifestyle changes which are important for hypertension prevention and control of hypertension should be employed

References

  • 1. Murray CJ, Lope AD. Evidence-based health policy-lessons from the global burden of disease study. Science 1996; 274: 740-3.
  • 2. Joint national committee on detection. Evaluation and treatment of high blood pressure. The seventh report of the Joint national committe on prevention. Detection and treatment of high blood pressure (JNC VII). JAMA 2003; 289: 2560-74.
  • 3. Guidelines Subcommittee of the World Health Organization: World Health Organization-International society of hypertension guidelines for the management of hypertension. J Hypertens 1999; 17: 151-83.
  • 4. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA 1996; 275: 1557-62.
  • 5. Altun B, Arıcı M, Nergizoglu G. Prevalence, awareness, treatment and control of hypertension in Turkey (the PatenT study) in 2003. Journal of hypertension 2005; 23: 1817-23.
  • 6. Onat A, Sansoy V, Yıldırım B. Erişkinlerimizde kan basıncı: 8-yıllık seyri, tedavi oranı, koroner kalp hastalığı ile bazı etkenlerle ilişkileri. Türk Kardiyoloji Derneği Arş 1999; 27: 136-43.
  • 7. Sağlam K, Yılmaz Mİ, Sönmez A, Baykal Y. Primer Hipertansiyon 2003; 37.
  • 8. Lascaux-Lefebvre V, Ruidavets J, Arveiler D. Influence of parental history of hypertension on blood pressure. J Hum Hypertens 1999; 13: 631-6.
  • 9. Tozawa M, Oshiro S, Iseki C. Family history of hypertension and blood pressure in a screened cohort. Hypertens Res 2001; 24: 93-8.
  • 10. Kikukawa N. Relationship between development of hypertension and a family history of high blood pressure in urban residents-analysis based on results of annual health examinations. Nippon Koshu Eisei Zasshi 2004; 51: 833-44.
  • 11. Al-Safi SA, Aboul-Enein FH, Aboul-Enein BH, Manuel B. Influence of family history and lifestyle on blood pressure and heart rate in young adults in Jordan. Public Health 2006; 120: 1027-32.
  • 12. Di Ruppo D, Farias, Guggisberg W, Delgado A. Family history as a risk factor for hypertension in adolescents. American Journal of Hypertension 2000; 13: 266.
  • 13. Bedir A, Arık N, Adam B. Angiotensin converting enzyme gene polymorphism and activity in Turkish patients with essential hypertension. American Journal of Hypertension 1999; 12: 1038-43.
  • 14. Maron DJ, Ridker PM, Pearson TA, Grundy S. Dislipidemi, Diğer Risk Faktörleri ve Koroner Kalp Hastalığının Önlenmesi: Fuster V. Alexander RW. O’Rourke RA: Hurst’s The Heart (10.baskı) McGraw-Hill 2002; 1131-60.
  • 15. Halperin RO, Sesso HD, Ma J. Dyslipidemia and the risk of incident hypertension in men. Hypertension 2006; 47: 45-50.
  • 16. Sesso HD, Buring JE, Chown MJ. A prospective study of plasma lipid levels and hypertension in women. Arch Intern Med 2005; 165: 2420-7.
  • 17. Ağaçhan B, Yılmaz H, Öztürk O. Aterosklerozda Apolipoprotein E, Okside-LDL ve Lipid Profili İlişkisinin Araştırılması F. Ü. Sağlık Bil. Dergisi 2005; 19: 193-7.
  • 18. Mahley RW. Apolipoprotein E: Cholesterol transport protein with expanding role in cell biology. Science 1988; 240: 622-30.
  • 19. Bhavani AB, Sastry KB, Reddy NK, Padma T. Lipid profile and apolipoprotein E polymorphism in essential hypertension. Indian Heart J 2005; 57: 151-7.
  • 20. Imazu M, Yamamoto H, Toyofuku M et al. Association of apolipoprotein E phenotype with hypertension in Japanese-Americans: Data from the Hawaii-Los Angeles-Hiroshima Study. Hypertens Res 2001; 24: 523-9.
  • 21. Lenzen HJ., Assman G, Buckwalsky R, Schulte H. Association of apolipoprotein E polymorphism, low density lipoprotein cholesterol, and coronary artery disease. Clin Chem 1986; 32/5: 778-81.
  • 22. Catto AJ, Kohler HP, Bannan S, Stickland M, Carter A, Grant PJ: Factor XIII Val34Leu. A novel association with primary intracerebral hemorrhage. Stroke 1998; 29: 813-6.
  • 23. Franco RF, Pazin-Filho A, Tavella MH, Simões MV, Marin-Neto JA, Zago MA.Factor XIII val34leu and the risk of myocardial infarction. Haematologica 2000; 85: 67-71.
  • 24. Braeckman L, De Bacquer D, Rosseneu M, De Bacquer G. Apolipoprotein E polymorphism in middle-aged Belgian men: Phenotype distribution and relation to serum lipids and lipoproteins. Atherosclerosis 1996; 120: 67-73.
  • 25. Davignon J, Greeg RE, Sing CF. Apolipoprotein E polymorphism and atherosclerosis. Atherosclerosis 1988; 8: 1-21.
  • 26. Hixson JE. Pathological Determinants of Atherosclerosis in Youth (PDAY) Research Group: Apolipoprotein E polymorphism affect atherosclerosis in young males. Arterioscler Thromb 1991; 11: 1237-44.
  • 27. Jemaa R, Elasmi M, Naouali C. Apolipoprotein E polymorphism in the Tunisian population: Frequency and effect on lipid parameters. Clin Biochem 2006; 39: 816-20.
  • 28. Yilmaz H, Isbir T, Ağaçhan B, Aydin M. Is epsilon4 allele of apolipoprotein E associated with more severe end-organ damage in essential hypertension? Cell Biochem Funct 2001; 19: 191-5.
  • 29. Catto AJ, Kohler HP, Coore J, Mansfiel MW, Stickland MH, Grant PJ: Association of a common polymorphism in the factor XIII gene with venous thrombosis. Blood 1999; 93: 906-8.

Hipertansif hastaların ailelerinde Apo E gen polimorfizmleri ve kan lipit profillerinin değerlendirilmesi

Year 2014, Volume: 36 Issue: 4, 459 - 465, 30.12.2014
https://doi.org/10.7197/cmj.v36i4.1008001689

Abstract

Özet

Amaç. Bu çalışmamızda, hipertansif hastaların ailelerinde Apo E gen polimorfizmleri ve kan lipit profillerinin değerlendirilmesi amaçlanmıştır. Yöntem. Çalışmamız iki aşamada planlandı. İlk aşamada; 45 yaş altı popülasyonda CVD (CardiovascularDisease) gen mutasyonunu değerlendirmek için, esansiyel hipertansiyona sahip 50 kişilik olgu grubu ve aynı yaş grubu ve cinsiyette tansiyonu normal sınırlarda olan 50 kişilik kontrol grubu seçildi. Çalışmanın ikinci aşamasında, olgu grubundaki ACE gen polimorfizmi DD homozigot olan hastaların birinci derece akrabalarında (50), genetik polimorfizm açısından değerlendirildi. Bulgular. Olgu grubunda ApoE3/E4 alleline sahip olanların %88,9’unda ailede hipertansiyon hikayesi mevcuidi. Aynı şekilde E3/E2 genotipine sahip olanların hepsinde aile hikayesi pozitif idi. Olgu grubunda, 5 kişide (%10) ApoE E3/E2 gen polimorfizmi, 9 kişide (%18) ApoE E3/E4 gen polimorfizmi mevcuttu. Kontrol grubunda bu sayılar sırasıyla 7 ve 3 (%14 ve %6) idi. Olgu grubunda ApoE3/E2 gen polimorfizmi, kontrol grubundan daha yüksekti (p>0,05). Olgu grubunda E3/E4 genotipi, kontrol grubundan yüksekti; ancak bu istatiksel olarak anlamlı bulunmadı. Total kolesterolü 200 mg/dL ve üzeri olanların %62,5’i olgu grubundaydı ve bu oran, kontrol grubuna göre (%37,5) istatistiksel olarak anlamlı şekilde yüksekti (p<0,05). Aile grubunda bu oran %66 idi. HDL ortalama değerleri 3 grupta da düşüktü (olgu grubunda 41,93 ± 11,22 mg/dL, aile grubunda 40,4 ± 13,4 ve kontrol grubunda 44,93 ± 15,24 mg/dL). Olgu grubunda LDL ortalaması 133,6 ± 32,2 mg/dL, aile grubunda 137,8±30,8 mg/dL ve kontrol grubunda 123,4 ± 32,9 mg/dL olarak belirlendi. Total kolesterol/HDL kolesterol oranı; olgu grubunda 4,9 ± 1,4, aile grubunda 5,7 ± 2,3 ve kontrol grubunda 4,7 ± 1,8 idi. Aile grubunda hipertansiyon prevalansı %56 idi (45 yaş ve altı bireylerde %37). 40 yaş öncesi hipertansiyon tanısı alanların oranı %42,9 idi. Sonuç. Hem olgu hem de aile grubunda kolesterol, LDL değerleri ve total kolesterol/HDL oranının yüksek, HDL değerlerinin düşük olması için gerekli hayat tarzı değişikliklerinin yapılması gerektiğini düşündürmektedir. Sonuç olarak, hipertansiyon etiyolojisi sorgulanırken, genetik faktörler de göz önünde tutulmalıdır ve hipertansiyondan sorumlu tutulan genlerle ilgili çalışmalar yapılmalıdır. Ayrıca hipertansif hastalar değerlendirilirken tüm aile bireylerinin taranması yapılarak, hipertansiyon ve diğer kardiyovasküler hastalıklar açısından takip edilmelidir. Özellikle 40 yaş öncesi hipertansiyon tanısı konmuş olan hastalar ve ailesi hem genetik açıdan, hem de diğer risk faktörleri (VKİ, lipid profili, sigara, alkol) açısından takip edilmeli ve hayat tarzı değişikliklerinin uygulanması sağlanmalıdır.

Anahtar sözcükler: Hipertansiyon, lipid profili, genetik yatkınlık

 

Abstract

Aim. It is observed in studies that hypertension is a feature of familial and a variety of gene polymorphism is associated with hypertension. Method. This study was planned in two stages.At the first stage; to evaluate gene mutation, in population under the age of 45 CVD (CardiovascularDisease) case group of 50 persons with essential hypertension and at the same age group and sex, within normal blood pressure limits in a control group of 50 people was selected.In the second stage, cases of first-degree relatives of patients with homozygous polimorfizm DD ACE gene group (parents and siblings) family group of 50 people, were evaluated for genetic polymorphism. Results. Those with cases of allele ApoE3/E4 group, 88.9% had a family history of hypertension. In the same way, in all of those with the E3/E2 genotype, family history was positive. In the case group, 5 people (10%) E3/E2 ApoE gene polymorphism, 9 patients (18%) had APOE E3/E4 gene polymorphism. In the control group, these numbers was about respectively, 7, and 3 (14% and 6%).In the control group, ApoE3/E2 gene polymorphism, higher than control group (p>0.05). Case group E3/E4 genotype, higher than the control group; but this difference was not statistically significant. Total cholesterol 200 mg/dL and above those 62.5% of people were in the case group and this ratio compared to control group (37.5%) were significantly higher (p<0.05). In the family group, this rate was 66%. The mean values of HDL was lower in the 3 groups (case group, 41.9 ± 11.2, family group, 40.4 ± 13.4 and control group 44.9 ± 15:24 mg/dL).Mean LDL values were determined as 133.6 ± 32.2 mg /dL in case group, 137.8 ± 30.8 mg/dL in family group, and 123.4 ± 32.9 mg /dL in control group. Total cholesterol/HDL cholesterol ratios were 4978 ± 1.41 in case group, 5.7 ± 2.3 in family group and 4670 ± 1.83 in control group. The prevalence of hypertension was 56% in family group, (37% in individuals 45 years and under). 42.9% of those diagnosed before the age of 40 had hypertension. Conclusion. Both the case and the family group, cholesterol, LDL levels and total cholesterol/HDL ratio is high, low HDL levels, lipid values should be within normal limits suggests that lifestyle changes are necessary to bring. As a result, while the etiology of hypertension is querying, also genetic factors should be considered in, and studies on genes and hypertension should be held responsible.In addition, hypertensive patients should be monitorized for hypertension and other cardiovascular diseases by screening of all family members while they are being evaluated. Especially patients with hypertension was diagnosed before the age of 40 and their families should be monitored for both genetic and other risk factors (BMI, lipid profile, smoking, alcohol). Lifestyle changes which are important for hypertension prevention and control of hypertension should be employed.

Keywords: Hypertension, lipid profile, genetic predisposition

References

  • 1. Murray CJ, Lope AD. Evidence-based health policy-lessons from the global burden of disease study. Science 1996; 274: 740-3.
  • 2. Joint national committee on detection. Evaluation and treatment of high blood pressure. The seventh report of the Joint national committe on prevention. Detection and treatment of high blood pressure (JNC VII). JAMA 2003; 289: 2560-74.
  • 3. Guidelines Subcommittee of the World Health Organization: World Health Organization-International society of hypertension guidelines for the management of hypertension. J Hypertens 1999; 17: 151-83.
  • 4. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA 1996; 275: 1557-62.
  • 5. Altun B, Arıcı M, Nergizoglu G. Prevalence, awareness, treatment and control of hypertension in Turkey (the PatenT study) in 2003. Journal of hypertension 2005; 23: 1817-23.
  • 6. Onat A, Sansoy V, Yıldırım B. Erişkinlerimizde kan basıncı: 8-yıllık seyri, tedavi oranı, koroner kalp hastalığı ile bazı etkenlerle ilişkileri. Türk Kardiyoloji Derneği Arş 1999; 27: 136-43.
  • 7. Sağlam K, Yılmaz Mİ, Sönmez A, Baykal Y. Primer Hipertansiyon 2003; 37.
  • 8. Lascaux-Lefebvre V, Ruidavets J, Arveiler D. Influence of parental history of hypertension on blood pressure. J Hum Hypertens 1999; 13: 631-6.
  • 9. Tozawa M, Oshiro S, Iseki C. Family history of hypertension and blood pressure in a screened cohort. Hypertens Res 2001; 24: 93-8.
  • 10. Kikukawa N. Relationship between development of hypertension and a family history of high blood pressure in urban residents-analysis based on results of annual health examinations. Nippon Koshu Eisei Zasshi 2004; 51: 833-44.
  • 11. Al-Safi SA, Aboul-Enein FH, Aboul-Enein BH, Manuel B. Influence of family history and lifestyle on blood pressure and heart rate in young adults in Jordan. Public Health 2006; 120: 1027-32.
  • 12. Di Ruppo D, Farias, Guggisberg W, Delgado A. Family history as a risk factor for hypertension in adolescents. American Journal of Hypertension 2000; 13: 266.
  • 13. Bedir A, Arık N, Adam B. Angiotensin converting enzyme gene polymorphism and activity in Turkish patients with essential hypertension. American Journal of Hypertension 1999; 12: 1038-43.
  • 14. Maron DJ, Ridker PM, Pearson TA, Grundy S. Dislipidemi, Diğer Risk Faktörleri ve Koroner Kalp Hastalığının Önlenmesi: Fuster V. Alexander RW. O’Rourke RA: Hurst’s The Heart (10.baskı) McGraw-Hill 2002; 1131-60.
  • 15. Halperin RO, Sesso HD, Ma J. Dyslipidemia and the risk of incident hypertension in men. Hypertension 2006; 47: 45-50.
  • 16. Sesso HD, Buring JE, Chown MJ. A prospective study of plasma lipid levels and hypertension in women. Arch Intern Med 2005; 165: 2420-7.
  • 17. Ağaçhan B, Yılmaz H, Öztürk O. Aterosklerozda Apolipoprotein E, Okside-LDL ve Lipid Profili İlişkisinin Araştırılması F. Ü. Sağlık Bil. Dergisi 2005; 19: 193-7.
  • 18. Mahley RW. Apolipoprotein E: Cholesterol transport protein with expanding role in cell biology. Science 1988; 240: 622-30.
  • 19. Bhavani AB, Sastry KB, Reddy NK, Padma T. Lipid profile and apolipoprotein E polymorphism in essential hypertension. Indian Heart J 2005; 57: 151-7.
  • 20. Imazu M, Yamamoto H, Toyofuku M et al. Association of apolipoprotein E phenotype with hypertension in Japanese-Americans: Data from the Hawaii-Los Angeles-Hiroshima Study. Hypertens Res 2001; 24: 523-9.
  • 21. Lenzen HJ., Assman G, Buckwalsky R, Schulte H. Association of apolipoprotein E polymorphism, low density lipoprotein cholesterol, and coronary artery disease. Clin Chem 1986; 32/5: 778-81.
  • 22. Catto AJ, Kohler HP, Bannan S, Stickland M, Carter A, Grant PJ: Factor XIII Val34Leu. A novel association with primary intracerebral hemorrhage. Stroke 1998; 29: 813-6.
  • 23. Franco RF, Pazin-Filho A, Tavella MH, Simões MV, Marin-Neto JA, Zago MA.Factor XIII val34leu and the risk of myocardial infarction. Haematologica 2000; 85: 67-71.
  • 24. Braeckman L, De Bacquer D, Rosseneu M, De Bacquer G. Apolipoprotein E polymorphism in middle-aged Belgian men: Phenotype distribution and relation to serum lipids and lipoproteins. Atherosclerosis 1996; 120: 67-73.
  • 25. Davignon J, Greeg RE, Sing CF. Apolipoprotein E polymorphism and atherosclerosis. Atherosclerosis 1988; 8: 1-21.
  • 26. Hixson JE. Pathological Determinants of Atherosclerosis in Youth (PDAY) Research Group: Apolipoprotein E polymorphism affect atherosclerosis in young males. Arterioscler Thromb 1991; 11: 1237-44.
  • 27. Jemaa R, Elasmi M, Naouali C. Apolipoprotein E polymorphism in the Tunisian population: Frequency and effect on lipid parameters. Clin Biochem 2006; 39: 816-20.
  • 28. Yilmaz H, Isbir T, Ağaçhan B, Aydin M. Is epsilon4 allele of apolipoprotein E associated with more severe end-organ damage in essential hypertension? Cell Biochem Funct 2001; 19: 191-5.
  • 29. Catto AJ, Kohler HP, Coore J, Mansfiel MW, Stickland MH, Grant PJ: Association of a common polymorphism in the factor XIII gene with venous thrombosis. Blood 1999; 93: 906-8.
There are 29 citations in total.

Details

Primary Language Turkish
Journal Section Medical Science Research Articles
Authors

Abdullah Doğan

Cem Yenicesu

Mustafa Sucaklı

Öztürk Özdemir

Yeltekin Demirel

Publication Date December 30, 2014
Published in Issue Year 2014Volume: 36 Issue: 4

Cite

AMA Doğan A, Yenicesu C, Sucaklı M, Özdemir Ö, Demirel Y. Hipertansif hastaların ailelerinde Apo E gen polimorfizmleri ve kan lipit profillerinin değerlendirilmesi. CMJ. December 2014;36(4):459-465. doi:10.7197/cmj.v36i4.1008001689