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Raynaud Fenomeni üzerine genetik yapı, östrojen ve toksik ajanların klinik etkileri

Year 2019, Volume: 12 Issue: 1, 143 - 149, 28.04.2019

Merih Akkapulu Ali Erdinç Yalın

https://doi.org/10.26559/mersinsbd.531295

Abstract

Raynaud Fenomeni (RF) soğuk kaynaklı vazokonstrüksiyonla
karakterize bir hastalıktır. Bu güçlendirilmiş vazokonstrüksiyon, sempatik
sinir sistemi yoluyla soğumaya karşı bir refleks cevabı ve Alfa2C (α2C)
adrenoreseptörlerinin lokal aktivasyonu ile gerçekleşmektedir. Bu hastalık
klinik olarak primer ve sekonder olarak sınıflandırılmaktadır. Primer RF
idiyopatiktir ve hastalığın en yaygın şeklidir. Sekonder RF, otoimmün veya
kanser gibi hastalıklara eşlik edebileceği gibi, sigara içimi ya da bazı
ilaçların kullanımı da sebebiyet verebilmektedir. Etkilenen bireyler, soğuk ve
stresin tetiklemesiyle birlikte, genellikle el parmaklarında, klasik üç renk
değişikliğiyle (solukluk, siyanoz ve hiperemi) ilişkili olan vazospastik
ataklardan muzdarip olmaktadırlar. Epidemiyolojik çalışmalardan elde edilen
veriler, RF prevalansı ile ilgili ilginç bulgular ortaya koymuştur. Yaşları
aynı olan kadınların, erkeklere göre anlamlı olarak daha yüksek bir insidansa
sahip olduğu belirlenmiştir. Bu derlemede, östrojenin, genetik yapının ve
kimyasal ajanların RF üzerine olan etkileri tartışılmıştır. Sonuç olarak, bu
hastalığa neden olan birçok faktör açıklanmasına rağmen, RF'nin başlangıcının
ve ilerlemesinin altında yatan moleküler mekanizmaların aydınlatılması için
daha fazla araştırmaya gereksinim duyulmaktadır.

Keywords

Raynaud fenomeni vazospazm Alfa2(α2) adrenoreseptörler östrojen

References

  • 1.Charkoudian N. Mechanisms and modifiers of reflex induced cutaneous vasodilation and vasoconstriction in humans. J. Appl. Physiol. 2010; 109(1985):1221–1228.
  • 2.Wigley FM, Flavahan NA.Raynaud’s phenomenon.N.Engl.J.Med. 2016;375:556–565.
  • 3.Herrick AL. The pathogenesis, diagnosis and treatment of Raynaud phenomenon. Nat. Rev. Rheumatol. 2012;8:469–479.
  • 4.Block JA, Sequeira W. Raynaud’s phenomenon. Lancet 2001;357:2042–2048.
  • 5. Roustit M, Khouri C, Blaise S, Villier C, Carpentier P, Cracowski JL. Pharmacology of Raynaud’s phenomenon. Therapie 2014;69:115–128.
  • 6. Prete M, Fatone MC, Favoino E, Perosa F. (2014). Raynaud’s phenomenon: from molecular pathogenesis to therapy. Autoimmun. Rev. 2014; 13:655–667.
  • 7. Black CM. Systemic sclerosis ‘state of the art’ 1995. Scand. J. Rheumatol. 1995;24:194–196.
  • 8. Garner R, Kumari R , Lanyon P, Doherty M, Zhang W. Prevalence, risk factors and associations of primary Raynaud’s phenomenon: systematic review and meta-analysis of observational studies. BMJ 2015; Open 5: e006389.
  • 9. Maverakis E, Patel F, Kronenberg DG, Chung L, Fiorentino D, Allanore Y, et al. (2014). International consensus criteria for the diagnosis of Raynaud’s phenomenon. J. Autoimmun. 2014;4:60–65.
  • 10. Fardoun MM, Nassif J, Issa K, Baydoun E, Eid AH. Raynaud’s Phenomenon: A brief review of the underlying mechanisms. Front. Pharmacol. 2016;7:438.
  • 11. Greenstein D, Jeffcote N, Ilsley D, Kester RC. The menstrual cycle and Raynaud’s phenomenon. Angiology. 1996;47:427–436.
  • 12. Wigley FM. Clinical practice. Raynaud’s phenomenon. N. Engl. J. Med. 2002;347:1001–1008.
  • 13. Easter M J, Marshall JM. Contribution of prostanoids to endothelium-dependent vasodilatation in the digital circulation of women with primary Raynaud’s disease. Clin. Sci. (Lond). 2005;109:45–54.
  • 14. Guimaraes S, Moura D. Vascular adrenoceptors: an update. Pharmacol. Rev. 2001;53:319–356.
  • 15. Ahles A, Engelhardt S. Polymorphic variants of adrenoceptors: pharmacology, physiology, and role in disease. Pharmacol. Rev. 2014;66:598–637.
  • 16. McCance KL, Huether SE. Pathophysiology: The Biologic Basis for Disease in Adults and Children. Amsterdam: Elsevier. 2013.
  • 17. Polonia JJ., Paiva MQ, Guimaraes S. Pharmacological characterization of postsynaptic alpha-adrenoceptor subtypes in five different dog arteries in-vitro. J. Pharm. Pharmacol. 1985;37:205–208.
  • 18. Johnson JM, Kellogg DLJr. Local thermal control of the human cutaneous circulation. J. Appl. Physiol. 2010;109:1229–1238.
  • 19. Freedman RR, Sabharwal SC, Moten M, Migaly P. Local temperature modulates alpha 1- and alpha 2-adrenergic vasoconstriction in men. Am. J. Physiol. 1992;263:H1197–H1200.20. MacDonald E, Kobilka BK, Scheinin M. Gene targeting–homing in on alpha2-adrenoceptor-subtype function.Trends Pharmacol. Sci. 1997;18:211–219.
  • 21. Chotani MA, Flavahan S, Mitra S, Daunt D, Flavahan NA. Silent alpha(2C)-adrenergic receptors enable cold-induced vasoconstriction in cutaneous arteries. Am. J. Physiol. Heart Circ. Physiol. 2000;278:H1075–H1083.
  • 22. Sallinen J, Link RE, Haapalinna A, Viitamaa T, Kulatunga M, Sjoholm B, et al. Genetic alteration of alpha 2C-adrenoceptor expression in mice: influence on locomotor, hypothermic, and neurochemical effects of dexmedetomidine, a subtype-nonselective alpha 2-adrenoceptor agonist. Mol. Pharmacol. 1997;51:36–46.
  • 23. Jeyaraj SC, Chotani MA, Mitra S, Gregg HE, Flavahan NA, Morrison KJ. Cooling evokes redistribution of alpha2C-adrenoceptors from Golgi to plasma membrane in transfected human embryonic kidney 293 cells. Mol. Pharmacol. 2001;60:1195–1200.
  • 24. Bailey SR, Eid AH, Mitra S, Flavahan S, Flavahan NA. Rho kinase mediates cold-induced constriction of cutaneous arteries: role of alpha2C-adrenoceptor translocation. Circ. Res. 2004;94:1367–1374.
  • 25. Maricq HR, Carpentier PH, Weinrich MC, Keil JE, Franco A, Drouet P, et al. Geographic variation in the prevalence of Raynaud’s phenomenon: Charleston, SC, USA, vs Tarentaise, Savoie, France. J. Rheumatol. 1993;20:70–76.
  • 26. Belch JJF, Ho M. “Vasospastic disorders and vasculitis,” in Vascular and Endovascular Surgery, eds J. D. Beard and P. A. Gaines (London: WB Saunders and Company). 2001;217–240.
  • 27. Garner R, Kumari R, Lanyon P, Doherty M, Zhang W. Prevalence, risk factors and associations of primary Raynaud’s phenomenon: systematic review and meta-analysis of observational studies. BMJ Open 5. 2015;e006389.
  • 28. Mayes MD. Epidemiologic studies of environmental agents and systemic autoimmune diseases. Environ. Health Perspect. 1999;107(Suppl. 5):743–748.
  • 29. Fraenkel L, Zhang Y, Chaisson CE, Evans SR, Wilson PW, Felson DT. The association of estrogen replacement therapy and the Raynaud phenomenon in postmenopausal women. Ann. Intern. Med. 1998;129:208–211.
  • 30. Chan NN, MacAllister RJ, Colhoun HM, Vallance P, Hingorani AD. Changes in endothelium-dependent vasodilatation and alpha- adrenergic responses in resistance vessels during the menstrual cycle in healthy women. J. Clin. Endocrinol. Metab. 2001;86:2499–2504.
  • 31. Li T, Xiao X, Zhang J, Zhu Y, Hu Y, Zang J, et al. Age and sex differences in vascular responsiveness in healthy and trauma patients: contribution of estrogen receptor-mediated Rho kinase and PKC pathways. Am. J. Physiol. Heart Circ. Physiol. 2014;306:H1105–H1115.
  • 32. Charkoudian N, Stachenfeld N. Sex hormone effects on autonomic mechanisms of thermoregulation in humans. Auton. Neurosci. 2016;196:75–80.
  • 33. Flavahan, N. A. A vascular mechanistic approach to understanding Raynaud phenomenon. Nat. Rev. Rheumatol. 2015;11:146–158.
  • 34. English KM, Jones RD, Jones TH, Morice AH, Channer KS. Gender differences in the vasomotor effects of different steroid hormones in rat pulmonary and coronary arteries. Horm. Metab. Res. 2001;33:645–652.
  • 35. Eid AH, Maiti K, Mitra S, Chotani MA, Flavahan S, Bailey SR, et al. Estrogen increases smooth muscle expression of alpha2C-adrenoceptors and cold-induced constriction of cutaneous arteries. Am. J. Physiol. Heart Circ. Physiol. 2007;293:H1955–H1961.
  • 36. Tan FK, Arnett FC. Genetic factors in the etiology of systemic sclerosis and Raynaud phenomenon. Curr. Opin. Rheumatol. 2000;12:511–519.
  • 37. Susol E, MacGregor AJ, Barrett JH, Wilson H, Black C, Welsh K, et al. A two-stage, genome-wide screen for susceptibility loci in primary Raynaud’s phenomenon. Arthritis Rheum. 2000;43:1641–1646.
  • 38. Pistorius MA, Planchon B, Schott JJ, Lemarec H. [Heredity and genetic aspects of Raynaud’s disease]. J. Mal. Vasc. 2006;31:10–15.
  • 39. Sharathkumar AA, Castillo-Caro P. Primary Raynaud’s phenomenon in an infant: a case report and review of literature. Pediatr. Rheumatol. Online J. 2011;9:16.
  • 40. Fontana L, Marion MJ, Ughetto S, Catilina P. Glutathione S-transferase M1 and GST T1 genetic polymorphisms and Raynaud’s phenomenon in French vinyl chloride monomer-exposed workers. J. Hum. Genet. 2006;51:879–886.

The clinical effects of genetic structure, estrogen, and toxic agents on Raynaud’s Phenomenon

Year 2019, Volume: 12 Issue: 1, 143 - 149, 28.04.2019

Merih Akkapulu Ali Erdinç Yalın

https://doi.org/10.26559/mersinsbd.531295

Abstract

Raynaud’s
phenomenon (RP) is characterized by cold-induced vasoconstriction. This
enhanced vasoconstriction is achieved by a reflex response to cooling through
the sympathetic nervous system and by local activation of Alpha2C (α2C)
adrenoreceptors. This disease is clinically
classified as primary and secondary. Primary RP is idiopathic and is the most
common form of the disease. Secondary RP may be associated with diseases such
as autoimmune diseases or cancer, and smoking or the use of certain medications
may also be cause. Affected individuals suffer from vasospastic attacks
associated with classical three colour changes (paleness, cyanosis, and hyperemia), often triggered by cold
and/or stress. The data from the epidemiological studies revealed interesting
findings related to the prevalence of RP. 

It was determined that women with the same age had a
significantly higher incidence than men. In this review, the effects of
oestrogen, genetic structure and chemical agents on RP were discussed. As a
result, although many factors have been described causing this disease, further
research is needed to elucidate the molecular mechanisms underlying the onset
and progression of RP.

Keywords

Raynaud's phenomenon vasospasm Alpha2 (α2) adrenoreceptors estrogen

References

  • 1.Charkoudian N. Mechanisms and modifiers of reflex induced cutaneous vasodilation and vasoconstriction in humans. J. Appl. Physiol. 2010; 109(1985):1221–1228.
  • 2.Wigley FM, Flavahan NA.Raynaud’s phenomenon.N.Engl.J.Med. 2016;375:556–565.
  • 3.Herrick AL. The pathogenesis, diagnosis and treatment of Raynaud phenomenon. Nat. Rev. Rheumatol. 2012;8:469–479.
  • 4.Block JA, Sequeira W. Raynaud’s phenomenon. Lancet 2001;357:2042–2048.
  • 5. Roustit M, Khouri C, Blaise S, Villier C, Carpentier P, Cracowski JL. Pharmacology of Raynaud’s phenomenon. Therapie 2014;69:115–128.
  • 6. Prete M, Fatone MC, Favoino E, Perosa F. (2014). Raynaud’s phenomenon: from molecular pathogenesis to therapy. Autoimmun. Rev. 2014; 13:655–667.
  • 7. Black CM. Systemic sclerosis ‘state of the art’ 1995. Scand. J. Rheumatol. 1995;24:194–196.
  • 8. Garner R, Kumari R , Lanyon P, Doherty M, Zhang W. Prevalence, risk factors and associations of primary Raynaud’s phenomenon: systematic review and meta-analysis of observational studies. BMJ 2015; Open 5: e006389.
  • 9. Maverakis E, Patel F, Kronenberg DG, Chung L, Fiorentino D, Allanore Y, et al. (2014). International consensus criteria for the diagnosis of Raynaud’s phenomenon. J. Autoimmun. 2014;4:60–65.
  • 10. Fardoun MM, Nassif J, Issa K, Baydoun E, Eid AH. Raynaud’s Phenomenon: A brief review of the underlying mechanisms. Front. Pharmacol. 2016;7:438.
  • 11. Greenstein D, Jeffcote N, Ilsley D, Kester RC. The menstrual cycle and Raynaud’s phenomenon. Angiology. 1996;47:427–436.
  • 12. Wigley FM. Clinical practice. Raynaud’s phenomenon. N. Engl. J. Med. 2002;347:1001–1008.
  • 13. Easter M J, Marshall JM. Contribution of prostanoids to endothelium-dependent vasodilatation in the digital circulation of women with primary Raynaud’s disease. Clin. Sci. (Lond). 2005;109:45–54.
  • 14. Guimaraes S, Moura D. Vascular adrenoceptors: an update. Pharmacol. Rev. 2001;53:319–356.
  • 15. Ahles A, Engelhardt S. Polymorphic variants of adrenoceptors: pharmacology, physiology, and role in disease. Pharmacol. Rev. 2014;66:598–637.
  • 16. McCance KL, Huether SE. Pathophysiology: The Biologic Basis for Disease in Adults and Children. Amsterdam: Elsevier. 2013.
  • 17. Polonia JJ., Paiva MQ, Guimaraes S. Pharmacological characterization of postsynaptic alpha-adrenoceptor subtypes in five different dog arteries in-vitro. J. Pharm. Pharmacol. 1985;37:205–208.
  • 18. Johnson JM, Kellogg DLJr. Local thermal control of the human cutaneous circulation. J. Appl. Physiol. 2010;109:1229–1238.
  • 19. Freedman RR, Sabharwal SC, Moten M, Migaly P. Local temperature modulates alpha 1- and alpha 2-adrenergic vasoconstriction in men. Am. J. Physiol. 1992;263:H1197–H1200.20. MacDonald E, Kobilka BK, Scheinin M. Gene targeting–homing in on alpha2-adrenoceptor-subtype function.Trends Pharmacol. Sci. 1997;18:211–219.
  • 21. Chotani MA, Flavahan S, Mitra S, Daunt D, Flavahan NA. Silent alpha(2C)-adrenergic receptors enable cold-induced vasoconstriction in cutaneous arteries. Am. J. Physiol. Heart Circ. Physiol. 2000;278:H1075–H1083.
  • 22. Sallinen J, Link RE, Haapalinna A, Viitamaa T, Kulatunga M, Sjoholm B, et al. Genetic alteration of alpha 2C-adrenoceptor expression in mice: influence on locomotor, hypothermic, and neurochemical effects of dexmedetomidine, a subtype-nonselective alpha 2-adrenoceptor agonist. Mol. Pharmacol. 1997;51:36–46.
  • 23. Jeyaraj SC, Chotani MA, Mitra S, Gregg HE, Flavahan NA, Morrison KJ. Cooling evokes redistribution of alpha2C-adrenoceptors from Golgi to plasma membrane in transfected human embryonic kidney 293 cells. Mol. Pharmacol. 2001;60:1195–1200.
  • 24. Bailey SR, Eid AH, Mitra S, Flavahan S, Flavahan NA. Rho kinase mediates cold-induced constriction of cutaneous arteries: role of alpha2C-adrenoceptor translocation. Circ. Res. 2004;94:1367–1374.
  • 25. Maricq HR, Carpentier PH, Weinrich MC, Keil JE, Franco A, Drouet P, et al. Geographic variation in the prevalence of Raynaud’s phenomenon: Charleston, SC, USA, vs Tarentaise, Savoie, France. J. Rheumatol. 1993;20:70–76.
  • 26. Belch JJF, Ho M. “Vasospastic disorders and vasculitis,” in Vascular and Endovascular Surgery, eds J. D. Beard and P. A. Gaines (London: WB Saunders and Company). 2001;217–240.
  • 27. Garner R, Kumari R, Lanyon P, Doherty M, Zhang W. Prevalence, risk factors and associations of primary Raynaud’s phenomenon: systematic review and meta-analysis of observational studies. BMJ Open 5. 2015;e006389.
  • 28. Mayes MD. Epidemiologic studies of environmental agents and systemic autoimmune diseases. Environ. Health Perspect. 1999;107(Suppl. 5):743–748.
  • 29. Fraenkel L, Zhang Y, Chaisson CE, Evans SR, Wilson PW, Felson DT. The association of estrogen replacement therapy and the Raynaud phenomenon in postmenopausal women. Ann. Intern. Med. 1998;129:208–211.
  • 30. Chan NN, MacAllister RJ, Colhoun HM, Vallance P, Hingorani AD. Changes in endothelium-dependent vasodilatation and alpha- adrenergic responses in resistance vessels during the menstrual cycle in healthy women. J. Clin. Endocrinol. Metab. 2001;86:2499–2504.
  • 31. Li T, Xiao X, Zhang J, Zhu Y, Hu Y, Zang J, et al. Age and sex differences in vascular responsiveness in healthy and trauma patients: contribution of estrogen receptor-mediated Rho kinase and PKC pathways. Am. J. Physiol. Heart Circ. Physiol. 2014;306:H1105–H1115.
  • 32. Charkoudian N, Stachenfeld N. Sex hormone effects on autonomic mechanisms of thermoregulation in humans. Auton. Neurosci. 2016;196:75–80.
  • 33. Flavahan, N. A. A vascular mechanistic approach to understanding Raynaud phenomenon. Nat. Rev. Rheumatol. 2015;11:146–158.
  • 34. English KM, Jones RD, Jones TH, Morice AH, Channer KS. Gender differences in the vasomotor effects of different steroid hormones in rat pulmonary and coronary arteries. Horm. Metab. Res. 2001;33:645–652.
  • 35. Eid AH, Maiti K, Mitra S, Chotani MA, Flavahan S, Bailey SR, et al. Estrogen increases smooth muscle expression of alpha2C-adrenoceptors and cold-induced constriction of cutaneous arteries. Am. J. Physiol. Heart Circ. Physiol. 2007;293:H1955–H1961.
  • 36. Tan FK, Arnett FC. Genetic factors in the etiology of systemic sclerosis and Raynaud phenomenon. Curr. Opin. Rheumatol. 2000;12:511–519.
  • 37. Susol E, MacGregor AJ, Barrett JH, Wilson H, Black C, Welsh K, et al. A two-stage, genome-wide screen for susceptibility loci in primary Raynaud’s phenomenon. Arthritis Rheum. 2000;43:1641–1646.
  • 38. Pistorius MA, Planchon B, Schott JJ, Lemarec H. [Heredity and genetic aspects of Raynaud’s disease]. J. Mal. Vasc. 2006;31:10–15.
  • 39. Sharathkumar AA, Castillo-Caro P. Primary Raynaud’s phenomenon in an infant: a case report and review of literature. Pediatr. Rheumatol. Online J. 2011;9:16.
  • 40. Fontana L, Marion MJ, Ughetto S, Catilina P. Glutathione S-transferase M1 and GST T1 genetic polymorphisms and Raynaud’s phenomenon in French vinyl chloride monomer-exposed workers. J. Hum. Genet. 2006;51:879–886.
There are 39 citations in total.

Details

Primary Language Turkish
Subjects Health Care Administration
Journal Section Articles
Authors

Merih Akkapulu 0000-0002-5884-2986

Ali Erdinç Yalın 0000-0002-3351-6885

Publication Date April 28, 2019
Submission Date February 22, 2019
Acceptance Date March 16, 2019
Published in Issue Year 2019 Volume: 12 Issue: 1

Cite

APA Akkapulu, M., & Yalın, A. E. (2019). Raynaud Fenomeni üzerine genetik yapı, östrojen ve toksik ajanların klinik etkileri. Mersin Üniversitesi Sağlık Bilimleri Dergisi, 12(1), 143-149. https://doi.org/10.26559/mersinsbd.531295
AMA Akkapulu M, Yalın AE. Raynaud Fenomeni üzerine genetik yapı, östrojen ve toksik ajanların klinik etkileri. Mersin Univ Saglık Bilim derg. April 2019;12(1):143-149. doi:10.26559/mersinsbd.531295
Chicago Akkapulu, Merih, and Ali Erdinç Yalın. “Raynaud Fenomeni üzerine Genetik yapı, östrojen Ve Toksik ajanların Klinik Etkileri”. Mersin Üniversitesi Sağlık Bilimleri Dergisi 12, no. 1 (April 2019): 143-49. https://doi.org/10.26559/mersinsbd.531295.
EndNote Akkapulu M, Yalın AE (April 1, 2019) Raynaud Fenomeni üzerine genetik yapı, östrojen ve toksik ajanların klinik etkileri. Mersin Üniversitesi Sağlık Bilimleri Dergisi 12 1 143–149.
IEEE M. Akkapulu and A. E. Yalın, “Raynaud Fenomeni üzerine genetik yapı, östrojen ve toksik ajanların klinik etkileri”, Mersin Univ Saglık Bilim derg, vol. 12, no. 1, pp. 143–149, 2019, doi: 10.26559/mersinsbd.531295.
ISNAD Akkapulu, Merih - Yalın, Ali Erdinç. “Raynaud Fenomeni üzerine Genetik yapı, östrojen Ve Toksik ajanların Klinik Etkileri”. Mersin Üniversitesi Sağlık Bilimleri Dergisi 12/1 (April 2019), 143-149. https://doi.org/10.26559/mersinsbd.531295.
JAMA Akkapulu M, Yalın AE. Raynaud Fenomeni üzerine genetik yapı, östrojen ve toksik ajanların klinik etkileri. Mersin Univ Saglık Bilim derg. 2019;12:143–149.
MLA Akkapulu, Merih and Ali Erdinç Yalın. “Raynaud Fenomeni üzerine Genetik yapı, östrojen Ve Toksik ajanların Klinik Etkileri”. Mersin Üniversitesi Sağlık Bilimleri Dergisi, vol. 12, no. 1, 2019, pp. 143-9, doi:10.26559/mersinsbd.531295.
Vancouver Akkapulu M, Yalın AE. Raynaud Fenomeni üzerine genetik yapı, östrojen ve toksik ajanların klinik etkileri. Mersin Univ Saglık Bilim derg. 2019;12(1):143-9.

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