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{{Sarcoidosis}}
{{Sarcoidosis}}
{{CMG}} {{AE}}"Roshan Dinparasti Saleh M.D."
{{CMG}} {{AE}}Roshan Dinparasti Saleh M.D.


==Overview==
==Overview==
Although [[sarcoidosis]] was first introduced as a clinical entity 140 years ago, the main cause of the disease remains elusive. The contributory factors are believed to be a combination of: antigens(environment), genetic factors, and the [[immune system]].
Although [[sarcoidosis]] was first introduced as a clinical entity 140 years ago, the main cause of the disease remains elusive. The contributory factors are believed to be a combination of: antigens(environment), genetic factors, and the [[immune system]].
==Causes==
==Causes==
'''Environmental factors '''
Because [[sarcoidosis]] commonly involves lung, eyes, and skin, several environmental/occupational exposures are believed to be associated with the risk for sarcoidosis:
* Rural setting, emmisions from wood-burning stove & [[firplace]], [[tree pollen]]<ref>Bresnitz EA, Strom BL. Epidemiology of sarcoidosis. Epidemiol Rev 1983;5:124-56.</ref><ref>Kajdasz DK, Lackland DT, Mohr LC, Judson MA: A current assessment of rurally linked exposures as potential risk factors for sarcoidosis. Ann Epidemiol 11(2):111–117, 2001.</ref>
* [[Inorganic particles]]<ref>Rybicki BA, Amend KL, Maliarik MJ, Iannuzzi MC. Photocopier exposure and risk of    sarcoidosis in  African-American sibs. Sarcoidosis Vasc Diffuse Lung Dis 2004;21:49-55.</ref>
* [[Pesticides]]<ref>Newman LS, Rose CS, Bresnitz EA, et al. A case control etiologic study of sarcoidosis: environmental and occupational risk factors. Am J  Respir Crit Care Med 2004;170:1324-30.</ref>
* [[Mold exposure]]<ref name="envir">Kucera GP, Rybicki BA, Kirkey KL, et al. Occupational risk factors for  sarcoidosis in  African-American siblings. Chest 2003;123:1527-35.</ref>
* [[Navy]] personnel<ref>Gorham ED, Garland CF, Garland FC, Kaiser K,  Travis WD, Centeno JA. Trends and occupational associations in  incidence of  hospitalized pulmonary sarcoidosis and other lung diseases in Navy personnel: a 27-year historical prospective study, 1975-2001. Chest 2004;126:1431-8</ref>
* [[Firefighters]] and first responders involved in [[World Trade Center]] disaster<ref>Prezant DJ, Dhala A, Goldstein A, et  al. The incidence, prevalence, and severity of sarcoidosis in  New York City firefighters. Chest 1999;116:1183-93.</ref><ref>Izbicki G, Chavko R, Banauch GI, et al: World Trade Center “sarcoidlike” granulomatous pulmonary disease in New York City Fire Department rescue workers. Chest 131(5):1414–1423, 2007.</ref><ref>Jordan HT, Stellman SD, Prezant D, et al: Sarcoidosis diagnosed after September 11, 2001, among adults exposed to the World Trade Center disaster. J Occup Environ Med 53(9):966–974, 2011.</ref><ref>Crowley LE, Herbert R, Moline JM, et al: “Sarcoid like” granulomatous
pulmonary disease in World Trade Center disaster responders. Am J Ind Med 54:175–184, 2011.</ref>
* [[Metalworking]] (especially [[tittanium]])<ref name="envir">Kucera GP, Rybicki BA, Kirkey KL, et al. Occupational risk factors for  sarcoidosis in  African-American siblings. Chest 2003;123:1527-35.</ref>
* [[Photocopie]]r exposure<ref>Rybicki BA, Amend KL, Maliarik MJ, Iannuzzi MC: Photocopier exposure and risk of sarcoidosis in African-American sibs. Sarcoidosis Vasc Diffuse Lung Dis 21(1):49–55, 2004.</ref>
* [[Hairdresser]]s<ref>Gowdy JM, Wagstaff MJ: Pulmonary iniltration due to aerosol thesaurosis. A survey of hairdressers. Arch Environ Health 25(2):101–108, 1972.</ref>
* Healthcare workers<ref>Bresnitz EA, Stolley PD, Israel HL, Soper K: Possible risk factors for sarcoidosis. A case-control study. Ann N Y Acad Sci 465:632–642, 1986.</ref>


* [[Propionibacterium acnes]]<ref>Yamada T, Eishi Y, Ikeda S, et al: In situ localization of Propionibacterium acnes DNA in lymph nodes from sarcoidosis patients by signal ampliication with catalysed reporter deposition. J Pathol 198(4):541–547, 2002.</ref>
* [[Mycobacteria]]<ref>Chen ES, Wahlstrom J, Song Z, et al: T cell responses to mycobacterial catalase-peroxidase proile a pathogenic antigen in systemic sarcoidosis. J Immunol 181(12):8784–8796, 2008.</ref><ref>Gupta D, Agarwal R, Aggarwal AN, Jindal SK: Molecular evidence for the role of mycobacteria in sarcoidosis: a meta-analysis. Eur Respir J 30(3):508–516, 2007.</ref><ref>Schurmann M, Reichel P, Muller-Myhsok B, et al: Angiotensinconverting enzyme (ACE) gene polymorphisms and familial occurrence of sarcoidosis. J Intern Med 249(1):77–83, 2001.</ref>.
* [[Hepatitis C virus]]<ref>Ramos-Casals M, Mana J, Nardi N, et al. Sarcoidosis in patients with chronic hepatitis C virus infection: analysis of 68 cases. Medicine(Baltimore) 2005;84:69-80.</ref>


'''Drug side effect'''
 
* [[Certolizumab pegol]]
'''Genetic factors'''
   
   
'''Environmental factors ''' - because [[sarcoidosis]] commonly involves lung, eyes, and skin, several environmental/occupational exposures are believed to be associated with the risk for sarcoidosis:
[[Sarcoidosis]] is the result of environmental triggers acting upon an immunogenetically susceptible host<ref name="sarc">McGrath DS, Goh N, Foley PJ, du Bois RM: Sarcoidosis genes and microbes—soil or seed. Sarcoidosis Vasc Diffuse Lung Dis 18:149–164, 2001.</ref>. The importance of genetic factors in pathophysiology of [[sarcoidosis]] is supported by familial clusters of [[sarcoidosis]]<ref>McGrath DS, Daniil Z, Foley P, et al: Epidemiology of familial sarcoidosis in the UK. Thorax 55(Sep):751–754, 2000</ref><ref>Rybicki BA, Iannuzzi MC, Frederick MM, et al: Familial aggregation of sarcoidosis: a case-control etiologic study of sarcoidosis (ACCESS). Am J Respir Crit Care Med 164:2085–2091, 2001</ref>.
# Rural setting, emmisions from wood-burning stove & [[firplace]], [[tree pollen]]<ref>Bresnitz EA, Strom BL. Epidemiology of sarcoidosis. Epidemiol Rev 1983;5:124-56.</ref><ref>Kajdasz DK, Lackland DT, Mohr LC, Judson MA: A current assessment of rurally linked exposures as potential risk factors for sarcoidosis. Ann Epidemiol 11(2):111–117, 2001.</ref>
* The first-degree relatives are belived to be have 5 fold increased risk of developing [[sarcoidosis]]<ref>Rybicki BA, Iannuzzi MC, Frederick MM, et al. Familial aggregation of sarcoidosis: A Case-Control Etiologic Study of Sarcoidosis(ACCESS). Am J Respir Crit Care Med 2001;164:2085-91.</ref>.
# [[Inorganic particles]]<ref>Rybicki BA, Amend KL, Maliarik MJ, Iannuzzi MC. Photocopier exposure and risk of   sarcoidosis in   African-American sibs. Sarcoidosis Vasc Diffuse Lung Dis 2004;21:49-55.</ref>
* [[HLA-DRB1*1101]] is associated with [[cardiac sarcoidosis]] and [[hypercalcemia]]<ref>Rossman MD, et al: HLA and environmental interactions in sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis 25:125–132, 2008.</ref>.
# [[Pesticides]]<ref>Newman LS, Rose CS, Bresnitz EA, et al. A case control etiologic study of sarcoidosis: environmental and occupational risk factors. Am J Respir Crit Care Med 2004;170:1324-30.</ref>
* [[HLA-DRB1*01]] and [[HLA-DRB1*04]] are protective against [[sarcoidosis]]<ref>Fischer A, et al: Genetics of sarcoidosis. Semin Respir Cri Care Med 35:296–306, 2014.</ref>.
# [[Mold exposure]]<ref name="envir">Kucera GP, Rybicki BA, Kirkey KL, et al. Occupational risk factors for  sarcoidosis in  African-American siblings. Chest 2003;123:1527-35.</ref>
* In patients diagnosed with [[Lofgren's Syndrome]], [[HLA-DRB1*03]] is 4 times higher than normal individuals<ref>Wysoczanska B, et al: Combined association between IFN-gamma 3,3 homozygosity and DRB1*03 in Löfgren’s syndrome patients. Immunol Lett 91:127–131, 2004.</ref>.<ref>Grunewald J, Eklund A: Lofgren’s syndrome: human leukocyte antigen strongly inluences the disease course. Am J Respir Crit Care Med 179(4):307–312, 2009.</ref><ref>Grunewald J, Brynedal B, Darlington P, et al: Different HLA-DRB1 allele distributions in distinct clinical subgroups of sarcoidosis patients. Respir Res 11:25, 2010</ref>.
# [[Navy]] personnel<ref>Gorham ED, Garland CF, Garland FC, Kaiser K,  Travis WD, Centeno JA. Trends and occupational associations in incidence of  hospitalized pulmonary sarcoidosis and other lung diseases in Navy personnel: a 27-year historical prospective study, 1975-2001. Chest 2004;126:1431-8</ref>
* [[BTNL-2]]([[butyrophilin-like 2]]) gene, is associated with 23% of [[sarcoidosis]] risk in German individuals<ref>Valentonyte R, Hampe J, Huse K, et al: Sarcoidosis is associated with a truncating splice site mutation in BTNL2. Nat Genet 37(4):357–364, 2005.</ref>.
# [[Firefighters]] and first responders involved in [[World Trade Center]] disaster<ref>Prezant DJ, Dhala A, Goldstein A, et al. The incidence, prevalence, and severity of sarcoidosis in  New York City firefighters. Chest 1999;116:1183-93.</ref><ref>Izbicki G, Chavko R, Banauch GI, et al: World Trade Center “sarcoidlike” granulomatous pulmonary disease in New York City Fire Department rescue workers. Chest 131(5):1414–1423, 2007.</ref><ref>Jordan HT, Stellman SD, Prezant D, et al: Sarcoidosis diagnosed after September 11, 2001, among adults exposed to the World Trade Center disaster. J Occup Environ Med 53(9):966–974, 2011.</ref><ref>Crowley LE, Herbert R, Moline JM, et al: “Sarcoid like” granulomatous
pulmonary disease in World Trade Center disaster responders. Am J Ind Med 54:175–184, 2011.</ref>
# [[Metalworking]] (especially [[tittanium]])<ref name="envir">Kucera GP, Rybicki BA, Kirkey KL, et al. Occupational risk factors for  sarcoidosis in  African-American siblings. Chest 2003;123:1527-35.</ref>
# [[Photocopie]]r exposure<ref>Rybicki BA, Amend KL, Maliarik MJ, Iannuzzi MC: Photocopier exposure and risk of sarcoidosis in African-American sibs. Sarcoidosis Vasc Diffuse Lung Dis 21(1):49–55, 2004.</ref>
# [[Hairdresser]]s<ref>Gowdy JM, Wagstaff MJ: Pulmonary iniltration due to aerosol thesaurosis. A survey of hairdressers. Arch Environ Health 25(2):101–108, 1972.</ref>
# Healthcare workers<ref>Bresnitz EA, Stolley PD, Israel HL, Soper K: Possible risk factors for sarcoidosis. A case-control study. Ann N Y Acad Sci 465:632–642, 1986.</ref>
* [[Propionibacterium acnes]]<ref>Yamada T, Eishi Y, Ikeda S, et al: In situ localization of Propionibacterium acnes DNA in lymph nodes from sarcoidosis patients by signal ampliication with catalysed reporter deposition. J Pathol 198(4):541–547, 2002.</ref>
* [[Mycobacteria]]<ref>Chen ES, Wahlstrom J, Song Z, et al: T cell responses to mycobacterial catalase-peroxidase proile a pathogenic antigen in systemic sarcoidosis. J Immunol 181(12):8784–8796, 2008.</ref><ref>Gupta D, Agarwal R, Aggarwal AN, Jindal SK: Molecular evidence for the role of mycobacteria in sarcoidosis: a meta-analysis. Eur Respir J 30(3):508–516, 2007.</ref>


'''Immune System'''


[[Sarcoidosis]] is the result of environmental triggers acting upon an immunogenetically susceptible host<ref name="sarc">McGrath DS, Goh N, Foley PJ, du Bois RM: Sarcoidosis genes and microbes—soil or seed. Sarcoidosis Vasc Diffuse Lung Dis 18:149–164, 2001.</ref>.
* Higher expression of [[serum amyloid A]] which originates from [[macrophages]] and [[giant cells]], is observed in [[sarcoidosis]] [[granuloma]]<ref>Chen ES, Song Z, Willett MH, et al: Serum amyloid A regulates granulomatous inlammation in sarcoidosis through Toll-like receptor-2. Am J Respir Crit Care Med 181(4):360–373, 2010.</ref>.
* [[Immune system exhaustion]] and failure of effective antigen clearence, is proposed as a contributing mechanism for the disease. [[NK  T-cells]] are depleted in [[sarcoidosis]]<ref>Snyder-Cappione JE, Nixon DF, Chi JC, et al: Invariant natural killer T (iNKT) cell exhaustion in sarcoidosis. Eur J Immunol 43(8):2194–2205, 2013.</ref>.


'''Drug side effect'''


* [[Adalimumab]]<ref>Bhargava S, Perlman DM, Allen TL, Ritter JH, Bhargava M. Adalimumab induced pulmonary sarcoid reaction. Respiratory Medicine Case Reports. 2013;10:53-55. doi:10.1016/j.rmcr.2013.07.002.</ref>
* [[Etanercept]]<ref>Burns AM, Green PJ, Pasternak S: Etanercept-induced cutaneous and pulmonary sarcoid-like granulomas resolving with adalimumab. Journal of cutaneous pathology 2012, 39(2):289-293.</ref><ref>Fonollosa A, Artaraz J, Les I, Martinez-Berriotxoa A, Izquierdo JP, Lopez AS, Gardeazaba J, Berasategui B, Martinez-Alday N: Sarcoid intermediate uveitis following etanercept treatment: a case report and review of the literature. Ocular immunology and inflammation 2012, 20(1):44-48.</ref>


* Ipilimumab<ref>Berthod G, Lazor R, Letovanec I, Romano E, Noirez L, Mazza Stalder J, Speiser DE, Peters S, Michielin O: Pulmonary sarcoid-like granulomatosis induced by ipilimumab. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2012, 30(17):e156-159.</ref>
* [[Infliximab]]<ref>Olivier A, Gilson B, Lafontaine S, Pautot JX, Bindi P: [Pulmonary and renal involvement in a TNFalpha antagonist drug-induced sarcoidosis]. La Revue de medecine interne 2012, 33(5):e25-27</ref>






'''Genetic factors''' -
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Latest revision as of 13:38, 4 April 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Roshan Dinparasti Saleh M.D.

Overview

Although sarcoidosis was first introduced as a clinical entity 140 years ago, the main cause of the disease remains elusive. The contributory factors are believed to be a combination of: antigens(environment), genetic factors, and the immune system.

Causes

Environmental factors

Because sarcoidosis commonly involves lung, eyes, and skin, several environmental/occupational exposures are believed to be associated with the risk for sarcoidosis:


Genetic factors

Sarcoidosis is the result of environmental triggers acting upon an immunogenetically susceptible host[19]. The importance of genetic factors in pathophysiology of sarcoidosis is supported by familial clusters of sarcoidosis[20][21].

Immune System

Sarcoidosis is the result of environmental triggers acting upon an immunogenetically susceptible host[19].

Drug side effect


References

  1. ↑ Bresnitz EA, Strom BL. Epidemiology of sarcoidosis. Epidemiol Rev 1983;5:124-56.
  2. ↑ Kajdasz DK, Lackland DT, Mohr LC, Judson MA: A current assessment of rurally linked exposures as potential risk factors for sarcoidosis. Ann Epidemiol 11(2):111–117, 2001.
  3. ↑ Rybicki BA, Amend KL, Maliarik MJ, Iannuzzi MC. Photocopier exposure and risk of sarcoidosis in African-American sibs. Sarcoidosis Vasc Diffuse Lung Dis 2004;21:49-55.
  4. ↑ Newman LS, Rose CS, Bresnitz EA, et al. A case control etiologic study of sarcoidosis: environmental and occupational risk factors. Am J Respir Crit Care Med 2004;170:1324-30.
  5. ↑ 5.0 5.1 Kucera GP, Rybicki BA, Kirkey KL, et al. Occupational risk factors for sarcoidosis in African-American siblings. Chest 2003;123:1527-35.
  6. ↑ Gorham ED, Garland CF, Garland FC, Kaiser K, Travis WD, Centeno JA. Trends and occupational associations in incidence of hospitalized pulmonary sarcoidosis and other lung diseases in Navy personnel: a 27-year historical prospective study, 1975-2001. Chest 2004;126:1431-8
  7. ↑ Prezant DJ, Dhala A, Goldstein A, et al. The incidence, prevalence, and severity of sarcoidosis in New York City firefighters. Chest 1999;116:1183-93.
  8. ↑ Izbicki G, Chavko R, Banauch GI, et al: World Trade Center “sarcoidlike” granulomatous pulmonary disease in New York City Fire Department rescue workers. Chest 131(5):1414–1423, 2007.
  9. ↑ Jordan HT, Stellman SD, Prezant D, et al: Sarcoidosis diagnosed after September 11, 2001, among adults exposed to the World Trade Center disaster. J Occup Environ Med 53(9):966–974, 2011.
  10. ↑ Crowley LE, Herbert R, Moline JM, et al: “Sarcoid like” granulomatous pulmonary disease in World Trade Center disaster responders. Am J Ind Med 54:175–184, 2011.
  11. ↑ Rybicki BA, Amend KL, Maliarik MJ, Iannuzzi MC: Photocopier exposure and risk of sarcoidosis in African-American sibs. Sarcoidosis Vasc Diffuse Lung Dis 21(1):49–55, 2004.
  12. ↑ Gowdy JM, Wagstaff MJ: Pulmonary iniltration due to aerosol thesaurosis. A survey of hairdressers. Arch Environ Health 25(2):101–108, 1972.
  13. ↑ Bresnitz EA, Stolley PD, Israel HL, Soper K: Possible risk factors for sarcoidosis. A case-control study. Ann N Y Acad Sci 465:632–642, 1986.
  14. ↑ Yamada T, Eishi Y, Ikeda S, et al: In situ localization of Propionibacterium acnes DNA in lymph nodes from sarcoidosis patients by signal ampliication with catalysed reporter deposition. J Pathol 198(4):541–547, 2002.
  15. ↑ Chen ES, Wahlstrom J, Song Z, et al: T cell responses to mycobacterial catalase-peroxidase proile a pathogenic antigen in systemic sarcoidosis. J Immunol 181(12):8784–8796, 2008.
  16. ↑ Gupta D, Agarwal R, Aggarwal AN, Jindal SK: Molecular evidence for the role of mycobacteria in sarcoidosis: a meta-analysis. Eur Respir J 30(3):508–516, 2007.
  17. ↑ Schurmann M, Reichel P, Muller-Myhsok B, et al: Angiotensinconverting enzyme (ACE) gene polymorphisms and familial occurrence of sarcoidosis. J Intern Med 249(1):77–83, 2001.
  18. ↑ Ramos-Casals M, Mana J, Nardi N, et al. Sarcoidosis in patients with chronic hepatitis C virus infection: analysis of 68 cases. Medicine(Baltimore) 2005;84:69-80.
  19. ↑ 19.0 19.1 McGrath DS, Goh N, Foley PJ, du Bois RM: Sarcoidosis genes and microbes—soil or seed. Sarcoidosis Vasc Diffuse Lung Dis 18:149–164, 2001.
  20. ↑ McGrath DS, Daniil Z, Foley P, et al: Epidemiology of familial sarcoidosis in the UK. Thorax 55(Sep):751–754, 2000
  21. ↑ Rybicki BA, Iannuzzi MC, Frederick MM, et al: Familial aggregation of sarcoidosis: a case-control etiologic study of sarcoidosis (ACCESS). Am J Respir Crit Care Med 164:2085–2091, 2001
  22. ↑ Rybicki BA, Iannuzzi MC, Frederick MM, et al. Familial aggregation of sarcoidosis: A Case-Control Etiologic Study of Sarcoidosis(ACCESS). Am J Respir Crit Care Med 2001;164:2085-91.
  23. ↑ Rossman MD, et al: HLA and environmental interactions in sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis 25:125–132, 2008.
  24. ↑ Fischer A, et al: Genetics of sarcoidosis. Semin Respir Cri Care Med 35:296–306, 2014.
  25. ↑ Wysoczanska B, et al: Combined association between IFN-gamma 3,3 homozygosity and DRB1*03 in Löfgren’s syndrome patients. Immunol Lett 91:127–131, 2004.
  26. ↑ Grunewald J, Eklund A: Lofgren’s syndrome: human leukocyte antigen strongly inluences the disease course. Am J Respir Crit Care Med 179(4):307–312, 2009.
  27. ↑ Grunewald J, Brynedal B, Darlington P, et al: Different HLA-DRB1 allele distributions in distinct clinical subgroups of sarcoidosis patients. Respir Res 11:25, 2010
  28. ↑ Valentonyte R, Hampe J, Huse K, et al: Sarcoidosis is associated with a truncating splice site mutation in BTNL2. Nat Genet 37(4):357–364, 2005.
  29. ↑ Chen ES, Song Z, Willett MH, et al: Serum amyloid A regulates granulomatous inlammation in sarcoidosis through Toll-like receptor-2. Am J Respir Crit Care Med 181(4):360–373, 2010.
  30. ↑ Snyder-Cappione JE, Nixon DF, Chi JC, et al: Invariant natural killer T (iNKT) cell exhaustion in sarcoidosis. Eur J Immunol 43(8):2194–2205, 2013.
  31. ↑ Bhargava S, Perlman DM, Allen TL, Ritter JH, Bhargava M. Adalimumab induced pulmonary sarcoid reaction. Respiratory Medicine Case Reports. 2013;10:53-55. doi:10.1016/j.rmcr.2013.07.002.
  32. ↑ Burns AM, Green PJ, Pasternak S: Etanercept-induced cutaneous and pulmonary sarcoid-like granulomas resolving with adalimumab. Journal of cutaneous pathology 2012, 39(2):289-293.
  33. ↑ Fonollosa A, Artaraz J, Les I, Martinez-Berriotxoa A, Izquierdo JP, Lopez AS, Gardeazaba J, Berasategui B, Martinez-Alday N: Sarcoid intermediate uveitis following etanercept treatment: a case report and review of the literature. Ocular immunology and inflammation 2012, 20(1):44-48.
  34. ↑ Berthod G, Lazor R, Letovanec I, Romano E, Noirez L, Mazza Stalder J, Speiser DE, Peters S, Michielin O: Pulmonary sarcoid-like granulomatosis induced by ipilimumab. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2012, 30(17):e156-159.
  35. ↑ Olivier A, Gilson B, Lafontaine S, Pautot JX, Bindi P: [Pulmonary and renal involvement in a TNFalpha antagonist drug-induced sarcoidosis]. La Revue de medecine interne 2012, 33(5):e25-27

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