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{{CMG}} {{AE}}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==
==Causes==
Sarcoidosis involves a dysregulated immune response to environmental agents in a genetically susceptible host.
'''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>
 


'''Immunological factors'''- The sarcoid granulomas indicate cell mediated immune response. Anergy to common skin test antigens like Candida and Tuberculosis purified protein derivative (PPD) is seen in sarcoidosis patient.It was demonstrated that the mycobacterial virulence factors, ESAT-6 and katG, when presented by DRB1*1101 are recognized by sarcoidosis CD4+ T cells.<ref name="pmid19536643">{{cite journal| author=Oswald-Richter K, Sato H, Hajizadeh R, Shepherd BE, Sidney J, Sette A et al.| title=Mycobacterial ESAT-6 and katG are recognized by sarcoidosis CD4+ T cells when presented by the American sarcoidosis susceptibility allele, DRB1*1101. | journal=J Clin Immunol | year= 2010 | volume= 30 | issue= 1 | pages= 157-66 | pmid=19536643 | doi=10.1007/s10875-009-9311-y | pmc=PMC2821522 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19536643  }} </ref>
'''Genetic factors'''
   
   
'''Environmental factors ''' - Several environmental exposures are believed to be associated with the risk for sarcoidosis:mold or mildew, musty odors at work, agricultural employment, and pesticide-using industries.
[[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>.
* 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>.
* [[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>.
* [[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>.
* 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>.
* [[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>.
 
'''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''' - Recent pangenomic studies highlight some regions of the genome such as 6p21 where are located important immune genes: MHC, BTNL2 and TNF-α . Sarcoidosis is more common and severe in blacks than whites.<ref name="pmid23461074">{{cite journal| author=Judson MA, Boan AD, Lackland DT| title=The clinical course of sarcoidosis: presentation, diagnosis, and treatment in a large white and black cohort in the United States. | journal=Sarcoidosis Vasc Diffuse Lung Dis | year= 2012 | volume= 29 | issue= 2 | pages= 119-27 | pmid=23461074 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23461074  }} </ref>It was recently found that non-synonymous single-nucleotide polymorphism (SNP), rs1049550, within the annexin A11 (ANXA11) gene was associated with susceptibility to sarcoidosis<ref name="pmid23151485">{{cite journal| author=Levin AM, Iannuzzi MC, Montgomery CG, Trudeau S, Datta I, McKeigue P et al.| title=Association of ANXA11 genetic variation with sarcoidosis in African Americans and European Americans. | journal=Genes Immun | year= 2013 | volume= 14 | issue= 1 | pages= 13-8 | pmid=23151485 | doi=10.1038/gene.2012.48 | pmc=PMC3595044 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23151485  }} </ref>.Sarcoidosis likely results from an interplay of environmental and genetic factors.


==References==
==References==
{{Reflist|2}}


{{Reflist|2}}
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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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