Sarcoidosis causes
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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:
- Rural setting, emmisions from wood-burning stove & firplace, tree pollen[1][2]
- Inorganic particles[3]
- Pesticides[4]
- Mold exposure[5]
- Navy personnel[6]
- Firefighters and first responders involved in World Trade Center disaster[7][8][9][10]
- Metalworking (especially tittanium)[5]
- Photocopier exposure[11]
- Hairdressers[12]
- Healthcare workers[13]
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].
- The first-degree relatives are belived to be have 5 fold increased risk of developing sarcoidosis[22].
- HLA-DRB1*1101 is associated with cardiac sarcoidosis and hypercalcemia[23].
- HLA-DRB1*01 and HLA-DRB1*04 are protective against sarcoidosis[24].
- In patients diagnosed with Lofgren's Syndrome, HLA-DRB1*03 is 4 times higher than normal individuals[25].[26][27].
- BTNL-2(butyrophilin-like 2) gene, is associated with 23% of sarcoidosis risk in German individuals[28].
Immune System
Sarcoidosis is the result of environmental triggers acting upon an immunogenetically susceptible host[19].
- Higher expression of serum amyloid A which originates from macrophages and giant cells, is observed in sarcoidosis granuloma[29].
- 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[30].
Drug side effect
- Ipilimumab[34]
- Infliximab[35]
References
- ↑ Bresnitz EA, Strom BL. Epidemiology of sarcoidosis. Epidemiol Rev 1983;5:124-56.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 5.0 5.1 Kucera GP, Rybicki BA, Kirkey KL, et al. Occupational risk factors for sarcoidosis in African-American siblings. Chest 2003;123:1527-35.
- ↑ 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
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Gowdy JM, Wagstaff MJ: Pulmonary iniltration due to aerosol thesaurosis. A survey of hairdressers. Arch Environ Health 25(2):101–108, 1972.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 19.0 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.
- ↑ McGrath DS, Daniil Z, Foley P, et al: Epidemiology of familial sarcoidosis in the UK. Thorax 55(Sep):751–754, 2000
- ↑ 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
- ↑ 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.
- ↑ Rossman MD, et al: HLA and environmental interactions in sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis 25:125–132, 2008.
- ↑ Fischer A, et al: Genetics of sarcoidosis. Semin Respir Cri Care Med 35:296–306, 2014.
- ↑ 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.
- ↑ 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.
- ↑ 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
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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