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Comparison of accepted autoimmune diseases
Disease name Aetiology Pathophysiology Epidemiology Tissues affected Treatment Prognosis
Acute disseminated encephalomyelitis[1] Unknown Disturbance of the blood-brain barrier and IL-1β, Il-2, IL-4, IL-5, IL-6, IL-8, IL-10, IFN-γ, TNF-α, and MIP-1β appear to be involved.[1] Children tend to be most often affected. Incidence is <1/100,000. Brain and spinal cord. Corticosteroids and intravenous immunoglobulin. Generally favourable; 1.5% mortality rate.
Antiphospholipid syndrome[2] Unknown Antiphospholipid antibody-mediated assault on phospholipids that make up blood cells.[3] Female predominance, more common in Hispanics and African Americans, it is more common in young-middle aged patients. Blood and foetus Anticoagulants, hydroxychloroquine, cyclophosphamide, prednisone, rituximab and intravenous immunoglobulin.[4][5][6][7][8][9][10][11][12][13][14][15][16] Highly fatal, due to venous thromboembolisms.
Atopic dermatitis Unknown, genes and environment contribute. People with a family or personal history of atopic dermatitis, asthma, food allergies and hay fever are at a heightened risk for the condition. Predominantly TH2-mediated pathology.[17][18][19][20] 15-30% of children are affected. Only 1-3% of adults are affected, although.[21][22] Skin Lukewarm baths, moisturisers, corticosteroids, tacrolimus, ciclosporin, azathioprine, methotrexate, rituximab, infliximab and pimecrolimus.[22][23][24][25][26][27] Generally favourable, although relapses are common.
Autoimmune haemolytic anaemia[28] Unknown; infectious and malignant expected. Immunoglobulin G and Immunoglobulin M involved. Annual incidence is about 1/100,000.[29] Red blood cells. Corticosteroid, azathioprine, cyclophosphamide, ciclosporin, mycophenolate mofetil, rituximab and immunoglobulins.[29] Generally favourable. 10% fatality rate overall.
Autoimmune hepatitis Unknown; genetics and environment likely play a role.[30] T-cell mediated destruction of hepatocytes. Frequency is about 0.015-1.2/100,000.[30][31] Liver Corticosteroids, azathioprine, mycophenolate mofetil, tacrolimus and ciclosporin.[32][33] Generally unfavourable; cirrhosis is present in 30% of cases at the time of diagnosis.[30]
Autoimmune inner ear disease[34] Unknown; infectious agents believed to contribute. Unknown Most commonly affects people between the ages of 20-50, especially females with other autoimmune conditions.[34] Inner ear Corticosteroids, azathioprine, mycophenolate mofetil, cyclophosphamide and methotrexate.[35] Unknown
Autoimmune lymphoproliferative syndrome
[36][37][38][39][40]		 Genetic; mutations in the Fas signalling pathway. Mutations in the fas signalling pathway allows for the accumulation of malfunctioning lymphocytes in the tissues. Most commonly presents in childhood and runs in over 300 families worldwide. Haematopoietic, liver and lymphatics (including spleen). Corticosteroids, cyclophosphamide, ciclosporin, mycophenolate mofetil and immunoglobulins. Favourable. Mortality usually occurs as a result of cytopenias or malignancies.
Autoimmune pancreatitis[41][42] Unknown Type I is mediated by immunoglobulin G produced by plasma cells and increased production of T cells. Type II is mediated by granulocytes. Type I is more common in Asia; type II in Europe/North America. Type I usually occurs in one's 60s or 70s. Type I is 2.85 times more common in men than in women. Type II has no such sexual predilection. Type I has a prevalence of 0.82/100,000 in Japan. Pancreas. Corticosteroids (both types); type I with azathioprine, mercaptopurine, mycophenolate mofetil and rituximab. Favourable for type II; unfavourable for type I. Type I has a high rate of re-occurrence.
Autoimmune polyglandular syndrome[43] Genetic Inflammation, destroying the various exocrine and endocrine glands of the body. Type I: <1/100,000. Type II: 5/100,000. Type I is more common in Iranian Jews (prevalence: 1:600-9,000) and Finns (prevalence: 1:25,000) and usually first presents in children, it has no sexual predilection. Type II occurs predominantly in women, and is more frequent than type I with an incidence of 5/100,000. Various endocrine glands including the pancreas, parathyroid, gonads, pituitary and thyroid; and the exocrine glands, the parotids. Supportive care with hormone replacement therapy. Favourable. With hormone replacement therapy to help with the various symptoms.
Autoimmune thrombocytopenic purpura
[44][45][46][47][48]		 Unknown Immunoglobulin G-mediated platelet lysis. It is more common in males than females when it comes to children, whereas in adults it is more common in females than males, the peak age for it is 1-6 years and 30-40 years. Brain and bone marrow. Corticosteroids, thrombopoietin receptor agonists (e.g. eltrombopag, romiplostim), platelet transfusions, intravenous immunoglobulin G, azathioprine, cyclophosphamide, danazol (mostly postmenopausal women) and rituximab. Haemorrhage is the major cause of death. About 0.9% of kids with it die at presentation; overall >80% of patients will respond favourably to treatment.
Behcet's disease[49] Unknown; genes and infectious agents are believed to contribute. T cells (especially Th1), NK cells and neutrophils are all involved, as are IL-2, IL-8, IL-12, IL-21, TNF-α and IFN-γ.[50] Turks and Asians appear to be a high-risk group. Turks have an incidence of 420/100,000; Asians 13.5-22/100,000. North American and European frequency is estimated to be 0.2-7/100,000. Mean age is between 20 and 40; most commonly affects males (3-6 times more frequently than females). Joints, eyes and skin are most commonly affected; although, the central nervous system, cardiovascular system, GI tract and genitourinary system may also be affected.[51][52][53] Corticosteroids, azathioprine, cyclophosphamide, methotrexate, chlorambucil, thalidomide, colchicine, ciclosporin, infliximab and adalimumab.[54][55] 5% die; more are permanently disabled by either eye or CNS involvement.
Coeliac disease
[56][57][58]
[59]		 Genes contribute, including HLA-DQ2 and HLA-DQ8.[60] Immunoglobulin A and T cell-mediated response to gluten.[61][62][63] Incidence is fairly constant across the races with a prevalence of about 0.15-1%.[64] Intestines Corticosteroids and gluten avoidance.[65][66][67][68][69][70] Excellent, if gluten is avoided. Increased incidence of cavities, type I diabetes mellitus,[71] inefficacy of hepatitis B vaccination,[72] non-Hodgkin's lymphoma, sepsis, juvenile rheumatoid arthritis and depression.[73][74]
Cold agglutinin disease[75][76][77] Idiophathic or infection/cancer. Unknown Annual incidence: 1/300,000. Blood and liver. Prednisone, cyclophosphamide, rituximab and interferon alfa-2b. Generally favourable. Few have complete remissions, however.
Crohn disease Unknown. Genes, diet, microbial and environment (especially cigarette smoking, contraception and NSAIDs) contribute.[78][79] Th1-mediated chronic assault on the GI tract, TNF-alpha is believed to be involved, along with other cytokine messengers. Granulomas form in the GIT.[80][81] Annual incidence is about 10-150/100,000 in the Europe, with a prevalence of 322/100,000. The prevalence is about 320-511/100,000 in the US, and the annual incidence is about 43/100,000 for children and 201/100,000 for adults. In Asia the annual incidence is about 0.5-4.2/100,000, whereas in South Africa the prevalence is 0.3-2.6/100,000 and in Latin America its prevalence is about 0-0.03/100,000. It is more common in Ashkenazi Jews.[82] GI tract Corticosteroids, aminosalicylates, azathioprine, mercaptopurine, methotrexate, tacrolimus, infliximab, adalimumab and certolizumab.[83][84][85][86][87][88][89][90][91][92] Generally favourable, although it causes significant disability in 25% of patients during the year when the diagnosis is made. Increased risk of lung and colorectal cancers, COPD, liver, genitourinary and GI disease.[93]
Dermatomyositis Unknown, genes are believed to contribute. Humoural assault on the skin. TNF-alfa appears to contribute too.[94][95][96][97][98] Annual incidence is estimated to be 9.63/1,000,000. Peak ages for onset are 5-10 years and 50 years. Lung, skin, joints, skeletal muscle and heart. Glucocorticoid,azathioprine, methotrexate, rituximab, mycophenolate mofetil, tacrolimus, ciclosporin, hydroxychloroquine,cyclophosphamide and intravenous immunoglobulins.[99][100][101][102] Generally unfavourable, only 20-40% of affected individuals achieve a remission and 5% die. 60-80% of persons suffer chronic disease.[103] Malignancies are more common in persons with dermatomyositis than in the general population.[104]
Diabetes mellitus type I Genetic and environmental factors involved.[105] 2-3% of children who's mother has the disease will develop it and 5-6% of children who's father has it will develop it.[106] 85% have antibody-mediated destruction of the islet cells.[106] Fewer than 1% of Chinese/Japanese individuals with diabetes mellitus have type I. Whereas 20% of Scandinavians with diabetes mellitus have type II. In the US the annual incidence is 15-20/100,000.[106] Pancreas Regular insulin injections and dietary changes. Generally positive; irreversible and deadly if ignored. Increased risk of various malignancies has been observed, particularly bladder, gastric and pancreatic cancer.[107][108][109]
IgA nephropathy
[110][111][112][113][114][115]
[116]		 Unknown Immunoglobulin A-mediated reaction.[117] It is significantly more common in Asia and Europe than in North America. The annual incidence is about 0.5-1/100,000 in the US, whereas the incidence in Japan the incidence is about 5-10/100,000. Kidney. Symptomatic (with ACE inhibitors), corticosteroids,cyclophosphamide, azathioprine, mycophenolate mofetil, anticoagulants, omega-3 fatty acids, leflunomide and ciclosporin.[118] The 10-year progression rate to end-stage kidney disease is about 15%, whereas the 20-year progression rate is 20%.
  1. ^ a b Rust, RS, Jr (30 September 2013). Luzzio, C; Talavera, F; Lopate, G; Benbadis, SR; Keegan, BM (ed.). "Acute Disseminated Encephalomyelitis". Medscape Reference. WebMD. Retrieved 26 February 2014.{{cite web}}: CS1 maint: multiple names: authors list (link)
  2. ^ Belilos, E; Carsons, S (19 January 2012). Lozada, CJ; Talavera, F; Brent, LH; Mechaber, AJ; Tokayer, A; Diamond, HS (ed.). "Antiphospholipid Syndrome". Medscape Reference. WebMD. Retrieved 2 March 2014.{{cite web}}: CS1 maint: multiple names: authors list (link)
  3. ^ Oku, Kenji; Amengual, Olga; Atsumi, Tatsuya (October 2012). "Pathophysiology of thrombosis and pregnancy morbidity in the antiphospholipid syndrome" (PDF). European Journal of Clinical Investigation. 42 (10): 1126–35. doi:10.1111/j.1365-2362.2012.02697.x. PMID 22784367.
  4. ^ Giannakopoulos, Bill; Krilis, Steven A. (3 September 2009). "How I treat the antiphospholipid syndrome". Blood. 114 (10): 2020–30. doi:10.1182/blood-2009-05-220756. PMID 19587374.
  5. ^ Rodríguez García, J.L.; Khamashta, M.A. (March 2013). "Avances de interés clínico en el diagnóstico y tratamiento de los pacientes con síndrome antifosfolípido". Revista Clínica Española. 213 (2): 108–113. doi:10.1016/j.rce.2012.04.003. PMID 22673391.
  6. ^ Wijetilleka, Sonali; Scoble, Tina; Khamashta, Munther (September 2012). "Novel insights into pathogenesis, diagnosis and treatment of antiphospholipid syndrome". Current Opinion in Rheumatology. 24 (5): 473–81. doi:10.1097/BOR.0b013e328354ae8c. PMID 22585233.
  7. ^ Pericleous, Charis; Ioannou, Yiannis (December 2010). "New therapeutic targets for the antiphospholipid syndrome". Expert Opinion on Therapeutic Targets. 14 (12): 1291–1299. doi:10.1517/14728222.2010.524207. PMID 20874375.
  8. ^ Giannakopoulos, Bill; Krilis, Steven A. (14 March 2013). "The Pathogenesis of the Antiphospholipid Syndrome". New England Journal of Medicine. 368 (11): 1033–1044. doi:10.1056/NEJMra1112830. PMID 23484830.
  9. ^ Erkan, Doruk; Aguiar, Cassyanne L.; Andrade, Danieli; Cohen, Hannah; Cuadrado, Maria J.; Danowski, Adriana; Levy, Roger A.; Ortel, Thomas L.; Rahman, Anisur; Salmon, Jane E.; Tektonidou, Maria G.; Willis, Rohan; Lockshin, Michael D. (21 January 2014). "14th International Congress on Antiphospholipid Antibodies Task Force Report on Antiphospholipid Syndrome Treatment Trends". Autoimmunity Reviews. 13 (6): 685–696. doi:10.1016/j.autrev.2014.01.053. PMID 24468415.
  10. ^ Tuthill, Josephine I.; Khamashta, Munther A. (September 2009). "Management of antiphospholipid syndrome". Journal of Autoimmunity. 33 (2): 92–98. doi:10.1016/j.jaut.2009.05.002. PMID 19559568.
  11. ^ Palomo, I.; Segovia, F.; Ortega, C.; Pierangeli, S. (July–August 2009). "Antiphospholipid syndrome: a comprehensive review of a complex and multisystemic disease". Clinical and Experimental Rheumatology. 27 (4): 668–77. PMID 19772805.
  12. ^ George, Diane; Erkan, Doruk (September 2009). "Antiphospholipid Syndrome". Progress in Cardiovascular Diseases. 52 (2): 115–125. doi:10.1016/j.pcad.2009.06.005. PMID 19732604.
  13. ^ Erkan, Doruk; Aguiar, Cassyanne L.; Andrade, Danieli; Cohen, Hannah; Cuadrado, Maria J.; Danowski, Adriana; Levy, Roger A.; Ortel, Thomas L.; Rahman, Anisur; Salmon, Jane E.; Tektonidou, Maria G.; Willis, Rohan; Lockshin, Michael D. (24 January 2014). "14th International Congress on Antiphospholipid Antibodies Task Force Report on Antiphospholipid Syndrome Treatment Trends". Autoimmunity Reviews. 13 (6): 685–696. doi:10.1016/j.autrev.2014.01.053. PMID 24468415.
  14. ^ Palomo, I.; Segovia, F.; Ortega, C.; Pierangeli, S. (July–August 2009). "Antiphospholipid syndrome: a comprehensive review of a complex and multisystemic disease" (PDF). Clinical and Experimental Rheumatology. 27 (4): 668–77. PMID 19772805.
  15. ^ Tuthill, Josephine I.; Khamashta, Munther A. (September 2009). "Management of antiphospholipid syndrome". Journal of Autoimmunity. 33 (2): 92–8. doi:10.1016/j.jaut.2009.05.002. PMID 19559568.
  16. ^ George, Diane; Erkan, Doruk (September 2009). "Antiphospholipid Syndrome". Progress in Cardiovascular Diseases. 52 (2): 115–125. doi:10.1016/j.pcad.2009.06.005. PMID 19732604.
  17. ^ Garnacho-Saucedo, G.; Salido-Vallejo, R.; Moreno-Giménez, J. C. (January 2013). "Atopic dermatitis: update and proposed management algorithm" (PDF). Actas Dermo-Sifiliograficas. 104 (1): 4–16. doi:10.1016/j.ad.2011.12.008. PMID 22578294.
  18. ^ Harskamp, Caitlin; Armstrong, April (September 2013). "Immunology of atopic dermatitis: novel insights into mechanisms and immunomodulatory therapies" (PDF). Seminars in Cutaneous Medicine and Surgery. 32 (3): 132–9. doi:10.12788/j.sder.0018. PMID 24175400.
  19. ^ Auriemma, Matteo; Vianale, Giovina; Amerio, Paolo; Reale, Marcella (March 2013). "Cytokines and T cells in atopic dermatitis" (PDF). European Cytokine Network. 24 (1): 37–44. doi:10.1684/ecn.2013.0333. PMID 23608610.
  20. ^ Kasraie, Sadaf; Werfel, Thomas (2013). "Role of Macrophages in the Pathogenesis of Atopic Dermatitis". Mediators of Inflammation. 2013: 942375. doi:10.1155/2013/942375. PMC 3603294. PMID 23533313.
  21. ^ Flohr, C.; Mann, J. (January 2014). "New insights into the epidemiology of childhood atopic dermatitis" (PDF). Allergy. 69 (1): 3–16. doi:10.1111/all.12270. PMID 24417229.
  22. ^ a b Berke, R.; Singh, A.; Guralnick, M. (1 July 2012). "Atopic dermatitis: an overview" (PDF). American Family Physician. 86 (1): 35–42. PMID 22962911.
  23. ^ Cookson, H.; Smith, C. (April 2012). "Systemic treatment of adult atopic dermatitis" (PDF). Clinical Medicine. 12 (2): 172–6. doi:10.2500/aap.2012.33.3569. PMC 4954107. PMID 22586797.
  24. ^ Varothai, S.; Nitayavardhana, S.; Kulthanan, K. (June 2013). "Moisturizers for patients with atopic dermatitis" (PDF). Asian Pacific Journal of Allergy and Immunology. 31 (2): 91–8. PMID 23859407.
  25. ^ Carr, WW (August 2013). "Topical calcineurin inhibitors for atopic dermatitis: review and treatment recommendations". Paediatric Drugs. 15 (4): 303–10. doi:10.1007/s40272-013-0013-9. PMC 3715696. PMID 23549982.
  26. ^ Comarmond, Cloé; Cacoub, Patrice (May 2013). "Antiphospholipid syndrome: From pathogenesis to novel immunomodulatory therapies". Autoimmunity Reviews. 12 (7): 752–757. doi:10.1016/j.autrev.2012.12.006. PMID 23282546.
  27. ^ Ruiz-Irastorza, Guillermo; Crowther, Mark; Branch, Ware; Khamashta, Munther A. (October 2010). "Antiphospholipid syndrome". The Lancet. 376 (9751): 1498–1509. doi:10.1016/S0140-6736(10)60709-X. PMID 20822807.
  28. ^ Schick, P (21 February 2013). Talavera, F; Sacher, RA; Besa, EC (ed.). "Hemolytic Anemia". Medscape Reference. WebMD. Retrieved 26 February 2014.{{cite web}}: CS1 maint: multiple names: editors list (link)
  29. ^ a b Zeerleder, S (April 2011). "Autoimmune haemolytic anaemia - a practical guide to cope with a diagnostic and therapeutic challenge" (PDF). The Netherlands Journal of Medicine. 69 (4): 177–84. PMID 21527804.
  30. ^ a b c Gossard, A. A.; Lindor, K. D. (May 2012). "Autoimmune hepatitis: a review". Journal of Gastroenterology. 47 (5): 498–503. doi:10.1007/s00535-012-0586-z. PMID 22526272.
  31. ^ Wolf, DC; Raghuraman, UV; Anand, BS; Baldassano, R; Cuffari, C; El-Baba, MF; Sukerek, HH; Talavera, F; Windle, MF (29 July 2013). Katz, J (ed.). "Autoimmune Hepatitis". Medscape Reference. WebMD. Retrieved 26 February 2014.{{cite web}}: CS1 maint: multiple names: authors list (link)
  32. ^ Selvarajah, V.; Montano-Loza, A. J.; Czaja, A. J. (October 2012). "Systematic review: managing suboptimal treatment responses in autoimmune hepatitis with conventional and nonstandard drugs". Alimentary Pharmacology & Therapeutics. 36 (8): 691–707. doi:10.1111/apt.12042. PMID 22973822.
  33. ^ Jothimani, Dinesh; Cramp, Matthew E.; Mitchell, Jonathon D.; Cross, Tim J S. (April 2011). "Treatment of autoimmune hepatitis: A review of current and evolving therapies". Journal of Gastroenterology and Hepatology. 26 (4): 619–627. doi:10.1111/j.1440-1746.2010.06579.x. PMID 21073674.
  34. ^ a b Mathur, NN; Jaquish, S; Meyerhoff, WL (2 April 2012). Battista, RA; Talavera, F; Roland, PS; Slack, CL; Meyers, AD (ed.). "Autoimmune Disease of the Inner Ear". Medscape Reference. WebMD. Retrieved 26 February 2014.{{cite web}}: CS1 maint: multiple names: authors list (link)
  35. ^ Buniel, M. C.; Geelan-Hansen, K.; Weber, P. C.; Tuohy, V. K. (May 2009). "Immunosuppressive therapy for autoimmune inner ear disease". Immunotherapy. 1 (3): 425–34. doi:10.2217/imt.09.12. PMC 2747333. PMID 19885385.
  36. ^ Teachey, David T.; Seif, Alix E.; Grupp, Stephan A. (January 2010). "Advances in the management and understanding of autoimmune lymphoproliferative syndrome (ALPS)". British Journal of Haematology. 148 (2): 205–16. doi:10.1111/j.1365-2141.2009.07991.x. PMC 2929682. PMID 19930184.
  37. ^ Teachey, DT (February 2012). "New advances in the diagnosis and treatment of autoimmune lymphoproliferative syndrome". Current Opinion in Pediatrics. 24 (1): 1–8. doi:10.1097/MOP.0b013e32834ea739. PMC 3673763. PMID 22157362.
  38. ^ Rao, V. Koneti; Oliveira, João Bosco (24 November 2011). "How I treat autoimmune lymphoproliferative syndrome" (PDF). Blood. 118 (22): 5741–51. doi:10.1182/blood-2011-07-325217. PMC 3228494. PMID 21885601.
  39. ^ Worth, Austen; Thrasher, Adrian J.; Bobby Gaspar, H. (April 2006). "Autoimmune lymphoproliferative syndrome: molecular basis of disease and clinical phenotype" (PDF). British Journal of Haematology. 133 (2): 124–40. doi:10.1111/j.1365-2141.2006.05993.x. PMID 16611303.
  40. ^ Webb, LM; Schwartz, DJ; Rao, VK; Windle, ML (2 August 2012). Jyonouchi, H (ed.). "Autoimmune Lymphoproliferative Syndrome". Medscape Reference. WebMD. {{cite web}}: Missing or empty |url= (help)CS1 maint: multiple names: authors list (link)
  41. ^ Sugumar, Aravind; Chari, Suresh T. (September 2011). "Autoimmune pancreatitis". Journal of Gastroenterology and Hepatology. 26 (9): 1368–73. doi:10.1111/j.1440-1746.2011.06843.x. PMID 21884246.
  42. ^ Wang, Qian; Zhang, Xuan; Zhang, Fengchun (March 2013). "Autoimmune pancreatitis: current concepts" (PDF). Science China. Life Sciences. 56 (3): 246–53. doi:10.1007/s11427-013-4450-z. PMID 23526391.
  43. ^ Kahaly, GJ (July 2009). "Polyglandular autoimmune syndromes" (PDF). European Journal of Endocrinology / European Federation of Endocrine Societies. 161 (1): 11–20. doi:10.1530/EJE-09-0044. PMID 19411300.
  44. ^ Anoop, P (2012 Oct). "Immune thrombocytopenic purpura: historical perspective, current status, recent advances and future directions" (PDF). Indian Pediatrics. 49 (10): 811–8. doi:10.1007/s13312-012-0195-1. PMID 23144100. {{cite journal}}: Check date values in: |date= (help)
  45. ^ Bredlau, AL (1 August 2011). "Management of immune thrombocytopenic purpura in children: potential role of novel agents". Paediatric Drugs. 13 (4): 213–23. doi:10.2165/11591640-000000000-00000. PMID 21692546. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  46. ^ Wang, Tingting; Wang, Zhao; Yang, Renchi (March 2011). "Thrombopoietic growth factors in the treatment of immune thrombocytopenic purpura". Critical Reviews in Oncology/Hematology. 77 (3): 172–83. doi:10.1016/j.critrevonc.2010.03.001. PMID 20378370.
  47. ^ Terrell, Deirdra R.; Beebe, Laura A.; Vesely, Sara K.; Neas, Barbara R.; Segal, Jodi B.; George, James N. (March 2010). "The incidence of immune thrombocytopenic purpura in children and adults: A critical review of published reports" (PDF). American Journal of Hematology. 85 (3): 174–80. doi:10.1002/ajh.21616. PMID 20131303.
  48. ^ Blanchette, Victor; Bolton-Maggs, Paula (February 2010). "Childhood immune thrombocytopenic purpura: diagnosis and management" (PDF). Hematology/Oncology Clinics of North America. 24 (1): 249–73. doi:10.1016/j.hoc.2009.11.004. PMID 20113906.
  49. ^ Alnaimat, FA; Lisse, JR; Posadas, AC (1 July 2013). Lohr, KM; Talavera, F; Brent, LH; Mechaber, AJ; Diamond, HS (ed.). "Behcet disease". Medscape Reference. WebMD. Retrieved 26 February 2014.{{cite web}}: CS1 maint: multiple names: authors list (link)
  50. ^ Pineton De Chambrun, Marc; Wechsler, Bertrand; Geri, Guillaume; Cacoub, Patrice; Saadoun, David (August 2012). "New insights into the pathogenesis of Behçet's disease". Autoimmunity Reviews. 11 (10): 687–698. doi:10.1016/j.autrev.2011.11.026. PMID 22197900.
  51. ^ Yuan, SM (30 January 2014). "Cardiothoracic interventions in Behçet's disease". Clinical and Experimental Rheumatology. PMID 24480592.
  52. ^ Park, JJ (September 2013). "Outcome predictors for intestinal Behçet's disease". Yonsei Medical Journal. 54 (5): 1084–90. doi:10.1016/j.autrev.2014.01.056. PMC 3743188. PMID 23918555. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  53. ^ Mora, Paolo; Menozzi, Chiara; Orsoni, Jelka G.; Rubino, Pierangela; Ruffini, Livia; Carta, Arturo (29 January 2013). "Neuro-Behçet's disease in childhood: a focus on the neuro-ophthalmological features". Orphanet Journal of Rare Diseases. 8: 18. doi:10.1186/1750-1172-8-18. PMC 3567996. PMID 23360593.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  54. ^ Saadoun, David; Wechsler, Bertrand (12 April 2012). "Behçet's disease" (PDF). Orphanet Journal of Rare Diseases. 7: 20. doi:10.1186/1750-1172-7-20. PMC 3472229. PMID 22497990.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  55. ^ Benitah, Nicole R.; Sobrin, Lucia; Papaliodis, George N. (July–September 2011). "The use of biologic agents in the treatment of ocular manifestations of Behcet's disease". Seminars in Ophthalmology. 26 (4–5): 295–303. doi:10.3109/08820538.2011.588665. PMID 21958178.
  56. ^ Kneepkens, C. M. Frank; von Blomberg, B. Mary E. (16 March 2012). "Clinical practice". European Journal of Pediatrics. 171 (7): 1011–1021. doi:10.1007/s00431-012-1714-8. PMC 3378840. PMID 22422192.
  57. ^ Ludvigsson, Jonas F.; Leffler, Daniel A.; Bai, Julio C.; Biagi, Federico; Fasano, Alessio; Green, Peter H R.; Hadjivassiliou, Marios; Kaukinen, Katri; Kelly, Ciaran P.; Leonard, Jonathan N.; Lundin, Knut Erik Aslaksen; Murray, Joseph A.; Sanders, David S.; Walker, Marjorie M.; Zingone, Fabiana; Ciacci, Carolina (16 February 2012). "The Oslo definitions for coeliac disease and related terms". Gut. 62 (1): 43–52. doi:10.1136/gutjnl-2011-301346. PMC 3440559. PMID 22345659.
  58. ^ Rubio-Tapia, Alberto; Murray, Joseph A. (March 2010). "Celiac disease". Current Opinion in Gastroenterology. 26 (2): 116–122. doi:10.1097/MOG.0b013e3283365263. PMC 2830645. PMID 20040864.
  59. ^ Tjon, Jennifer May-Ling; Van Bergen, Jeroen; Koning, Frits (27 July 2010). "Celiac disease: how complicated can it get?". Immunogenetics. 62 (10): 641–651. doi:10.1007/s00251-010-0465-9. PMC 2944025. PMID 20661732.
  60. ^ Kumar, Vinod; Wijmenga, Cisca; Withoff, Sebo (14 May 2012). "From genome-wide association studies to disease mechanisms: celiac disease as a model for autoimmune diseases". Seminars in Immunopathology. 34 (4): 567–580. doi:10.1007/s00281-012-0312-1. PMC 3410018. PMID 22580835.
  61. ^ Kupfer, Sonia S.; Jabri, Bana (October 2012). "Pathophysiology of Celiac Disease". Gastrointestinal Endoscopy Clinics of North America. 22 (4): 639–660. doi:10.1016/j.giec.2012.07.003. PMC 3872820. PMID 23083984.
  62. ^ Denham, Jolanda M.; Hill, Ivor D. (17 May 2013). "Celiac Disease and Autoimmunity: Review and Controversies". Current Allergy and Asthma Reports. 13 (4): 347–353. doi:10.1007/s11882-013-0352-1. PMC 3725235. PMID 23681421.
  63. ^ Pozo-Rubio, Tamara; Olivares, Marta; Nova, Esther; De Palma, Giada; Mujico, Jorge R.; Ferrer, Maria Desamparados; Marcos, Ascensión; Sanz, Yolanda (2012). "Immune Development and Intestinal Microbiota in Celiac Disease". Clinical and Developmental Immunology. 2012: 654143. doi:10.1155/2012/654143. PMC 3447214. PMID 23008734.
  64. ^ Barada, K (2010). "Celiac disease in Middle Eastern and North African countries: A new burden?". World Journal of Gastroenterology. 16 (12): 1449. doi:10.3748/wjg.v16.i12.1449. PMC 2846249. PMID 20333784.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  65. ^ Rashtak, S.; Murray, J. A. (April 2012). "Review article: coeliac disease, new approaches to therapy". Alimentary Pharmacology & Therapeutics. 35 (7): 768–781. doi:10.1111/j.1365-2036.2012.05013.x. PMC 3912561. PMID 22324389.
  66. ^ Rubio-Tapia, A.; Murray, J. A. (23 March 2010). "Classification and management of refractory coeliac disease". Gut. 59 (4): 547–557. doi:10.1136/gut.2009.195131. PMC 2861306. PMID 20332526.
  67. ^ Sollid, L. M.; Khosla, C. (June 2011). "Novel therapies for coeliac disease". Journal of Internal Medicine. 269 (6): 604–613. doi:10.1111/j.1365-2796.2011.02376.x. PMC 3101315. PMID 21401739.
  68. ^ Freeman, HJ (21 April 2010). "Risk factors in familial forms of celiac disease". World Journal of Gastroenterology. 16 (15): 1828–31. doi:10.3748/wjg.v16.i15.1828. PMC 2856821. PMID 20397258.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  69. ^ Mooney, P. D.; Evans, K. E.; Singh, S.; Sanders, D. S. (June 2012). "Treatment failure in coeliac disease: a practical guide to investigation and treatment of non-responsive and refractory coeliac disease" (PDF). Journal of Gastrointestinal and Liver Diseases. 21 (2): 197–203. PMID 22720310.
  70. ^ Fasano, A (2012). "Novel Therapeutic/Integrative Approaches for Celiac Disease and Dermatitis Herpetiformis". Clinical and Developmental Immunology. 2012: 1–7. doi:10.1155/2012/959061. PMC 3474991. PMID 23093980.
  71. ^ Camarca, Maria Erminia; Mozzillo, Enza; Nugnes, Rosa; Zito, Eugenio; Falco, Mariateresa; Fattorusso, Valentina; Mobilia, Sara; Buono, Pietro; Valerio, Giuliana; Troncone, Riccardo; Franzese, Adriana (2012). "Celiac disease in type 1 diabetes mellitus". Italian Journal of Pediatrics. 38 (1): 10. doi:10.1186/1824-7288-38-10. PMC 3348012. PMID 22449104.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  72. ^ Vitaliti, G (2013). "Hepatitis B vaccine in celiac disease: Yesterday, today and tomorrow". World Journal of Gastroenterology. 19 (6): 838. doi:10.3748/wjg.v19.i6.838. PMC 3574880. PMID 23430309.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  73. ^ Fouda, M. A.; Khan, A. A.; Sultan, M. S.; Rios, L. P.; McAssey, K.; Armstrong, D. (November 2012). "Evaluation and management of skeletal health in celiac disease: position statement". Canadian Journal of Gastroenterology. 26 (11): 819–29. doi:10.1155/2012/823648. PMC 3495700. PMID 23166906.
  74. ^ Rostami-Nejad, Mohammad; Haldane, Thea; Aldulaimi, David; Alavian, Seyed Moayed; Zali, Mohammad Reza; Rostami, Kamran (2013). "The Role of Celiac Disease in Severity of Liver Disorders and Effect of a Gluten Free Diet on Diseases Improvement". Hepatitis Monthly. 13 (10): e11893. doi:10.5812/hepatmon.11893. PMC 3842525. PMID 24348636.
  75. ^ Aljubran, SA; Lockey, RJ (25 January 2013). Kaliner, MA; Camilo, NA; Coppes, MJ; Crouch, GD; Georgy, S; Harper, JL; Jones, GR; Kishiyama, JL; Loew, TW; McKenna, R; Messmore, HL, Jr.; Talavera, F; Windle, ML (ed.). "Cold Agglutinin Disease". Medscape Reference. WebMD. {{cite web}}: Missing or empty |url= (help)CS1 maint: multiple names: authors list (link)
  76. ^ Swiecicki, Paul L.; Hegerova, Livia T.; Gertz, Morie A. (15 August 2013). "Cold agglutinin disease". Blood. 122 (7): 1114–21. doi:10.1182/blood-2013-02-474437. PMID 23757733.
  77. ^ Berentsen, S (May 2011). "How I manage cold agglutinin disease". British Journal of Haematology. 153 (3): 309–317. doi:10.1111/j.1365-2141.2011.08643.x. PMID 21385173.
  78. ^ Hovde, Øistein (21 April 2012). "Epidemiology and clinical course of Crohn's disease: Results from observational studies". World Journal of Gastroenterology. 18 (15): 1723–1731. doi:10.3748/wjg.v18.i15.1723. PMC 3332285. PMID 22553396.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  79. ^ Lapaquette, Pierre; Brest, Patrick; Hofman, Paul; Darfeuille-Michaud, Arlette (September 2012). "Etiology of Crohn's disease: many roads lead to autophagy". Journal of Molecular Medicine. 90 (9): 987–96. doi:10.1007/s00109-012-0934-8. PMID 22797958.
  80. ^ Stappenbeck, T. S.; Rioux, J. D.; Mizoguchi, A.; Saitoh, T.; Huett, A.; Darfeuille-Michaud, A.; Wileman, T.; Mizushima, N.; Carding, S.; Akira, S.; Parkes, M.; Xavier, R. J. (April 2011). "Crohn disease: a current perspective on genetics, autophagy and immunity". Autophagy. 7 (4): 355–74. doi:10.4161/auto.7.2.13074 (inactive 2023-08-02). PMC 3574590. PMID 20729636.{{cite journal}}: CS1 maint: DOI inactive as of August 2023 (link)
  81. ^ Vilela, Eduardo Garcia; Torres, H. O.; Martins, F. P.; Ferrari Mde, L.; Andrade, M. M.; Cunha, A. S. (7 March 2012). "Evaluation of inflammatory activity in Crohn's disease and ulcerative colitis". World Journal of Gastroenterology. 18 (9): 872–81. doi:10.3748/wjg.v18.i9.872. PMC 3297045. PMID 22408345.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  82. ^ Baumgart, Daniel C.; Sandborn, William J. (November 2012). "Crohn's disease". The Lancet. 380 (9853): 1590–1605. doi:10.1016/S0140-6736(12)60026-9. PMID 22914295.
  83. ^ Wilkins, T.; Jarvis, K.; Patel, J. (2011 Dec 15). "Diagnosis and management of Crohn's disease" (PDF). American Family Physician. 84 (12): 1365–75. PMID 22230271. {{cite journal}}: Check date values in: |date= (help)
  84. ^ Lakatos, PL (21 October 2011). "Current status of thiopurine analogues in the treatment in Crohn's disease". World Journal of Gastroenterology. 17 (39): 4372. doi:10.3748/wjg.v17.i39.4372. PMC 3218150. PMID 22110262.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  85. ^ Bandzar, Sean; Gupta, Shabnam; Platt, Manu O. (November–December 2013). "Crohn's disease: a review of treatment options and current research". Cellular Immunology. 286 (1–2): 45–52. doi:10.1016/j.cellimm.2013.11.003. PMID 24321565.
  86. ^ Dassopoulos, Themistocles; Sultan, Shahnaz; Falck–Ytter, Yngve T.; Inadomi, John M.; Hanauer, Stephen B. (December 2013). "American Gastroenterological Association Institute technical review on the use of thiopurines, methotrexate, and anti-TNF-α biologic drugs for the induction and maintenance of remission in inflammatory Crohn's disease". Gastroenterology. 145 (6): 1464–78.e1–5. doi:10.1053/j.gastro.2013.10.046. PMID 24267475.
  87. ^ Cheifetz, AS (22 May 2013). "Management of active Crohn disease". JAMA. 309 (20): 2150–8. doi:10.1001/jama.2013.4466. PMID 23695484.
  88. ^ Rogler, G (2013). "Top-down or step-up treatment in Crohn's disease?". Digestive Diseases. 31 (1): 83–90. doi:10.1159/000347190. PMID 23797128.
  89. ^ Panaccione, Remo; Hibi, Toshifumi; Peyrin-Biroulet, Laurent; Schreiber, Stefan (February 2012). "Implementing changes in clinical practice to improve the management of Crohn's disease". Journal of Crohn's & Colitis. 6 (Suppl 2): S235-42. doi:10.1016/S1873-9946(12)60503-0. PMID 22463930.
  90. ^ Baran, Bulent; Karaca, Cetin (2013). "Practical Medical Management of Crohn's Disease". ISRN Gastroenterology. 2013: 208073. doi:10.1155/2013/208073. PMC 3838825. PMID 24307950.
  91. ^ Kansal, S.; Wagner, J.; Kirkwood, C. D.; Catto-Smith, A. G. (2013). "Enteral Nutrition in Crohn's Disease: An Underused Therapy". Gastroenterology Research and Practice. 2013: 482108. doi:10.1155/2013/482108. PMC 3870077. PMID 24382954.
  92. ^ Cottone, Mario; Renna, Sara; Orlando, Ambrogio; Mocciaro, Filippo (November 2011). "Medical management of Crohn's disease". Expert Opinion on Pharmacotherapy. 12 (16): 2505–25. doi:10.1517/14656566.2011.609556. PMID 21988215.
  93. ^ Mills, S. C.; von Roon, A. C.; Tekkis, P. P.; Orchard, T. R. (27 April 2011). "Crohn's disease". Clinical Evidence. 2011: 0416. PMC 3217808. PMID 21524318.
  94. ^ Rosa Neto, Nilton Salles; Goldenstein-Schainberg, Cláudia (June 2010). "Dermatomiosite juvenil: revisão e atualização em patogênese e tratamento" (PDF). Revista Brasileira de Reumatologia. 50 (3): 299–312. doi:10.1590/S0482-50042010000300010. PMID 21125166.
  95. ^ Greenberg, SA (16 April 2010). "Dermatomyositis and Type 1 Interferons". Current Rheumatology Reports. 12 (3): 198–203. doi:10.1007/s11926-010-0101-6. PMC 2929916. PMID 20425524.
  96. ^ Wedderburn, Lucy R.; Rider, Lisa G. (October 2009). "Juvenile dermatomyositis: new developments in pathogenesis, assessment and treatment". Best Practice & Research Clinical Rheumatology. 23 (5): 665–678. doi:10.1016/j.berh.2009.07.007. PMC 774891. PMID 19853831.
  97. ^ Nagaraju, Kanneboyina; Lundberg, Ingrid E. (May 2011). "Polymyositis and Dermatomyositis: Pathophysiology". Rheumatic Disease Clinics of North America. 37 (2): 159–171. doi:10.1016/j.rdc.2011.01.002. PMID 21444017.
  98. ^ Mammen, AL (January 2010). "Dermatomyositis and polymyositis". Annals of the New York Academy of Sciences. 1184 (1): 134–153. doi:10.1111/j.1749-6632.2009.05119.x. PMID 20146695.
  99. ^ Marie, Isabelle; Mouthon, Luc (November 2011). "Therapy of polymyositis and dermatomyositis". Autoimmunity Reviews. 11 (1): 6–13. doi:10.1016/j.autrev.2011.06.007. PMID 21740984.
  100. ^ Femia, Alisa N.; Vleugels, Ruth Ann; Callen, Jeffrey P. (11 June 2013). "Cutaneous Dermatomyositis: An Updated Review of Treatment Options and Internal Associations". American Journal of Clinical Dermatology. 14 (4): 291–313. doi:10.1007/s40257-013-0028-6. PMID 23754636.
  101. ^ Gordon, Patrick A.; Winer, John B.; Hoogendijk, Jessica E.; Choy, Ernest HS (15 August 2012). "Immunosuppressant and immunomodulatory treatment for dermatomyositis and polymyositis". The Cochrane Database of Systematic Reviews. 8 (8): CD003643. doi:10.1002/14651858.CD003643.pub4. PMC 7144740. PMID 22895935.
  102. ^ Hak, A. E.; De Paepe, B.; De Bleecker, J. L.; Tak, P. P.; De Visser, M. (October 2011). "Dermatomyositis and polymyositis: new treatment targets on the horizon" (PDF). The Netherlands Journal of Medicine. 69 (10): 410–21. PMID 22058260.
  103. ^ Marie, I (13 March 2012). "Morbidity and Mortality in Adult Polymyositis and Dermatomyositis". Current Rheumatology Reports. 14 (3): 275–285. doi:10.1007/s11926-012-0249-3. PMID 22410829.
  104. ^ Zampieri, S.; Valente, M.; Adami, N.; Biral, D.; Ghirardello, A.; Rampudda, M.E.; Vecchiato, M.; Sarzo, G.; Corbianco, S.; Kern, H.; Carraro, U.; Bassetto, F.; Merigliano, S.; Doria, A. (April 2010). "Polymyositis, dermatomyositis and malignancy: A further intriguing link". Autoimmunity Reviews. 9 (6): 449–453. doi:10.1016/j.autrev.2009.12.005. PMID 20026430.
  105. ^ Stankov, Karmen; Benc, Damir; Draskovic, Dragan (December 2013). "Genetic and epigenetic factors in etiology of diabetes mellitus type 1". Pediatrics. 132 (6): 1112–22. doi:10.1542/peds.2013-1652. PMID 24190679.
  106. ^ a b c Khardori, R; Bessen, HA; Brenner, BE; Hussain, AN; Peters, AL; Schalch, DS; Schraga, ED; Talavera, F; Vincent, MT; Votey, SR; Ziel, FH (16 December 2013). Griffing, GT (ed.). "Type 1 Diabetes Mellitus". Medscape Reference. WebMD. Retrieved 3 March 2014.{{cite web}}: CS1 maint: multiple names: authors list (link)
  107. ^ Pezzilli, Raffaele (August 2013). "Is diabetes mellitus a risk factor for pancreatic cancer?". World Journal of Gastroenterology. 19 (30): 4861. doi:10.3748/wjg.v19.i30.4861. PMC 3740415. PMID 23946590.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  108. ^ Zhu, Zhaowei; Wang, Xianjin; Shen, Zhoujun; Lu, Yingli; Zhong, Shan; Xu, Chen (June 2013). "Risk of bladder cancer in patients with diabetes mellitus: an updated meta-analysis of 36 observational studies". BMC Cancer. 13: 310. doi:10.1186/1471-2407-13-310. PMC 3699355. PMID 23803148.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  109. ^ Yoon, Jae Moon; Son, K. Y.; Eom, C. S.; Durrance, D.; Park, S. M. (2013). "Pre-existing diabetes mellitus increases the risk of gastric cancer: A meta-analysis". World Journal of Gastroenterology. 19 (6): 936–945. doi:10.3748/wjg.v19.i6.936. PMC 3574893. PMID 23429469.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  110. ^ Yu, Hsin-Hui; Chiang, Bor-Luen (13 January 2014). "Diagnosis and classification of IgA nephropathy". Autoimmunity Reviews. 13 (4–5): 556–559. doi:10.1016/j.autrev.2014.01.030. PMID 24434362.
  111. ^ Wyatt, Robert J.; Julian, Bruce A. (20 June 2013). "IgA nephropathy". The New England Journal of Medicine. 368 (25): 2402–14. doi:10.1056/NEJMra1206793. PMID 23782179.
  112. ^ Lv, Jicheng; Shi, Sufang; Xu, Damin; Zhang, Hong; Troyanov, Stéphan; Cattran, Daniel C.; Wang, Haiyan (November 2013). "Evaluation of the Oxford Classification of IgA nephropathy: a systematic review and meta-analysis". American Journal of Kidney Diseases : The Official Journal of the National Kidney Foundation. 62 (5): 891–9. doi:10.1053/j.ajkd.2013.04.021. PMID 23820066.
  113. ^ Kiryluk, Krzysztof; Julian, Bruce A.; Wyatt, Robert J.; Scolari, Francesco; Zhang, Hong; Novak, Jan; Gharavi, Ali G. (November 2010). "Genetic studies of IgA nephropathy: past, present, and future". Pediatric Nephrology. 25 (11): 2257–68. doi:10.1007/s00467-010-1500-7. PMC 2937145. PMID 20386929.
  114. ^ Yu, Hsin-Hui; Chu, Kuan-Hua; Yang, Yao-Hsu; Lee, Jyh-Hong; Wang, Li-Chieh; Lin, Yu-Tsan; Chiang, Bor-Luen (October 2011). "Genetics and immunopathogenesis of IgA nephropathy". Clinical Reviews in Allergy & Immunology. 41 (2): 198–213. doi:10.1007/s12016-010-8232-0. PMID 21188648.
  115. ^ Suzuki, Hitoshi; Kiryluk, Krzysztof; Novak, Jan; Moldoveanu, Zina; Herr, Andrew B.; Renfrow, Matthew B.; Wyatt, Robert J.; Scolari, Francesco; Mestecky, Jiri; Gharavi, Ali G.; Julian, Bruce A. (23 September 2011). "The Pathophysiology of IgA Nephropathy" (PDF). Journal of the American Society of Nephrology. 22 (10): 1795–1803. doi:10.1681/ASN.2011050464. PMC 3892742. PMID 21949093.
  116. ^ Rosselli, Jennifer L.; Thacker, Stacey M.; Karpinski, Julie P.; Petkewicz, Katherine A. (27 September 2011). "Treatment of IgA Nephropathy: An Update". Annals of Pharmacotherapy. 45 (10): 1284–1296. doi:10.1345/aph.1Q122. PMID 21954446.
  117. ^ Suzuki, Hitoshi; Kiryluk, Krzysztof; Novak, Jan; Moldoveanu, Zina; Herr, Andrew B.; Renfrow, Matthew B.; Wyatt, Robert J.; Scolari, Francesco; Mestecky, Jiri; Gharavi, Ali G.; Julian, Bruce A. (October 2011). "The pathophysiology of IgA nephropathy" (PDF). Journal of the American Society of Nephrology. 22 (10): 1795–803. doi:10.1681/ASN.2011050464. PMC 3892742. PMID 21949093.
  118. ^ Floege, Jürgen; Eitner, Frank (October 2011). "Current therapy for IgA nephropathy" (PDF). Journal of the American Society of Nephrology. 22 (10): 1785–94. doi:10.1681/ASN.2011030221. PMID 21903997.
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