User:Fuse809/sandbox6

Source: Wikipedia, the free encyclopedia.
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
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,
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,
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,
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,
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
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
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,
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,
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,
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,
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. PMID 22784367
    .
  4. PMID 19587374
    .
  5. PMID 22673391
    .
  6. PMID 22585233
    .
  7. PMID 20874375
    .
  8. PMID 23484830
    .
  9. PMID 24468415
    .
  10. PMID 19559568
    .
  11. PMID 19772805
    .
  12. PMID 19732604
    .
  13. PMID 24468415
    .
  14. PMID 19772805
    .
  15. PMID 19559568
    .
  16. PMID 19732604
    .
  17. PMID 22578294
    .
  18. PMID 24175400
    .
  19. PMID 23608610
    .
  20. PMID 23533313
    .
  21. PMID 24417229
    .
  22. ^
    PMID 22962911
    .
  23. PMID 22586797
    .
  24. PMID 23859407
    .
  25. PMID 23549982
    .
  26. PMID 23282546
    .
  27. 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. ^
    PMID 21527804
    .
  30. ^
    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. PMID 22973822
    .
  33. 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. PMID 19885385
    .
  36. PMID 19930184
    .
  37. PMID 22157362
    .
  38. PMID 21885601
    .
  39. 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. PMID 21884246
    .
  42. PMID 23526391
    .
  43. PMID 19411300
    .
  44. PMID 23144100. {{cite journal}}: Check date values in: |date= (help
    )
  45. PMID 21692546. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help
    )
  46. PMID 20378370
    .
  47. PMID 20131303
    .
  48. 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. PMID 22197900
    .
  51. PMID 24480592
    .
  52. PMID 23918555. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help
    )
  53. PMID 23360593.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  54. PMID 22497990.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  55. PMID 21958178
    .
  56. PMID 22422192
    .
  57. PMID 22345659
    .
  58. PMID 20040864
    .
  59. PMID 20661732
    .
  60. PMID 22580835
    .
  61. PMID 23083984
    .
  62. PMID 23681421
    .
  63. PMID 23008734
    .
  64. PMID 20333784.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  65. PMID 22324389
    .
  66. PMID 20332526
    .
  67. PMID 21401739
    .
  68. PMID 20397258.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  69. PMID 22720310
    .
  70. PMID 23093980
    .
  71. PMID 22449104.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  72. PMID 23430309.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  73. PMID 23166906
    .
  74. 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. PMID 23757733
    .
  77. PMID 21385173
    .
  78. PMID 22553396.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  79. PMID 22797958
    .
  80. PMID 20729636.{{cite journal}}: CS1 maint: DOI inactive as of August 2023 (link
    )
  81. PMID 22408345.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  82. PMID 22914295
    .
  83. PMID 22230271. {{cite journal}}: Check date values in: |date= (help
    )
  84. PMID 22110262.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  85. PMID 24321565
    .
  86. PMID 24267475
    .
  87. PMID 23695484
    .
  88. PMID 23797128
    .
  89. PMID 22463930
    .
  90. PMID 24307950
    .
  91. PMID 24382954
    .
  92. PMID 21988215
    .
  93. PMID 21524318
    .
  94. PMID 21125166
    .
  95. PMID 20425524
    .
  96. PMID 19853831
    .
  97. PMID 21444017
    .
  98. PMID 20146695
    .
  99. PMID 21740984
    .
  100. PMID 23754636
    .
  101. PMID 22895935
    .
  102. PMID 22058260
    .
  103. PMID 22410829
    .
  104. PMID 20026430
    .
  105. 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. PMID 23946590.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  108. PMID 23803148.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  109. PMID 23429469.{{cite journal}}: CS1 maint: unflagged free DOI (link
    )
  110. PMID 24434362
    .
  111. PMID 23782179
    .
  112. PMID 23820066
    .
  113. PMID 20386929
    .
  114. PMID 21188648
    .
  115. PMID 21949093
    .
  116. PMID 21954446
    .
  117. PMID 21949093
    .
  118. PMID 21903997
    .
Retrieved from "https://en.wikipedia.org/w/index.php?title=User:Fuse809/sandbox6&oldid=1168402755"