Hemolytic-uremic syndrome risk factors: Difference between revisions
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{{CMG}}; {{AE}} {{AHS}} | {{CMG}}; {{AE}} {{S.G.}}, {{AHS}} | ||
==Overview== | ==Overview== | ||
The most potent risk factor in the development of Hemolytic | The most potent risk factor in the development of [[Hemolytic-uremic syndrome|hemolytic uremic syndrome]] ([[Hemolytic-uremic syndrome|HUS]]) in childhood is [[infection]] with [[verocytotoxin]] ([[shiga-like toxin]])-producing [[bacteria]], usually [[Escherichia coli|enterohemorrhagic ''Escherichia coli'']] (VTEC/[[STEC]]),and in some tropical regions [[Shigella dysenteriae type 1|Shigella dysenteriae type I]] . Other risk factors include [[genetic mutations]] in [[complement]] factors, pnemumococcal [[Infection|infections]], [[Autoimmune disease|autoimmune diseases]] like [[SLE]] and [[antiphospholipid syndrome]], [[pregnancy]], [[antineoplastic]] and [[Immunosuppressive drug|immunosupressive drugs]], [[Human Immunodeficiency Virus (HIV)|HIV]] [[HIV AIDS|infection]] and [[Organ transplant|organ transplantation]]. | ||
==Risk Factors== | ==Risk Factors== | ||
The most potent risk factor in the development of HUS is | The most potent [[risk factor]] in the development of [[Hemolytic-uremic syndrome|HUS]] is [[etiology]] advanced and [[clinical]] associations. | ||
'''etiology advance ''' | '''etiology advance ''' | ||
*'''Infection induced''' | *'''Infection induced'''<ref name="pmid24750096">{{cite journal| author=Majowicz SE, Scallan E, Jones-Bitton A, Sargeant JM, Stapleton J, Angulo FJ et al.| title=Global incidence of human Shiga toxin-producing Escherichia coli infections and deaths: a systematic review and knowledge synthesis. | journal=Foodborne Pathog Dis | year= 2014 | volume= 11 | issue= 6 | pages= 447-55 | pmid=24750096 | doi=10.1089/fpd.2013.1704 | pmc=4607253 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24750096 }}</ref><ref name="pmid18493800">{{cite journal| author=Mark Taylor C| title=Enterohaemorrhagic Escherichia coli and Shigella dysenteriae type 1-induced haemolytic uraemic syndrome. | journal=Pediatr Nephrol | year= 2008 | volume= 23 | issue= 9 | pages= 1425-31 | pmid=18493800 | doi=10.1007/s00467-008-0820-3 | pmc=2459235 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18493800 }}</ref> | ||
#Shiga and verocytotoxin (shiga-like toxin)-producing bacteria;enterohemorrhagic Escherichia coli, Shigella dysenteriaen type 1,Citrobacter | #[[Shiga-like toxin-producing E. coli|Shiga]] and [[verocytotoxin]] ([[shiga-like toxin]])-producing [[bacteria]]; [[Enterohemorrhagic Escherichica coli|enterohemorrhagic Escherichia coli,]] [[Shigella Dysentery|Shigella dysenteriaen type 1]], [[Citrobacter]] | ||
#Streptococcus pneumoniae, neuraminidase, and T-antigen exposure | #[[Streptococcus pneumoniae]], [[neuraminidase]], and T-[[antigen]] [[Exposure (photography)|exposure]] | ||
*'''Disorders of complement regulatio'''n | *'''Disorders of complement regulatio'''n<ref name="pmid24594571">{{cite journal| author=Frémeaux-Bacchi V| title=[Pathophysiology of atypical hemolytic uremic syndrome. Ten years of progress, from laboratory to patient]. | journal=Biol Aujourdhui | year= 2013 | volume= 207 | issue= 4 | pages= 231-40 | pmid=24594571 | doi=10.1051/jbio/2013027 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24594571 }}</ref><ref name="pmid17599974">{{cite journal| author=Sellier-Leclerc AL, Fremeaux-Bacchi V, Dragon-Durey MA, Macher MA, Niaudet P, Guest G et al.| title=Differential impact of complement mutations on clinical characteristics in atypical hemolytic uremic syndrome. | journal=J Am Soc Nephrol | year= 2007 | volume= 18 | issue= 8 | pages= 2392-400 | pmid=17599974 | doi=10.1681/ASN.2006080811 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17599974 }}</ref> | ||
**Complement factor H (CFH) mutation/ | **[[Complement|Complement factor H (CFH) mutation/ factor H defeciency (autosomal dominant)]] | ||
**Complement | **[[Complement]] [[Complement factor I|factor I]](CFI) defeciency ([[acquired]] [[antibody]] mediated) | ||
**Membrane co-factor protein | **[[Membrane]] co-factor [[protein]] defeciency (MCP; [[CD46]]) | ||
**Factor B | **[[Factor B]] overactivity ([[Complement System|Complement]] [[factor B]] [[mutation]]) | ||
**Diacylglycerol | **[[Diacylglycerol kinase]] epsilon [[gene]] [[mutations]] | ||
*'''von Willebrand proteinase, ADAMTS13 deficiency''' | *'''von Willebrand proteinase, ADAMTS13 deficiency''' | ||
# Genetic disorders of ADAMTS13 | # [[Genetic disorder|Genetic disorders]] of [[ADAMTS13]]<ref name="pmid23847193">{{cite journal| author=Feng S, Eyler SJ, Zhang Y, Maga T, Nester CM, Kroll MH et al.| title=Partial ADAMTS13 deficiency in atypical hemolytic uremic syndrome. | journal=Blood | year= 2013 | volume= 122 | issue= 8 | pages= 1487-93 | pmid=23847193 | doi=10.1182/blood-2013-03-492421 | pmc=3750341 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23847193 }}</ref> | ||
#Acquired von Willebrand proteinase deficiency; autoimmune, drug induced | #[[Acquired]] [[Von Willebrand's|von Willebrand]] proteinase [[deficiency]]; [[autoimmune]], [[drug]] induced | ||
*'''Defective cobalamine metabolism'''. | *'''Defective cobalamine metabolism'''<ref name="pmid27324188">{{cite journal| author=Adrovic A, Canpolat N, Caliskan S, Sever L, Kıykım E, Agbas A et al.| title=Cobalamin C defect-hemolytic uremic syndrome caused by new mutation in MMACHC. | journal=Pediatr Int | year= 2016 | volume= 58 | issue= 8 | pages= 763-5 | pmid=27324188 | doi=10.1111/ped.12953 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27324188 }}</ref>. | ||
'''Clinical associations with following diseases:''' | '''Clinical associations with following diseases:''' | ||
#Malignancy, cancer chemotherapy and ionizing radiation | #[[Malignancy]], [[Cancer (disease)|cancer]] [[chemotherapy]] and [[ionizing radiation]] | ||
#Calcineurin | #[[Calcineurin inhibitor]]<nowiki/>s and [[transplantation]] | ||
#Pregnancy, HELLP syndrome and oral contraceptive pill | #[[Pregnancy]], [[HELLP syndrome]] and [[oral contraceptive pill]] | ||
#Systemic lupus erythematosis and antiphospholipid antibody syndrome | #[[Systemic lupus erythematosis]] and [[Antiphospholipid syndrome|antiphospholipid antibody syndrome]] | ||
#Glomerulopathy | #[[Glomerulopathy]] | ||
#Familial, not included in part 1 | #[[Familial]], not included in part 1 | ||
#Unclassified | #Unclassified | ||
Latest revision as of 04:01, 20 September 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2], Anila Hussain, MD [3]
Overview
The most potent risk factor in the development of hemolytic uremic syndrome (HUS) in childhood is infection with verocytotoxin (shiga-like toxin)-producing bacteria, usually enterohemorrhagic Escherichia coli (VTEC/STEC),and in some tropical regions Shigella dysenteriae type I . Other risk factors include genetic mutations in complement factors, pnemumococcal infections, autoimmune diseases like SLE and antiphospholipid syndrome, pregnancy, antineoplastic and immunosupressive drugs, HIV infection and organ transplantation.
Risk Factors
The most potent risk factor in the development of HUS is etiology advanced and clinical associations.
etiology advance
- Shiga and verocytotoxin (shiga-like toxin)-producing bacteria; enterohemorrhagic Escherichia coli, Shigella dysenteriaen type 1, Citrobacter
- Streptococcus pneumoniae, neuraminidase, and T-antigen exposure
- Disorders of complement regulation[3][4]
- Complement factor H (CFH) mutation/ factor H defeciency (autosomal dominant)
- Complement factor I(CFI) defeciency (acquired antibody mediated)
- Membrane co-factor protein defeciency (MCP; CD46)
- Factor B overactivity (Complement factor B mutation)
- Diacylglycerol kinase epsilon gene mutations
- von Willebrand proteinase, ADAMTS13 deficiency
- Genetic disorders of ADAMTS13[5]
- Acquired von Willebrand proteinase deficiency; autoimmune, drug induced
- Defective cobalamine metabolism[6].
Clinical associations with following diseases:
- Malignancy, cancer chemotherapy and ionizing radiation
- Calcineurin inhibitors and transplantation
- Pregnancy, HELLP syndrome and oral contraceptive pill
- Systemic lupus erythematosis and antiphospholipid antibody syndrome
- Glomerulopathy
- Familial, not included in part 1
- Unclassified
References
- ↑ Majowicz SE, Scallan E, Jones-Bitton A, Sargeant JM, Stapleton J, Angulo FJ; et al. (2014). "Global incidence of human Shiga toxin-producing Escherichia coli infections and deaths: a systematic review and knowledge synthesis". Foodborne Pathog Dis. 11 (6): 447–55. doi:10.1089/fpd.2013.1704. PMC 4607253. PMID 24750096.
- ↑ Mark Taylor C (2008). "Enterohaemorrhagic Escherichia coli and Shigella dysenteriae type 1-induced haemolytic uraemic syndrome". Pediatr Nephrol. 23 (9): 1425–31. doi:10.1007/s00467-008-0820-3. PMC 2459235. PMID 18493800.
- ↑ Frémeaux-Bacchi V (2013). "[Pathophysiology of atypical hemolytic uremic syndrome. Ten years of progress, from laboratory to patient]". Biol Aujourdhui. 207 (4): 231–40. doi:10.1051/jbio/2013027. PMID 24594571.
- ↑ Sellier-Leclerc AL, Fremeaux-Bacchi V, Dragon-Durey MA, Macher MA, Niaudet P, Guest G; et al. (2007). "Differential impact of complement mutations on clinical characteristics in atypical hemolytic uremic syndrome". J Am Soc Nephrol. 18 (8): 2392–400. doi:10.1681/ASN.2006080811. PMID 17599974.
- ↑ Feng S, Eyler SJ, Zhang Y, Maga T, Nester CM, Kroll MH; et al. (2013). "Partial ADAMTS13 deficiency in atypical hemolytic uremic syndrome". Blood. 122 (8): 1487–93. doi:10.1182/blood-2013-03-492421. PMC 3750341. PMID 23847193.
- ↑ Adrovic A, Canpolat N, Caliskan S, Sever L, Kıykım E, Agbas A; et al. (2016). "Cobalamin C defect-hemolytic uremic syndrome caused by new mutation in MMACHC". Pediatr Int. 58 (8): 763–5. doi:10.1111/ped.12953. PMID 27324188.