Hemolytic-uremic syndrome causes: Difference between revisions
No edit summary |
|||
Line 5: | Line 5: | ||
==Overview== | ==Overview== | ||
The major cause of [[HUS]] in childhood is [[gastrointestinal]] [[infection]] with [[verocytotoxin]] ([[Shiga-like toxin]])-producing [[bacteria]], usually [[enterohemorrhagic]] [[Escherichia coli]] (VTEC/[[Escherichia coli enteritis|STEC]]), and in some tropical regions [[Shigella dysenteriae type 1|Shigella dysenteriae type I]].[[Verocytotoxin]]-producing [[citrobacter freundii]] has also been reported. In America and the UK, most cases are associated with [[E. coli]] [[serotype]] [[O157:H7]], while other [[serotype]]<nowiki/>s such as O26, O111, O103, and O145 are increasingly reported in Europe and elsewhere. | The major cause of [[HUS]] in childhood is [[gastrointestinal]] [[infection]] with [[verocytotoxin]] ([[Shiga-like toxin]])-producing [[bacteria]], usually [[enterohemorrhagic]] [[Escherichia coli]] (VTEC/[[Escherichia coli enteritis|STEC]]), and in some tropical regions [[Shigella dysenteriae type 1|Shigella dysenteriae type I]].[[Verocytotoxin]]-producing [[citrobacter freundii]] has also been reported. In America and the UK, most cases are associated with [[E. coli]] [[serotype]] [[O157:H7]], while other [[serotype]]<nowiki/>s such as O26, O111, O103, and O145 are increasingly reported in Europe and elsewhere. | ||
VTEC [[strain]]<nowiki/>s produce various [[toxin]]<nowiki/>s, the major ones being [[verocytotoxin]]-1 (Stx1) and [[verocytotoxin]]-2 (Stx2). [[Verocytotoxin]]-1 differs by one [[amino acid]] from [[Shiga toxin]] produced by [[Shigella dysenteriae type 1]]. [[Verocytotoxin]]-2 has multiple variants that are closely related to each other but have 55–60% [[homology]] to [[verocytotoxin]]1. [[HUS]] is mostly caused by [[verocytotoxin]]-2-producing [[strains]].[[HUS]] can occur in the course of [[Systemic disease|systemic diseases]] or physiopathological conditions such as [[pregnancy]], after [[transplantation]] or after drug assumption. | VTEC [[strain]]<nowiki/>s produce various [[toxin]]<nowiki/>s, the major ones being [[verocytotoxin]]-1 (Stx1) and [[verocytotoxin]]-2 (Stx2). [[Verocytotoxin]]-1 differs by one [[amino acid]] from [[Shiga toxin]] produced by [[Shigella dysenteriae type 1]]. [[Verocytotoxin]]-2 has multiple variants that are closely related to each other but have 55–60% [[homology]] to [[verocytotoxin]]1. [[HUS]] is mostly caused by [[verocytotoxin]]-2-producing [[strains]].[[HUS]] can occur in the course of [[Systemic disease|systemic diseases]] or physiopathological conditions such as [[pregnancy]], after [[transplantation]] or after drug assumption. |
Revision as of 15:11, 22 August 2018
Hemolytic-uremic syndrome Microchapters |
Differentiating Hemolytic-uremic syndrome from other Diseases |
---|
Diagnosis |
Treatment |
Case Studies |
Hemolytic-uremic syndrome causes On the Web |
American Roentgen Ray Society Images of Hemolytic-uremic syndrome causes |
Risk calculators and risk factors for Hemolytic-uremic syndrome causes |
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 major cause of HUS in childhood is gastrointestinal infection with verocytotoxin (Shiga-like toxin)-producing bacteria, usually enterohemorrhagic Escherichia coli (VTEC/STEC), and in some tropical regions Shigella dysenteriae type I.Verocytotoxin-producing citrobacter freundii has also been reported. In America and the UK, most cases are associated with E. coli serotype O157:H7, while other serotypes such as O26, O111, O103, and O145 are increasingly reported in Europe and elsewhere.
VTEC strains produce various toxins, the major ones being verocytotoxin-1 (Stx1) and verocytotoxin-2 (Stx2). Verocytotoxin-1 differs by one amino acid from Shiga toxin produced by Shigella dysenteriae type 1. Verocytotoxin-2 has multiple variants that are closely related to each other but have 55–60% homology to verocytotoxin1. HUS is mostly caused by verocytotoxin-2-producing strains.HUS can occur in the course of systemic diseases or physiopathological conditions such as pregnancy, after transplantation or after drug assumption.
Causes
Common Causes
Common causes of HUS may include:[1][2][3][4]
- E. coli (70%)- Shiga-Toxin producing E.Coli (STEC)
- Primary source of infection is usually undercooked or raw ground meat products, raw milk, or fecal contamination of vegetables
- Other sources include swimming pools or lakes contaminated with feces
- Usually cause self-limiting infection but can lead to HUS in some, particularly in young children and elderly
- STEC is heat sensitive and destroyed by thorough cooking and WHO recommended guidelines for safer food should be used to prevent infections with foodborne organisms like STEC[5].
- Other Shiga-Toxin bacteria like Shigella dysenteriae type-1
Less Common Causes
Less common causes of HUS include [6][7][8][9]
- Genetic mutations of complement genes/ complement factor abnormalities
- Infection with Campylobacter Jejuni or Salmonella Typhi
- Pneumococcal infection (commonly pneumonia, empyema, meningitis, and less commonly pericarditis, peritonitis, otitis media and bacteremia
- Pregnancy
- Autoimmune disease such as SLE, Antiphospholipid Syndrome
- Drug associated
- Organ Transplantation
- Human immunodeficiency viral infection such as HIV/AIDS
Causes in Alphabetical Order
List the causes of the disease in alphabetical order:
References
- ↑ Shannon E. Majowicz, Elaine Scallan, Andria Jones-Bitton, Jan M. Sargeant, Jackie Stapleton, Frederick J. Angulo, Derrick H. Yeung & Martyn D. Kirk (2014). "Global incidence of human Shiga toxin-producing Escherichia coli infections and deaths: a systematic review and knowledge synthesis". Foodborne pathogens and disease. 11 (6): 447–455. doi:10.1089/fpd.2013.1704. PMID 24750096. Unknown parameter
|month=
ignored (help) - ↑ Chantal Loirat, Fadi Fakhouri, Gema Ariceta, Nesrin Besbas, Martin Bitzan, Anna Bjerre, Rosanna Coppo, Francesco Emma, Sally Johnson, Diana Karpman, Daniel Landau, Craig B. Langman, Anne-Laure Lapeyraque, Christoph Licht, Carla Nester, Carmine Pecoraro, Magdalena Riedl, Nicole C. A. J. van de Kar, Johan Van de Walle, Marina Vivarelli & Veronique Fremeaux-Bacchi (2016). "An international consensus approach to the management of atypical hemolytic uremic syndrome in children". Pediatric nephrology (Berlin, Germany). 31 (1): 15–39. doi:10.1007/s00467-015-3076-8. PMID 25859752. Unknown parameter
|month=
ignored (help) - ↑ Fadi Fakhouri, Julien Zuber, Veronique Fremeaux-Bacchi & Chantal Loirat (2017). "Haemolytic uraemic syndrome". Lancet (London, England). 390 (10095): 681–696. doi:10.1016/S0140-6736(17)30062-4. PMID 28242109. Unknown parameter
|month=
ignored (help) - ↑ Lopes da Silva, Rodrigo (2011). "Viral-associated thrombotic microangiopathies". Hematology/Oncology and Stem Cell Therapy. 4 (2): 51–59. doi:10.5144/1658-3876.2011.51. ISSN 1658-3876.
- ↑ http://www.who.int/news-room/fact-sheets/detail/e-coli
- ↑ P. J. Medina, J. M. Sipols & J. N. George (2001). "Drug-associated thrombotic thrombocytopenic purpura-hemolytic uremic syndrome". Current opinion in hematology. 8 (5): 286–293. PMID 11604563. Unknown parameter
|month=
ignored (help) - ↑ Fadi Fakhouri, Lubka Roumenina, Francois Provot, Marion Sallee, Sophie Caillard, Lionel Couzi, Marie Essig, David Ribes, Marie-Agnes Dragon-Durey, Frank Bridoux, Eric Rondeau & Veronique Fremeaux-Bacchi (2010). "Pregnancy-associated hemolytic uremic syndrome revisited in the era of complement gene mutations". Journal of the American Society of Nephrology : JASN. 21 (5): 859–867. doi:10.1681/ASN.2009070706. PMID 20203157. Unknown parameter
|month=
ignored (help) - ↑ Christine Skerka, Mihaly Jozsi, Peter F. Zipfel, Marie-Agnes Dragon-Durey & Veronique Fremeaux-Bacchi (2009). "Autoantibodies in haemolytic uraemic syndrome (HUS)". Thrombosis and haemostasis. 101 (2): 227–232. PMID 19190803. Unknown parameter
|month=
ignored (help) - ↑ 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.