Budd-Chiari syndrome risk factors: Difference between revisions
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{{Budd-Chiari syndrome}} | {{Budd-Chiari syndrome}} | ||
{{CMG}} | {{CMG}}; {{AE}}{{Mazia}} | ||
==Overivew== | |||
Approximately 80 percent of [[patients]] with the Budd-Chiari syndrome have an underlying [[disorder]]. Many patients may have more than one [[risk factor]]. Same patients may have multiple [[causes]] that predispose to the [[development]] of Budd-Chiari Syndrome. Associated risk factors include [[hematologic]] disorders, [[coagulopathies]], [[chronic]] [[infections]], [[chronic]] [[inflammatory diseases]], [[tumors]], [[congenital]] membranous obstructions. | |||
==Risk Factors== | ==Risk Factors== | ||
* | *Approximately 80 percent of [[patients]] with the [[Budd-Chiari syndrome]] have an underlying disorder. Many [[patients]] may have more than one [[Risk factors|risk factor]]. Same [[patient]] may have multiple [[causes]] that predispose to the [[development]] of Budd-Chiari Syndrome.<ref name="pmid26668741">{{cite journal |vauthors=Martens P, Nevens F |title=Budd-Chiari syndrome |journal=United European Gastroenterol J |volume=3 |issue=6 |pages=489–500 |year=2015 |pmid=26668741 |pmc=4669515 |doi=10.1177/2050640615582293 |url=}}</ref><ref name="pmid27326316">{{cite journal |vauthors=Shin N, Kim YH, Xu H, Shi HB, Zhang QQ, Colon Pons JP, Kim D, Xu Y, Wu FY, Han S, Lee BB, Li LS |title=Redefining Budd-Chiari syndrome: A systematic review |journal=World J Hepatol |volume=8 |issue=16 |pages=691–702 |year=2016 |pmid=27326316 |pmc=4909431 |doi=10.4254/wjh.v8.i16.691 |url=}}</ref> | ||
*Associated [[risk factors]] include: | |||
*[[Hematologic]] disorders including: | |||
**[[Polycythemia rubra vera]] | |||
**[[Paroxysmal nocturnal hemoglobinuria]] | |||
**[[Myeloproliferative disease|myeloproliferative disorder]] | |||
**[[Antiphospholipid antibody syndrome]] | |||
**[[Essential thrombocytosis]] | |||
**[[Inherited]] [[thrombotic]] diathesis | |||
*[[Coagulopathies]] include the following: | |||
**[[Protein C deficiency]] | |||
**[[Protein S deficiency]] | |||
**[[Antithrombin III]] [[deficiency]] | |||
**[[Factor V Leiden]] [[deficiency]] | |||
*[[Chronic]] [[infections]] like: | |||
**[[Hydatid cyst|Hydatid cysts]] | |||
**[[Aspergillosis]] | |||
**[[Amoebic liver abscess causes|Amebic abscess]] | |||
**[[Syphilis]] | |||
**[[Tuberculosis]] | |||
*[[Chronic]] [[inflammatory diseases]] such as: | |||
**[[Behçet disease]] | |||
**[[Inflammatory bowel disease]] | |||
**[[Sarcoidosis]] | |||
**[[Systemic lupus erythematosus]] | |||
**[[Sjögren's Syndrome|Sjögren syndrome]] | |||
**[[Mixed connective tissue disease|Mixed connective-tissue disease]] | |||
*[[Tumors]] such as | |||
**[[Hepatocellular carcinoma|Hepatocellular carcinoma (HCC)]] | |||
**[[Renal cell carcinoma]] | |||
**[[Leiomyosarcoma]] | |||
**[[Adrenal carcinoma]] | |||
**[[Wilms' tumor|Wilms tumor]] | |||
**[[Right atrial myxoma]] | |||
*[[Congenital]] membranous obstructions that include the following: | |||
**Type I: Thin membrane is present in the [[vena cava]] or the [[atrium]] | |||
**Type II: A part of the [[vena cava]] is absent | |||
**Type III: The [[Inferior vena cava|inferior vena cava (IVC)]] cannot be filled, and [[collaterals]] have developed | |||
*Miscellaneous [[risk factors]] of Budd-Chiari syndrome include the following: | |||
**[[Alpha1-antitrypsin deficiency]] | |||
**[[Dacarbazine]] | |||
**Urethane | |||
**[[Hypoplasia]] of the [[Hepatic veins|suprahepatic veins]] | |||
**[[Postsurgical]] [[obstruction]] | |||
**Posttraumatic [[obstruction]] | |||
**[[Total parenteral nutrition|Total parenteral nutrition (TPN)]]: Budd-Chiari syndrome can be a [[complication]] of [[total parenteral nutrition]] ([[TPN]]) via an [[inferior vena cava]] ([[Inferior vena cava|IVC]]) [[catheter]] in a [[neonate]] | |||
==References== | ==References== | ||
{{Reflist|2}} | |||
[[Category:Gastroenterology]] | [[Category:Gastroenterology]] | ||
[[Category:Hepatology]] | |||
[[Category:Needs overview]] | [[Category:Needs overview]] | ||
[[Category:Needs content]] | |||
{{WS}} | |||
{{WH}} | |||
Latest revision as of 18:02, 30 November 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]
Overivew
Approximately 80 percent of patients with the Budd-Chiari syndrome have an underlying disorder. Many patients may have more than one risk factor. Same patients may have multiple causes that predispose to the development of Budd-Chiari Syndrome. Associated risk factors include hematologic disorders, coagulopathies, chronic infections, chronic inflammatory diseases, tumors, congenital membranous obstructions.
Risk Factors
- Approximately 80 percent of patients with the Budd-Chiari syndrome have an underlying disorder. Many patients may have more than one risk factor. Same patient may have multiple causes that predispose to the development of Budd-Chiari Syndrome.[1][2]
- Associated risk factors include:
- Hematologic disorders including:
- Coagulopathies include the following:
- Chronic infections like:
- Chronic inflammatory diseases such as:
- Tumors such as
- Congenital membranous obstructions that include the following:
- Type I: Thin membrane is present in the vena cava or the atrium
- Type II: A part of the vena cava is absent
- Type III: The inferior vena cava (IVC) cannot be filled, and collaterals have developed
- Miscellaneous risk factors of Budd-Chiari syndrome include the following:
- Alpha1-antitrypsin deficiency
- Dacarbazine
- Urethane
- Hypoplasia of the suprahepatic veins
- Postsurgical obstruction
- Posttraumatic obstruction
- Total parenteral nutrition (TPN): Budd-Chiari syndrome can be a complication of total parenteral nutrition (TPN) via an inferior vena cava (IVC) catheter in a neonate
References
- ↑ Martens P, Nevens F (2015). "Budd-Chiari syndrome". United European Gastroenterol J. 3 (6): 489–500. doi:10.1177/2050640615582293. PMC 4669515. PMID 26668741.
- ↑ Shin N, Kim YH, Xu H, Shi HB, Zhang QQ, Colon Pons JP, Kim D, Xu Y, Wu FY, Han S, Lee BB, Li LS (2016). "Redefining Budd-Chiari syndrome: A systematic review". World J Hepatol. 8 (16): 691–702. doi:10.4254/wjh.v8.i16.691. PMC 4909431. PMID 27326316.