Spontaneous bacterial peritonitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
SBP is thought to result from a combination of factors inherent in cirrhosis and ascites, such as prolonged [[bacteremia]] secondary to compromised host defenses, intrahepatic shunting of colonized [[blood]], and defective bactericidal activity within the ascitic fluid.<ref name="pmid6500513">{{cite journal | author = Runyon BA, Hoefs JC | title = Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis | journal = Hepatology | volume = 4 | issue = 6 | pages = 1209–11 | year = 1984 | pmid = 6500513 | doi = 10.1002/hep.1840040619| url = | issn = }}</ref> Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.<ref name="pmid3371881">{{cite journal | author = Runyon BA | title = Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis | journal = Hepatology | volume = 8 | issue = 3 | pages = 632–5 | year = 1988 | pmid = 3371881 | doi = 10.1002/hep.1840080332| url = | issn = }}</ref> | |||
With respect to compromised [[immune system|host defenses]], patients with severe acute or chronic liver disease are often deficient in [[Complement system|complement]] and may also have malfunctioning of the [[neutrophil]]ic and [[reticuloendothelial systems]].<ref name="pmid19561863">{{cite journal | author = Alaniz C, Regal RE | title = Spontaneous Bacterial Peritonitis: A Review of Treatment Options | journal = P T | volume = 34 | issue = 4 | pages = 204–210 | year = 2009 | month = April | pmid = 19561863 | pmc = 2697093 | doi = | url = | issn = }}</ref> | |||
As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.<ref name="pmid3770358">{{cite journal | author = Runyon BA | title = Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis | journal = Gastroenterology | volume = 91 | issue = 6 | pages = 1343–6 | year = 1986 | month = December | pmid = 3770358 | doi = | url = | issn = }}</ref> It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.<ref name="pmid4018735">{{cite journal | author = Runyon BA, Morrissey RL, Hoefs JC, Wyle FA | title = Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis | journal = Hepatology | volume = 5 | issue = 4 | pages = 634–7 | year = 1985 | pmid = 4018735 | doi = 10.1002/hep.1840050419| url = | issn = }}</ref> Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.<ref name="pmid19561863"/> | |||
==References== | ==References== | ||
Revision as of 15:09, 31 July 2012
{{Spontaneous bacterial peritonitis))
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: {{ADI}
Overview
Pathophysiology
SBP is thought to result from a combination of factors inherent in cirrhosis and ascites, such as prolonged bacteremia secondary to compromised host defenses, intrahepatic shunting of colonized blood, and defective bactericidal activity within the ascitic fluid.[1] Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.[2]
With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.[3]
As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.[4] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[5] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[3]
References
- ↑ Runyon BA, Hoefs JC (1984). "Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis". Hepatology. 4 (6): 1209–11. doi:10.1002/hep.1840040619. PMID 6500513.
- ↑ Runyon BA (1988). "Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis". Hepatology. 8 (3): 632–5. doi:10.1002/hep.1840080332. PMID 3371881.
- ↑ 3.0 3.1 Alaniz C, Regal RE (2009). "Spontaneous Bacterial Peritonitis: A Review of Treatment Options". P T. 34 (4): 204–210. PMC 2697093. PMID 19561863. Unknown parameter
|month=ignored (help) - ↑ Runyon BA (1986). "Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis". Gastroenterology. 91 (6): 1343–6. PMID 3770358. Unknown parameter
|month=ignored (help) - ↑ Runyon BA, Morrissey RL, Hoefs JC, Wyle FA (1985). "Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis". Hepatology. 5 (4): 634–7. doi:10.1002/hep.1840050419. PMID 4018735.