Spontaneous bacterial peritonitis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
SBP is the culmination of the inability of the gut to contain bacteria and failure of the immune | SBP is the culmination of the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped.<ref name="pmid15920324">{{cite journal| author=Sheer TA, Runyon BA| title=Spontaneous bacterial peritonitis. | journal=Dig Dis | year= 2005 | volume= 23 | issue= 1 | pages= 39-46 | pmid=15920324 | doi=10.1159/000084724 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15920324 }} </ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
SBP is the culmination of the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped.[1]
Pathophysiology
Spontaneous bacterial peritonitis is thought to result from a combination of factors related to 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.[2] 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.[3]
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.[4]
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.[5] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[6] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[4]
References
- ↑ Sheer TA, Runyon BA (2005). "Spontaneous bacterial peritonitis". Dig Dis. 23 (1): 39–46. doi:10.1159/000084724. PMID 15920324.
- ↑ 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.
- ↑ 4.0 4.1 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.