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| | ==Physical examination== |
| | ==References== |
| | {{reflist|2}} |
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| __NOTOC__
| | {{WH}} |
| {{Irritable bowel syndrome}} | | {{WS}} |
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| {{CMG}}; {{AE}}
| | ==References== |
| ==Overview== | | {{Reflist|2}} |
| The exact pathogenesis of [disease name] is not fully understood.
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| OR
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| It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
| | ===Pathophysiology prev=== |
| | <div style="-webkit-user-select: none;"> |
| | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
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| | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
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| | |} |
| | __NOTOC__ |
| | {{Cirrhosis}} |
| | {{CMG}} {{AE}} |
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| OR
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| [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
| | ===Pathophysiology prev=== |
| | <div style="-webkit-user-select: none;"> |
| | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
| | |- |
| | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
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| | __NOTOC__ |
| | {{Cirrhosis}} |
| | {{CMG}} {{AE}} |
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| | == History and Symptoms == |
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| Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
| | * History should include: |
| | ** Appearance of bowel movements |
| | ** Travel history |
| | ** Associated symptoms |
| | ** Immune status |
| | ** Woodland exposure |
| | ==References== |
| | {{reflist|2}} |
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| OR
| | {{WH}} |
| | {{WS}} |
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| | ==Other Imaging Findings== |
| | * [[Endoscopy]] |
| | * [[Barium enema]] |
| | * [[Colonoscopy]] |
| | * [[Sigmoidoscopy]] |
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| [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
| | ==Other diagnostic studies== |
| | == Other Diagnostic Studies == |
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| OR
| | * Breath hydrogen test |
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| The progression to [disease name] usually involves the [molecular pathway].
| | * [[HIV test]]ing for those patients suspected of having HIV |
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| OR
| | == |
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| The pathophysiology of [disease/malignancy] depends on the histological subtype.
| | ==Overview== |
| | |
| ==Pathophysiology== | |
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| ===Pathogenesis===
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| The exact pathogenesis of Irritable Bowel Syndrome (IBS) is uncertain. It is understood that IBS is caused by the interaction of various factors:
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| *'''Gastrointestinal motor abnormalities'''
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| **IBS is referred to as ‘spastic colon’ due to changes in colonic motor function.
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| **Manometry recordings from the transverse, descending and sigmoid colon have shown that spastic colon leads to changed patterns of colonic and small intestinal motor function such as increased frequency and irregularity of luminal contractions.<ref name="pmid8789897">{{cite journal |vauthors=Schmidt T, Hackelsberger N, Widmer R, Meisel C, Pfeiffer A, Kaess H |title=Ambulatory 24-hour jejunal motility in diarrhea-predominant irritable bowel syndrome |journal=Scand. J. Gastroenterol. |volume=31 |issue=6 |pages=581–9 |year=1996 |pmid=8789897 |doi= |url=}}</ref><ref name="pmid2865504">{{cite journal |vauthors=Kumar D, Wingate DL |title=The irritable bowel syndrome: a paroxysmal motor disorder |journal=Lancet |volume=2 |issue=8462 |pages=973–7 |year=1985 |pmid=2865504 |doi= |url=}}</ref><ref name="pmid11215731">{{cite journal |vauthors=Simrén M, Castedal M, Svedlund J, Abrahamsson H, Björnsson E |title=Abnormal propagation pattern of duodenal pressure waves in the irritable bowel syndrome (IBS) [correction of (IBD)] |journal=Dig. Dis. Sci. |volume=45 |issue=11 |pages=2151–61 |year=2000 |pmid=11215731 |doi= |url=}}</ref>
| |
| **Peak amplitude of high-amplitude propagating contractions (HAPCs) in diarrhea-prone IBS patients is higher, compared to healthy subjects.<ref name="pmid18456567">{{cite journal |vauthors=Camilleri M, McKinzie S, Busciglio I, Low PA, Sweetser S, Burton D, Baxter K, Ryks M, Zinsmeister AR |title=Prospective study of motor, sensory, psychologic, and autonomic functions in patients with irritable bowel syndrome |journal=Clin. Gastroenterol. Hepatol. |volume=6 |issue=7 |pages=772–81 |year=2008 |pmid=18456567 |pmc=2495078 |doi=10.1016/j.cgh.2008.02.060 |url=}}</ref><ref name="pmid3569764">{{cite journal |vauthors=Kellow JE, Phillips SF |title=Altered small bowel motility in irritable bowel syndrome is correlated with symptoms |journal=Gastroenterology |volume=92 |issue=6 |pages=1885–93 |year=1987 |pmid=3569764 |doi= |url=}}</ref>
| |
| **Diarrhea prone IBS patients have increased responses to ingestion, CRH(Corticotropin releasing hormone)<ref name="pmid7379673">{{cite journal |vauthors=Whitehead WE, Engel BT, Schuster MM |title=Irritable bowel syndrome: physiological and psychological differences between diarrhea-predominant and constipation-predominant patients |journal=Dig. Dis. Sci. |volume=25 |issue=6 |pages=404–13 |year=1980 |pmid=7379673 |doi= |url=}}</ref><ref name="pmid9691924">{{cite journal |vauthors=Fukudo S, Nomura T, Hongo M |title=Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome |journal=Gut |volume=42 |issue=6 |pages=845–9 |year=1998 |pmid=9691924 |pmc=1727153 |doi= |url=}}</ref>, CCK(cholecystokinin)<ref name="pmid11374689">{{cite journal |vauthors=Chey WY, Jin HO, Lee MH, Sun SW, Lee KY |title=Colonic motility abnormality in patients with irritable bowel syndrome exhibiting abdominal pain and diarrhea |journal=Am. J. Gastroenterol. |volume=96 |issue=5 |pages=1499–506 |year=2001 |pmid=11374689 |doi=10.1111/j.1572-0241.2001.03804.x |url=}}</ref> and present with abdominal discomfort and accelerated transit through the colon.
| |
| **On the other hand, constipation prone IBS patients show fewer HAPCs, delayed transit through the colon and decreased motility.<ref name="pmid18456567">{{cite journal |vauthors=Camilleri M, McKinzie S, Busciglio I, Low PA, Sweetser S, Burton D, Baxter K, Ryks M, Zinsmeister AR |title=Prospective study of motor, sensory, psychologic, and autonomic functions in patients with irritable bowel syndrome |journal=Clin. Gastroenterol. Hepatol. |volume=6 |issue=7 |pages=772–81 |year=2008 |pmid=18456567 |pmc=2495078 |doi=10.1016/j.cgh.2008.02.060 |url=}}</ref>
| |
| **It has been demonstrated that more than 90% of HAPCs are associated with abdominal pain.<ref name="pmid11374689">{{cite journal |vauthors=Chey WY, Jin HO, Lee MH, Sun SW, Lee KY |title=Colonic motility abnormality in patients with irritable bowel syndrome exhibiting abdominal pain and diarrhea |journal=Am. J. Gastroenterol. |volume=96 |issue=5 |pages=1499–506 |year=2001 |pmid=11374689 |doi=10.1111/j.1572-0241.2001.03804.x |url=}}</ref>
| |
| | |
| *'''CNS dysregulation'''
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| ** The conceptualization of IBS being a brain gut disorder is reinforced by the following:
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| *** Epidemiological studies suggest that IBS occurs in individuals who have experienced childhood trauma, with symptom exacerbation occurring in patients with emotional disturbances or stress.<ref name="pmid27061107">{{cite journal |vauthors=Park SH, Videlock EJ, Shih W, Presson AP, Mayer EA, Chang L |title=Adverse childhood experiences are associated with irritable bowel syndrome and gastrointestinal symptom severity |journal=Neurogastroenterol. Motil. |volume=28 |issue=8 |pages=1252–60 |year=2016 |pmid=27061107 |pmc=4956522 |doi=10.1111/nmo.12826 |url=}}</ref>
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| *** Traumatic experiences before the age of 18 can directly shape adult connectivity in the executive control network. The effects on structures such as the insula, anterior cingulate cortex and the thalamus have been implicated in the pathophysiology of central pain amplification.<ref name="pmid25003944">{{cite journal |vauthors=Gupta A, Kilpatrick L, Labus J, Tillisch K, Braun A, Hong JY, Ashe-McNalley C, Naliboff B, Mayer EA |title=Early adverse life events and resting state neural networks in patients with chronic abdominal pain: evidence for sex differences |journal=Psychosom Med |volume=76 |issue=6 |pages=404–12 |year=2014 |pmid=25003944 |pmc=4113723 |doi=10.1097/PSY.0000000000000089 |url=}}</ref>
| |
| *** IBS has been found to have a high association with pre-existing psychiatric and psychological conditions like anxiety and depression.<ref name="pmid27144627">{{cite journal |vauthors=Mearin F, Lacy BE, Chang L, Chey WD, Lembo AJ, Simren M, Spiller R |title=Bowel Disorders |journal=Gastroenterology |volume= |issue= |pages= |year=2016 |pmid=27144627 |doi=10.1053/j.gastro.2016.02.031 |url=}}</ref> However, studies have shown that even when patients are not anxious or depressed, the dorsolateral prefrontal cortex activity is reduced, pointing directly towards CNS dysfunction and increased susceptibility to stressors.<ref name="pmid22108191">{{cite journal |vauthors=Larsson MB, Tillisch K, Craig AD, Engström M, Labus J, Naliboff B, Lundberg P, Ström M, Mayer EA, Walter SA |title=Brain responses to visceral stimuli reflect visceral sensitivity thresholds in patients with irritable bowel syndrome |journal=Gastroenterology |volume=142 |issue=3 |pages=463–472.e3 |year=2012 |pmid=22108191 |pmc=3288538 |doi=10.1053/j.gastro.2011.11.022 |url=}}</ref>
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| *** Psychological therapies that act on cerebral cortical sites and antidepressants have proven to be one of the mainstays of therapy for patients. The role of probiotics in modifying signal processing in the brain also proves that IBS is a brain gut disorder. <ref name="pmid23474283">{{cite journal |vauthors=Tillisch K, Labus J, Kilpatrick L, Jiang Z, Stains J, Ebrat B, Guyonnet D, Legrain-Raspaud S, Trotin B, Naliboff B, Mayer EA |title=Consumption of fermented milk product with probiotic modulates brain activity |journal=Gastroenterology |volume=144 |issue=7 |pages=1394–401, 1401.e1–4 |year=2013 |pmid=23474283 |pmc=3839572 |doi=10.1053/j.gastro.2013.02.043 |url=}}</ref>
| |
| *** Studies using advanced brain imaging techniques have analyzed differences in brain activity and have helped us appreciate that the mid-cingulate cortex (responsible for attention processes and responses) and the prefrontal cortex(responsible for vigilance and alertness of the human brain) are involved in IBS. <ref name="pmid25003944" />
| |
| *** Modulation of the mid-cingulate cortex is associated with alterations in the subjective sensations of pain whereas prefrontal cortex modulation may lead to increased perception of visceral pain.<ref name="pmid25003944">{{cite journal |vauthors=Gupta A, Kilpatrick L, Labus J, Tillisch K, Braun A, Hong JY, Ashe-McNalley C, Naliboff B, Mayer EA |title=Early adverse life events and resting state neural networks in patients with chronic abdominal pain: evidence for sex differences |journal=Psychosom Med |volume=76 |issue=6 |pages=404–12 |year=2014 |pmid=25003944 |pmc=4113723 |doi=10.1097/PSY.0000000000000089 |url=}}</ref>
| |
| *** Patients with IBS have aberrant processing of central information,<ref name="pmid23864686">{{cite journal |vauthors=Hong JY, Kilpatrick LA, Labus J, Gupta A, Jiang Z, Ashe-McNalley C, Stains J, Heendeniya N, Ebrat B, Smith S, Tillisch K, Naliboff B, Mayer EA |title=Patients with chronic visceral pain show sex-related alterations in intrinsic oscillations of the resting brain |journal=J. Neurosci. |volume=33 |issue=29 |pages=11994–2002 |year=2013 |pmid=23864686 |pmc=3713732 |doi=10.1523/JNEUROSCI.5733-12.2013 |url=}}</ref> with decreased feedback on the emotional arousal network that controls the autonomic modulation of gastrointestinal function.<ref name="pmid20003075">{{cite journal |vauthors=Hall GB, Kamath MV, Collins S, Ganguli S, Spaziani R, Miranda KL, Bayati A, Bienenstock J |title=Heightened central affective response to visceral sensations of pain and discomfort in IBS |journal=Neurogastroenterol. Motil. |volume=22 |issue=3 |pages=276–e80 |year=2010 |pmid=20003075 |doi=10.1111/j.1365-2982.2009.01436.x |url=}}</ref>These have been seen as irregularities on diffusion tensor imaging<ref name="pmid23721972">{{cite journal |vauthors=Ellingson BM, Mayer E, Harris RJ, Ashe-McNally C, Naliboff BD, Labus JS, Tillisch K |title=Diffusion tensor imaging detects microstructural reorganization in the brain associated with chronic irritable bowel syndrome |journal=Pain |volume=154 |issue=9 |pages=1528–41 |year=2013 |pmid=23721972 |pmc=3758125 |doi=10.1016/j.pain.2013.04.010 |url=}}</ref> in the white matter of the brain.
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| *** Rectal balloon distension in patients has shown the increased involvement of regions of the brain associated with attentional and behavioral responses to the arrival of such stimuli.<ref name="pmid20600024">{{cite journal |vauthors=Elsenbruch S, Rosenberger C, Bingel U, Forsting M, Schedlowski M, Gizewski ER |title=Patients with irritable bowel syndrome have altered emotional modulation of neural responses to visceral stimuli |journal=Gastroenterology |volume=139 |issue=4 |pages=1310–9 |year=2010 |pmid=20600024 |doi=10.1053/j.gastro.2010.06.054 |url=}}</ref><ref name="pmid19651629">{{cite journal |vauthors=Elsenbruch S, Rosenberger C, Enck P, Forsting M, Schedlowski M, Gizewski ER |title=Affective disturbances modulate the neural processing of visceral pain stimuli in irritable bowel syndrome: an fMRI study |journal=Gut |volume=59 |issue=4 |pages=489–95 |year=2010 |pmid=19651629 |doi=10.1136/gut.2008.175000 |url=}}</ref><ref name="pmid22108191">{{cite journal |vauthors=Larsson MB, Tillisch K, Craig AD, Engström M, Labus J, Naliboff B, Lundberg P, Ström M, Mayer EA, Walter SA |title=Brain responses to visceral stimuli reflect visceral sensitivity thresholds in patients with irritable bowel syndrome |journal=Gastroenterology |volume=142 |issue=3 |pages=463–472.e3 |year=2012 |pmid=22108191 |pmc=3288538 |doi=10.1053/j.gastro.2011.11.022 |url=}}</ref>
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| | |
| * '''Visceral hypersensitivity'''
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| ** Visceral hypersensitivity is an important factor in the pathogenesis of pain perception in IBS patients<ref name="pmid2323511">{{cite journal |vauthors=Whitehead WE, Holtkotter B, Enck P, Hoelzl R, Holmes KD, Anthony J, Shabsin HS, Schuster MM |title=Tolerance for rectosigmoid distention in irritable bowel syndrome |journal=Gastroenterology |volume=98 |issue=5 Pt 1 |pages=1187–92 |year=1990 |pmid=2323511 |doi= |url=}}</ref>. IBS is associated with a decreased threshold for perception of visceral stimuli<ref name="pmid18456567">{{cite journal |vauthors=Camilleri M, McKinzie S, Busciglio I, Low PA, Sweetser S, Burton D, Baxter K, Ryks M, Zinsmeister AR |title=Prospective study of motor, sensory, psychologic, and autonomic functions in patients with irritable bowel syndrome |journal=Clin. Gastroenterol. Hepatol. |volume=6 |issue=7 |pages=772–81 |year=2008 |pmid=18456567 |pmc=2495078 |doi=10.1016/j.cgh.2008.02.060 |url=}}</ref><ref name="pmid21537962">{{cite journal |vauthors=Barbara G, Cremon C, De Giorgio R, Dothel G, Zecchi L, Bellacosa L, Carini G, Stanghellini V, Corinaldesi R |title=Mechanisms underlying visceral hypersensitivity in irritable bowel syndrome |journal=Curr Gastroenterol Rep |volume=13 |issue=4 |pages=308–15 |year=2011 |pmid=21537962 |doi=10.1007/s11894-011-0195-7 |url=}}</ref> (i.e. visceral hypersensitivity).
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| ** Studies in IBS patients have shown that rectal balloon inflation produces painful and non-painful sensations at lower volumes as compared to healthy controls, suggesting the presence of afferent pathway disturbances in visceral innervation<ref name="pmid7797041">{{cite journal |vauthors=Mertz H, Naliboff B, Munakata J, Niazi N, Mayer EA |title=Altered rectal perception is a biological marker of patients with irritable bowel syndrome |journal=Gastroenterology |volume=109 |issue=1 |pages=40–52 |year=1995 |pmid=7797041 |doi= |url=}}</ref><ref name="pmid2338274">{{cite journal |vauthors=Prior A, Maxton DG, Whorwell PJ |title=Anorectal manometry in irritable bowel syndrome: differences between diarrhoea and constipation predominant subjects |journal=Gut |volume=31 |issue=4 |pages=458–62 |year=1990 |pmid=2338274 |pmc=1378424 |doi= |url=}}</ref><ref name="pmid17919487">{{cite journal |vauthors=Posserud I, Syrous A, Lindström L, Tack J, Abrahamsson H, Simrén M |title=Altered rectal perception in irritable bowel syndrome is associated with symptom severity |journal=Gastroenterology |volume=133 |issue=4 |pages=1113–23 |year=2007 |pmid=17919487 |doi=10.1053/j.gastro.2007.07.024 |url=}}</ref><ref name="pmid12055583">{{cite journal |vauthors=Bouin M, Plourde V, Boivin M, Riberdy M, Lupien F, Laganière M, Verrier P, Poitras P |title=Rectal distention testing in patients with irritable bowel syndrome: sensitivity, specificity, and predictive values of pain sensory thresholds |journal=Gastroenterology |volume=122 |issue=7 |pages=1771–7 |year=2002 |pmid=12055583 |doi= |url=}}</ref>. Many factors contribute to visceral hyperalgesia(i.e increased sensitivity of the intestines to normal sensations):
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| *** Spinal hyperexcitability due to activation of an N-methyl D aspartate(NMDA) receptor, Nitric oxide and possibly other neurotransmitters.
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| *** Activation of specific gastrointestinal mediators like kinins and serotonin that lead to afferent nerve fiber sensitization.
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| *** Central (brainstem and cortical) modulation with increased activation of anterior circulate cortex, thalamus and insula, involved in processing of pain, translating into long term hypersensitivity due to neuroplasticity, causing semipermanent changes in the neural response to all kinds of visceral stimulation. These findings have been proven by brain imaging studies. (e.g. functional magnetic resonance imaging, positron emission tomography'')<ref name="pmid21537962">{{cite journal |vauthors=Barbara G, Cremon C, De Giorgio R, Dothel G, Zecchi L, Bellacosa L, Carini G, Stanghellini V, Corinaldesi R |title=Mechanisms underlying visceral hypersensitivity in irritable bowel syndrome |journal=Curr Gastroenterol Rep |volume=13 |issue=4 |pages=308–15 |year=2011 |pmid=21537962 |doi=10.1007/s11894-011-0195-7 |url=}}</ref><ref name="pmid10784583">{{cite journal |vauthors=Mertz H, Morgan V, Tanner G, Pickens D, Price R, Shyr Y, Kessler R |title=Regional cerebral activation in irritable bowel syndrome and control subjects with painful and nonpainful rectal distention |journal=Gastroenterology |volume=118 |issue=5 |pages=842–8 |year=2000 |pmid=10784583 |doi= |url=}}</ref> ''
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| *** Recruitment of peripheral silent nociceptors causing increased end organ sensitivity due to hormonal or immune activation<ref name="pmid21537962">{{cite journal |vauthors=Barbara G, Cremon C, De Giorgio R, Dothel G, Zecchi L, Bellacosa L, Carini G, Stanghellini V, Corinaldesi R |title=Mechanisms underlying visceral hypersensitivity in irritable bowel syndrome |journal=Curr Gastroenterol Rep |volume=13 |issue=4 |pages=308–15 |year=2011 |pmid=21537962 |doi=10.1007/s11894-011-0195-7 |url=}}</ref>.
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| * '''Immune activation and mucosal inflammation'''
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| ** The high prevalence of IBS in patients with history of inflammatory bowel disease, celiac disease or microscopic colitis points towards the fact that immune activation and mucosal inflammation play an important role in the pathogenesis of IBS.<ref name="pmid19997094">{{cite journal |vauthors=Coëffier M, Gloro R, Boukhettala N, Aziz M, Lecleire S, Vandaele N, Antonietti M, Savoye G, Bôle-Feysot C, Déchelotte P, Reimund JM, Ducrotté P |title=Increased proteasome-mediated degradation of occludin in irritable bowel syndrome |journal=Am. J. Gastroenterol. |volume=105 |issue=5 |pages=1181–8 |year=2010 |pmid=19997094 |doi=10.1038/ajg.2009.700 |url=}}</ref><ref name="pmid12055584">{{cite journal |vauthors=Chadwick VS, Chen W, Shu D, Paulus B, Bethwaite P, Tie A, Wilson I |title=Activation of the mucosal immune system in irritable bowel syndrome |journal=Gastroenterology |volume=122 |issue=7 |pages=1778–83 |year=2002 |pmid=12055584 |doi= |url=}}</ref><ref name="pmid17383420">{{cite journal |vauthors=Liebregts T, Adam B, Bredack C, Röth A, Heinzel S, Lester S, Downie-Doyle S, Smith E, Drew P, Talley NJ, Holtmann G |title=Immune activation in patients with irritable bowel syndrome |journal=Gastroenterology |volume=132 |issue=3 |pages=913–20 |year=2007 |pmid=17383420 |doi=10.1053/j.gastro.2007.01.046 |url=}}</ref><ref name="pmid12454854">{{cite journal |vauthors=Törnblom H, Lindberg G, Nyberg B, Veress B |title=Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome |journal=Gastroenterology |volume=123 |issue=6 |pages=1972–9 |year=2002 |pmid=12454854 |doi=10.1053/gast.2002.37059 |url=}}</ref><ref name="pmid17005763">{{cite journal |vauthors=Guilarte M, Santos J, de Torres I, Alonso C, Vicario M, Ramos L, Martínez C, Casellas F, Saperas E, Malagelada JR |title=Diarrhoea-predominant IBS patients show mast cell activation and hyperplasia in the jejunum |journal=Gut |volume=56 |issue=2 |pages=203–9 |year=2007 |pmid=17005763 |pmc=1856785 |doi=10.1136/gut.2006.100594 |url=}}</ref><ref name="pmid14988823">{{cite journal |vauthors=Barbara G, Stanghellini V, De Giorgio R, Cremon C, Cottrell GS, Santini D, Pasquinelli G, Morselli-Labate AM, Grady EF, Bunnett NW, Collins SM, Corinaldesi R |title=Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome |journal=Gastroenterology |volume=126 |issue=3 |pages=693–702 |year=2004 |pmid=14988823 |doi= |url=}}</ref><ref name="pmid17383420">{{cite journal |vauthors=Liebregts T, Adam B, Bredack C, Röth A, Heinzel S, Lester S, Downie-Doyle S, Smith E, Drew P, Talley NJ, Holtmann G |title=Immune activation in patients with irritable bowel syndrome |journal=Gastroenterology |volume=132 |issue=3 |pages=913–20 |year=2007 |pmid=17383420 |doi=10.1053/j.gastro.2007.01.046 |url=}}</ref>
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| ** Moreover, psychological stress can significantly impact the release of proinflammatory cytokines, thereby affecting intestinal permeability and reinforcing a functional link existing between immune activation, psychological symptoms and symptoms in patients with IBS.<ref name="pmid19997094">{{cite journal |vauthors=Coëffier M, Gloro R, Boukhettala N, Aziz M, Lecleire S, Vandaele N, Antonietti M, Savoye G, Bôle-Feysot C, Déchelotte P, Reimund JM, Ducrotté P |title=Increased proteasome-mediated degradation of occludin in irritable bowel syndrome |journal=Am. J. Gastroenterol. |volume=105 |issue=5 |pages=1181–8 |year=2010 |pmid=19997094 |doi=10.1038/ajg.2009.700 |url=}}</ref>
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| ** Patients are found to have higher mucosal counts of lymphocytes (T cells, B cells), mast cells and immune mediators such as prostanoids, proteases, cytokines and histamines. <ref name="pmid17383420">{{cite journal |vauthors=Liebregts T, Adam B, Bredack C, Röth A, Heinzel S, Lester S, Downie-Doyle S, Smith E, Drew P, Talley NJ, Holtmann G |title=Immune activation in patients with irritable bowel syndrome |journal=Gastroenterology |volume=132 |issue=3 |pages=913–20 |year=2007 |pmid=17383420 |doi=10.1053/j.gastro.2007.01.046 |url=}}</ref><ref name="pmid20427395">{{cite journal |vauthors=Marshall JK, Thabane M, Garg AX, Clark WF, Moayyedi P, Collins SM |title=Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery |journal=Gut |volume=59 |issue=5 |pages=605–11 |year=2010 |pmid=20427395 |doi=10.1136/gut.2009.202234 |url=}}</ref><ref name="pmid21911849">{{cite journal |vauthors=Wensaas KA, Langeland N, Hanevik K, Mørch K, Eide GE, Rortveit G |title=Irritable bowel syndrome and chronic fatigue 3 years after acute giardiasis: historic cohort study |journal=Gut |volume=61 |issue=2 |pages=214–9 |year=2012 |pmid=21911849 |doi=10.1136/gutjnl-2011-300220 |url=}}</ref><ref name="pmid19711225">{{cite journal |vauthors=Mearin F, Perelló A, Balboa A, Perona M, Sans M, Salas A, Angulo S, Lloreta J, Benasayag R, García-Gonzalez MA, Pérez-Oliveras M, Coderch J |title=Pathogenic mechanisms of postinfectious functional gastrointestinal disorders: results 3 years after gastroenteritis |journal=Scand. J. Gastroenterol. |volume=44 |issue=10 |pages=1173–85 |year=2009 |pmid=19711225 |doi=10.1080/00365520903171276 |url=}}</ref><ref name="pmid12631663">{{cite journal |vauthors=Gwee KA, Collins SM, Read NW, Rajnakova A, Deng Y, Graham JC, McKendrick MW, Moochhala SM |title=Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome |journal=Gut |volume=52 |issue=4 |pages=523–6 |year=2003 |pmid=12631663 |pmc=1773606 |doi= |url=}}</ref>
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| ** '''Lymphocytes:'''
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| *** Patients with IBS have increased B lymphocyte activation in the blood.<ref name="pmid19222763">{{cite journal |vauthors=Ohman L, Lindmark AC, Isaksson S, Posserud I, Strid H, Sjövall H, Simrén M |title=B-cell activation in patients with irritable bowel syndrome (IBS) |journal=Neurogastroenterol. Motil. |volume=21 |issue=6 |pages=644–50, e27 |year=2009 |pmid=19222763 |doi=10.1111/j.1365-2982.2009.01272.x |url=}}</ref> However, activation of humoral immunity in IBS is specific for the gastrointestinal tract<ref name="pmid25209656">{{cite journal |vauthors=Vicario M, González-Castro AM, Martínez C, Lobo B, Pigrau M, Guilarte M, de Torres I, Mosquera JL, Fortea M, Sevillano-Aguilera C, Salvo-Romero E, Alonso C, Rodiño-Janeiro BK, Söderholm JD, Azpiroz F, Santos J |title=Increased humoral immunity in the jejunum of diarrhoea-predominant irritable bowel syndrome associated with clinical manifestations |journal=Gut |volume=64 |issue=9 |pages=1379–88 |year=2015 |pmid=25209656 |doi=10.1136/gutjnl-2013-306236 |url=}}</ref> as increased numbers of lymphocytes have been found in the small intestine and colon of patients.<ref name="pmid12055584">{{cite journal |vauthors=Chadwick VS, Chen W, Shu D, Paulus B, Bethwaite P, Tie A, Wilson I |title=Activation of the mucosal immune system in irritable bowel syndrome |journal=Gastroenterology |volume=122 |issue=7 |pages=1778–83 |year=2002 |pmid=12055584 |doi= |url=}}</ref><ref name="pmid12454854">{{cite journal |vauthors=Törnblom H, Lindberg G, Nyberg B, Veress B |title=Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome |journal=Gastroenterology |volume=123 |issue=6 |pages=1972–9 |year=2002 |pmid=12454854 |doi=10.1053/gast.2002.37059 |url=}}</ref>
| |
| *** In addition to this, IBS patients with diarrhea<ref name="pmid25209656">{{cite journal |vauthors=Vicario M, González-Castro AM, Martínez C, Lobo B, Pigrau M, Guilarte M, de Torres I, Mosquera JL, Fortea M, Sevillano-Aguilera C, Salvo-Romero E, Alonso C, Rodiño-Janeiro BK, Söderholm JD, Azpiroz F, Santos J |title=Increased humoral immunity in the jejunum of diarrhoea-predominant irritable bowel syndrome associated with clinical manifestations |journal=Gut |volume=64 |issue=9 |pages=1379–88 |year=2015 |pmid=25209656 |doi=10.1136/gutjnl-2013-306236 |url=}}</ref> have enhanced mucosal humoral activity, associated with activation and proliferation of B cells and immunoglobulin production, identified by microarray profiling.
| |
| *** IBS patients with severe disease have an increase in lymphocyte infiltration in the myentric plexus,<ref name="pmid12454854">{{cite journal |vauthors=Törnblom H, Lindberg G, Nyberg B, Veress B |title=Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome |journal=Gastroenterology |volume=123 |issue=6 |pages=1972–9 |year=2002 |pmid=12454854 |doi=10.1053/gast.2002.37059 |url=}}</ref> in studies where full-thickness jejunal biopsies were obtained.
| |
| *** Mediators released by lymphocytes include histamine, proteases and nitric oxide. The stimulation of the enteric nervous system by these mediators leads to abnormal visceral and motor responses within the gastrointestinal tract.<ref name="pmid12055584" />
| |
| *** Examination of stool in patients with diarrhea prominent IBS have high levels of serine protease activity.<ref name="pmid18924448">{{cite journal |vauthors=Bueno L |title=Protease activated receptor 2: a new target for IBS treatment |journal=Eur Rev Med Pharmacol Sci |volume=12 Suppl 1 |issue= |pages=95–102 |year=2008 |pmid=18924448 |doi= |url=}}</ref><ref name="pmid18194983">{{cite journal |vauthors=Gecse K, Róka R, Ferrier L, Leveque M, Eutamene H, Cartier C, Ait-Belgnaoui A, Rosztóczy A, Izbéki F, Fioramonti J, Wittmann T, Bueno L |title=Increased faecal serine protease activity in diarrhoeic IBS patients: a colonic lumenal factor impairing colonic permeability and sensitivity |journal=Gut |volume=57 |issue=5 |pages=591–9 |year=2008 |pmid=18194983 |doi=10.1136/gut.2007.140210 |url=}}</ref>When fecal extracts are intra colonically infused into mice, there is increased visceral pain and colonic cellular permeability. <ref name="pmid18924448" />
| |
| *** Serine protease inhibitors prevent effects mediated by high levels of serine protease. Studies have shown that mononuclear cell supernatants in the peripheral blood from healthy controls have greater inhibitory effects on colorectal sensory afferent nerve endings than in IBS patients.<ref name="pmid18194983" /><ref name="pmid18924448" />
| |
| ** '''Mast cells:'''
| |
| *** Studies have shown an increased number of mast cells in IBS patients in the jejunum, terminal ileum and colon.<ref name="pmid14988823">{{cite journal |vauthors=Barbara G, Stanghellini V, De Giorgio R, Cremon C, Cottrell GS, Santini D, Pasquinelli G, Morselli-Labate AM, Grady EF, Bunnett NW, Collins SM, Corinaldesi R |title=Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome |journal=Gastroenterology |volume=126 |issue=3 |pages=693–702 |year=2004 |pmid=14988823 |doi= |url=}}</ref>
| |
| *** Higher numbers of activated mast cells are found in proximity to colonic nerve fibres in the mucosa of the gastrointestinal tract of IBS patients. <ref name="pmid14988823">{{cite journal |vauthors=Barbara G, Stanghellini V, De Giorgio R, Cremon C, Cottrell GS, Santini D, Pasquinelli G, Morselli-Labate AM, Grady EF, Bunnett NW, Collins SM, Corinaldesi R |title=Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome |journal=Gastroenterology |volume=126 |issue=3 |pages=693–702 |year=2004 |pmid=14988823 |doi= |url=}}</ref><ref name="pmid17005763">{{cite journal |vauthors=Guilarte M, Santos J, de Torres I, Alonso C, Vicario M, Ramos L, Martínez C, Casellas F, Saperas E, Malagelada JR |title=Diarrhoea-predominant IBS patients show mast cell activation and hyperplasia in the jejunum |journal=Gut |volume=56 |issue=2 |pages=203–9 |year=2007 |pmid=17005763 |pmc=1856785 |doi=10.1136/gut.2006.100594 |url=}}</ref>
| |
| ** '''Proinflammatory cytokines:'''
| |
| *** Cytokines are proteinaceous mediators of the immune response. Increased levels of cytokines have been found in IBS patients.<ref name="pmid12631663">{{cite journal |vauthors=Gwee KA, Collins SM, Read NW, Rajnakova A, Deng Y, Graham JC, McKendrick MW, Moochhala SM |title=Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome |journal=Gut |volume=52 |issue=4 |pages=523–6 |year=2003 |pmid=12631663 |pmc=1773606 |doi= |url=}}</ref><ref name="pmid19711225">{{cite journal |vauthors=Mearin F, Perelló A, Balboa A, Perona M, Sans M, Salas A, Angulo S, Lloreta J, Benasayag R, García-Gonzalez MA, Pérez-Oliveras M, Coderch J |title=Pathogenic mechanisms of postinfectious functional gastrointestinal disorders: results 3 years after gastroenteritis |journal=Scand. J. Gastroenterol. |volume=44 |issue=10 |pages=1173–85 |year=2009 |pmid=19711225 |doi=10.1080/00365520903171276 |url=}}</ref>
| |
| *** Higher amounts of of tumor necrosis factor are produced by the peripheral blood mononuclear cells of IBS patients.<ref name="pmid16472586">{{cite journal |vauthors=Dinan TG, Quigley EM, Ahmed SM, Scully P, O'Brien S, O'Mahony L, O'Mahony S, Shanahan F, Keeling PW |title=Hypothalamic-pituitary-gut axis dysregulation in irritable bowel syndrome: plasma cytokines as a potential biomarker? |journal=Gastroenterology |volume=130 |issue=2 |pages=304–11 |year=2006 |pmid=16472586 |doi=10.1053/j.gastro.2005.11.033 |url=}}</ref><ref name="pmid17383420">{{cite journal |vauthors=Liebregts T, Adam B, Bredack C, Röth A, Heinzel S, Lester S, Downie-Doyle S, Smith E, Drew P, Talley NJ, Holtmann G |title=Immune activation in patients with irritable bowel syndrome |journal=Gastroenterology |volume=132 |issue=3 |pages=913–20 |year=2007 |pmid=17383420 |doi=10.1053/j.gastro.2007.01.046 |url=}}</ref>
| |
| *** In studies conducted using supernatants from cultured peripheral blood mononuclear cells in IBS patients,the TNF antagonist infliximab has been found to block the mechanical hypersensitivity of the mouse colonic afferent nerve endings. <ref name="pmid25063707">{{cite journal |vauthors=Hughes PA, Moretta M, Lim A, Grasby DJ, Bird D, Brierley SM, Liebregts T, Adam B, Blackshaw LA, Holtmann G, Bampton P, Hoffmann P, Andrews JM, Zola H, Krumbiegel D |title=Immune derived opioidergic inhibition of viscerosensory afferents is decreased in Irritable Bowel Syndrome patients |journal=Brain Behav. Immun. |volume=42 |issue= |pages=191–203 |year=2014 |pmid=25063707 |doi=10.1016/j.bbi.2014.07.001 |url=}}</ref>
| |
| *** Other cytokines such as interleukin 1β, interleukin 6, interleukin 10 and TNFα have been found in increased amounts on analysis of the supernatants from IBS patients with diarrhea, as compared to healthy controls.Increased concentration of these cytokines is directly proportional to the severity and frequency of pain.<ref name="pmid17383420">{{cite journal |vauthors=Liebregts T, Adam B, Bredack C, Röth A, Heinzel S, Lester S, Downie-Doyle S, Smith E, Drew P, Talley NJ, Holtmann G |title=Immune activation in patients with irritable bowel syndrome |journal=Gastroenterology |volume=132 |issue=3 |pages=913–20 |year=2007 |pmid=17383420 |doi=10.1053/j.gastro.2007.01.046 |url=}}</ref><ref name="pmid25063707">{{cite journal |vauthors=Hughes PA, Moretta M, Lim A, Grasby DJ, Bird D, Brierley SM, Liebregts T, Adam B, Blackshaw LA, Holtmann G, Bampton P, Hoffmann P, Andrews JM, Zola H, Krumbiegel D |title=Immune derived opioidergic inhibition of viscerosensory afferents is decreased in Irritable Bowel Syndrome patients |journal=Brain Behav. Immun. |volume=42 |issue= |pages=191–203 |year=2014 |pmid=25063707 |doi=10.1016/j.bbi.2014.07.001 |url=}}</ref><ref name="pmid16472586">{{cite journal |vauthors=Dinan TG, Quigley EM, Ahmed SM, Scully P, O'Brien S, O'Mahony L, O'Mahony S, Shanahan F, Keeling PW |title=Hypothalamic-pituitary-gut axis dysregulation in irritable bowel syndrome: plasma cytokines as a potential biomarker? |journal=Gastroenterology |volume=130 |issue=2 |pages=304–11 |year=2006 |pmid=16472586 |doi=10.1053/j.gastro.2005.11.033 |url=}}</ref>
| |
| ** '''Altered gut microbiota'''
| |
| *** It is postulated that altered fecal microflora may be associated with IBS.<ref name="pmid20117111">{{cite journal |vauthors=Ford AC, Thabane M, Collins SM, Moayyedi P, Garg AX, Clark WF, Marshall JK |title=Prevalence of uninvestigated dyspepsia 8 years after a large waterborne outbreak of bacterial dysentery: a cohort study |journal=Gastroenterology |volume=138 |issue=5 |pages=1727–36; quiz e12 |year=2010 |pmid=20117111 |doi=10.1053/j.gastro.2010.01.043 |url=}}</ref><ref name="pmid20427395">{{cite journal |vauthors=Marshall JK, Thabane M, Garg AX, Clark WF, Moayyedi P, Collins SM |title=Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery |journal=Gut |volume=59 |issue=5 |pages=605–11 |year=2010 |pmid=20427395 |doi=10.1136/gut.2009.202234 |url=}}</ref> There are numerous studies that suggest that altered fecal microflora in IBS patients differ from healthy controls. <ref name="pmid17631127">{{cite journal |vauthors=Kassinen A, Krogius-Kurikka L, Mäkivuokko H, Rinttilä T, Paulin L, Corander J, Malinen E, Apajalahti J, Palva A |title=The fecal microbiota of irritable bowel syndrome patients differs significantly from that of healthy subjects |journal=Gastroenterology |volume=133 |issue=1 |pages=24–33 |year=2007 |pmid=17631127 |doi=10.1053/j.gastro.2007.04.005 |url=}}</ref><ref name="pmid15667495">{{cite journal |vauthors=Malinen E, Rinttilä T, Kajander K, Mättö J, Kassinen A, Krogius L, Saarela M, Korpela R, Palva A |title=Analysis of the fecal microbiota of irritable bowel syndrome patients and healthy controls with real-time PCR |journal=Am. J. Gastroenterol. |volume=100 |issue=2 |pages=373–82 |year=2005 |pmid=15667495 |doi=10.1111/j.1572-0241.2005.40312.x |url=}}</ref><ref name="pmid21820992">{{cite journal |vauthors=Rajilić-Stojanović M, Biagi E, Heilig HG, Kajander K, Kekkonen RA, Tims S, de Vos WM |title=Global and deep molecular analysis of microbiota signatures in fecal samples from patients with irritable bowel syndrome |journal=Gastroenterology |volume=141 |issue=5 |pages=1792–801 |year=2011 |pmid=21820992 |doi=10.1053/j.gastro.2011.07.043 |url=}}</ref><ref name="pmid21741921">{{cite journal |vauthors=Saulnier DM, Riehle K, Mistretta TA, Diaz MA, Mandal D, Raza S, Weidler EM, Qin X, Coarfa C, Milosavljevic A, Petrosino JF, Highlander S, Gibbs R, Lynch SV, Shulman RJ, Versalovic J |title=Gastrointestinal microbiome signatures of pediatric patients with irritable bowel syndrome |journal=Gastroenterology |volume=141 |issue=5 |pages=1782–91 |year=2011 |pmid=21741921 |pmc=3417828 |doi=10.1053/j.gastro.2011.06.072 |url=}}</ref><ref name="pmid22180058">{{cite journal |vauthors=Jeffery IB, O'Toole PW, Öhman L, Claesson MJ, Deane J, Quigley EM, Simrén M |title=An irritable bowel syndrome subtype defined by species-specific alterations in faecal microbiota |journal=Gut |volume=61 |issue=7 |pages=997–1006 |year=2012 |pmid=22180058 |doi=10.1136/gutjnl-2011-301501 |url=}}</ref>
| |
| *** Inoculation of germ free animals with fecal microbiota from IBS patients has demonstrated increased colonic hypersensitivity, as compared to samples inoculated from healthy controls. <ref name="pmid23433203">{{cite journal |vauthors=Crouzet L, Gaultier E, Del'Homme C, Cartier C, Delmas E, Dapoigny M, Fioramonti J, Bernalier-Donadille A |title=The hypersensitivity to colonic distension of IBS patients can be transferred to rats through their fecal microbiota |journal=Neurogastroenterol. Motil. |volume=25 |issue=4 |pages=e272–82 |year=2013 |pmid=23433203 |doi=10.1111/nmo.12103 |url=}}</ref>
| |
| *** Studies have also shown that the fecal microbiota in patients with post infectious IBS differs markedly from healthy controls, with decrease in the diversity of the fecal microbiome, correlated with increased numbers of CD8 and CD4RA-positive intraepithelial lymphocytes. <ref name="pmid25521822">{{cite journal |vauthors=Sundin J, Rangel I, Fuentes S, Heikamp-de Jong I, Hultgren-Hörnquist E, de Vos WM, Brummer RJ |title=Altered faecal and mucosal microbial composition in post-infectious irritable bowel syndrome patients correlates with mucosal lymphocyte phenotypes and psychological distress |journal=Aliment. Pharmacol. Ther. |volume=41 |issue=4 |pages=342–51 |year=2015 |pmid=25521822 |doi=10.1111/apt.13055 |url=}}</ref>
| |
| *** IBS patients who have undergone colonoscopy, with sampling from the colon and terminal ileum have been found to have colonic spirochaetosis with a unique pathology of increased lymphoid follicles and eosinophils as compared to healthy controls.<ref name="pmid25540866">{{cite journal |vauthors=Walker MM, Talley NJ, Inganäs L, Engstrand L, Jones MP, Nyhlin H, Agréus L, Kjellstrom L, Öst Å, Andreasson A |title=Colonic spirochetosis is associated with colonic eosinophilia and irritable bowel syndrome in a general population in Sweden |journal=Hum. Pathol. |volume=46 |issue=2 |pages=277–83 |year=2015 |pmid=25540866 |doi=10.1016/j.humpath.2014.10.026 |url=}}</ref>
| |
| *** IBS with diarrhea is sometimes preceded by acute enteric infections and therefore, benefit from probiotics that serve to alter metabolism and composition of the microflora.<ref name="pmid22315951">{{cite journal |vauthors=Chassard C, Dapoigny M, Scott KP, Crouzet L, Del'homme C, Marquet P, Martin JC, Pickering G, Ardid D, Eschalier A, Dubray C, Flint HJ, Bernalier-Donadille A |title=Functional dysbiosis within the gut microbiota of patients with constipated-irritable bowel syndrome |journal=Aliment. Pharmacol. Ther. |volume=35 |issue=7 |pages=828–38 |year=2012 |pmid=22315951 |doi=10.1111/j.1365-2036.2012.05007.x |url=}}</ref><ref name="pmid18806702">{{cite journal |vauthors=Camilleri M |title=Probiotics and irritable bowel syndrome: rationale, mechanisms, and efficacy |journal=J. Clin. Gastroenterol. |volume=42 Suppl 3 Pt 1 |issue= |pages=S123–5 |year=2008 |pmid=18806702 |doi=10.1097/MCG.0b013e3181574393 |url=}}</ref> Administration of probiotics in patients decreases flatulence relative to Lactobacillus.<ref name="pmid10811333">{{cite journal |vauthors=Nobaek S, Johansson ML, Molin G, Ahrné S, Jeppsson B |title=Alteration of intestinal microflora is associated with reduction in abdominal bloating and pain in patients with irritable bowel syndrome |journal=Am. J. Gastroenterol. |volume=95 |issue=5 |pages=1231–8 |year=2000 |pmid=10811333 |doi=10.1111/j.1572-0241.2000.02015.x |url=}}</ref> A probiotic yogurt containing a mixture of Bacteroides species has been shown to improve symptoms in IBS patients.<ref name="pmid22713265">{{cite journal |vauthors=Maccaferri S, Candela M, Turroni S, Centanni M, Severgnini M, Consolandi C, Cavina P, Brigidi P |title=IBS-associated phylogenetic unbalances of the intestinal microbiota are not reverted by probiotic supplementation |journal=Gut Microbes |volume=3 |issue=5 |pages=406–13 |year=2012 |pmid=22713265 |doi=10.4161/gmic.21009 |url=}}</ref>
| |
| *** Studies have been conducted suggesting that the switching on of a T-helper-2 immune-cell response may cause increased susceptibility to IBS after acute GI infection.<ref name="pmid26071133">{{cite journal |vauthors=Wouters MM, Van Wanrooy S, Nguyen A, Dooley J, Aguilera-Lizarraga J, Van Brabant W, Garcia-Perez JE, Van Oudenhove L, Van Ranst M, Verhaegen J, Liston A, Boeckxstaens G |title=Psychological comorbidity increases the risk for postinfectious IBS partly by enhanced susceptibility to develop infectious gastroenteritis |journal=Gut |volume=65 |issue=8 |pages=1279–88 |year=2016 |pmid=26071133 |doi=10.1136/gutjnl-2015-309460 |url=}}</ref><ref name="pmid26729548">{{cite journal |vauthors=Riddle MS, Welsh M, Porter CK, Nieh C, Boyko EJ, Gackstetter G, Hooper TI |title=The Epidemiology of Irritable Bowel Syndrome in the US Military: Findings from the Millennium Cohort Study |journal=Am. J. Gastroenterol. |volume=111 |issue=1 |pages=93–104 |year=2016 |pmid=26729548 |pmc=4759150 |doi=10.1038/ajg.2015.386 |url=}}</ref>
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| *** Abnormal serotonin pathways
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| *** Neuroimmune factors
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| *** Genetic factors- Mutations in SCN5A encode alpha subunit of voltage gated sodium channel NaV1.5
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| *** Bile acid malabsorption- causes alteration of the function of an apical ileal bile acid transporter
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| ==Genetics==
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| **
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| ==Genetics==
| |
| *[Disease name] is transmitted in [mode of genetic transmission] pattern.
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| *Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
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| *The development of [disease name] is the result of multiple genetic mutations.
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| ==Associated Conditions==
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| ==Gross Pathology==
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| *On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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| ==Microscopic Pathology==
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| *On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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| ==References== | | ==References== |
| {{Reflist|2}} | | {{reflist|2}} |
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| {{WH}} | | {{WH}} |
| {{WS}} | | {{WS}} |
| [[Category: (name of the system)]]
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| | ===Pathophysiology prev=== |
| <div style="-webkit-user-select: none;"> | | <div style="-webkit-user-select: none;"> |
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| | {{#ev:youtube|https://https://www.youtube.com/watch?v=9f5wxYW0Z3k|350}} | | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
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| | __NOTOC__ |
| | {{Cirrhosis}} |
| | {{CMG}} {{AE}} |
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| | ==Video codes== |
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| | ===Normal video=== |
| | {{#ev:youtube|x6e9Pk6inYI}} |
| | {{#ev:youtube|4uSSvD1BAHg}} |
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| | ===Video in table=== |
| | <div style="width:350px">{{#ev:youtube|5ucSlgqGAno}}</div> |
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| Initially, IBS was considered a psychosomatic illness, and the involvement of biological and pathogenic factors was not verified until the 1990s, a process common in the [[history of emerging infectious diseases]]. The risk of developing IBS increases six-fold after acute gastrointestinal infection. Post-infection, further risk factors are young age, prolonged [[fever]], [[anxiety]] and [[depression]].<ref>{{cite journal | author = Thabane M, Kottachchi DT, Marshall JK | title = The incidence and prognosis of post-infectious irritable bowel syndrome. | journal = Aliment Pharmacol Ther | volume = 26 | issue = 4 | pages = 535-44 | year = 2007 | pmid = 17661757}}</ref>
| | ===Floating video=== |
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| ===Psychosomatic illness===
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| One of the first references to the concept of an "Irritable Bowel" appeared in the Rocky Mountain Medical Journal in 1950.<ref name="BROWN_1950">{{cite journal |author=BROWN PW |title=The irritable bowel syndrome |journal=Rocky Mountain medical journal|volume=47 |issue=5 |pages=343-6 |year=1950 |pmid=15418074 |doi=}}</ref> The term was used to categorize patients who developed symptoms of diarrhea, abdominal pain, [[constipation]], but where no well-recognized infective cause could be found. Early theories suggested that the Irritable Bowel was caused by a [[Somatoform disorder|somatic]], or mental disorder. One paper from the 1980s investigated "learned illness behavior" in patients with IBS and [[peptic ulcers]].<ref name="WHITEHEAD_1982">{{cite journal |author=Whitehead WE, Winget C, Fedoravicius AS, Wooley S, Blackwell B|title=Learned illness behavior in patients with irritable bowel syndrome and peptic ulcer |journal=Dig. Dis. Sci. |volume=27|issue=3 |pages=202-8 |year=1982 |pmid=7075418 |doi=}}</ref> Another study suggested that both IBS and stomach ulcer patients would benefit from 15 months of [[psychotherapy]].<ref name="pmid3895386">{{cite journal |author=Svedlund J, Sjödin I |title=A psychosomatic approach to treatment in the irritable bowel syndrome and peptic ulcer disease with aspects of the design of clinical trials |journal=Scand. J. Gastroenterol. Suppl. |volume=109 |issue= |pages=147-51 |year=1985 |pmid=3895386 |doi=}}</ref> Later, it was found that most stomach ulcers were caused by a bacterial infection with ''[[Helicobacter pylori]].''<ref name="pmid9191460">{{cite journal |author=Damianos AJ, McGarrity TJ |title=Treatment strategies for Helicobacter pylori infection|journal=American family physician |volume=55 |issue=8 |pages=2765–74, 2784–6 |year=1997 |pmid=9191460 |doi=}}</ref>
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| Additional publications suggesting the role of brain-gut "axis" appeared in the 1990s, such as a study entitled ''Brain-gut response to stress and cholinergic stimulation in IBS'' published in the ''Journal of Clinical Gastrotnerology'' in 1993.<ref>{{cite journal|author=Fukudo S, Nomura T, Muranaka M, Taguchi F |title=Brain-gut response to stress and cholinergic stimulation in irritable bowel syndrome. A preliminary study |journal=J. Clin. Gastroenterol. |volume=17 |issue=2 |pages=133-41 |year=1993 |pmid=8031340|doi=}}</ref> A 1997 study published in ''Gut'' magazine suggested that IBS was associated with a "derailing of the brain-gut axis."<ref>{{cite journal |author=Orr WC, Crowell MD, Lin B, Harnish MJ, Chen JD |title=Sleep and gastric function in irritable bowel syndrome: derailing the brain-gut axis |journal=Gut |volume=41 |issue=3 |pages=390-3 |year=1997 |pmid=9378397 |doi=}}</ref>
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| {{"
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| |There was a greater improvement in the psychotherapy groups for patients with IBS after three months and for both IBS and PUD (peptic ulcer disease) patients after 15 months. The difference had become more pronounced after 15 months, with the patients given psychotherapy showing further improvement, and the patients who had received medical treatment only showing some deterioration.
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| |by J Svedlund, ''A psychosomatic approach to treatment in the irritable bowel syndrome and peptic ulcer disease with aspects of the design of clinical trials'', 1985.
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| }}
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| ''Most peptic ulcers are now treated with 1-2 weeks of antibiotic therapy, since it has been discovered that they are caused by a combination of a genetic trait in the patient and infection with the bacteria [[H. Pylori]].''<ref name="EL-OMAR_2000">{{cite journal |author=El-Omar EM, Carrington M, Chow WH, ''et al'' |title=Interleukin-1 polymorphisms associated with increased risk of gastric cancer |journal=Nature |volume=404 |issue=6776 |pages=398-402 |year=2000 |pmid=10746728 |doi=10.1038/35006081}} </ref>
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| </div>
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| ===Immune reaction===
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| From the late 1990s, research publications began identifying specific biochemical changes present in tissue biopsies and serum samples from IBS patients that suggested symptoms had an organic rather than [[psychosomatic]] cause. These studies identified [[cytokine]]s and secretory products in tissues taken from IBS patients. The cytokines identified in IBS patients produce [[inflammation]] and are associated with the body's [[Immunity (medical)|immune]] response.
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| * A study showed that intestinal [[biopsies]] from patients with constipation predominant IBS secreted higher levels of [[serotonin]] in-vitro.<ref>{{cite journal |author=Miwa J, Echizen H, Matsueda K, Umeda N |title=Patients with constipation-predominant irritable bowel syndrome (IBS) may have elevated serotonin concentrations in colonic mucosa as compared with diarrhea-predominant patients and subjects with normal bowel habits |journal=Digestion |volume=63 |issue=3 |pages=188-94|year=2001 |pmid=11351146 |doi=}}</ref> [[Serotonin]] plays a role in regulating gastrointestinal motility and water content and can be altered by some diseases and infections.<ref name="MCGOWAN_1983">{{cite journal |author=McGowan K, Kane A, Asarkof N, ''et al'' |title=Entamoeba histolytica causes intestinal secretion: role of serotonin |journal=Science |volume=221 |issue=4612|pages=762-4 |year=1983 |pmid=6308760 |doi=}} </ref><ref name="MCGOWAN_1985">{{cite journal |author=McGowan K, Guerina V, Wicks J, Donowitz M |title=Secretory hormones of Entamoeba histolytica |journal=Ciba Found. Symp. |volume=112 |issue= |pages=139-54|year=1985 |pmid=2861068 |doi=}} </ref><ref>{{cite journal |author=Banu, Naheed, et al. |title=Neurohumoral alterations and their role in amoebiasis. |journal=Indian J. Clin Biochem |volume=20 |issue=2 |pages=142-5 |year=2005|url=http://medind.nic.in/iaf/t05/i2/iaft05i2p142.pdf}}</ref>
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| * A study of rectal biopsy tissue from IBS patients showed increased levels of cellular structures involved in the production of the cytokine [[Interleukin 1]] Beta.<ref>{{cite journal |author=Gwee KA, Collins SM, Read NW, ''et al'' |title=Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome |journal=Gut |volume=52 |issue=4|pages=523-6 |year=2003 |pmid=12631663 |doi=}}</ref>
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| * A study of blood samples from IBS patients identified elevated levels of cytokines [[Tumor necrosis factor-alpha]], [[Interleukin 1]], and [[Interleukin 6]] in patients with IBS.<ref name="pmid17383420">{{cite journal |author=Liebregts T, Adam B, Bredack C, ''et al'' |title=Immune activation in patients with irritable bowel syndrome |journal=Gastroenterology |volume=132 |issue=3 |pages=913-20|year=2007 |pmid=17383420 |doi=10.1053/j.gastro.2007.01.046}}</ref>
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| * A study of intestinal biopsies from IBS patients showed increased levels of [[protease]] enzymes used by the body to digest proteins, and by infectious agents to combat the host's [[immune system]].<ref>{{cite journal |author=Cenac N, Andrews CN, Holzhausen M, ''et al'' |title=Role for protease activity in visceral pain in irritable bowel syndrome |journal=J. Clin. Invest.|volume=117 |issue=3 |pages=636-47 |year=2007 |pmid=17304351 |doi=10.1172/JCI29255}}</ref>
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| * A study of blood samples from IBS patients found elevated levels of [[antibodies]] to the [[protozoan]] ''[[Blastocystis]]''.<ref name="HUSSAIN_1997">{{cite journal |author=Hussain R, Jaferi W, Zuberi S, ''et al'' |title=Significantly increased IgG2 subclass antibody levels to Blastocystis hominis in patients with irritable bowel syndrome |journal=Am. J. Trop. Med. Hyg. |volume=56|issue=3 |pages=301-6 |year=1997 |pmid=9129532 |doi=}}</ref>
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| Specific forms of immune response that have been implicated in IBS symptoms include [[coeliac disease]] and other [[food allergy]] conditions.<ref name="Wangen_2006">Wangen, Dr. Stephen. ''The Irritable Bowel Syndrome Solution''. 2006. ISBN 0976853787. Excerpted with author's permission at [http://www.IBSTreatmentCenter.com/]</ref> [[Coeliac disease]] (also spelled "celiac") is an immunoglobulin type A-(IgA) mediated allergic response to the [[gliadin]] protein in gluten grains,which exhibits wide variety of symptoms and can present as IBS. "Some patients with diarrhea-predominant irritable bowel syndrome (IBS-D) may have undiagnosed celiac sprue (CS). Because the symptoms of CS respond to a gluten-free diet, testing for CS in IBS may prevent years of morbidity and attendant expense."<ref>{{cite journal |author=Spiegel BM, ''et al'' |title=Testing for celiac sprue in irritable bowel syndrome with predominant diarrhea: a cost-effectiveness analysis. |journal=Gastroenterology |volume=126 |issue=7 |pages=1721-32 |year=2004|pmid=15188167 |doi=}}</ref> "Coeliac disease is a common finding among patients labelled as having irritable bowel syndrome. In this sub-group, a gluten free diet may lead to a significant improvement in symptoms. Routine testing for coeliac disease may be indicated in all patients being evaluated for irritable bowel syndrome."<ref>{{cite journal |author=Shahbazkhani B, ''et al''|title=Coeliac disease presenting with symptoms of irritable bowel syndrome. |journal=Aliment Pharmacol Therapy |volume=18 |issue=2|pages=231-5 |year=2003 |pmid=12869084 |doi=}}</ref> Food allergies, particularly those mediated by IgE and IgG-type antibodies have been implicated in IBS.<ref>{{cite journal |author=Li H, ''et al'' |title=Allergen-IgE complexes trigger CD23-dependent CCL20 release from human intestinal epithelial cells. |journal=Gastroenterology |volume=133 |issue=6 |pages=1905-15 |year=2007|pmid=18054562 |doi=}}</ref><ref>{{cite journal |Yang CM, Li YQ |title=The therapeutic effects of eliminating allergic foods according to food-specific IgG antibodies in irritable bowel syndrome - Article in Chinese |journal=Zhonghua Nei Ke Za Zhi.|volume=46 |issue=8 |pages=641-3 |year=2007 |pmid=17967233 |doi=}}</ref><ref>{{cite journal |author=Drisko ''et al'' |title=Treating Irritable Bowel Syndrome with a Food Elimination Diet Followed by Food Challenge and Probiotics |journal=Journal of the American College of Nutrition |volume=25 |issue=6 |pages=514-22 |year=2006 |pmid=17229899 |doi=}}</ref>
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| ===Active infections===
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| <div class="noprint" style="clear: center; border: solid #aaa 1px; margin: 0 0 1em 1em; background: #efeff9; width: 50%; padding: 4px; text-align: left; float: right;">
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| {{"
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| |Clearly this study highlights a new concept in the potential pathogenesis of IBS. An infectious cause may offer a tremendous opportunity to manage an otherwise frustrating disease -- both for patients and their treating physician.
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| |by Dr. David A. Johnson, President of the [[American College of Gastroenterology]] , commenting on results from study of Rifaximin in treatment of IBS<ref>{{cite journal |author=Johnson, David. |title=Viewpoints: Efficacy of Rifaximin vs Placebo in Reducing Symptoms in Adults With IBS. |journal=Medscape Gastroenterology |volume=8 |issue=2 |year=2006|url=http://www.medscape.com/viewarticle/547055}}</ref>
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| }}
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| </div>
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| There is research to support IBS being caused by an as-yet undiscovered active infection. Most recently, a study has found that the antibiotic [[Rifaximin]] provides sustained relief for IBS patients.<ref name="pmid17043337">{{cite journal |author=Pimentel M, Park S, Mirocha J, Kane SV, Kong Y |title=The effect of a nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome: a randomized trial |journal=Ann. Intern. Med. |volume=145 |issue=8 |pages=557-63 |year=2006 |pmid=17043337 |doi=}}</ref> While some researchers see this as evidence that IBS is related to an undiscovered agent, others believe IBS patients suffer from overgrowth of [[Gut flora|intestinal flora]] and the antibiotics are effective in reducing the overgrowth (known as ''[[Small bowel bacterial overgrowth syndrome|small intestinal bacterial overgrowth]]'').<ref name="pmid17148502">{{cite journal |author=Posserud I, Stotzer PO, Björnsson ES, Abrahamsson H, Simrén M |title=Small intestinal bacterial overgrowth in patients with irritable bowel syndrome |journal=Gut |volume=56 |issue=6 |pages=802-8 |year=2007 |pmid=17148502 |doi=10.1136/gut.2006.108712}}</ref> Other researchers have focused on an unrecognized [[protozoa]]l infection as a cause of IBS<ref name="STARK_2007">{{cite journal|author=Stark D, van Hal S, Marriott D, Ellis J, Harkness J |title=Irritable bowel syndrome: a review on the role of intestinal protozoa and the importance of their detection and diagnosis |journal=Int. J. Parasitol. |volume=37 |issue=1 |pages=11-20 |year=2007|pmid=17070814 |doi=10.1016/j.ijpara.2006.09.009}}</ref> as certain protozoal infections occur more frequently in IBS patients.<ref name="YAKOOB_2004">{{cite journal |author=Yakoob J, Jafri W, Jafri N, ''et al'' |title=Irritable bowel syndrome: in search of an etiology: role of Blastocystis hominis |journal=Am. J. Trop. Med. Hyg. |volume=70 |issue=4 |pages=383-5 |year=2004 |pmid=15100450|doi=}}</ref><ref name="GIACOM_1999">{{cite journal |author=Giacometti A, Cirioni O, Fiorentini A, Fortuna M, Scalise G|title=Irritable bowel syndrome in patients with Blastocystis hominis infection |journal=Eur. J. Clin. Microbiol. Infect. Dis.|volume=18 |issue=6 |pages=436-9 |year=1999 |pmid=10442423 |doi=}}</ref> Two of the protozoa investigated have a high prevalence in industrialized countries and infect the bowel, but little is known about them as they are recently emerged pathogens.
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| ''[[Blastocystis]]'' is a single-celled organism which has been reported to produce symptoms of abdominal pain, constipation and diarrhea in patients, along with headaches and depression,<ref name="QADRI_1989">{{cite journal |author=Qadri SM, al-Okaili GA, al-Dayel F |title=Clinical significance of Blastocystis hominis |journal=J. Clin. Microbiol. |volume=27 |issue=11 |pages=2407-9|year=1989 |pmid=2808664 |doi=}}</ref> though these reports are contested by some physicians.<ref name="MARKELL_1986">{{cite journal|author=Markell EK, Udkow MP |title=Blastocystis hominis: pathogen or fellow traveler? |journal=Am. J. Trop. Med. Hyg. |volume=35|issue=5 |pages=1023-6 |year=1986 |pmid=3766850 |doi=}}</ref> Studies from research hospitals in various countries have identified high [[Blastocystis]] infection rates in IBS patients, with 38% being reported from [[London School of Hygiene & Tropical Medicine]],<ref name="WINDSOR_2007">{{cite journal |author=Windsor J |title=B. hominis and D. fragilis: Neglected human protozoa|journal=British Biomedical Scientist |pages=524-7 |year=2007 |pmid= |doi= |url=http://www.ibms.org/index.cfm?method=publications.biomedical_scientist&subpage=contents_2007_July}}</ref> 47% reported from the Department of Gastroenterology at [[Aga Khan University]] in Pakistan<ref name="YAKOOB_2004" /> and 18.1% reported from the Institute of Diseases and Public Health at [[University of Ancona]] in Italy.<ref name="GIACOM_1999" /> Reports from all three groups indicate a [[Blastocystis]] prevalence of approximately 7% in non-IBS patients. Researchers have noted that clinical diagnostics fail to identify infection,<ref name="STENSVOLD_2006">{{cite journal |author=Stensvold R, Brillowska-Dabrowska A, Nielsen HV, Arendrup MC |title=Detection of Blastocystis hominis in unpreserved stool specimens by using polymerase chain reaction |journal=J. Parasitol. |volume=92 |issue=5|pages=1081-7 |year=2006 |pmid=17152954 |doi=}}</ref> and ''Blastocystis'' may not respond to treatment with common antiprotozoals.<ref name="pmid15250669">{{cite journal |author=Yakoob J, Jafri W, Jafri N, Islam M, Asim Beg M |title=In vitro susceptibility of Blastocystis hominis isolated from patients with irritable bowel syndrome |journal=Br. J. Biomed. Sci. |volume=61|issue=2 |pages=75-7 |year=2004 |pmid=15250669 |doi=}}</ref><ref name="pmid10357863">{{cite journal |author=Haresh K, Suresh K, Khairul Anus A, Saminathan S |title=Isolate resistance of Blastocystis hominis to metronidazole |journal=Trop. Med. Int. Health|volume=4 |issue=4 |pages=274-7 |year=1999 |pmid=10357863 |doi=}}</ref><ref name="pmid3766850">{{cite journal |author=Markell EK, Udkow MP |title=Blastocystis hominis: pathogen or fellow traveler? |journal=Am. J. Trop. Med. Hyg. |volume=35 |issue=5 |pages=1023-6|year=1986 |pmid=3766850 |doi=}}</ref><ref name="pmid10566723">{{cite journal |author=Ok UZ, Girginkardeşler N, Balcioğlu C, Ertan P, Pirildar T, Kilimcioğlu AA |title=Effect of trimethoprim-sulfamethaxazole in Blastocystis hominis infection |journal=Am. J. Gastroenterol. |volume=94 |issue=11 |pages=3245-7 |year=1999 |pmid=10566723 |doi=}}</ref>
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| [[Image:Wiki ibs cause figures.jpg|thumb|800px|center|Prevalence of protozoal infections in industrialized countries (United States and Canada) in 21st century.<ref name="CMAJ_2006" /><ref name="pmid12224595">{{cite journal |author=Amin OM |title=Seasonal prevalence of intestinal parasites in the United States during 2000 |journal=Am. J. Trop. Med. Hyg. |volume=66 |issue=6|pages=799-803 |year=2002 |pmid=12224595 |doi=}}</ref>]]
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| ''[[Dientamoeba fragilis]]'' is a single-celled organism which produces abdominal pain and diarrhea. Studies have reported a high incidence of infection in developed countries, and symptoms of patients resolve following antibiotic treatment.<ref name="CMAJ_2006">{{cite journal |author=Lagacé-Wiens PR, VanCaeseele PG, Koschik C |title=Dientamoeba fragilis: an emerging role in intestinal disease |journal=CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne|volume=175 |issue=5 |pages=468-9 |year=2006 |pmid=16940260 |doi=10.1503/cmaj.060265}}</ref><ref name="STENSVOLD_2007f">{{cite journal |author=Stensvold CR, Arendrup MC, Mølbak K, Nielsen HV |title=The prevalence of Dientamoeba fragilis in patients with suspected enteroparasitic disease in a metropolitan area in Denmark |journal=Clin. Microbiol. Infect. |volume=13 |issue=8|pages=839-42 |year=2007 |pmid=17610603 |doi=10.1111/j.1469-0691.2007.01760.x}}</ref> One study reported on a large group of patients with IBS-like symptoms who were found to be infected with ''Dientamoeba fragilis'' and experienced resolution of symptoms following treatment.<ref name="BORODY_2002">{{cite journal |author=Borody T, Warren E, Wettstein A, et al. | title = Eradication of Dientamoeba fragilis can resolve IBS-like symptoms. | journal=J Gastroenterol Hepatol | year= 2002 | volume=17 | issue=Suppl; pages=A103}}</ref> Researchers have noted that methods used clinically may fail to detect some ''[[Dientamoeba fragilis]]'' infections.<ref name="STENSVOLD_2007f" />
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| ==Pathophysiology==
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| ===Pathogenesis===
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| *The exact pathogenesis of [disease name] is not fully understood.
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| OR
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| *It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
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| *[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
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| *Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
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| *[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
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| *The progression to [disease name] usually involves the [molecular pathway].
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| *The pathophysiology of [disease/malignancy] depends on the histological subtype.
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| __NOTOC__
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| {{CMG}}; {{AE}} {{Cherry}}
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| ==Overview==
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| ==Pathophysiology== | | ===Redirect=== |
| | #REDIRECT[[Esophageal web]] |
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| ==Diagnosis== | | ===synonym website=== |
| IBS is a [[diagnosis]] of <ref name="urlapi.isoa.org">{{cite web |url=https://api.isoa.org/docs/plans/2018/ISO-J_Exchange_Visitors_Plan_2017_2018.pdf |title=api.isoa.org |format= |work= |accessdate=}}</ref>
| | https://mq.b2i.sg/snow-owl/#!terminology/snomed/10743008 |
| <ref name="pmid17483191">{{cite journal |vauthors=Dorn SD, Palsson OS, Thiwan SI, Kanazawa M, Clark WC, van Tilburg MA, Drossman DA, Scarlett Y, Levy RL, Ringel Y, Crowell MD, Olden KW, Whitehead WE |title=Increased colonic pain sensitivity in irritable bowel syndrome is the result of an increased tendency to report pain rather than increased neurosensory sensitivity |journal=Gut |volume=56 |issue=9 |pages=1202–9 |year=2007 |pmid=17483191 |pmc=1954968 |doi=10.1136/gut.2006.117390 |url=}}</ref>
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| Visceral hypersensitivity may have been utilized as a clinical marker of IBS and could be represented by signs and symptoms of urgency for bowel movements, bloating and abdominal pain. The mechanisms that result in persistent visceral hypersensitivity in patients who have IBS are unclear. nonetheless, various working models might be considered
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| | ===Image=== |
| | [[Image: Normal versus Abnormal Barium study of esophagus.jpg|thumb|left|200px|Normal versus Abnormal Barium study of esophagus with varices]] |
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| | ===Image to the right=== |
| {{Xyz}} | | {| style="float: right; width: 350px;" |
| '''For patient information, click [[Xyz (patient information)|here]]'''
| | | [[Image:Coxiella burnetii.JPG|right|400px|C. burnetii, the Q fever causing agent]] |
| | |} |
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| {{CMG}}; {{AE}}
| | ===Image and text to the right=== |
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| {{SK}}
| | <figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline>[[File:Global distribution of leptospirosis.jpg|577x577px]]</figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> Recent out break of leptospirosis is reported in Bronx, New York and found 3 cases in the months January and February, 2017. |
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| ==[[Xyz overview|Overview]]== | | ===Gallery=== |
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| ==[[Xyz historical perspective|Historical Perspective]]== | | <gallery widths="250px"> |
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| ==[[Xyz classification|Classification]]==
| | Pancreatic insulinoma histology 2.JPG|Histopathology of a pancreatic endocrine tumor (insulinoma). ''Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas''<ref name=aaa> Neuroendocrine tumor of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas</ref> |
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| ==[[Xyz pathophysiology|Pathophysiology]]==
| | Pancreatic insulinoma histopathology 3.JPG|Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. ''Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas''<ref name=aaa> Neuroendocrine tumour of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas</ref> |
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| ==[[Xyz causes|Causes]]==
| | Pancreatic insulinoma histology 4.JPG|Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. ''Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas''<ref name=aaa> Neuroendocrine tumour of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas</ref> |
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| ==[[Xyz differential diagnosis|Differentiating Xyz from other Diseases]]== | | </gallery> |
| | ==References== |
| | {{Reflist|2}} |
| | {{WS}} |
| | {{WH}} |
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| ==[[Xyz epidemiology and demographics|Epidemiology and Demographics]]==
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| ==[[Xyz risk factors|Risk Factors]]==
| | REFERENCES |
| | | <references /> |
| ==[[Xyz screening|Screening]]==
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| ==[[Xyz natural history, complications and prognosis|Natural History, Complications, and Prognosis]]==
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| ==Diagnosis==
| | [[Category:Gastroenterology]] |
| [[Xyz history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]] | [[Xyz other imaging findings|Other Imaging Findings]] | | [[Category:Needs overview]] |
| | | [[Category:Hepatology]] |
| ==Treatment==
| | [[Category:Disease]] |
| [[Xyz medical therapy|Medical Therapy]] | [[Xyz surgery|Surgery]] | [[Xyz primary prevention|Primary Prevention]] | [[Xyz secondary prevention|Secondary Prevention]] | [[Xyz cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]] | |
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| ==Case Studies==
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| [[Xyz case study one|Case #1]] | |
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| [[Category: (name of the system)]] | |
| <references />
| |
</figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> Recent out break of leptospirosis is reported in Bronx, New York and found 3 cases in the months January and February, 2017.
![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/2/2f/Pancreatic_insulinoma_histology_2.JPG)
Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]![Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/a/a3/Pancreatic_insulinoma_histopathology_3.JPG)
Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]![Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/d/d5/Pancreatic_insulinoma_histology_4.JPG)
Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histology_2.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histopathology_3.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histology_4.JPG)