A Study of Intestinal Permeability in Relation to the Inflammatory Response and Plasma Endocab IgM Levels in Patients with Acute Pancreatitis

Penalva, J C; Martínez, Juan; Laveda, R; Esteban, Ángel; Muñoz, Carlos; Sáez, J.; Such, José; Navarro, Salvador; Feu, Faust; Sánchez‐Paya, José; Pérez‐Mateo, Miguel

doi:10.1097/01.mcg.0000129060.46654.e0

Cited by 48 publications

(47 citation statements)

References 41 publications

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“…17,25,29 Those clinical situations are clearly more severe than the mild biochemical cholestasis in our patients, who also had a less prominent increase in L/M ratio.…”

Section: Discussionmentioning

confidence: 89%

“…This test is considered a reproducible, reliable, and well-established noninvasive method for assessing intestinal passive permeability, and it has been used extensively to evaluate mucosal integrity in several disease states and in healthy individuals. 13,[15][16][17]25 Sucrose was added to the lactulose/ mannitol solution as a permeability probe for absorption through the stomach and proximal duodenum. [27][28][29][30][31][32][33] Permeability tests were carried out starting at 08:00 to 09:00 AM.…”

Section: Methodsmentioning

confidence: 99%

“…An increased intestinal permeability has been observed in patients with enteric damage, such as in inflammatory bowel disease and coeliac disease, in intestinal infections, during the intake of aspirin, nonsteroidal anti-inflammatory drugs, or alcohol, in malnourished individuals, after burns, during total parenteral nutrition, in critically ill patients, and also in various extraintestinal diseases. [5][6][7][8][9][10][11][12][13][14][15][16][17] These conditions determine a "leaky gut syndrome" with increased portal uptake of inflammatory mediators, bacteria, antigens, and toxins, enhancing the systemic distribution of potentially injurious macromolecules.…”

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confidence: 99%

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Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?†‡§

et al. 2006

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I ntrahepatic cholestasis of pregnancy (ICP) is a rare disorder of unknown cause that may develop during the third or second trimester of pregnancy and resolves rapidly after delivery. The chief complaint is pruritus, and serum liver tests reveal a mild cholestasis with increased levels of bile salts and aminotransferases. ICP may cause fetal distress, with stillbirths or premature deliveries leading to increased perinatal morbidity and mortality. 1,2 The pathogenesis of ICP appears to be multifactorial. Potential contributors include a genetic predisposition interacting with the effects of estrogen and progesterone metabolites on bile secretory mechanisms. 3 The influence of environmental factors has been suggested by the observation of a seasonal variability in the incidence of ICP, with highest rates reported during winter, a recurrence rate of only 45% to 70% in subsequent pregnancies of multiparous women, and the decrease in the prevalence of ICP detected in Sweden and Chile during recent decades. 4 Therefore, identifying factors that may explain these epidemiological changes appear to be important.The gastrointestinal mucosal epithelium is an essential barrier that normally restricts the passage of harmful molecules into the mucosa and systemic circulation. An increased intestinal permeability has been observed in patients with enteric damage, such as in inflammatory From the

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“…17,25,29 Those clinical situations are clearly more severe than the mild biochemical cholestasis in our patients, who also had a less prominent increase in L/M ratio.…”

Section: Discussionmentioning

confidence: 89%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?†‡§

et al. 2006

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“…This process, termed microbial translocation, has been observed in numerous diseases, including ulcerative colitis and Crohn's disease, 94 graft-versus-host disease, 95 and hepatitis 96 as well as after abdominal surgeries 97 and in pancreatitis. 98 Importantly, in many of these situations the microbial translocation is associated not only with local inflammation of the gut microenvironment but also with systemic immune activation. 99 In light of these findings, we recently investigated whether microbial translocation occurs in HIV infection and, if so, whether it is associated with chronic systemic immune activation.…”

Section: Enteropathy Revisitedmentioning

confidence: 99%

HIV infection and the gastrointestinal immune system

2008

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There has recently been a resurgence of interest in the gastrointestinal pathology observed in patients infected with HIV. The gastrointestinal tract is a major site of HIV replication, which results in massive depletion of lamina propria CD4 T cells during acute infection. Highly active antiretroviral therapy leads to incomplete suppression of viral replication and substantially delayed and only partial restoration of gastrointestinal CD4 T cells. The gastrointestinal pathology associated with HIV infection comprises significant enteropathy with increased levels of inflammation and decreased levels of mucosal repair and regeneration. Assessment of gut mucosal immune system has provided novel directions for therapeutic interventions that modify the consequences of acute HIV infection.The mucosal surface of the gastrointestinal (GI) tract forms a unique anatomical and physiological niche, serving as a predominant structural and immunological barrier against the microorganisms of the outside world. In addition, the tightly apposed enterocytes that form the single cell layer of the mucosal epithelium also absorb water and nutrients during the digestive process, which is critical to host survival. Hence, loss of the integrity of the mucosal surface results in multiple deleterious sequelae.

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“…Electron-microscopically manifested exuviation in microvillus of the intestinal mucosa, significantly reduced height, width and area of microvillus, damaged cell tight junction (Wu and Li, 1999;Yang and Gao, 2005), and increased apoptotic cells and other pathologic alternations. Therefore, it will lead to an increase of intestinal permeability (IP) (Wu and Li, 1999;Yang and Gao, 2005;Takahashi et al, 2005;Ammori et al, 2003;Penalva et al, 2004), causing translocation of bacteria and endotoxin, activation of endothelial cells, release of inflammatory mediators and cytokines, and initiation of SIRS (systemic inflammatory response syndrome) and MODS (Mole et al, 2005;Closa and Folch-Puy, 2004). Meanwhile, the process will further increase intestinal permeability and promote continuous invasion of intestinal bacteria and endotoxin into body to form an infernal circle.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

Zhang

Song

et al. 2007

J. Zhejiang Univ. - Sci. B

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Acute pancreatitis (AP) is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition.AP can cause an injury of intestinal mucosa barrier, leading to translocation of bacteria or endotoxin through multiple routes, bacterial translocation (BT), gutorigin endotoxaemia, and secondary infection of pancreatic tissue, and then cause systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), which are important factors influencing AP's severity and mortality. Meanwhile, the injury of intestinal mucosa barrier plays a key role in AP's process. Therefore, it is clinically important to study the relationship between the injury of intestinal mucosa barrier and AP. In addition, many factors such as microcirculation disturbance, ischemical reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier. In this review, we summarize studies on mechanisms of AP.

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A Study of Intestinal Permeability in Relation to the Inflammatory Response and Plasma Endocab IgM Levels in Patients with Acute Pancreatitis

Abstract: Patients with AP show an increased IP when compared with controls, being more relevant and persistent in severe cases. This seems related to an increase of endotoxemia late in the course of the disease, but not with an exacerbation of the systemic immune response.

Cited by 48 publications

References 41 publications

Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?†‡§

Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?†‡§

HIV infection and the gastrointestinal immune system

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

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