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Chua, Gerald Seng Wee; Lee, Kang-Hoe

doi:10.1186/cc2889

Cited by 46 publications

(9 citation statements)

References 11 publications

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“…An understanding of the intimate relationships of the innate immune system, cytokines, pathogen-associated molecular pattern compounds, glucocorticoids, and B-type natriuretic peptides may serve in the future as a clinically useful paradigm to alert physicians to the possibility of impeding fulminating septic shock. [46][47][48][49]…”

Section: Discussionmentioning

confidence: 99%

Pathophysiology of Mifepristone-Induced Septic Shock Due to Clostridium sordellii

Miech

2005

Ann Pharmacother

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OBJECTIVE: To explain the role of mifepristone in medical abortions that results in fulminant and lethal septic shock due to Clostridium sordellii. DATA SOURCES: MEDLINE, PubMed, and Google Scholar databases were searched (1984–March 2005%). Key search terms were mifepristone, RU38486, RU486, Mifeprex, medical abortion, septic shock, innate immune system, cytokines, and Clostridium sordellii. STUDY SELECTION AND DATA EXTRACTION: All articles identified from the data sources were evaluated and all information deemed relevant was included for the information related to the development of the understanding of the pathophysiology of mifepristone-induced septic shock due to C. sordellii. DATA SYNTHESIS: The mechanisms of action of mifepristone were incorporated into the pathophysiology of septic shock due to C. sordellii. Mifepristone, by blocking both progesterone and glucocorticoid receptors, interferes with the controlled release and functioning of cortisol and cytokines. Failure of physiologically controlled cortisol and cytokine responses results in an impaired innate immune system that results in disintegration of the body's defense system necessary to prevent the endometrial spread of C. sordellii infection. The abnormal cortisol and cytokine responses due to mifepristone coupled to the release of potent exotoxins and an endotoxin from C. sordellii are the major contributors to the rapid development of lethal septic shock. CONCLUSIONS: Theoretically, it appears that the mechanisms of mifepristone action favor the development of infection that leads to septic shock and intensifies the actions of multiple inflammatory cytokines, resulting in fulminant, lethal septic shock.

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Section: Discussionmentioning

confidence: 99%

Pathophysiology of Mifepristone-Induced Septic Shock Due to Clostridium sordellii

Miech

2005

Ann Pharmacother

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“…It is produced in the prohormone form, and before secretion is split into the inactive NT-proBNP and the active BNP [ 36 ]. Numerous studies demonstrated markedly elevated plasma levels of BNP and NT-proBNP in septic patients [ 37 , 38 ], and the increased plasma BNP and NT-proBNP concentrations were associated with myocardial depression and increased mortality in patients with sepsis [ 39 , 40 ]. These findings suggest that plasma BNP and NT-proBNP levels represent reliable markers for the identification of SIMD.…”

Section: Biomarkers Of Simdmentioning

confidence: 99%

Pathophysiology of sepsis-induced myocardial dysfunction

2016

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Sepsis-induced myocardial dysfunction is a common complication in septic patients and is associated with increased mortality. In the clinical setting, it was once believed that myocardial dysfunction was not a major pathological process in the septic patients, at least in part, due to the unavailability of suitable clinical markers to assess intrinsic myocardial function during sepsis. Although sepsis-induced myocardial dysfunction has been studied in clinical and basic research for more than 30 years, its pathophysiology is not completely understood, and no specific therapies for this disorder exist. The purpose of this review is to summarize our current knowledge of sepsis-induced myocardial dysfunction with a special focus on pathogenesis and clinical characteristics.

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“…Several reports have indicated that plasma ANF or BNP levels are increased in sepsis and in septic shock patients [61–64]. The increase in plasma NPs is partly due to cardiac dysfunction because plasma ANF or BNP was inversely correlated with cardiac function [65–67].…”

Section: Bnp In Sepsis and Following Lps Treatmentmentioning

confidence: 99%

Brain Natriuretic Peptide Production and Secretion in Inflammation

Ogawa

Bold

2012

Journal of Transplantation

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Gene expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are simultaneously upregulated in various cardiac disorders such as congestive heart failure, ischemic heart disease, and hypertensive heart disease, in which hemodynamic or neuroendocrine changes are key components in the progression of disease. However, during acute cardiac allograft rejection, plasma BNP levels are increased but not those of ANF. Successful treatment of the rejection episode decreases the elevated plasma BNP to prerejection values suggesting that substances related to inflammation may selectively influence BNP gene expression. Indeed, cytokines such as TNFα and IL-1β selectively stimulate cardiac BNP at the transcriptional and translational levels in cardiomyocyte cultures without affecting ANF. This selective BNP increase is seen in vivo, in addition to acute cardiac allograft rejection, in several circumstances where inflammation significantly contributes to the pathogenesis of disease such as in sepsis and in acute myocarditis.

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Untitled

Cited by 46 publications

References 11 publications

Pathophysiology of Mifepristone-Induced Septic Shock Due to Clostridium sordellii

Pathophysiology of Mifepristone-Induced Septic Shock Due to Clostridium sordellii

Pathophysiology of sepsis-induced myocardial dysfunction

Brain Natriuretic Peptide Production and Secretion in Inflammation

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