Pub Date : 2009-11-18DOI: 10.3109/17471060902980760
Christopher S. Stevenson
Chronic obstructive pulmonary disease (COPD) is a complex disorder predominantly affecting smokers and is characterized by progressive airflow obstruction that is largely irreversible. Approximately 25% of smokers are believed to be susceptible to developing the disease, suggesting that there are at present unknown genetic, epigenetic and/or environmental factors which underlie an individual's risk for developing the disease. COPD is a multifactorial disease and susceptibility is therefore likely to be determined by the expression of a number of allelic variants that leave an individual less capable of handling the damaging effects of chronic smoking. It is proposed herein that intrinsic aerobic (exercise) capacity is the primary trait which determines an individual's risk for developing this disease. This polygenetic characteristic comprises an individual's ability to metabolize oxygen and detoxify its reactive species. Pathways regulating these processes are damaged by smoking; thus individuals with low...
{"title":"Chronic obstructive pulmonary disease susceptibility: Is it due to poor oxygen metabolism?","authors":"Christopher S. Stevenson","doi":"10.3109/17471060902980760","DOIUrl":"https://doi.org/10.3109/17471060902980760","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is a complex disorder predominantly affecting smokers and is characterized by progressive airflow obstruction that is largely irreversible. Approximately 25% of smokers are believed to be susceptible to developing the disease, suggesting that there are at present unknown genetic, epigenetic and/or environmental factors which underlie an individual's risk for developing the disease. COPD is a multifactorial disease and susceptibility is therefore likely to be determined by the expression of a number of allelic variants that leave an individual less capable of handling the damaging effects of chronic smoking. It is proposed herein that intrinsic aerobic (exercise) capacity is the primary trait which determines an individual's risk for developing this disease. This polygenetic characteristic comprises an individual's ability to metabolize oxygen and detoxify its reactive species. Pathways regulating these processes are damaged by smoking; thus individuals with low...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"16 1","pages":"218-223"},"PeriodicalIF":0.0,"publicationDate":"2009-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78962185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-11-18DOI: 10.3109/17471060902859113
I. Hilmi, J. Kellum, R. Planinsic, D. Foster, A. Abdullah, D. Damian, S. Gligor, D. Klein, K. Abu-Elmagd
Objective. Patients undergoing orthotopic liver transplantation (OLT) and multi-visceral transplantation (MVT) may have an increased incidence of endotoxemia due to translocation of endotoxin from the intestine, in combination with impaired hepatic clearance. We sought to evaluate the presence of endotoxemia in the perioperative period, using the Endotoxin Activity Assay™ (EAA) to understand the association of endotoxin activity (EA) with clinical course and outcome. Material and methods. In this prospective observational pilot study we measured EA in 40 patients undergoing OLT or MVT during the perioperative period. As a control, the EAA was performed on 10 healthy adult volunteers. We analyzed the relationships between EA and graft function, episodes of rejection, infection and outcome. Results. Mean EA in the control group was 0.21±0.05 u (range 0.16–0.27 u). For patients, baseline pre-transplant EA was significantly greater than that in controls at 0.50±0.17 u (range 0.10–0.80 u) (p=0.001) and further...
{"title":"Endotoxemia is common following abdominal organ transplantation and is associated with reperfusion and rejection","authors":"I. Hilmi, J. Kellum, R. Planinsic, D. Foster, A. Abdullah, D. Damian, S. Gligor, D. Klein, K. Abu-Elmagd","doi":"10.3109/17471060902859113","DOIUrl":"https://doi.org/10.3109/17471060902859113","url":null,"abstract":"Objective. Patients undergoing orthotopic liver transplantation (OLT) and multi-visceral transplantation (MVT) may have an increased incidence of endotoxemia due to translocation of endotoxin from the intestine, in combination with impaired hepatic clearance. We sought to evaluate the presence of endotoxemia in the perioperative period, using the Endotoxin Activity Assay™ (EAA) to understand the association of endotoxin activity (EA) with clinical course and outcome. Material and methods. In this prospective observational pilot study we measured EA in 40 patients undergoing OLT or MVT during the perioperative period. As a control, the EAA was performed on 10 healthy adult volunteers. We analyzed the relationships between EA and graft function, episodes of rejection, infection and outcome. Results. Mean EA in the control group was 0.21±0.05 u (range 0.16–0.27 u). For patients, baseline pre-transplant EA was significantly greater than that in controls at 0.50±0.17 u (range 0.10–0.80 u) (p=0.001) and further...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"1 1","pages":"254-260"},"PeriodicalIF":0.0,"publicationDate":"2009-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81121740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-11-18DOI: 10.3109/17471060902968526
S. Tschoeke, T. Drogies, Bjoern Meyer, M. Hellmuth, W. Ertel, P. Stahel, A. Oberholzer, A. Hostmann
Objective. To investigate the influence of traumatic brain injury (TBI) on immune function and viability of human peripheral monocytes in polytraumatized patients. Material and methods. This was a prospective, randomized, controlled clinical study conducted in a Level I trauma center. Multiply injured patients (n=42; mean age 42.4±15.5 years) with a mean Injury Severity Score (ISS) of 32.3±9.6 were compared to healthy controls (n=20; mean age 36.3±8.4 years). The methods used were clinical evaluation, scoring of injury severity (ISS, abbreviated injury scores), multiple organ dysfunction score, real-time reverse transcription polymerase chain reaction, Western blotting and fluorescent-activated cell sorting analyses of negatively isolated monocytes. The main outcome measures were overall clinical outcome, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) staining, expression of the Fas and tumor necrosis factor receptor I, expression of the mitochondrial proteins Bax and Bcl-2, ...
{"title":"Severe head injury promotes early caspase-dependent apoptosis in peripheral blood monocytes from multiply injured patients","authors":"S. Tschoeke, T. Drogies, Bjoern Meyer, M. Hellmuth, W. Ertel, P. Stahel, A. Oberholzer, A. Hostmann","doi":"10.3109/17471060902968526","DOIUrl":"https://doi.org/10.3109/17471060902968526","url":null,"abstract":"Objective. To investigate the influence of traumatic brain injury (TBI) on immune function and viability of human peripheral monocytes in polytraumatized patients. Material and methods. This was a prospective, randomized, controlled clinical study conducted in a Level I trauma center. Multiply injured patients (n=42; mean age 42.4±15.5 years) with a mean Injury Severity Score (ISS) of 32.3±9.6 were compared to healthy controls (n=20; mean age 36.3±8.4 years). The methods used were clinical evaluation, scoring of injury severity (ISS, abbreviated injury scores), multiple organ dysfunction score, real-time reverse transcription polymerase chain reaction, Western blotting and fluorescent-activated cell sorting analyses of negatively isolated monocytes. The main outcome measures were overall clinical outcome, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) staining, expression of the Fas and tumor necrosis factor receptor I, expression of the mitochondrial proteins Bax and Bcl-2, ...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"1 1","pages":"261-272"},"PeriodicalIF":0.0,"publicationDate":"2009-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83549195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-15DOI: 10.1080/17471060701342550
G. Wolf, F. Ziyadeh
Glomerulosclerosis, interstitial fibrosis, and tubular atrophy occur together with end-stage kidney failure, irrespective of the primary etiology. Transforming growth factor (TGF)-β is a key factor in these alterations either directly, by stimulating synthesis of extracellular matrix components and/or impairing turnover of extracellular matrix, or indirectly, through other profibrogenic factors such as connective tissue growth factor. TGF-β is important for the proliferation of renal interstitial fibroblasts and the epithelial–mesenchymal transition, through which tubular cells acquire fibroblastic properties. In addition, TGF-β can modulate the immune response in inflammatory renal diseases. Many humoral factors induce TGF-β expression in the kidney, chief among them being various members of the renin–angiotensin–aldosterone system. Proof of the concept that TGF-β is the main mediator of renal fibrosis stems originally from experimental and clinical observations in diabetic nephropathy, and more recently...
{"title":"Transforming growth factor- and diabetic nephropathy","authors":"G. Wolf, F. Ziyadeh","doi":"10.1080/17471060701342550","DOIUrl":"https://doi.org/10.1080/17471060701342550","url":null,"abstract":"Glomerulosclerosis, interstitial fibrosis, and tubular atrophy occur together with end-stage kidney failure, irrespective of the primary etiology. Transforming growth factor (TGF)-β is a key factor in these alterations either directly, by stimulating synthesis of extracellular matrix components and/or impairing turnover of extracellular matrix, or indirectly, through other profibrogenic factors such as connective tissue growth factor. TGF-β is important for the proliferation of renal interstitial fibroblasts and the epithelial–mesenchymal transition, through which tubular cells acquire fibroblastic properties. In addition, TGF-β can modulate the immune response in inflammatory renal diseases. Many humoral factors induce TGF-β expression in the kidney, chief among them being various members of the renin–angiotensin–aldosterone system. Proof of the concept that TGF-β is the main mediator of renal fibrosis stems originally from experimental and clinical observations in diabetic nephropathy, and more recently...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2009-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86870067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-15DOI: 10.1080/17471060701721985
J. Liebhart, R. Dobek
Chronic obstructive pulmonary disease (COPD) is a highly prevalent airway disorder. However, the mechanisms of the pathogenesis of COPD have not been completely elucidated to date. Transforming growth factor (TGF)-β is a pleiotropic, multifunctional cytokine participating in cell differentiation, apoptosis, survival and proliferation. TGF-β is involved in many diseases, including carcinogenesis and fibrosis. Although the most important risk factor for COPD is cigarette smoking, only 10–15% of all smokers develop the disease. This finding raises suspicion that some host or genetic factors may be involved in the pathogenesis of the disease. Thus, special attention has recently been focused on the role in COPD of TGF-β, which is active in inflammation of the airways and particularly in lung remodeling. TGF-β induces chemotaxis of mast cells and macrophages, regulates cell apoptosis and influences the protease/antiprotease balance inhibiting matrix metalloproteinase-9. TGF-β is heavily involved in repair proc...
{"title":"Transforming growth factor-beta in the pathogenesis of chronic obstructive pulmonary disease","authors":"J. Liebhart, R. Dobek","doi":"10.1080/17471060701721985","DOIUrl":"https://doi.org/10.1080/17471060701721985","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is a highly prevalent airway disorder. However, the mechanisms of the pathogenesis of COPD have not been completely elucidated to date. Transforming growth factor (TGF)-β is a pleiotropic, multifunctional cytokine participating in cell differentiation, apoptosis, survival and proliferation. TGF-β is involved in many diseases, including carcinogenesis and fibrosis. Although the most important risk factor for COPD is cigarette smoking, only 10–15% of all smokers develop the disease. This finding raises suspicion that some host or genetic factors may be involved in the pathogenesis of the disease. Thus, special attention has recently been focused on the role in COPD of TGF-β, which is active in inflammation of the airways and particularly in lung remodeling. TGF-β induces chemotaxis of mast cells and macrophages, regulates cell apoptosis and influences the protease/antiprotease balance inhibiting matrix metalloproteinase-9. TGF-β is heavily involved in repair proc...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"16 4","pages":"161-170"},"PeriodicalIF":0.0,"publicationDate":"2009-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72607986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-15DOI: 10.1080/17471060701682310
G. Sullivan, J. Linden
Neutrophils [polymorphonuclear leukocytes (PMNs)] express several purinergic receptors, including the nucleotide receptors P2Y2 and P2X7 and the adenosine receptor subtypes A1, A2A and A3. Activation of these receptors modulates PMN function and ultimately, in concert with other cells, affects the host's innate inflammatory response. PMN activities that can be altered by purinergic receptor stimulation include adhesion, aggregation, migration, phagocytosis, microbicidal function, release of tissue-damaging products and apoptosis. Interventions that alter PMN purinergic receptor stimulation are being developed to reduce organ dysfunction in conditions such as sepsis, ischemia–reperfusion injury and the acute respiratory distress syndrome.
{"title":"Role of neutrophil purinergic receptors in organ dysfunction","authors":"G. Sullivan, J. Linden","doi":"10.1080/17471060701682310","DOIUrl":"https://doi.org/10.1080/17471060701682310","url":null,"abstract":"Neutrophils [polymorphonuclear leukocytes (PMNs)] express several purinergic receptors, including the nucleotide receptors P2Y2 and P2X7 and the adenosine receptor subtypes A1, A2A and A3. Activation of these receptors modulates PMN function and ultimately, in concert with other cells, affects the host's innate inflammatory response. PMN activities that can be altered by purinergic receptor stimulation include adhesion, aggregation, migration, phagocytosis, microbicidal function, release of tissue-damaging products and apoptosis. Interventions that alter PMN purinergic receptor stimulation are being developed to reduce organ dysfunction in conditions such as sepsis, ischemia–reperfusion injury and the acute respiratory distress syndrome.","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"141 1","pages":"147-160"},"PeriodicalIF":0.0,"publicationDate":"2009-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80417085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-15DOI: 10.1080/17471060701682245
C. Bai, Xiang-dong Wang
5-Lipoxygenase (5-LO) is an important enzyme that dominates the metabolism of arachidonic acid and the synthesis of leukotrienes, of which leukotriene B4 (LTB4) is suggested to be one of the most potent chemoattractants and activators of leukocytes. 5-LO is normally limited to hematopoetic cells, e.g. granulocytes and macrophages, where LTB4 is produced. Leukotrienes play an important role in the innate defense system, in the antimicrobial defense system, and in intercellular signaling. Under pathophysiological conditions, overproduction of LTB4 was noted in multiple cells. It is known that 5-LO and its production of LTB4 are involved in the maintenance of normal host defense, initiation of inflammation, migration of leukocytes, development of endothelial barrier dysfunction, hyperresponsiveness of smooth muscle cells, stimulation of mucus secretion, reduction of mucociliary clearance, and tissue remodeling. In order to understand the role of 5-LO and its production in functions of the innate host defense...
{"title":"Role of 5-lipoxygenase and its production of leukotriene B4 in innate host defense and diseases","authors":"C. Bai, Xiang-dong Wang","doi":"10.1080/17471060701682245","DOIUrl":"https://doi.org/10.1080/17471060701682245","url":null,"abstract":"5-Lipoxygenase (5-LO) is an important enzyme that dominates the metabolism of arachidonic acid and the synthesis of leukotrienes, of which leukotriene B4 (LTB4) is suggested to be one of the most potent chemoattractants and activators of leukocytes. 5-LO is normally limited to hematopoetic cells, e.g. granulocytes and macrophages, where LTB4 is produced. Leukotrienes play an important role in the innate defense system, in the antimicrobial defense system, and in intercellular signaling. Under pathophysiological conditions, overproduction of LTB4 was noted in multiple cells. It is known that 5-LO and its production of LTB4 are involved in the maintenance of normal host defense, initiation of inflammation, migration of leukocytes, development of endothelial barrier dysfunction, hyperresponsiveness of smooth muscle cells, stimulation of mucus secretion, reduction of mucociliary clearance, and tissue remodeling. In order to understand the role of 5-LO and its production in functions of the innate host defense...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"10 1","pages":"140-146"},"PeriodicalIF":0.0,"publicationDate":"2009-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73329182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-15DOI: 10.1080/17471060701850529
Xiaoling Li, I. Chaudry, M. Choudhry
This article reviews studies dealing with gut barrier dysfunction following major trauma and alcohol exposure. An association between alcohol exposure and traumatic injury has been recognized in many studies. The gut is the major reservoir of bacteria within the body but, under healthy conditions, it maintains a barrier which prevents these bacteria from crossing the intestinal lumen. The findings reviewed herein indicate that this barrier is lost in conditions such as major trauma and alcohol exposure. Furthermore, studies also indicate that alcohol intoxication at the time of injury causes a further deterioration in intestinal barrier function as determined by intestinal permeability and bacterial translocation. A precise mechanism for impaired barrier function following alcohol exposure, either alone or in combination with major trauma or burn injury, remains unknown. However, the findings discussed in this article indicate that this could result from: (i) an increase in bacterial growth; (ii) a decrea...
{"title":"Gut dysfunction following alcohol exposure and trauma","authors":"Xiaoling Li, I. Chaudry, M. Choudhry","doi":"10.1080/17471060701850529","DOIUrl":"https://doi.org/10.1080/17471060701850529","url":null,"abstract":"This article reviews studies dealing with gut barrier dysfunction following major trauma and alcohol exposure. An association between alcohol exposure and traumatic injury has been recognized in many studies. The gut is the major reservoir of bacteria within the body but, under healthy conditions, it maintains a barrier which prevents these bacteria from crossing the intestinal lumen. The findings reviewed herein indicate that this barrier is lost in conditions such as major trauma and alcohol exposure. Furthermore, studies also indicate that alcohol intoxication at the time of injury causes a further deterioration in intestinal barrier function as determined by intestinal permeability and bacterial translocation. A precise mechanism for impaired barrier function following alcohol exposure, either alone or in combination with major trauma or burn injury, remains unknown. However, the findings discussed in this article indicate that this could result from: (i) an increase in bacterial growth; (ii) a decrea...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"30 1","pages":"171-181"},"PeriodicalIF":0.0,"publicationDate":"2009-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88639501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-09-15DOI: 10.1080/17471060701649962
Jingfei Cheng, J. Grande
In addition to their critical role in embryogenesis of the kidney, members of the transforming growth factor (TGF)-β superfamily direct a number of pathways important in the maintenance of homeostasis in the differentiated kidney. TGF-β family members also play an important role in cell-cycle regulation. Through induction of cyclin-dependent kinase inhibitors, TGF-β promotes a hypertrophic response of renal tubular epithelial cells and glomerular mesangial cells. This TGF-β-driven hypertrophic response, which occurs in diabetic nephropathy, may have deleterious effects on the kidney. In contrast, many human cancers are associated with loss of the growth inhibitory effects of TGF-β. TGF-β may promote or inhibit inflammation, an outcome which appears to depend on the cell type(s) involved and on potential interactions with other signaling pathways that regulate inflammatory responses. In recent studies, TGF-β has been implicated as a key mediator of the epithelial to mesenchymal transition, a process throug...
{"title":"Transforming growth factor-β and kidney dysfunction","authors":"Jingfei Cheng, J. Grande","doi":"10.1080/17471060701649962","DOIUrl":"https://doi.org/10.1080/17471060701649962","url":null,"abstract":"In addition to their critical role in embryogenesis of the kidney, members of the transforming growth factor (TGF)-β superfamily direct a number of pathways important in the maintenance of homeostasis in the differentiated kidney. TGF-β family members also play an important role in cell-cycle regulation. Through induction of cyclin-dependent kinase inhibitors, TGF-β promotes a hypertrophic response of renal tubular epithelial cells and glomerular mesangial cells. This TGF-β-driven hypertrophic response, which occurs in diabetic nephropathy, may have deleterious effects on the kidney. In contrast, many human cancers are associated with loss of the growth inhibitory effects of TGF-β. TGF-β may promote or inhibit inflammation, an outcome which appears to depend on the cell type(s) involved and on potential interactions with other signaling pathways that regulate inflammatory responses. In recent studies, TGF-β has been implicated as a key mediator of the epithelial to mesenchymal transition, a process throug...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"83 1","pages":"182-192"},"PeriodicalIF":0.0,"publicationDate":"2009-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81949790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-07-11DOI: 10.1080/17471060802449346
R. Agha-Jaffar, C. Hinds
Multiple organ dysfunction syndrome (MODS) is associated with a marked catabolic response. Although, initially, aspects of this response are likely to be advantageous, the relentless loss of lean tissue and protein-wasting soon become functionally important, leading to increases in morbidity and mortality. Because standard nutritional support does little to limit protein-wasting in patients with MODS, investigators have sought to develop alternative treatment strategies. Amongst the many factors implicated in the adverse effects of prolonged catabolism, the role of the hypothalamic–anterior–pituitary axis has stimulated considerable research and debate. In view of the well-documented anabolic properties of growth hormone, the efficacy of treatment with recombinant human growth hormone (rhGH) has been extensively investigated in the critically ill. Results have been disappointing however, and prospective randomized controlled trials have clearly demonstrated the dangers of administering ‘pharmacological’ d...
{"title":"Growth hormone and multiple organ dysfunction syndrome","authors":"R. Agha-Jaffar, C. Hinds","doi":"10.1080/17471060802449346","DOIUrl":"https://doi.org/10.1080/17471060802449346","url":null,"abstract":"Multiple organ dysfunction syndrome (MODS) is associated with a marked catabolic response. Although, initially, aspects of this response are likely to be advantageous, the relentless loss of lean tissue and protein-wasting soon become functionally important, leading to increases in morbidity and mortality. Because standard nutritional support does little to limit protein-wasting in patients with MODS, investigators have sought to develop alternative treatment strategies. Amongst the many factors implicated in the adverse effects of prolonged catabolism, the role of the hypothalamic–anterior–pituitary axis has stimulated considerable research and debate. In view of the well-documented anabolic properties of growth hormone, the efficacy of treatment with recombinant human growth hormone (rhGH) has been extensively investigated in the critically ill. Results have been disappointing however, and prospective randomized controlled trials have clearly demonstrated the dangers of administering ‘pharmacological’ d...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"143 1","pages":"17-25"},"PeriodicalIF":0.0,"publicationDate":"2009-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91179431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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