The impact of diabetes on the pathogenesis of sepsis

Koh, Gavin; Peacock, Sharon J.; Poll, Tom van der; Wiersinga, W. Joost

doi:10.1007/s10096-011-1337-4

Cited by 185 publications

(158 citation statements)

References 144 publications

(143 reference statements)

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“…The risk of infectious diseases can be exaggerated in patients with DM owing to well-documented defects in neutrophil function, such as chemotaxis, phagocytosis and killing, attributable to hyperglycemia. 35 Non-transplant diabetic patients have a significantly increased risk of infectious diseases, including infections of the respiratory and urinary tracts, skin and mucosa. [35][36][37] Infection-related mortality, 38 as well as pneumonia-related hospitalization, are also increased in patients with DM.…”

Section: Risk Of Infectious Diseasesmentioning

confidence: 99%

“…35 Non-transplant diabetic patients have a significantly increased risk of infectious diseases, including infections of the respiratory and urinary tracts, skin and mucosa. [35][36][37] Infection-related mortality, 38 as well as pneumonia-related hospitalization, are also increased in patients with DM. A Danish population-based study showed that patients with DM had an increased relative risk of infectious diseases with each 1-mmol/L increase in plasma glucose at baseline.…”

Section: Risk Of Infectious Diseasesmentioning

confidence: 99%

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How do I manage hyperglycemia/post-transplant diabetes mellitus after allogeneic HSCT

Fuji

Rovó

Ohashi

et al. 2016

Bone Marrow Transplant

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Allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipients frequently develop glucose intolerance and post-transplant diabetes mellitus (PTDM). The clinical importance of PTDM and its detrimental impact on HSCT outcomes are underrecognized. After allo-HSCT, various mechanisms can contribute to the development of PTDM. Here we review information about hyperglycemia and PTDM after allo-HSCT as well as PTDM after solid organ transplantation and describe ways to manage hyperglycemia/PTDM after allogeneic HSCT. Taking into consideration a lack of well-established evidence in the field of allo-HSCT, more studies should be conducted in the future, which will require closer multidisciplinary collaboration between hematologists, endocrinologists and nutritionists.

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Section: Risk Of Infectious Diseasesmentioning

confidence: 99%

Section: Risk Of Infectious Diseasesmentioning

confidence: 99%

How do I manage hyperglycemia/post-transplant diabetes mellitus after allogeneic HSCT

Fuji

Rovó

Ohashi

et al. 2016

Bone Marrow Transplant

View full text Add to dashboard Cite

show abstract

“…It has been recently reported that the immune response (within the nasal mucosa) to attenuated influenza virus vaccine were suppressed in smokers as compared to nonsmokers [20]. Furthermore, it has been reported that cigarette smokers are susceptible to infection and sepsis [21]. Some immunologic disorders have been shown in cigarette smokers.…”

Section: Figure 1: Distribution Of Subjects According To Anti-tetanusmentioning

confidence: 99%

Lower immunity to tetanus in cigarette smoker subjects

Jafarzadeh

Shabani

Hassanabadi

et al. 2012

JOHE

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Received: February 2013, Accepted: October 2013 Background: Cigarette smoking has been linked with the suppression of immune responses and increased susceptibility to numerous infections in humans. Tetanus is also a major public health problem in many countries. The aim of the present study was to evaluate the serum levels of antitetanus toxin antibodies in cigarette smoking and healthy non-smoking people. Materials and Methods: A total of 100 cigarette smokers and 100 age-matched healthy nonsmoker individuals were enrolled in this descriptive study. A blood sample was collected from each participant. The samples were tested for the levels of anti-tetanus toxin antibodies by use of enzyme linked immunosorbent assay. Results: The seroprotective rate of anti-tetanus toxin antibodies in non-smoking group (99%) was significantly higher than that observed in cigarette smoking group (78%, P<0.0001). The mean titer of anti-tetanus toxin antibodies in non-smoking group (5.32± 0.26 IU/ml) was also significantly higher than that in smoker subjects (1.03 ± 0.16 IU/ml; P<0.0001). The mean titer of anti-tetanus toxin antibodies in individuals with smoking duration >10 years was significantly lower than that among smokers with smoking duration ≤10 years (0.59 ± 0.12 IU/ml vs 1.98 ± 0.41 IU/ml; P<0.001). The seroprotection rate was also significantly lower in persons with smoking duration >10 years in comparison to smokers with smoking duration ≤10 years (72.1% vs 90.6%; P=0.037). The mean titer of anti-tetanus toxin antibodies in individuals with daily smoking >10 cigarettes was also significantly lower in comparison to smokers with daily smoking ≤10 cigarettes (0.68 ± 0.15 IU/ml vs 1.63 ± 0.36 IU/ml; P<0.001). Conclusion: These results showed lower levels of anti-tetanus toxin antibodies in cigarette smokers which represents cigarette smoking as a risk factor for susceptibility to tetanus. A negative association was also observed between the immunity to tetanus and smoking burden.

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“…5,6,26 The rationale for insulin use in hyperglycemic septic states is based mainly on its direct antiinflammatory role and its inhibitory effect on glycogen synthase kinase 3β. 5,6 However, current evidence states that intensive insulin therapy (IIT) with target glucose between 80-110 mg/dL compared to a moderately hyperglycemic goal (140-180 mg/dL) offered no apparent benefits, but instead increased the risk of hypoglycemia.…”

mentioning

confidence: 99%

Endocrine dysfunction in sepsis: a beneficial or deleterious host response?

Gheorghiță¹,

Gheorghiu

et al. 2015

GERMS

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Sepsis is a systemic, deleterious inflammatory host response triggered by an infective agent leading to severe sepsis, septic shock and multi-organ failure. The host response to infection involves a complex, organized and coherent interaction between immune, autonomic, neuroendocrine and behavioral systems. Recent data have confirmed that disturbances of the autonomic nervous and neuroendocrine systems could contribute to sepsis-induced organ dysfunction.Through this review, we aimed to summarize the current knowledge about the endocrine dysfunction as response to sepsis, specifically addressed to vasopressin, copeptin, cortisol, insulin and leptin. We searched the following readily accessible, clinically relevant databases: PubMed, UpToDate, BioMed Central.The immune system could be regarded as a "diffuse sensory organ" that signals the presence of pathogens to the brain through different pathways, such as the vagus nerve, endothelial activation/dysfunction, cytokines and neurotoxic mediators and the circumventricular organs, especially the neurohypophysis. The hormonal profile changes substantially as a consequence of inflammatory mediators and microorganism products leading to inappropriately low levels of vasopressin, sick euthyroid syndrome, reduced adrenal responsiveness to ACTH, insulin resistance, hyperglycemia as well as hyperleptinemia.In conclusion, clinical diagnosis of this "pan-endocrine illness" is frequently challenging due to the many limiting factors. The most important benefits of endocrine markers in the management of sepsis may be reflected by their potential to be used as biomarkers in different scoring systems to estimate the severity of the disease and the risk of death.

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The impact of diabetes on the pathogenesis of sepsis

Cited by 185 publications

References 144 publications

How do I manage hyperglycemia/post-transplant diabetes mellitus after allogeneic HSCT

How do I manage hyperglycemia/post-transplant diabetes mellitus after allogeneic HSCT

Lower immunity to tetanus in cigarette smoker subjects

Endocrine dysfunction in sepsis: a beneficial or deleterious host response?

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