Association Between Blood Glucose Levels and Development of Candidemia in Hospitalized Patients

Shoham, Shmuel; Han, Grace Y.; Granek, Tal; Walsh, Thomas J.; Magee, Michelle F.

doi:10.4158/ep.15.2.111

Cited by 7 publications

(3 citation statements)

References 28 publications

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“…We found that patients with hyperglycemia requiring insulin therapy were at increased risk to develop invasive fusariosis until day 40 posttransplant. Hyperglycemia exerts various deleterious effects in the innate immune system, including impairment in neutrophil function [27], and has been identified as a risk factor for candidemia [28], mucormycosis [29], and infectious complications (including IFD) in patients with acute leukemia [30,31].…”

Section: Discussionmentioning

confidence: 99%

Risk Factors for Invasive Fusariosis in Patients With Acute Myeloid Leukemia and in Hematopoietic Cell Transplant Recipients

Garnica

Cunha²,

Portugal

et al. 2014

Clinical Infectious Diseases

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Section: Discussionmentioning

confidence: 99%

Risk Factors for Invasive Fusariosis in Patients With Acute Myeloid Leukemia and in Hematopoietic Cell Transplant Recipients

Garnica

Cunha²,

Portugal

et al. 2014

Clinical Infectious Diseases

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“…Some secondary conditions not directly related to T cells or IL-17 also predispose to CMC, such as hyper-glycemia or long-term use of broad-spectrum antibiotics [67,68]. Moreover, the salivary gland plays a critical role in oral mucosal immunity.…”

Section: Other Causes Of Chronic Mucocutaneous Candidiasismentioning

confidence: 99%

Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy

2012

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IL-17 and related cytokines are direct and indirect targets of selective immunosuppressive agents for the treatment of autoimmune diseases and other diseases of pathologic inflammation. Insights into the potential adverse effects of IL-17 blockade can be drawn from the experience of patients with deficiencies in the IL-17 pathway. A unifying theme of susceptibility to mucocutaneous candidiasis is seen in both mice and humans with a variety of genetic defects that converge on this pathway. Mucocutaneous candidiasis is a superficial infection of mucosal, nail or skin surfaces usually caused by the fungal pathogen Candida albicans. The morbidity of the disease includes significant pain, weight loss and secondary complications, including carcinoma and aneurysms. This review describes the known human diseases associated with chronic mucocutaneous candidiasis (CMC) as well as the known and proposed connections to IL-17 signaling. The human diseases include defects in IL-17 signaling due to autoantibodies (AIRE deficiency), receptor mutations (IL-17 receptor mutations) or mutations in the cytokine genes (IL17F and IL17A). Hyper-IgE syndrome is characterized by elevated serum IgE, dermatitis and recurrent infections, including CMC due to impaired generation of IL-17-producing Th17 cells. Mutations in STAT1, IL12B and IL12RB1 result in CMC secondary to decreased IL-17 production through different mechanisms. Dectin-1 defects and CARD9 defects result in susceptibility to C. albicans because of impaired host recognition of the pathogen and subsequent impaired generation of IL-17-producing T cells. Thus, recent discoveries of genetic predisposition to CMC have driven the recognition of the role of IL-17 in protection from mucosal fungal infection and should guide counseling and management of patients treated with pharmacologic IL-17 blockade.

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“…Elevated serum glucose may lead to impaired neutrophil and monocyte adherence, chemotaxis, phagocytosis, pathogen killing, and respiratory burst and has been associated with development of candidemia. [26][27][28][29][30][31] Renal failure is associated with phagocyte dysfunction, and uremia may contribute to development of candidemia. [32][33][34][35] Mononuclear cells from uremic patients have decreased responsiveness to Candida antigens, and uremic plasma inhibits phagocytosis of C albicans by previously healthy monocytes.…”

Section: Host/pathogen Interactionsmentioning

confidence: 99%

Invasive Fungal Infections in the ICU

Shoham

Marwaha

2009

J Intensive Care Med

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Invasive fungal infections are major causes of morbidity and mortality in critically ill patients. Foremost among these is invasive candidiasis. In recent years, invasive aspergillosis (IA) and zygomycosis have emerged as major problems in susceptible, critically ill patients. Risk factors for invasive fungal infections, including disrupted anatomic barriers, suppressed antifungal host responses, and exposure to potentially opportunistic fungi are common in critically ill patients. The expanded antifungal armamentarium and advent of rapid diagnostic techniques are altering the approach to invasive fungal infections in the intensive care unit (ICU). Herein, we review recent developments in the field of antifungal host defenses, the changing epidemiology of fungal infections in the ICU, the pharmacology of antifungal agents of importance to critically ill patients, and the evolving approaches to therapy in this setting.

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Association Between Blood Glucose Levels and Development of Candidemia in Hospitalized Patients

Cited by 7 publications

References 28 publications

Risk Factors for Invasive Fusariosis in Patients With Acute Myeloid Leukemia and in Hematopoietic Cell Transplant Recipients

Risk Factors for Invasive Fusariosis in Patients With Acute Myeloid Leukemia and in Hematopoietic Cell Transplant Recipients

Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy

Invasive Fungal Infections in the ICU

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