leptin and Systemic-Inflammatory-Response-Syndrome

Preeclampsia is a syndrome occurring only in pregnancy characterized by systemic maternal inflammation and associated with the presence of the placenta. How these 2 aspects of the disease are linked has been the subject of numerous theories and ideas. Recently, there has been increasing interest in DNA shed from the placenta into the maternal circulation as a potential agent initiating the inflammatory response. This review will discuss the current evidence and future directions for placental DNA as the linking factor in preeclampsia in the context of other hypotheses.

Topics: Cell-Derived Microparticles; Cytokines; DNA; Female; Humans; Hypoxia; Leptin; Placenta; Pre-Eclampsia; Pregnancy; Systemic Inflammatory Response Syndrome; Trophoblasts; Vascular Endothelial Growth Factor Receptor-1

There is general agreement that central, as opposed to peripheral, adipose tissue confers the most cardiometabolic risk. Although the basis of this differential risk has not been established, the pattern of gene expression and secretory products in visceral fat would be predicted to be more atherogenic compared with that in subcutaneous peripheral fat. Adipose tissue is, in fact, now recognized not simply a store of excess energy but a major endocrine and secretory organ, releasing a wide range of protein factors and signals, termed adipokines, in addition to fatty acids and other lipid moieties. These factors are derived from adipocyte or non-adipocyte fractions, and include proteins, metabolites and hormones. This paper reviews some of the advances in the understanding of biologically active molecules produced by adipose tissue and how dysregulated production of these factors could be implicated in the association between central adiposity, cardiovascular pathology and comorbidities, including metabolic syndrome, type 2 diabetes and systemic inflammation.

Topics: Adipocytes; Adipokines; Adiponectin; Adipose Tissue; Animals; Atherosclerosis; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Humans; Leptin; Metabolic Syndrome; Obesity; Systemic Inflammatory Response Syndrome

Leptin was originally identified as an adipocyte-derived cytokine with a key role in the regulation of the energy balance. Subsequent research revealed that leptin's biological action is not restricted to its effects on appetite and food intake, but instead has a much more pleiotropic character. There is now ample evidence that leptin has important functions in reproduction, hematopoiesis, HPA-axis endocrinology and angiogenesis. In this review we have focused on the effects of leptin in the antigen-specific immunity and in the inflammatory effector system.

Topics: Adaptation, Physiological; alpha-MSH; Animals; Anorexia; Humans; Immunity; Inflammation; Leptin; Macrophages; Metallothionein; Monocytes; Receptors, Cell Surface; Receptors, Leptin; Starvation; Systemic Inflammatory Response Syndrome; T-Lymphocytes

Systemic inflammatory response syndrome and the resulting complications continue to be important causes of morbidity in surgical patients. A favourable prognosis of patients with postoperative inflammatory intraabdominal complications is limited by forwardness if diagnosis of this severe complication. Cytokines play a significant role not only in regulating pathogenic mechanisms, during the rising of SIRS, but can themselves directly lead to tissue damage. Increased concentrations of inflammatory cytokines observed in the initial phase of postoperative complications have great significance in the early diagnosis of systemic complications. Procalcitonin, alongside to cytokines, appears as a significant parameter. Despite lots of its pathophysiological points are unclear it is a highly selective and specific indicator of systemic bacterial inflammation. Leptin is not only a hormone of adipocytes but also a member of inflammatory network of cytokines and acute phase reactants. Leptin is possibly a necessary factor for adequate course of acute phase reaction. Proinflammatory cytokines as interleukin-1 or tumour necrosis factor-alpha are the main regulatory factors of leptin in this period.

Topics: Acute-Phase Proteins; Calcitonin; Calcitonin Gene-Related Peptide; Cytokines; Humans; Leptin; Postoperative Complications; Protein Precursors; Surgical Procedures, Operative; Systemic Inflammatory Response Syndrome

Leptin was originally identified as an adipocyte-derived cytokine with a key role in the regulation of the energy balance. Subsequent research has, however, revealed that leptin's biological action is not restricted to its effects on appetite and food intake, but rather has a much more pleiotropic character. Evidence is now accumulating that it has important functions in reproduction, hematopoiesis, HPA-axis endocrinology and angiogenesis. In this review, we have focused on the effects of leptin in the immune system, which can be found in both the antigen-specific immunity and in the inflammatory effector system.

Topics: Adaptation, Physiological; Animals; Humans; Immunity; Immunity, Cellular; Inflammation; Leptin; Metallothionein; Neuropeptide Y; Starvation; Systemic Inflammatory Response Syndrome; T-Lymphocytes

Cardiac surgery involving cardiopulmonary bypass (CPB) causes a systemic inflammatory process which can lead to multiple organ failure and postoperative morbidity. Recent animal and human studies suggested a possible involvement of leptin in the systemic inflammatory response.. To characterize the response of leptin to open heart surgery (OHS) and the relationship between the time course of leptin levels and the post-operative clinical course, and to examine the effect of exogenous glucocorticoids.. Forty-seven pediatric patients, undergoing OHS for congenital heart disease were studied. Thirty-four patients (Group 1) received methylprednisolone during CPB while 13 (group 2) did not. Serial blood samples were collected perioperatively and up to 24 h after surgery, and assayed for leptin and cortisol.. All patients' leptin levels decreased significantly during CPB (to 44-48% of baseline, p<0.001); they then increased, peaking at 12 h post-operatively. The levels of groups 1 and 2 were similar up to 8 h post-operatively; thereafter, those of group 1 were significantly higher. Recovery of leptin levels in patients with a more complicated post-operative course was comparatively slower. Cortisol levels of all patients increased significantly during CPB (p<0.001), gradually decreasing afterwards. Cortisol and leptin levels were inversely correlated in both patients' groups.. CPB is associated with acute changes in circulating leptin levels. A complicated postoperative course is associated with lower leptin levels which are inversely correlated with cortisol levels. Leptin may participate in post-CPB inflammatory and hemodynamic responses.

Topics: Adolescent; Cardiopulmonary Bypass; Child; Child, Preschool; Female; Glucocorticoids; Heart Defects, Congenital; Humans; Infant; Infant, Newborn; Inflammation; Leptin; Male; Methylprednisolone; Postoperative Complications; Postoperative Period; Prognosis; Systemic Inflammatory Response Syndrome

Topics: Adult; Aged; Female; Humans; Interleukin-6; Leptin; Male; Middle Aged; Systemic Inflammatory Response Syndrome; Tumor Necrosis Factor-alpha

A key feature of post-polio syndrome (PPS) is progressive loss of muscle strength. In other chronic diseases systemic inflammation has been linked to muscle wasting. In this study plasma TNF-α, IL-6, IL-8, and leptin levels were significantly increased in PPS-patients compared to healthy controls. There was however no association between these raised systemic levels of inflammatory mediators and long-term decline in quadriceps strength or other clinical parameters. In conclusion, there is evidence for systemic inflammation in PPS, yet the relationship with clinical deterioration remains tenuous.

Topics: Adult; Cohort Studies; Cytokines; Electromyography; Female; Humans; Leptin; Male; Middle Aged; Muscle Strength; Postpoliomyelitis Syndrome; Systemic Inflammatory Response Syndrome; Walking

The involvement of a systemic inflammatory response, as evidenced by the Glasgow Prognostic Score (GPS), is associated with weight loss and poor outcome in patients with non-small cell lung cancer. There is good evidence that nutritional and functional decline in patients with advanced malignant disease is associated with catabolic changes in metabolism. However, defects in anabolism may also contribute towards nutritional decline in patients with cancer. The aim of the present study was to examine the relationship between IGF-1 and IGFBP-3, performance status, mGPS and survival in patients with inoperable NSCLC.. 56 patients with inoperable NSCLC were studied. The plasma concentrations of IGF-1, IGFBP-3 and leptin were measured using ELISA and RIA.. The patients were predominantly male (61%), over 60 years old (80%), with advanced (stage III or IV) disease (98%), with a BMI> or =20 (84%), an ECOG-ps of 0 or 1 (79%), a haemoglobin (59%) and white cell count (79%) in the reference range. On follow-up 43 patients died of their cancer. On univariate analysis, BMI (p<0.05), Stage (p<0.05), ECOG-ps (p<0.05), haemoglobin (p<0.05), white cell count (p<0.05) and mGPS (p<0.05) were associated with cancer specific survival. There was no association between age, sex, treatment, IGF-1, IGFBP-3, IGF-1:IGFBP-3 ratio, or leptin and cancer specific survival. With an increasing mGPS concentrations of haemoglobin (p<0.005) and IGFBP-3 (p<0.05) decreased. mGPS was not associated with either IGF-1(p>0.20), or leptin (p>0.20).. In summary, the results of this study suggest that anabolism (IGF-1 axis) does not play a significant role in the relationship between nutritional and functional decline, systemic inflammation and poor survival in patients with inoperable NSCLC.

Topics: Aged; Body Mass Index; Carcinoma, Non-Small-Cell Lung; Female; Hemoglobins; Humans; Insulin-Like Growth Factor Binding Protein 3; Insulin-Like Growth Factor Binding Proteins; Insulin-Like Growth Factor I; Leptin; Leukocyte Count; Male; Middle Aged; Neoplasm Staging; Prognosis; Severity of Illness Index; Survival Analysis; Systemic Inflammatory Response Syndrome; Weight Loss

Severe infection and sepsis are common causes of morbidity and mortality. Early diagnosis in critically ill patients is important to reduce these complications. The present study was conducted to determine the role of serum leptin at early diagnosis and differentiation between patients with manifestations of systemic inflammatory response syndrome (SIRS) and those with sepsis in patients suffering from a broad range of diseases in the intensive care unit (ICU) and its correlation with other biomarkers, such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).. One hundred and six adult ICU patients were observed. CRP, leptin, IL-6 and TNF-alpha were compared among the following groups: sepsis group (n = 40), SIRS group (n = 34) and non-SIRS group (n = 32). Patients were classified into these groups at the time of blood analysis for these biomarkers.. Non-significant differences were observed among patients in different groups regarding biomarkers on the day of ICU admission. On the second day of ICU admission, significant elevation of leptin, IL-6 and TNF-alpha occurred in the SIRS and sepsis groups. Delayed elevation of CRP started on the fourth day of ICU admission in patients with sepsis. At the end of the first week, only CRP level was elevated in septic patients.. Serum leptin correlates well with serum level of IL-6 and TNF-alpha. Leptin helps to differentiate SIRS from non-SIRS patients. CRP is a classic marker of sepsis but is of late onset.

Topics: Adult; Biomarkers; C-Reactive Protein; Critical Illness; Diagnosis, Differential; Early Diagnosis; Egypt; Female; Humans; Intensive Care Units; Interleukin-6; Leptin; Male; Middle Aged; Monitoring, Physiologic; Observation; Predictive Value of Tests; Prospective Studies; Sepsis; Systemic Inflammatory Response Syndrome; Tumor Necrosis Factor-alpha

Topics: Acute Disease; Aged; C-Reactive Protein; Cholecystitis; Diabetes Mellitus, Type 2; Diagnostic Imaging; Female; Humans; Leptin; Systemic Inflammatory Response Syndrome

Previously we reported an impaired energy balance in patients with chronic obstructive pulmonary disease (COPD) during an acute disease exacerbation, but limited data are available on the underlying mechanisms. Experimental and clinical research supports the hypothesis of involvement of the hormone leptin in body weight and energy balance homeostasis. The aim of this study was to investigate the course of the energy balance in relation to leptin and the soluble tumor necrosis factor (TNF) receptors (sTNF-R) 55 and 75, plasma glucose, and serum insulin in patients with severe COPD during the first 7 d of hospitalization for an acute exacerbation (n = 17, 11 men, age mean [SD] 66 [10] yr, FEV(1) 36 [12] %pred). For reference values of the laboratory parameters, blood was collected from 23 (16 men) healthy, elderly subjects. On admission, the dietary intake/resting energy expenditure (REE) ratio was severely depressed (1.28 [0.57]), but gradually restored until Day 7 (1.65 [0. 45], p = 0.005 versus Day 1). Glucose and insulin concentrations were elevated on admission, but on Day 7 only plasma glucose was decreased. The sTNF-Rs were not different from healthy subjects and did not change. Plasma leptin, adjusted for fat mass expressed as percentage of body weight (%FM), was elevated on Day 1 compared with healthy subjects (1.82 [3.85] versus 0.32 [0.72] ng%/ml, p = 0.008), but decreased significantly until Day 7 (1.46 [3.77] ng%/ml, p = 0. 015 versus Day 1). On Day 7, sTNF-R55 was, independently of %FM, correlated with the natural logarithm (LN) of leptin (r = 0.65, p = 0.041) and with plasma glucose (r = 0.81, p = 0.015). In addition, the dietary intake/REE ratio was not only inversely related with LN leptin (-0.74, p = 0.037), but also with sTNF-R55 (r = -0.93, p = 0. 001) on day seven. In conclusion, temporary disturbances in the energy balance were seen during an acute exacerbation of COPD, related to increased leptin concentrations as well as to the systemic inflammatory response. Evidence was found that the elevated leptin concentrations were in turn under control of the systemic inflammatory response, and, presumably, the high-dose systemic glucocorticosteroid treatment.

Topics: Acute Disease; Aged; Blood Glucose; Body Weight; Energy Metabolism; Female; Homeostasis; Humans; Leptin; Lung Diseases, Obstructive; Lung Volume Measurements; Male; Middle Aged; Respiratory Insufficiency; Risk Factors; Systemic Inflammatory Response Syndrome

Recent animal and human studies have suggested that leptin secretion is closely linked to the functions of the hypothalamic-pituitary-adrenal (HPA) axis and the immune system, both of which are crucial in influencing the course and outcome of critical illness. Therefore, we measured basal plasma leptin levels and examined the circadian secretion of leptin, in parallel with the hormones of the HPA axis and a key cytokine, interleukin-6, in critically ill patients with acute sepsis. Sixteen critically ill patients from the University of Leipzig Intensive Care Unit were recruited for this study. All of these patients fulfilled the standard diagnostic criteria for sepsis. Plasma leptin levels were measured in all patients and controls at 09:00. In addition, in a subgroup of eight critically ill patients and all of the nine controls plasma leptin, cortisol, ACTH and interleukin-6 concentrations were measured every 4 hours for 24 hours. Mean plasma leptin levels were three-fold higher (18.9 +/- 4.5 ng/ml) in critically ill patients than controls (3.8 +/- 1.0 ng/ml, p < 0.05). Similarly, ACTH levels were lower (7.8 +/- 3.4 pmol/l) in patients than in controls (17.1 +/- 1.5 pmol/l, p < .001), while plasma cortisol levels were increased (947.6 +/- 144 nmol/l) in patients compared to controls (361.1 +/- 29, p < 0.001). Morning plasma interleukin-6 levels were markedly elevated in all patients with sepsis (1238.0 +/- 543.1 pg/ml) versus controls (6.4 +/- 1.7, p < 0.001). The controls exhibited a nyctohemeral fluctuation in plasma leptin levels with peak levels at 23:00; in contrast, septic patients, had no nocturnal rise of leptin. In healthy controls, plasma leptin and cortisol had reciprocal circadian rhythms with high nocturnal leptin levels and low nocturnal cortisol concentrations; in critically ill patients, this relation was abolished. Mean leptin levels were three-fold higher in patients who survived the septic episode (25.5 +/- 6.2, n = 10) than in non-survivors (8.0 +/- 3.7, n = 6, p < 0.01). We conclude that in addition to its function as an anti-obesity factor, leptin may play a role in a severe stress state such as acute sepsis.

Topics: Biomarkers; Circadian Rhythm; Critical Illness; Follow-Up Studies; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Leptin; Pituitary-Adrenal System; Proteins; Reference Values; Survivors; Systemic Inflammatory Response Syndrome