Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Trauma and surgery induce extensive physiological changes, commonly denominated the acute phase reaction (APR). This APR is activated by various kinds of stimuli, namely nociceptive stimulations, tissue injury, tissue ischaemia and reperfusion as well as by haemodynamic disturbances which occur commonly in such patients. APR is mainly characterised by the release of counter-regulatory hormones, complex metabolic changes and by the hepatic synthesis of numerous acute phase factors (C-reactive protein, haptoglobin, complement protein, etc). In addition, fever is typically present and there is a resistance to the nutritional support. The intensity of APR is variable, according to the extent of surgery, the subsequent course, occurrence of complications and to various factors related to the patient and its treatment. In patients with non complicated surgery and low or moderate severity trauma, the metabolic changes are minor and self-limited. In such a condition, there is no need for nutritional support. Conservely, in patients with complicated surgery or major trauma, there is an extensive APR, which can be very prolonged. This results in important and sustained metabolic changes, leading to extensive catabolism and progressive loss of body cell mass. The latter is amplified by the decreased body ability to adapt to starvation and by the resistance to the nutritional support that typically occur in complicated postoperative and trauma patients. Total parenteral nutrition does not prevent from metabolic changes occurring in surgical patients. By contrast, several experimental and human studies have shown that early enteral nutrition may alleviate both the endocrine and metabolic responses in such conditions. Regional anaesthesia, particularly by the epidural route, may also decrease but not abolish the extent of APR.
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PMID:[Consequences of surgery on nutritional status]. 748 33

We investigated the effects of acute starvation on mitogen-induced T-cell activation and Th1/Th2 cytokine responses in rheumatoid arthritis (RA) patients. Ten RA patients with active disease underwent a 7-day fast followed by a 2-week refeeding period. Immunological, hormonal, laboratory and clinical evaluations were carried out on days 0, 7 and 21. Using flow cytometry, mitogen-stimulated T-cell activation was assessed in fresh heparinised blood via analysis of CD69 expression. Production of Th1 (interferon-gamma) and Th2 (interleukin-4, IL-4) cytokines was also assessed by ELISA. The 7-day fast significantly decreased the erythrocyte sedimentation rate, C-reactive protein level, joint count, morning stiffness, body weight, CD4+ and CD8+ counts and CD69+ expression on mitogen stimulated CD4+ lymphocytes. A significant increase in mitogen-induced IL-4 production after fasting was found. The fast markedly reduced serum leptin and insulin-like growth factor-1 concentrations. No significant differences occurred in serum cortisol or prolactin before and after fasting. Decreases in CD4+ lymphocyte activation during fasting correlated with decreases in body weight. Our results suggest that the clinical and laboratory improvements in fasting RA patients may be attributed to decreased CD4+ T-cell activation and an increase in the number and/or function of IL-4-producing Th2 cells. Factors associated with loss of body weight during acute starvation appear to have an inhibitory effect on CD4+ lymphocyte activation.
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PMID:Decreased CD4+ lymphocyte activation and increased interleukin-4 production in peripheral blood of rheumatoid arthritis patients after acute starvation. 1052 54

Changes in plasma protein composition normally associated with malnutrition, specifically hypoalbuminemia and reduced levels of tranferrin and prealbumin, usually only occur in the presence of preterminal starvation in the absence of inflammation. Thus, reduced levels of any of these proteins suggest that the inflammatory response has been activated. Inflammation also alters lipoprotein structure and function, and oxidation of low-density lipoprotein (LDL). This decreases high-density lipoprotein (HDL) levels and reduces its capacity to function as an antioxidant, and increases the levels of proteins, such as fibrinogen, associated with vascular disease. Cytokines and acute phase proteins, such as C-reactive protein (CRP), also up-regulate expression of adhesion molecules on the vascular endothelium, making them more effective targets for macrophage adhesion. Leukocyte-derived myeloperoxidase functions as an "NO oxidase" in the inflamed vasculature and contributes to decreased NO bioavailability and compromises vascular reactivity. The link between inflammation and apparent malnutrition explains the relationship between low levels of albumin, prealbumin, and transferrin with subsequent cardiovascular risk.
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PMID:Effects of inflammation on plasma composition and endothelial structure and function. 1564 15

Acute pancreatitis is a dynamic, often progressive disease; 14-20% require intensive care in its severe form due to multiorgan dysfunction and/or failure. This review was created using systematic literature review of articles published on this subject in the last 5 years. The outcome of severe acute pancreatitis is determined by the inflammatory response and multiorgan dysfunction - the prognostic scores (Acute Physiology and Chronic Health Evaluation, Glasgow Prognostic Index, Sepsis-related Organ Failure Assessment, Multi Organ Dysfunction Syndrome Scale, Ranson Scale) can be used to determine outcome. Clinical signs (age, coexisting diseases, confusion, obesity) and biochemistry values (serum amylase, lipase, C-reactive protein, procalcitonin, creatinine, urea, calcium) have important prognostic roles as well. Early organ failure increases the risk of late abdominal complications and mortality. Intensive care can provide appropriate multi-function patient monitoring which helps in early recognition of complications and appropriate target-controlled treatment. Treatment of severe acute pancreatitis aims at reducing systemic inflammatory response and multiorgan dysfunction and, on the other side, at increasing the anti-inflammatory response. Oral starvation for 24-48 hours is effective in reducing the exocrine activity of the pancreas; the efficacy of protease inhibitors is questionable. Early intravascular volume resuscitation and stable haemodynamics improve microcirculation. Early oxygen therapy and mechanical ventilation provide adequate oxygenation. Electrolyte and acid-base control can be as important as tight glucose control. Adequate pain relief can be achieved by thoracic epidural catheterization. Early enteral nutrition with immunonutrition should be used. There is evidence that affecting the coagulation cascade by activated protein C can play a role in reducing the inflammatory response. The complex therapy of acute pancreatitis includes appropriate antibiotics, thrombo-embolic prophylaxis and in certain cases plasmapheresis and/or haemofiltration. Reducing intraabdominal pressure may be necessary in the acute phase. Intensive care multidisciplinary teamwork can reduce the mortality of severe acute pancreatitis from 30% to 10%.
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PMID:[Principles of intensive care in severe acute pancreatitis in 2008]. 1900 43

Cancer-induced cachexia (CIC) is a paraneoplastic syndrome that may account for up to 20% of deaths in cancer patients. Cachexia includes distinct metabolic changes that are the result of an acute-phase response (APR) mounted by the host as a reaction to tumor cells. These changes include increased muscle proteolysis, increased fat lipolysis, and increased hepatic production of acute-phase proteins such as C-reactive protein and fibrinogen. This APR pathogenesis is an important consideration in trying to treat cachectic patients as most therapies do not target the APR and its subsequent metabolic effects. Although there is currently no cure for CIC, the oncologist frequently encounters cachectic patients in practice, and evidence-based management is needed. We review the current data for assessment of starvation and cachexia, providing guidelines for management that include serum markers and functional assessment. In addition, a review of current therapies is provided, including hypercaloric feeding and nutritional intervention to address starvation, as well as data on appetite stimulants such as corticosteroids and megestrol acetate. Experimental therapies are also discussed, including nonsteroidal antiinflammatory drugs, tumor necrosis factor alpha antagonists, tetrahydrocannabinol, growth hormone, ghrelin, oxandrolone, and omega-3 fatty acids.
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PMID:Cancer-induced cachexia: a guide for the oncologist. 1988 31

Nutritional status is often impaired in ambulatory rehabilitation patients. Wasting conditions can be classified as starvation, sarcopenia or cachexia but differences between these are not well defined, and misdiagnosis may lead to inappropriate intervention. A secondary analysis of data from 187 ambulatory rehabilitation patients aged >=60 years aimed to identify patients with one or more wasting condition, and investigate the impact on common rehabilitation outcomes. Starvation was defined by fat-free mass index and the Council on Nutrition Appetite Questionnaire score; sarcopenia by fat-free mass index and quadriceps strength; and cachexia by fat-free mass index and serum C-reactive protein. Selected rehabilitation outcomes were compared for those who were, and those who were not, identified as having one or more wasting condition. Of those identified with starvation (n=30), all were also identified as sarcopenic and 20 as cachectic; of those identified as sarcopenic (n=75), 30 had starvation and 37 were cachectic; and of those identified as cachectic (n=37), 20 had starvation and all were sarcopenic. Twenty participants were identified as having all three conditions. Those with starvation had higher level of depression (p=0.003), lower self-rated health (p=0.032), and lower levels of physical function (motor p=0.006; process p=0.004) than those with no evidence of a wasting condition. Those who had sarcopenia had lower physical function (motor p=0.012; process p=0.003) as did those with cachexia (motor p=0.025; process p=0.042). Results suggest problems in operationalising definitions in an ambulatory clinical setting. The overlap identified in this analysis suggests that up to 40% (75/187) of patients could be misidentified and prescribed inappropriate nutritional support.
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PMID:The complexity of treating wasting in ambulatory rehabilitation: Is it starvation, sarcopenia, cachexia or a combination of these conditions? 2270 28

C-reactive protein (CRP) acts as a biomarker reflecting different degrees of inflammation. Accumulating reports have suggested that there is a close relationship between CRP and various cancers. However, the influence of CRP on the development of tongue squamous cell carcinoma (TSCC) remains unclear. The purpose of this study was to investigate the role of CRP in TSCC. The results of immunohistochemical staining and statistical analyses showed that CRP expression was associated with TSCC tumor size, lymph node metastasis and pathological differentiation. Cell Counting Kit-8 (CCK-8) assay revealed that CRP could enhance TSCC cell proliferation in a dose- and time-dependent manner. Moreover, with CRP stimulation, proliferating cell nuclear antigen (PCNA) expression patterns presented a notable time-dependent up-regulation. In addition, CRP could enhance the invasion and migration of TSCC cells, as revealed by transwell and wound-healing assays, respectively. Annexin V-FITC/PI staining showed that CRP could protect TSCC cells from starvation- and drug-induced apoptosis. With CRP stimulation, the protein expression levels of phosphorylated protein kinase B (pAkt), phosphorylated mammalian target of rapamycin (pmTOR) and phosphorylated S6 ribosomal protein (pS6) were significantly increased, as demonstrated by western blot analysis. Our data suggest that CRP may play an important role in the development of TSCC. Moreover, the biological effects of CRP on TSCC cells might be related to Akt, mTOR, and S6.
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PMID:C-reactive protein is associated with the development of tongue squamous cell carcinoma. 2938 6