Inflammatory response markers

Inflammatory response markers have been detected with 2D/MS in the urine of stroke-prone rats at least 4 weeks before a stroke occurred and before the appearance of anomalous features could be detected in the brain by MRI (S4). The specificity of inflammatory response markers still needs to be determined however, this study suggests that proteins in a readily obtainable body fluid can be used as early diagnostic markers. 

The wide range of inflammation-related factors that adipocytes secrete is linked to the inflammatory response that the tissue exhibits in obesity [1]. Obesity in general, like an increasing number of other diseases, is characterised by a state of mild chronic inflammation, and adipose tissue plays a central role in this. The production of most inflammation-related adipokines increases markedly in obesity and there is an elevated circulating level of a number of these factors as well as of other inflammatory markers such as C-reactive protein (CRP). The increased production of inflammatory adipokines (and decreased production of adiponectin with its anti-inflammatory action) in the obese is considered to play a critical role in the development of the obesity-associated pathologies, particularly type 2 diabetes and the metabolic syndrome [1]. 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

Pyuria The presence of white blood cells in the urine, a known marker of inflammatory response to bacterial infection. 

Corticosteroids have a complex mechanism of action. They can affect the production of cytokines, leukotrienes and prostaglandins. This affects the production of eosinophils and release of other markers of the inflammatory response. Corticosteroids can affect other areas of the body and hence have a range of side-effects. 

Numerous biochemical markers of neuroinflammation have also been found in ALS tissue. The families of compounds include cytokines, chemokines, complement proteins, prostaglandins, interleukins, interferons, integrins, acute phase reactants, apolipoproteins, and (Table 27.1). Many of these biochemical markers have also been found in Alzheimer s disease tissues, suggesting that the inflammatory response in the two conditions may be similar (Eikelenboom and van Gool 2004). 

In clinical practice, only a few laboratory tests are of value in tlie assessment of protein-energy status It is particularly important to recognize that serum protein concentrations are not helpful in sick patients with any form of inflammatory process (see Chapter 20). Although serum albumin is often measured and reported as an indicator of protein-energy status, factors such as increased transcapillary escape and reduced hepatic synthesis malce it of little value as a nutritional marker. Serum albumin is, however, a valuable prognostic marker and is frequently used as part of prognostic indices. Short half-life proteins, such as transthyretin (prealbumin) also may be of some limited value in patients with no inflammatory response. 

Reminiscent of the above experimental studies, inflammatory responses are also seen in those clinical scenarios where coronary microembolization is likely to occur, i.e. nuclear factor - v.B is activated in patients with unstable angina79 and serum C-reactive protein is increased in patients who died from an acute coronary syndrome80. Interleukin-6 was higher up to 48 h in patients with unstable angina who experienced a major adverse cardiac event.81 These markers of inflammation were assumed to originate from... 

Overall, results from all these studies suggest that the long-term reduction in fat consumption improved both in vivo and ex vivo measures of immune functions. Increased response in these immune functions will generally indicate increased protection that may be of clinical significance. Only one study has compared the effects of lipid infusion on ex vivo measures of immune functions and the in vivo markers for diseases (van der Poll et al., 1995). In this study, intralipid infusion caused up to a 70% reduction in the in vitro secretion of IL-lp, IL-6, and TNF-ot however, it did not influence inflammatory responses to endotoxin (fever, leukocytosis, release of TNF and its receptor) and even potentiated plasma endotoxin responses (release of IL-6 and IL-8 and neutrophil degranulation). The authors concluded that hypertriglyceridemia does not inhibit the in vivo responses to endotoxin. 

Ascorbic Acid Deficiency. Scurvy is the classical disease associated with ascorbate deficiency. It is a disease of the connective tissue and probably is caused by inadequate crosslinking attributed to a lack of hydroxy-lated proline and lysine. Many consider scurvy to be an advanced stage of ascorbate deficiency. Chronic deficiencies may also (l)in-crease risk for malignancies, as evidenced by oxidized DNA markers and increased concentrations of reactive oxygen species (2) decreased immune function, as evidenced by less vitamin in neutrophils and lymphocytes (3) cardiovascular disease caused by the inflammatory response on the blood vessel walls and (4) cataract formation caused by decreased concentrations of ascorbate in the ocular tissues. 

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