Evaluation of Intercellular adhesion molecule-1 (ICAM-1), Tumor necrosis factor α (TNF-α), Interleukins (IL-6, IL-8) and C-reactive protein (CRP) Levels in Neonatal calves with presumed Septicemia

Helicobacter pylori is a Gram-negative spiral-shaped bacterium that infects from 30% to 50% of the world’s population and it is one of the most important in dyspeptic syndrome causes of gastritis and peptic ulcer. H. pylori is one of the most common chronic bacterial infections especially in the development countries because the socioeconomic contribute to chronic disease. The infection induces an acute polymorphonuclear infiltration in the gastric mucosa. Infection with H. pylori has been epidemiologically linked to some extra digestive conditions, including ischemic heart disease, diabetes mellitus (DM), and others. The patients with DM are at risk for H. pylori infection, since they have coupled susceptibility of to a wide range of infections as a result of chronic elevation of blood glucose level and impairment of immune functions. Chronic inflammation is a risk factor for coronary heart disease, because inflammation, vascular injury and thrombosis are considered to cause atherosclerosis. The risk of cardiovascular events is associated with increased levels of the acute phase proteins, C-reactive protein (CRP), and pro-inflammatory cytokines. Interleukin 6 (IL-6), a major pro-inflammatory cytokine is produced in a variety of tissues, including activated leukocytes, adipocytes, and endothelial cells. CRP is the principal downstream mediator of the acute phase response and is primarily derived through IL-6-dependent hepatic biosynthesis. Tumor necrosis factor-α (TNF-α), as an important inflammatory factor, has been shown to play a central role in the pathogenesis of diabetes. CRP and IL-6 were determinant of risk for the development of type 2 DM in apparently healthy middle-aged women. Since the prevalence of infected persons with H. pylori in Kosovo is high, the aim of this study was the evaluation of cytokines (IL1, TNF-α) and CRP in diabetic type 2 patients with positive H. pylori.

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Evaluation of tumor necrosis factor-α (TNF-α) and C-reactive protein over lipase amylase ratio for acute pancreatitis in north Indian population

Journal of Medical Science And clinical Research ◽

10.18535/jmscr/v5i7.68 ◽

2017 ◽

Vol 5 (7) ◽

Author(s):

Sweta Kumari ◽

Keyword(s):

Acute Pancreatitis ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Indian Population ◽

North Indian Population ◽

C Reactive Protein ◽

Reactive Protein ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

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Blood Levels of Nitric Oxide, C-Reactive Protein, and Tumor Necrosis Factor-α Are Upregulated in Patients with Malignancy-Associated Hypercoagulable State: Pathophysiologic Implications

Clinical and Applied Thrombosis/Hemostasis ◽

10.1177/107602960401000408 ◽

2004 ◽

Vol 10 (4) ◽

pp. 357-364 ◽

Cited By ~ 9

Author(s):

D. Fareed ◽

O. Iqbal ◽

M. Tobu ◽

D. A. Hoppensteadt ◽

J. Fareed

Keyword(s):

Nitric Oxide ◽

Cancer Patients ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Hypercoagulable State ◽

C Reactive Protein ◽

Reactive Protein ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

Endogenous generation of nitric oxide (NO) plays an important role in the regulation of cardiovascular and inflammatory responses. This mediator is synthesized by a family of enzymes collectively known as NO synthase. Several isoforms of this enzyme have been identified and can be grouped as constitutive or inducible. Increased production of NO is reported in several inflammatory disorders, such as sepsis, arthritis, thrombotic thrombocytopenic purpura (TTP), and antiphospholipid syndrome. In addition, NO upregulates cyclo-oxygenase-2 and synthesis of several other inflammatory cytokines. Inflammation and thrombotic complications are usually associated with malignancy. Earlier reports indicate the upregulation of tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), and tissue factor (TF) in patients with malignancy. To determine the relationship between inflammatory cytokines and NO in cancer patients with hypercoagulable states, baseline plasma samples from 160 patients with confirmed malignancy and hypercoagulable state were analyzed for NO levels. A chemical method based on a chemiluminescent reaction between NO and ozone using a highly sensitive gas phase NO analyzer was used. CRP, TF, and TNF-α were measured using enzyme-linked immunosorbent assay methods. Of the 160 patients who were plasma tested, the baseline NO levels ranged from 13.7 to 98.6 μM (63.1±15.9 μM, mean±SD) in contrast to age-matched control, which ranged from 9.1 to 34.6 μM (19.8±6.2 μM, mean±SD, n=138). Cancer patients also showed marked variations in the NO levels. Eighteen of 60 cancer patients exhibited greater than 60 μM NO levels. The CRP, TNF-α and TF were also significantly elevated. A correlation between CRP (r2=0.73) and NO levels was noted in cancer patients with hypercoagulable state. These data suggest that the pathogenesis associated with malignancy/hypercoagulable state is associated with an inflammatory component. In addition, the observed hemodynamic changes in some of the cancer patients may be due to increased NO production.

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