Concentrations of Cytokines, Soluble Interleukin-2 Receptor, and Soluble CD30 in Sera of Patients with Hepatitis B Virus Infection during Acute and Convalescent Phases
“…One cannot discard, however, the possibility that besides the hypothesis of the existence of a defect in the generation of cGMP, other sources of could be contributing to its serum level via the expression of induced NO-synthase by inflammatory cells (macrophages, neutrophils, and vascular muscle cells, among others). Furthermore, the findings of raised levels of sIL-2R in diabetic patients are in accordance with those reported by Doganay et al [ 17 ] and this indicates activation of T lymphocytes [ 18 ]. Taken together, these findings suggest that this group of diabetic patients present a low-grade inflammation triggered by the diabetic mellitus state, which is favouring the progression of accelerated atherosclerosis.…”
This study compared the results of tumour necrosis factor alpha (TNF-α), interleukin-2 soluble receptor (sIL-2R), nitric oxide
metabolites (), C-reactive protein (CRP), and lipids (total cholesterol, high-density lipoprotein (HDL-cholesterol), lowdensity
lipoprotein (LDL-cholesterol), and triglycerides) between control group (nondiabetic subjects) and overweight type 2
DM subjects. To restrict the influence of variables that could interfere in the interpretation of data, subjects with obesity and/or
acute or chronic inflammatory disease, haemoglobinopathies, recent use of antibiotics, antiinflammatory drugs, and trauma were
excluded. Type 2 DM patients (n = 39; age 53.3 ± 9.0 years; median glycated haemoglobin A1c < 8%) presented higher
levels of TNF-α, triglycerides (P < .01), and sIL-2R (P < .05) than control group (n = 28; age 39.7 ± 14.1 years). CRP, LDL-cholesterol,
total cholesterol, and HDL-cholesterol did not differ among groups. Diabetic women
(n = 21) had higher levels of TNF-α, total
cholesterol, LDL-cholesterol, and HDL-cholesterol than diabetic
men (n = 18) (P < .05), but there were no differences among
sexes in the control group. This study indicates that increased level of proinflammatory markers occurs in type 2 DM even in the
absence of obesity and marked hyperglycaemia, confirming that the inflammation course of the atherosclerotic process is more
severe in diabetic patients than in nondiabetic subjects.
“…One cannot discard, however, the possibility that besides the hypothesis of the existence of a defect in the generation of cGMP, other sources of could be contributing to its serum level via the expression of induced NO-synthase by inflammatory cells (macrophages, neutrophils, and vascular muscle cells, among others). Furthermore, the findings of raised levels of sIL-2R in diabetic patients are in accordance with those reported by Doganay et al [ 17 ] and this indicates activation of T lymphocytes [ 18 ]. Taken together, these findings suggest that this group of diabetic patients present a low-grade inflammation triggered by the diabetic mellitus state, which is favouring the progression of accelerated atherosclerosis.…”
This study compared the results of tumour necrosis factor alpha (TNF-α), interleukin-2 soluble receptor (sIL-2R), nitric oxide
metabolites (), C-reactive protein (CRP), and lipids (total cholesterol, high-density lipoprotein (HDL-cholesterol), lowdensity
lipoprotein (LDL-cholesterol), and triglycerides) between control group (nondiabetic subjects) and overweight type 2
DM subjects. To restrict the influence of variables that could interfere in the interpretation of data, subjects with obesity and/or
acute or chronic inflammatory disease, haemoglobinopathies, recent use of antibiotics, antiinflammatory drugs, and trauma were
excluded. Type 2 DM patients (n = 39; age 53.3 ± 9.0 years; median glycated haemoglobin A1c < 8%) presented higher
levels of TNF-α, triglycerides (P < .01), and sIL-2R (P < .05) than control group (n = 28; age 39.7 ± 14.1 years). CRP, LDL-cholesterol,
total cholesterol, and HDL-cholesterol did not differ among groups. Diabetic women
(n = 21) had higher levels of TNF-α, total
cholesterol, LDL-cholesterol, and HDL-cholesterol than diabetic
men (n = 18) (P < .05), but there were no differences among
sexes in the control group. This study indicates that increased level of proinflammatory markers occurs in type 2 DM even in the
absence of obesity and marked hyperglycaemia, confirming that the inflammation course of the atherosclerotic process is more
severe in diabetic patients than in nondiabetic subjects.
“…By in vitro and in vivo studies, it has been shown that these inflammatory cells especially cytotoxic T‐lymphocytes produce a number of cytokines including TNF‐α and IFN‐γ which mediate the inflammatory process and contribute to the successful clearance of the virus. Additionally, these cytokines are also produced by injured endogenous cells, such as kuppfer cells, endothelial cells, hepatocytes and bile duct epithelial cells (1,6,10,11).…”
Although both chronic active hepatitis-B (CAH-B) and liver cirrhosis (LC) are characterised by various degrees of inflammation and hepatocyte necrosis, in advanced stage cirrhosis, marked fibrosis develops and inflammation and tissue necrosis diminishes. In this study, we aimed to investigate serum tumour necrosis factor-alpha (TNF-alpha) concentration in patients with CAH-B and LC and its relationship to disease activity. Serum samples were taken from 30 patients with CAH-B and 30 with LC at different stages of the disease. TNF-alpha concentrations were measured by the ELISA technique. Results were compared with those of 30 healthy controls. Mean plasma TNF-alpha levels were found as 2.47 +/- 2.98, 0.8 +/- 1.21 and 0.72 +/- 1.08 pg/ml in CAH-B, LC and control groups, respectively. TNF-alpha levels were significantly higher in CAH-B group than LC and control groups (p <0.01 and p < 0.05, respectively). Although mean plasma TNF-alpha level of cirrhotic patients at Child-A stage was markedly high (3.31 +/- 0.15), no significant difference has been found between LC and control groups (p > 0.05). TNF-alpha concentrations were positively correlated with hepatitis activity index (Knodell's score) in CAH-B group whereas negatively correlated with Child-Pugh score in LC group (r =0.73, p < 0.01 and r = -0.42, p < 0.05, respectively). Our study showed that TNF-alpha level increases in patients with CAH-B correlated with histologic activity index. So it can be used to evaluate disease activity. Additionally, marked reduction of TNF-alpha concentration in advanced cirrhosis suggested that TNF-alpha production is determined by hepatic damage and inflammation.
“…In children, sIL‐2R has been used as a diagnostic or prognostic marker of various immunological disorders, such as refractory Kawasaki disease, hemophagocytic syndrome, and macrophage activation syndrome caused by systemic juvenile idiopathic arthritis . It was also reported that the serum level of sIL‐2R is elevated in patients with acute hepatitis B virus infection . Lobo‐Yeo et al .…”
This survey clarified that the clinical profile of pediatric AIH in Japan is not only different from that of adult AIH in Japan but is also different from that of pediatric AIH in other countries.
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