Tumor Necrosis Factor In Patients Research Articles

Five commonly used traditional Chinese medicine formulas in the treatment of ulcerative colitis: A network meta-analysis.

Currently, traditional Chinese medicine (TCM) formulas are commonly being used as adjunctive therapy for ulcerative colitis in China. Network meta-analysis, a quantitative and comprehensive analytical method, can systematically compare the effects of different adjunctive treatment options for ulcerative colitis, providing scientific evidence for clinical decision-making. To evaluate the clinical efficacy and safety of commonly used TCM for the treatment of ulcerative colitis (UC) in clinical practice through a network meta-analysis. Clinical randomized controlled trials of these TCM formulas used for the adjuvant treatment of UC were searched from the establishment of the databases to July 1, 2022. Studies that met the inclusion criteria were screened and evaluated for literature quality and risk of bias according to the Cochrane 5.1 standard. The methodological quality of the studies was assessed using ReviewManager (RevMan) 5.4, and a funnel plot was constructed to test for publication bias. ADDIS 1.16 statistical software was used to perform statistical analysis of the treatment measures and derive the network relationship and ranking diagrams of the various intervention measures. A total of 64 randomized controlled trials involving 5456 patients with UC were included in this study. The adjuvant treatment of UC using five TCM formulations was able to improve the clinical outcome of the patients. Adjuvant treatment with Baitouweng decoction (BTWT) showed a significant effect [mean difference = 36.22, 95% confidence interval (CI): 7.63 to 65.76]. For the reduction of tumor necrosis factor in patients with UC, adjunctive therapy with BTWT (mean difference = -9.55, 95%CI: -17.89 to -1.41), Shenlingbaizhu powder [SLBZS; odds ratio (OR) = 0.19, 95%CI: 0.08 to 0.39], and Shaoyao decoction (OR = -23.02, 95%CI: -33.64 to -13.14) was effective. Shaoyao decoction was more effective than BTWT (OR = 0.12, 95%CI: 0.03 to 0.39), SLBZS (OR = 0.19, 95%CI: 0.08 to 0. 39), and Xi Lei powder (OR = 0.34, 95%CI: 0.13 to 0.81) in reducing tumor necrosis factor and the recurrence rate of UC. TCM combined with mesalazine is more effective than mesalazine alone in the treatment of UC.

The Relationship of immunoglobulin-e and tumor necrosis factor in patients with allergic rhinitis in Babylon province

Abstract Background: Rhinitis is defined as inflammation of the mucous membranes of the nose usually that is accompanied by swelling of the mucosa and a nasal discharge. It is caused by immunoglobulin E (IgE)-mediated reactions to inhaled allergens, smoking and alcohol use, gender, age, overweight, adoption of pets, race, educational achievement, and family history can represent a risk factor for allergic rhinitis (AR). Objectives: To find the effect of electrolytes tumor necrosis factor (TNF)-α and IgE on AR and study the influence of smoking, gender, and obesity (as a risk factor on AR) on the levels of TNF-α and IgE. Materials and Methods: Eighty subjects for this study were enrolled; 40 of those who have AR age ranged between 18 and 50 years. A control group of 40 subjects who appear to be in good health was selected. This study is a case–control study. TNF-alpha concentration and immunoglobulin-E were measured in serum by an enzyme-linked immunosorbent assay (ELISA) technique also The electrolytes concentrations were measured in the serum using an Abbott device with Integrated Chip Technology (ICT) human kit. The electrolytes were also measured in the serum using the Abbott device. Full history was taken from all patients, which include age, residence, smoking, body mass index, and family history of AR. Results: The results reveal a significant difference (P < 0.05) in levels of TNF-α, Ig-E between patients and controls, There was no significant difference between smoker and non- smoker, normal weight and overweight groups in patients and controls groups.

Autoantibodies to Tumor Necrosis Factor in Patients with Active Pulmonary Tuberculosis.

Tumor necrosis factor (TNF) plays an important role in immune responses to the causative agent of tuberculosis, Mycobacterium tuberculosis. Additionally, TNF can also mediate many negative disease manifestations. The aim of this study was to assess the contribution of anti-TNF autoantibodies to the pathogenesis of active pulmonary tuberculosis (TB). The levels of anti-TNF autoantibody classes and subclasses were determined by applying enzyme-linked immunosorbent assays (ELISAs). The levels of TNF and of its soluble receptors were also evaluated using commercial ELISA kits. The levels of both types of soluble TNF receptors were lower patients with TB than in healthy donors. Patients with TB had higher titers of immunoglobulin (Ig)G class and IgG3 subclass anti-TNF autoantibodies in comparison with healthy donors. Patients who had a disseminated TB infection had higher TNF level and IgG, IgG1 and IgG3 autoantibody titers compared with patients who had a localized TB infection. Changes in the titers of anti-TNF autoantibody classes and subclasses were noted in patients with TB, suggesting their possible contribution to the disease pathogenesis of TB.

Molecular and Genetic Characterization of Tumor Samples from Patients with Relapsed or Refractory Follicular Lymphoma Identifies Factors Influencing Response to Tazemetostat

Molecular and Genetic Characterization of Tumor Samples from Patients with Relapsed or Refractory Follicular Lymphoma Identifies Factors Influencing Response to Tazemetostat

Expansion of CD4 T Lymphocytes Expressing Interleukin 17 and Tumor Necrosis Factor in Patients with Major Depressive Disorder.

Background: We have investigated the distribution of the Th1, Th2 and Th17 subsets in circulating CD4+ T lymphocytes and their naïve (TN), effector (TE), central (TCM) and effector memory (TEM) activation/differentiation stages in patients with major depressive disorder (MDD). Methods: Thirty MDD patients and 30 healthy controls were studied. The counts of circulating CD4+ T lymphocytes and their distribution on the TN, TE, TCM and TEM activation/differentiation stages were analyzed by polychromatic flow cytometry. The intracytoplasmic interferon gamma (IFNγ), interleukin (IL)-4, IL-17A and tumor necrosis factor alpha (TNF-alpha) and membrane CD28 expression were also measured. The serum IFNγ, IL-4, Il-17A and TNF-alpha were measured by Luminex, respectively. Results: MDD patients had normal counts of CD4+ T lymphocytes and of their TN, TCM and TEM subsets but increased number and percentage of TE CD4+ subset. CD4+ T lymphocytes had significantly enhanced percentage of cells that express IL-17 and TNF-alpha explained by the expansions found in the TN, TCM and, TEM and TCM, TEM and TE activation/differentiation stages, respectively. A selective increase in the percentages of TCM and TEM expressing IFNγ was also observed. We found a significant correlation between the percentages of CD4+ T lymphocytes expressing IFNγ and TNF-alpha in these patients. MDD patients showed increased serum levels of IL-17 and TNF-alpha, but normal IFNγ and IL-4 concentration. Limitations: the cross-sectional nature of the study could be considered a limitation. Conclusions: MDD patients have abnormal circulating CD4+ T lymphocytes with expansion of the IL-17 and TNF-alpha expressing cells as well as increased levels of circulating IL-17 and TNF-alpha.

The level of proinflammatory cytokines: interleukins 12, 23, 17 and tumor necrosis factor α in patients with metabolic syndrome accompanying severe psoriasis and psoriatic arthritis.

IntroductionThe incidence of metabolic syndrome is estimated at 15–24% in the general population and at 30–50% in patients with psoriasis. A probable cause of the described correlation is a constant release in chronic dermatosis of proinflammatory cytokines and their influence on individual systems and organs.AimAssessment of the concentration of the proinflammatory cytokines (IL-12, IL-23, IL-17 and TNF-α) in blood serum and their correlation with the intensity of skin lesions, the presence of psoriatic arthritis and the risk of development of obesity and metabolic syndrome.Material and methodsThe concentrations of subunit p70 IL-12, IL-17 and IL-23, and TNF-α in subjects with psoriasis and metabolic syndrome were determined.ResultsThe level of the studied cytokines, IL-17, IL-23 and TNF-α was higher in patients diagnosed with psoriasis. Higher levels of IL-17, IL-23 and TNF-α were observed in patients with metabolic syndrome accompanying psoriasis. A higher level of IL-17 and IL-23 was found in sera of patients with psoriatic arthritis in comparison to normal psoriasis.ConclusionsIn the study, a higher level of IL-17 and IL-23 was also shown in patients with psoriatic arthritis in comparison to patients with normal psoriasis. The effectiveness of anti-IL12/23 drugs in psoriatic arthritis is a confirmation of the obtained results of the studies. Additionally, the increased level of IL-17, both in patients with metabolic syndrome and with psoriasis, could indirectly indicate an increased cardiovascular risk in patients with affected joints in comparison to psoriasis affecting only the skin.

High levels of soluble GPR56/ADGRG1 are associated with positive rheumatoid factor and elevated tumor necrosis factor in patients with rheumatoid arthritis.

GPR56/ADGRG1 is a member of the adhesion-class G protein-coupled receptor (aGPCR) family important in brain development, oncogenesis and tumor metastasis. Like other aGPCRs, GPR56 is cleaved at the GPCR proteolysis site (GPS) motif into an N-terminal fragment (NTF) and a C-terminal fragment (CTF). Existence of soluble GPR56 (sGPR56) has been shown invitro, however the underlying mechanism and its pathophysiologic role remains undetermined. To assess the presence of sGPR56 in human serum using ELISA assay and compare the serum sGPR56 levels among patients of various chronic inflammatory diseases and healthy subjects. In this study, serum samples from patients with systemic lupus erythematosus (SLE) (n=57), rheumatoid arthritis (RA) (n=95), Sjögren's syndrome (SS) (n=29), ankylosing spondylitis (AS) (n=51), and normal controls (n=81) were analyzed using sGPR56-specific ELISA. We show that serum sGPR56 levels are increased in patients of RA, but not in those with SLE, SS and AS. Intriguingly, serum sGPR56 levels in RA patients correlated with positive rheumatoid factor, a marker of bone erosion and poor outcome. In addition, an elevated sGPR56 level is also noted in RA patients with higher tumor necrosis factor level. we conclude that sGPR56 is present invivo and sGPR56 level is elevated in certain chronic inflammatory diseases such as RA. Hence, sGPR56 might be considered a potential biomarker for RA disease progression.

295. Paradoxically Elevated Levels of Tumour Necrosis Factor in Patients with Juvenile Idiopathic Arthritis on Etanercept

295. Paradoxically Elevated Levels of Tumour Necrosis Factor in Patients with Juvenile Idiopathic Arthritis on Etanercept

Frontotemporal dementia—time to target inflammation?

Systemic inflammation has been associated with dementia. A new study has found an increased rate of autoimmune disorders and elevated serum levels of tumour necrosis factor in patients with frontotemporal dementia associated with TDP-43 pathology. These findings help in understanding disease mechanisms and in identification of biomarkers of this heterogeneous disease.

Effects of invigorating Qi and promoting blood circulation drugs combined with compound triamcinolone acetonide on interleukin 2 and tumor necrosis factor in patients With oral lichen planus

Objective To observe the effects of invigorating qi and promoting blood circulation drugs combined with compound triamcinolone acetonide on the interleukin 2 and tumor necrosis factor in patients with oral lichen planus. Methods 43 patients with oral lichen planus were randomly recurited into two groups by means of random number table.The control group was treated with prednisone orally, 30 mg/d, then reduced to IS mg/d at first two weeks, and further reduced to S mg/d at first three weeks. Maintained the dose for four to eight weeks. While the treatment group was treated with 40 mg compound triamcinolone acetonide at injury area by local injection,which was mixed with 2% lidocaine hydrochloride injection, once a week, continuous therapy for 2 months. Qi regulating and blood activating drugs were also added to the treatment group, with 150ml each time, once a day for 2 months. The clinical symptoms were observed, serum interleukin 2 and tumor necrosis factor were detected before and after the treatment. Results Compared with the control group, serum interleukin 2 and tumor necrosis factor in the treatment group decreased significantly after treatment [IL-2 (2.58± 0.32)ug/L, TNF(156.45+13.67)ng/L,P＜0.05]. Serum interleukin 2 and tumor necrosis factor decreased significantly after the treatment in the control group [IL-2(5.21±0.53) μg/L, TNF (205.02±15.75) ng/L,P＜ 0.05]. The total effective rate of the treatment group and the control group was 86.4% and 66.7% respectively, there was a significant difference (x2=3.321,P＜0.05).Conclusion Invigorating qi and promoting blood circulation drugs combined with compound triamcinolone acetonide on oral lichen planus was better than prednisone. Key words: Oral lichen planus; Chinese medicine; Compound triamcinolone acetonide

Autoantibodies to Tumor Necrosis Factor in Patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus

To detect autoantibodies to tumor necrosis factor (TNF) in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), and to determine their clinical correlates. Ninety-two patients with RA and 62 with SLE were studied. Sera were examined for autoantibodies to TNF by enzyme linked immunoassay. Levels of these autoantibodies were analyzed in respect to markers of inflammation such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and joint erosions, as well as other clinical, laboratory, and therapeutic aspects of RA and SLE. Anti-TNF levels were higher in those RA patients without erosions, but did not correlate with ESR or CRP. These observations suggest that autoantibody anti-TNF may be part of the innate immune system and may contribute to decreased inflammation in patients with RA.

Takayasu’s arteritis

Takayasu's arteritis is a rare disease that causes arterial inflammation with resulting stenosis or aneurysm of affected vessels. It primarily affects young females and has a predilection for the aorta, its primary branches, and the pulmonary arteries. Patients may present with symptoms of organ ischemia, such as stroke or claudication, or with signs of arterial stenosis, such as absent pulses or asymmetric blood pressures. Most patients require chronic immunosuppressive therapy to control inflammation. The foundation of therapy is glucocorticoids, which are often used in combination with other immunosuppressive agents, such as methotrexate, azathioprine, or mycophenolate mofetil. The goal of systemic therapy is to induce and maintain disease remission, often defined as the absence of new arterial lesions, lack of systemic symptoms, and ability to taper prednisone to less than 10 mg/d. Promising results have been seen with the use of agents directed against tumor necrosis factor in patients who have failed to maintain remission with standard therapies. Revascularization procedures such as percutaneous transluminal angioplasty (PTA) or bypass grafting are reserved for patients who have critical organ ischemia or severe extremity claudication. Bypass grafting has a lower restenosis rate than PTA and is the preferred method of restoring blood flow to affected organs. Frequent laboratory testing is recommended to monitor for drug toxicity and signs of disease relapse. At each clinic visit, physicians should auscultate for bruits over primary arterial branches and evaluate for asymmetry between arm and leg blood pressures. Biannual radiographic imaging with magnetic resonance or CT angiography is helpful to examine for evidence of new aortic aneurysms or arterial stenoses.

Controlling malignant pericardial effusion by intrapericardial administration of recombinant mutant human tumor necrosis factor in patients with carcinoma

Objective To evaluate the therapeutic efficacy of injecting recombinant mutant human tumor necrosis factor (rmhTNF) into pericardial cavity of carcinoma patients with malignant pericardial effusion.

Targeted Anticytokine Therapy and the Failing Heart

Recent studies have identified the importance of proinflammatory mediators in the development and progression of chronic heart failure (CHF). The growing appreciation of the pathophysiologic consequences of sustained expression of proinflammatory mediators in preclinical and clinical CHF models culminated in a series of multicenter clinical trials that used targeted approaches to neutralize tumor necrosis factor in patients with moderate-to-advanced CHF. However, these targeted approaches have resulted in worsening CHF, thereby raising a number of important questions about what role, if any, proinflammatory cytokines play in the pathogenesis of CHF. This review summarizes what has been learned from the negative clinical trials, as well as the potential direction of future research in this area.

Strategies for targeting tumour necrosis factor in IBD

Tumour necrosis factor (TNF) plays an important role in mediating the inflammation of inflammatory bowel disease, in particular, Crohn's disease. Strategies aimed at reducing tumour necrosis factor in patients with inflammatory bowel disease include the mouse/human chimeric monoclonal antibody infliximab, the humanized monoclonal antibody CDP571, the human soluble TNF p55 receptor onercept, the human monoclonal antibody D2E7 (adalimumab), the anti-TNF human antibody Fab′ fragment–polyethelene glycol (PEG) conjugate CDP870, and the small molecules thalidomide and CNI-1493 (MAP-kinase inhibitor). Infliximab is effective for treating active Crohn's disease, maintaining remission, closing fistulas, maintaining fistula closure, and treating ankylosing spondylitis. Infliximab is also being investigated for the treatment of ulcerative colitis. Side-effects occurring in patients treated with infliximab include human anti-chimeric antibodies, infusion reactions, delayed hypersensitivity reactions, formation of autoantibodies, and, in rare circumstances, drug-induced lupus and serious infections, including tuberculosis. CDP571 is effective for treating active Crohn's disease, steroid sparing, and possibly for closing fistulas and maintaining remission. Side-effects occurring in patients treated with CDP571 include anti-idiotype antibodies, infusion reactions and the formation of autoantibodies. A controlled trial of etanercept in patients with Crohn's disease was negative. Pilot studies with onercept, thalidomide, and CNI-1493 have suggested benefit for Crohn's disease. There are no published data on the efficacy of adalimumab (D2E7) or CDP870 for either Crohn's disease or ulcerative colitis. Anti-tumour necrosis factor therapies are effective for the treatment of Crohn's disease and are being investigated for ulcerative colitis.

Inflammatory mediators and the failing heart: past, present, and the foreseeable future.

Recent studies have identified the importance of proinflammatory mediators in the development and progression of heart failure. The growing appreciation of the pathophysiological consequences of sustained expression of proinflammatory mediators in preclinical and clinical heart failure models culminated in a series of multicenter clinical trials that used "targeted" approaches to neutralize tumor necrosis factor in patients with moderate to advanced heart failure. However, these targeted approaches have resulted in worsening heart failure, thereby raising a number of important questions about what role, if any, proinflammatory cytokines play in the pathogenesis of heart failure. This review will summarize the tremendous growth of knowledge that has taken place in this field, with a focus on what we have learned from the negative clinical trials, as well as the potential direction of future research in this area.

Effect of phosphodiesterase III inhibitor on plasma concentrations of endothelin-1 and tumour necrosis factor in patients with acute heart failure

Objective — Effects of loprinone hydrochloride on plasma ET-1 and TNF-a levels were assessed in patients with acute heart failure (AHF).Methods and results — Thirty patients with AHF were divided into 2 groups and treated with loprinone hydrochloride (0.3 μg/kg/min) (n = 15) or placebo (n = 15).Twenty healthy controls were also included. Plasma ET-1 and TNF-a were significantly higher in the 30 AHF patients than in the healthy controls. In AHF patients, loprinone hydrochloride lowered plasma ET-1 and TNF-a (p < 0.01).Conclusion — ET-1 and TNF-a may play pathophysiological roles in the progression of AHF.Loprinone hydrochloride is effective in reducing plasma ET-1 and TNF-a levels in AHF patients.

The change of interleukin-6 and tumor necrosis factor in patients with obstructive sleep apnea syndrome.

The levels of lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) expression in culture of peripheral blood mononuclear cells (PBMC) and the plasma levels of IL-6 and TNF-alpha in the patients with obstructive sleep apnea syndrome (OSAS) were measured and the relationship between OSAS and IL-6 or TNF-alpha expression studied. Both IL-6 and TNF-alpha were detected by using ELISA in 22 patients with OSAS and 16 normal controls. The levels of LPS-induced IL-6 (787.82 +/- 151.97 pg/ml) and TNF-alpha (4165.45 +/- 1501.43 pg/ml) expression in the supernatant of the culture of PBMC and plasma level of IL-6 (50.67 +/- 4.70 pg/ml) and TNF-alpha (299.09 +/- 43.57 pg/ml) in the patients with OSAS were significantly higher than those in the normal controls (in the supernatant of the culture of PBMC: 562.69 +/- 197.54 pg/ml and 1596.25 +/- 403.08 pg/ml respectively; in the plasma; 12.69 +/- 2.75 pg/ml and 101.88 +/- 21.27 pg/ml respectively). There were significantly positive correlation between the levels of IL-6 and TNF-alpha and the percentage of time of apnea and hyponea, as well as the percentage of time spending at SaO2 below 90% in the total sleep time. It was concluded that LPS-induced IL-6 and TNF-alpha levels as well as plasma IL-6 and TNF-alpha levels in the patients with OSAS were up-regulated, which may be associated with the pathogenesis of OSAS.

Elevated circulating levels of tumor necrosis factor in patients with mitral valve disease and ventricular septum defect.

Elevated levels of circulating tumor necrosis factor (TNF)-alpha have been reported in patients with decreased left ventricular ejection fraction. Also, TNF has been reported to depress myocardial contractility. In our previous study, no correlation was found between the plasma level of TNF and clinical parameters in patients with cardiomyopathy. In the present study, we detected elevated levels of circulating TNF-alpha in 5 out of 15 patients with mitral valve disease and in 1 patient with ventricular septal defect whose left ventricular ejection fraction was within the normal range. The levels of TNF-alpha were not correlated with any hemodynamic parameters. Further studies are necessary to clarify the mechanisms of the regulation and effects of TNF-alpha in patients with chronic heart failure.

Plasma Inhibitory Activity against Tumour Necrosis Factor in Fulminant Hepatic Failure

1. Soluble tumour necrosis factor receptors released into the circulation inhibit the effects of excess tumour necrosis factor-alpha and represent an important protective response. 2. In this study we have measured the levels of tumour necrosis factor and soluble tumour necrosis factor receptors p55 and p75 in the plasma of 10 patients with fulminant hepatic failure and 10 healthy control subjects. The capacity of the plasmas at varying dilutions to inhibit the biological activity of 1000 pg/ml of recombinant tumour necrosis factor in a tumour necrosis factor cytotoxicity assay in vitro was also determined. 3. The mean plasma levels of tumour necrosis factor in patients with fulminant hepatic failure (48.4 +/- 10.9 pg/ml) were significantly increased compared with normal control subjects (6.1 +/- 1.04 pg/ml, P < 0.01). Plasma soluble tumour necrosis factor receptors p55 and p75 were also significantly elevated in patients with fulminant hepatic failure (18.16 +/- 9.94 ng/ml and 16.06 +/- 9.93 ng/ml respectively) when compared with normal control subjects (1.28 +/- 0.24 ng/ml and 1.62 +/- 0.91 ng/ml, P < 0.001). 4. Fulminant hepatic failure plasma had a much lower capacity to inhibit tumour necrosis factor bioactivity in vitro, with a statistically significant difference between the inhibitory capacity of the fulminant hepatic failure and normal plasma seen at plasma dilutions of 1:5 and 1:20 (P < 0.05). 5. The reduced tumour necrosis factor neutralization capacity observed in fulminant hepatic failure, despite the increased levels of soluble tumour necrosis factor receptors, suggests enhanced susceptibility to the potential deleterious effects of tumour necrosis factor in fulminant hepatic failure.