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Increased serum tumor necrosis factor ? levels in patients with lenalidomide-induced hypothyroidism.

ABSTRACT: As the use of lenalidomide expands, the poorly understood phenomenon of lenalidomide-induced thyroid abnormalities will increase. In this study, we compared rates of therapy-induced hypothyroidism in 329 patients with diffuse large B-cell lymphoma (DLBCL) treated with conventional chemotherapy (DLBCL-c) or conventional chemotherapy plus lenalidomide (DLBCL-len). We measured serum levels of tumor necrosis factor ?, interferon gamma, interleukin 6, interleukin 12, and interleukin 15 before and after treatment. We found a significantly higher rate of therapy-induced hypothyroidism in the DLBCL-len group (25.8% vs. 1.3%), and we found a statistically significant increase in serum tumor necrosis factor ? in patients with lenalidomide-induced hypothyroidism.

SUBMITTER: Iams WT

PROVIDER: S-EPMC5002942 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature

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Increased serum tumor necrosis factor α levels in patients with lenalidomide-induced hypothyroidism.

Iams Wade T WT Hames Megan L ML Tsai Judy P JP Dahlman Kimberly B KB Talbott Mahsa S MS Richards Kristy L KL Reddy Nishitha M NM

Experimental hematology 20141028 2

As the use of lenalidomide expands, the poorly understood phenomenon of lenalidomide-induced thyroid abnormalities will increase. In this study, we compared rates of therapy-induced hypothyroidism in 329 patients with diffuse large B-cell lymphoma (DLBCL) treated with conventional chemotherapy (DLBCL-c) or conventional chemotherapy plus lenalidomide (DLBCL-len). We measured serum levels of tumor necrosis factor α, interferon gamma, interleukin 6, interleukin 12, and interleukin 15 before and aft ...[more]

PMID: 25448491

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Association of increased levels of plasma tumor necrosis factor alpha with primary open-angle glaucoma.

Project description:Purpose:Retinal ganglion cell (RGC) death is a key feature of glaucoma. Elevated levels of tumor necrosis factor alpha (TNF-?), a pro-inflammatory cytokine, can induce RGC apoptosis and play a critical role in glaucomatous neurodegeneration. Based on the possible role of inflammation and oxidative stress in the pathogenesis of primary open-angle glaucoma (POAG), we investigated the association between plasma levels of TNF-? and POAG or its clinical indices in comparison to non-glaucomatous controls. Patients and methods:In a case-control retrospective cohort of 51 POAG cases and 88 controls, plasma TNF-? levels were measured using an enzyme-linked immunosorbent assay (ELISA). The assay was performed in duplicates on an automated ELISA analyzer. Results:Mean TNF-? level was significantly elevated in POAG cases (1.88 ± 2.17 pg/mL) than the controls (0.93 ± 1.49 pg/mL; p = 0.003). The overall dose-response trend was significant (?2 = 6.12, df = 2; p = 0.047). No statistical difference was seen in age, gender and systemic disease distribution. A modest negative and significant correlation was seen between TNF-? level and number of antiglaucoma medications, an important clinical index of POAG severity. Moreover, logistic regression analysis showed that the risk of POAG was most significantly affected by TNF-? level and not by age and sex. Conclusion:High systemic level of an inflammatory cytokine, TNF-?, is associated with POAG; however, its possible use as a biomarker for early glaucoma diagnosis and/or disease severity needs further investigation.

| S-EPMC5905466 | biostudies-literature

High Serum Tumor Necrosis Factor-Alpha Levels in Women with Polycystic Ovary Syndrome: A Meta-Analysis.

Project description:The objective of the study is to assess the TNF-? levels in PCOS patients and healthy controls. A comprehensive electronic search in Medline, Embase, and the Cochrane Library database was conducted up to July 2016. Random-effects model was used to estimate the standardized mean differences (SMDs) with 95% confidence intervals (CIs). Twenty-nine studies with a total of 1960 participants (1046 PCOS patients and 914 controls) were included in this meta-analysis. The TNF-? levels in PCOS patients were significantly higher than those in controls (random-effects, SMD = 0.60, 95% CI = 0.28-0.92, P<0.001). With regard to the subgroup analyses stratified by ethnicity, study quality, methods, and BMI, significantly high TNF-? levels were found in patients with PCOS in almost all of these subgroups. In the subgroup stratified by HOMA-IR ratio and T ratio, significant differences were only observed in the subgroups with HOMA-IR ratio of >1.72(SMD = 0.967, 95% CI = 0.103-1.831, P = 0.028, I2 = 93.5%) and T ratio>2.10 (SMD = 1.420, 95% CI = 0.429-2.411, P = 0.005, I2 = 96.1%). By meta-regression it was suggested that ethnicity might contribute little to the heterogeneity between the included studies. Through cumulative meta-analysis and sensitivity analysis it was supposed that the higher TNF-? levels of PCOS patients compared to healthy controls was stable and reliable. This meta-analysis suggests that the circulating TNF-? levels in women with PCOS are significantly higher than those in healthy controls. It may be involved in promoting insulin resistance and androgen excess of PCOS.

| S-EPMC5072730 | biostudies-literature

Alteration in Serum Levels of Tumor Necrosis Factor Alpha is associated with Histopathologic Progression of Gastric Cancer

Project description:BackgroundThe role of inflammatory cytokines, such as tumor necrosis-α (TNF-α) and IL-8, in gastric carcinogenesis has been investigated, but their impact remains to be further elucidated.MethodsIn this study, we measured the serum concentrations of these cytokines and H. pylori serostatus in dyspeptic patients, presenting with normal mucosa (NM = 53), chronic gastritis (CG = 94), and gastric cancer (GC = 82), by ELISA.ResultsModerate levels of TNF-α were detected in the NM group (19.9 ± 19.5 pg/ml), which were nearly doubled in patients with CG (35.7 ± 28.0 pg/ml) and drastically declined in GC patients (1.8 ± 5.9 pg/ml). The serum levels of IL-8, however, were not statistically different amongst these three groups.ConclusionTNF-α serum concentration seemed to undergo up- and downregulation, when moving from NM to CG and from CG to GC, respectively. If confirmed in a prospective study, this cytokine can behave as a serum indicator of gastric inflammation and malignant transformation.

| S-EPMC9971713 | biostudies-literature

Serum levels of tumor necrosis factor alpha in patients with IgA nephropathy are closely associated with disease severity.

Project description:BackgroundTumor necrosis factor alpha (TNF-α) is considered to play an important role in the pathogenesis in IgA nephropathy (IgAN). The correlations between serum TNF-α and disease severity in patients with IgAN remain controversial.MethodsConcentrations of serum TNF-α of 147 patients with IgAN and 126 healthy subjects were measured by chemiluminescence immunoassay. Correlations with clinicopathological features of patients with IgAN were evaluated.ResultsSerum levels of TNF-α [9.20 (7.70-10.60) pg/mL vs. 6.04 (5.11-7.23) pg/mL, P < 0.0001] were higher in patients with IgAN than that in healthy subjects. Receiver operating characteristic curve analysis revealed that TNF-α had better discrimination between patients with IgAN and healthy controls than estimated glomerular filtration rate [TNF-α: (AUC, 0.87; 95% CI, 0.83-0.91; P < 0.0001) vs. estimated glomerular filtration rate: (AUC, 0.76; 95% CI, 0.71-0.82; P < 0.0001), P = 0.007]. Multivariate linear regression analyses showed that serum levels of TNF-α were positively correlated with 24-h urine protein excretion (r = 0.33, P = 0.04), urinary protein to serum creatinine ratio (r = 0.33, P = 0.03), serum creatinine (r = 0.46, P < 0.0001) and Cystatin C (r = 0.59, P < 0.0001) in IgAN and negatively correlated with estimated glomerular filtration rate (r = - 0.49, P < 0.0001) after adjustment for sex, systolic blood pressure and diastolic blood pressure. Patients with higher mesangial hypercellularity or tubular atrophy/interstitial fibrosis score according to Oxford classification showed higher serum levels of TNF-α.ConclusionsOur data showed that serum levels of TNF-α detected by chemiluminescence immunoassay was a potential biomarker for evaluating the disease severity in IgAN.

| S-EPMC6236996 | biostudies-literature

Tumor necrosis factor alpha-induced inflammation is increased but apoptosis is inhibited by common food additive carrageenan.

Project description:Tumor necrosis factor (TNF)-?, a homotrimeric, pleiotropic cytokine, is secreted in response to inflammatory stimuli in diseases such as rheumatoid arthritis and inflammatory bowel disease. TNF-? mediates both apoptosis and inflammation, stimulating an inflammatory cascade through the non-canonical pathway of NF-?B activation, leading to increased nuclear RelB and p52. In contrast, the common food additive carrageenan (CGN) stimulates inflammation through both the canonical and non-canonical pathways of NF-?B activation and utilizes the adaptor molecule BCL10 (B-cell leukemia/lymphoma 10). In a series of experiments, colonic epithelial cells and mouse embryonic fibroblasts were treated with TNF-? and carrageenan in order to simulate the possible effects of exposure to dietary CGN in the setting of a TNF-?-mediated inflammatory disease process. A marked increase in secretion of IL-8 occurred, attributable to synergistic effects on phosphorylated NF-?B-inducing kinase (NIK) in the non-canonical pathway. TNF-? induced the ubiquitination of TRAF2 (TNF receptor-associated factor 2), which interacts with NIK, and CGN induced phosphorylation of BCL10, leading to increased NIK phosphorylation. These results suggest that TNF-? and CGN in combination act to increase NIK phosphorylation, thereby increasing activation of the non-canonical pathway of NF-?B activation. In contrast, the apoptotic effects of TNF-?, including activation of caspase-8 and PARP-1 (poly(ADP-ribose) polymerase 1) fragmentation, were markedly reduced in the presence of CGN, and CGN caused reduced expression of Fas. These findings demonstrate that exposure to CGN drives TNF-?-stimulated cells toward inflammation rather than toward apoptotic cell death and suggest that CGN exposure may compromise the effectiveness of anti-TNF-? therapy.

| S-EPMC2998126 | biostudies-literature

Enhanced serum levels of tumor necrosis factor-α, interleukin-1β, and -6 in sarcopenia: alleviation through exercise and nutrition intervention.

Project description:BackgroundLimited research has been conducted on the post-intervention inflammatory status in sarcopenic patients, despite previous studies revealing elevated pro-inflammatory markers. This study aimed to investigate the potential elevation of specific pro-inflammatory cytokines in sarcopenic patients and evaluate the effects of exercise and nutritional support interventions on these cytokine levels.MethodsIn this post-hoc analysis of a randomized controlled trial (RCT), 57 individuals with sarcopenia from the RCT and 57 non-sarcopenic participants from the same geriatric community cohort that did not participate in the RCT were enrolled. Grip strength and body composition measurements were recorded. Tumor necrotizing factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-15 levels were assessed at baseline for both groups and after a 12-week intervention consisting of resistive exercise and supplementation with branched-chain amino acids, calcium, and vitamin D3 in the patients with sarcopenia.ResultsThe sarcopenic group demonstrated significantly lower body weight, body mass index, grip strength, and skeletal muscle mass index. Moreover, sarcopenic patients exhibited higher levels of TNF-α (p=0.007), IL-1β (p<0.001), and IL-6 (p<0.001), while no significant difference was observed in IL-15 (p=0.345) between participants with and those without sarcopenia. Following the intervention, the sarcopenic group experienced significant improvements in grip strength and skeletal muscle mass index with a notable reduction in TNF-α (p=0.003), IL-1β (p=0.012) and IL-6 (p=0.001) levels.ConclusionsSarcopenic patients exhibit elevated levels of TNF-α, IL-1β, and IL-6, which declined after nutrition support and exercise interventions. However, further research is necessary to evaluate the long-term impact of these interventions on cytokine levels.

| S-EPMC10713395 | biostudies-literature

Mechanisms of Tumor Necrosis Factor-Alpha Inhibitor-Induced Systemic Lupus Erythematosus

Project description:Systemic lupus erythematosus induced by biologics mainly results from tumor necrosis factor-alpha remains unclear. The objectives of the study were to investigate the mechanisms of tumor necrosis factor-alpha inhibitor-induced systemic lupus erythematosus. Peripheral blood mononuclear cells obtained from thirteen psoriasis patients were cultured and treated with the following: untreated control, Streptococcus pyogenes with or without different biologics. The supernatants were collected for cytokines assay. Analysis of cytokine expression revealed that IL-2 and IL-10 levels decreased only in the TNF-α inhibitor-treated groups but not in the groups treated with biologics involving IL-17, IL-12/IL-23 or IL-23 inhibitor mechanisms (p < 0.001, p < 0.05). The IFN-γ/IL-13 ratio increased significantly in patients with SLE inducing biologics to S. pyogenes induction only compared with non-SLE inducing biologics to S. pyogenes induction only (p = 0.001). IL-2 and IL-10 depletion and a shift to the Th-1 pathway in the innate response are the correlated mechanism for tumor necrosis factor-alpha inhibitor-induced systemic lupus erythematosus.

| S-EPMC9208548 | biostudies-literature

Osteopontin Deficiency Suppresses Tumor Necrosis Factor-α-Induced Apoptosis in Chondrocytes.

Project description:ObjectiveApoptosis of chondrocytes in articular cartilage has been observed in rheumatoid arthritis patients. However, molecules involved in such chondrocyte apoptosis in arthritic joints have not been fully understood. We previously observed that apoptosis of chondrocytes is enhanced in a murine arthritis model induced by injection with anti-type II collagen antibodies and lipopolysaccharide (mAbs/LPS), and osteopontin (OPN) deficiency suppresses chondrocyte apoptosis in this arthritis model in vivo. To understand how OPN deficiency renders resistance against chondrocyte apoptosis, we examined the cellular basis for this protection.DesignChondrocytes were prepared from wild-type and OPN-deficient mouse ribs, and tumor necrosis factor (TNF)-α-induced cell death was examined based on lactate dehydrogenase (LDH) release assay and TUNEL assay.ResultsTNF-α treatment induced LDH release in wild-type chondrocytes, while OPN deficiency suppressed such LDH release in the cultures of these cells. TNF-α-induced increase in the number of TUNEL-positive cells was observed in wild-type chondrocytes, while OPN deficiency in chondrocytes suppressed the TNF-α induction of TUNEL-positive cells. OPN deficiency suppressed TNF-α-induced increase in caspase-3 activity in chondrocytes in culture. Furthermore, OPN overexpression in chondrocytes enhanced TNF-α-induced apoptosis.ConclusionThese results indicated that the presence of OPN in chondrocytes is involved in the susceptibility of these cells to TNF-α-induced apoptosis.

| S-EPMC4297182 | biostudies-literature

Elevated levels of plasma tumor necrosis factor alpha in patients with pseudoexfoliation glaucoma.

Project description:Background:Tumor necrosis factor alpha (TNF-?) is a pro-inflammatory cytokine, which plays a role in glaucomatous neurodegeneration. Based on the plausible role of inflammation in the pathogenesis of pseudoexfoliation glaucoma (PEG), we investigated whether there is any relationship between the levels of plasma TNF-? and PEG or any of its clinical indices in comparison to normal controls. Methods:The study was designed as a retrospective analysis. Plasma samples from 49 PEG patients and 88 non-glaucomatous controls were evaluated for TNF-? levels using an enzyme-linked immunosorbent assay (ELISA). The assay was performed in duplicates on a biochemical/ELISA analyzer. Results:The two study groups were similar in age, sex and systemic disease distribution. The mean TNF-? concentration was significantly higher in the PEG patients (5.54±4.58 pg/mL) than in the control subjects (0.93±1.49 pg/mL; 95% confidence interval [CI] =3.50-5.72; p=0.000). The overall dose-response trend was significant (?2=57.07, df=2; p=0.000). A moderate positive and significant correlation was seen between TNF-? level and cup/disc ratio, an important clinical index for PEG. Besides, binary logistic regression analysis showed that the risk of PEG was most significantly affected by TNF-? level as compared to no association with age and sex. In receiver operating characteristic analysis, the area under the curve was 0.777 (95% CI =0.682-0.872) and statistically significant (p=0.000). Conclusion:Elevated systemic levels of inflammatory marker, TNF-?, are associated with PEG and may possibly serve as a biomarker for undiagnosed early glaucoma and/or as a marker for disease progression.

| S-EPMC5775737 | biostudies-literature

Tumor Necrosis Factor Alpha (TNFα) Gene Promoter Polymorphisms and Haplotypes are Associated with the Febrile Seizure (FS) and TNFα Serum Levels.

Project description:ObjectivesFebrile seizure (FS) is a neuroinflammatory disease involving fever-induced seizures affecting children in the early stages of life. TNFα is a pro-inflammatory cytokine reported to be elevated in FS. Specific promoter variants of TNFα could be associated with its elevated cytokine expression and susceptibility to FS. The present study analyzed the association of specific TNFα variants, including TNFα -238 G/A (rs361525), TNFα -308 G/A (rs1800629), and TNFα -376 G/A (rs1800750) promoter polymorphisms, with FS susceptibility, and TNFα serum levels in an Iranian population.Materials & methodsSixty-eight FS patients and 136 controls were enrolled. The SSP-PCR method was utilized to analyze TNFα promoter genotypes. This research also confirmed the genotyping results by sequencing samples of ten patients and normal controls.ResultsThe GG genotype of -238 SNP was associated with the increased risk of FS [OR = 12.65, 95% CI (2.83-56.60), P-value = 0.0012]. The AA genotype in the-308 region was increased in patients with FS and associated with the disease [OR = 4.62, 95% CI (1.46-14.56), P-value = 0.028]. The increased occurrence of heterozygous AG in the -376 SNP among control groups has been linked to a decreased risk of FS [OR = 0.22, 95% CI (0.11-0.43), P-value = 0.0001]. This study revealed that AGA (-238/ -308/ -376) haplotype with the highest frequency in controls was associated with a decreased risk of FS, while GAA (-238/ -308/ -376) carriers were more susceptible to FS.ConclusionThe current study suggested that TNFα gene promoter variants at rs361525, rs1800629, and rs1800750 could be associated with the susceptibility to FS and altered serum levels of TNFα.

| S-EPMC10704284 | biostudies-literature

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