PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33995584-7 2021 Clinical guidelines for SARS-CoV-2-negative patients advocate the use of steroids, calcineurin inhibitors, or tumor necrosis factor alpha (TNF-alpha)-antagonists as induction therapy, and experiences from the current three cases show that steroids and TNF-alpha-antagonists could also be used in patients with COVID-19. Steroids 239-247 tumor necrosis factor Homo sapiens 139-148 2485698-6 1989 These are important precursors for placental steroid synthesis which are mainly provided by the fetal adrenals during normal gestation, and the results thus suggest a role for TNF in the regulation of steroidogenesis in the human fetoplacentary unit. Steroids 45-52 tumor necrosis factor Homo sapiens 176-179 3350575-1 1988 We have investigated the modulating effect of steroids on the in vitro production of tumour necrosis factor (TNF) by lipopolysaccharide (LPS)-stimulated human monocytes. Steroids 46-54 tumor necrosis factor Homo sapiens 85-107 3350575-1 1988 We have investigated the modulating effect of steroids on the in vitro production of tumour necrosis factor (TNF) by lipopolysaccharide (LPS)-stimulated human monocytes. Steroids 46-54 tumor necrosis factor Homo sapiens 109-112 33995584-7 2021 Clinical guidelines for SARS-CoV-2-negative patients advocate the use of steroids, calcineurin inhibitors, or tumor necrosis factor alpha (TNF-alpha)-antagonists as induction therapy, and experiences from the current three cases show that steroids and TNF-alpha-antagonists could also be used in patients with COVID-19. Steroids 239-247 tumor necrosis factor Homo sapiens 252-261 32426829-8 2021 At 12 months, steroid-free clinical and biochemical remission on the same anti-TNF occurred in 53.9% of the IM group vs 26.8% in the No-IM group (P = 0.025). Steroids 14-21 tumor necrosis factor Homo sapiens 79-82 32426829-12 2021 CONCLUSIONS: Pediatric patients with inflammatory bowel disease on anti-TNF monotherapy who started an IM for significant ADA levels exhibited longer anti-TNF durability and a higher likelihood of steroid-free clinical and biochemical remission on the same anti-TNF. Steroids 197-204 tumor necrosis factor Homo sapiens 72-75 33553650-7 2021 Stimulation with IL-4 and TNF-alpha induced the generation of PGE2 in supernatants of conjunctival fibroblasts, and this production was significantly downregulated by ketotifen fumarate or steroids. Steroids 189-197 tumor necrosis factor Homo sapiens 26-35 32963592-3 2020 Topical steroids are an effective treatment; however, recurrent or refractory cases may need conventional disease-modifying antirheumatic drugs or biological treatment with monoclonal tumor necrosis factor (TNF) inhibitors, thus also influencing treatment strategy of the underlying SpA. Steroids 8-16 tumor necrosis factor Homo sapiens 184-205 33283312-8 2021 Predictors of infections in anti-TNFalpha-exposed patients were concomitant use of systemic steroids (OR 1.9, p=0.02) or azathioprine (OR 2.6, p=0.01) and a BMI<18.5 at time of infection (OR 2.2, p=0.01). Steroids 92-100 tumor necrosis factor Homo sapiens 33-41 32356680-3 2020 Tumor necrosis factor (TNF) is an important cytokine involved in the pathogenesis of GVHD, and medications such as infliximab (Remicade ) have been utilized as second-line treatment options in patients with steroid-refractory GHVD. Steroids 207-214 tumor necrosis factor Homo sapiens 0-21 32356680-3 2020 Tumor necrosis factor (TNF) is an important cytokine involved in the pathogenesis of GVHD, and medications such as infliximab (Remicade ) have been utilized as second-line treatment options in patients with steroid-refractory GHVD. Steroids 207-214 tumor necrosis factor Homo sapiens 23-26 32356680-9 2020 Although we had important limitations, this case report supports the use of anti-TNF agents in highly mortal steroid-refractory acute GI GVHD and that replacement of infliximab with its biosimilars is feasible. Steroids 109-116 tumor necrosis factor Homo sapiens 81-84 33226355-18 2020 SUMMARY: INTRODUCTION: Anti-tumor necrosis factor-alpha (anti-TNFalpha) treatment is reserved for steroid-dependent or steroid/immunomodulator-refractory inflammatory bowel diseases patients. Steroids 99-106 tumor necrosis factor Homo sapiens 29-56 33226355-18 2020 SUMMARY: INTRODUCTION: Anti-tumor necrosis factor-alpha (anti-TNFalpha) treatment is reserved for steroid-dependent or steroid/immunomodulator-refractory inflammatory bowel diseases patients. Steroids 99-106 tumor necrosis factor Homo sapiens 63-71 33226355-18 2020 SUMMARY: INTRODUCTION: Anti-tumor necrosis factor-alpha (anti-TNFalpha) treatment is reserved for steroid-dependent or steroid/immunomodulator-refractory inflammatory bowel diseases patients. Steroids 120-127 tumor necrosis factor Homo sapiens 29-56 33226355-18 2020 SUMMARY: INTRODUCTION: Anti-tumor necrosis factor-alpha (anti-TNFalpha) treatment is reserved for steroid-dependent or steroid/immunomodulator-refractory inflammatory bowel diseases patients. Steroids 120-127 tumor necrosis factor Homo sapiens 63-71 32723069-4 2020 The effectiveness of the anti-TNF agent was defined as a composite outcome combining steroid-free drug persistence with no use of new biologics or immunomodulators, hospital admission, surgery or endoscopic therapy during follow-up. Steroids 85-92 tumor necrosis factor Homo sapiens 30-33 33120729-0 2020 Use of steroids to treat anti-tumor necrosis factor alpha induced tuberculosis-associated immune reconstitution inflammatory syndrome: Case report and literature review. Steroids 7-15 tumor necrosis factor Homo sapiens 30-57 32963592-3 2020 Topical steroids are an effective treatment; however, recurrent or refractory cases may need conventional disease-modifying antirheumatic drugs or biological treatment with monoclonal tumor necrosis factor (TNF) inhibitors, thus also influencing treatment strategy of the underlying SpA. Steroids 8-16 tumor necrosis factor Homo sapiens 207-210 32782876-3 2020 Biologic agents are considered to be appropriate alternatives for treatment in steroid-refractory sarcoidosis and uveitis due to the role of tumor necrosis factor (TNF) in mediating the inflammatory cascade seen in both conditions. Steroids 79-86 tumor necrosis factor Homo sapiens 164-167 32999670-1 2020 Purpose: To report a case with rapid regression of scleral melting associated with tumor necrosis factor-alpha (TNF-alpha) in a surgically induced necrotizing scleritis (SINS) patient treated with local steroid therapy. Steroids 203-210 tumor necrosis factor Homo sapiens 83-110 32999670-1 2020 Purpose: To report a case with rapid regression of scleral melting associated with tumor necrosis factor-alpha (TNF-alpha) in a surgically induced necrotizing scleritis (SINS) patient treated with local steroid therapy. Steroids 203-210 tumor necrosis factor Homo sapiens 112-121 31728510-6 2020 RESULTS: Early intervention with anti-TNF-alpha treatment was more costly, with an incremental cost of CAD$31,112 (95% confidence interval [CI], $2939-$91,715), and more effective, with 11.3 more weeks in steroid-free remission (95% CI, 10.6-11.6) compared with standard care, resulting in an incremental cost per steroid-free remission-week gained of CAD$2756 from an Ontario public health care perspective and CAD$2968 from a societal perspective. Steroids 205-212 tumor necrosis factor Homo sapiens 38-47 31728510-6 2020 RESULTS: Early intervention with anti-TNF-alpha treatment was more costly, with an incremental cost of CAD$31,112 (95% confidence interval [CI], $2939-$91,715), and more effective, with 11.3 more weeks in steroid-free remission (95% CI, 10.6-11.6) compared with standard care, resulting in an incremental cost per steroid-free remission-week gained of CAD$2756 from an Ontario public health care perspective and CAD$2968 from a societal perspective. Steroids 314-321 tumor necrosis factor Homo sapiens 38-47 32586650-15 2020 However, anti-TNF-alpha agents could be proposed as an alternative in cases of severe inflammation or initial high level of steroid dependency. Steroids 124-131 tumor necrosis factor Homo sapiens 14-23 32719413-8 2020 In conclusion, TAC and anti-TNF agents promoted similar short-term effects, but anti-TNF agents ensured better long-term outcomes at first-time treatment of steroid-refractory UC patients. Steroids 157-164 tumor necrosis factor Homo sapiens 85-88 32246833-7 2020 CONCLUSIONS: Our findings indicate that TNFalpha treatment reduces steroid hormone production in MG63 cells (but not in HOB) at the level of lanosterol-demethylation during cholesterol biosynthesis. Steroids 67-82 tumor necrosis factor Homo sapiens 40-48 32141941-1 2020 PURPOSE: To investigative the effects of sex steroids on hyperosmolar stress-induced proinflammatory cytokine expression of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-8, and IL-6, and on the mitogen-activated protein kinase pathway in immortalized human corneal epithelial cells (hCECs). Steroids 45-53 tumor necrosis factor Homo sapiens 124-151 32507783-3 2020 Here, we report a case of steroid-refractory CD after umbilical cord blood transplantation (CBT), which was dramatically improved with administration of anti-tumor necrosis factor-alpha (anti-TNF-alpha) antibodies. Steroids 26-33 tumor necrosis factor Homo sapiens 158-185 32507783-3 2020 Here, we report a case of steroid-refractory CD after umbilical cord blood transplantation (CBT), which was dramatically improved with administration of anti-tumor necrosis factor-alpha (anti-TNF-alpha) antibodies. Steroids 26-33 tumor necrosis factor Homo sapiens 192-201 31988197-0 2020 Association of anti-TNF with decreased survival in steroid refractory ipilimumab and anti-PD1 treated patients in the Dutch Melanoma Treatment Registry. Steroids 51-58 tumor necrosis factor Homo sapiens 20-23 31988197-8 2020 Among patients experiencing severe toxicity, survival was significantly decreased in patients who received anti-TNF +/- steroids for steroid-refractory toxicity compared to patients who were managed with steroids only (HRadj 1.61; 95%CI 1.03-2.51), with a median OS of 17 months and 27 months, respectively. Steroids 120-128 tumor necrosis factor Homo sapiens 112-115 31988197-10 2020 However, this survival advantage is abrogated when anti-TNF is administered for steroid-refractory toxicity. Steroids 80-87 tumor necrosis factor Homo sapiens 56-59 32246833-8 2020 By contrast, TNFalpha treatment of HOB cells (but not in MG63) leads to the upregulation of several key enzymes involved in the biosynthesis of sex steroids, which is proposed to lead to higher levels of estrogen production. Steroids 148-156 tumor necrosis factor Homo sapiens 13-21 31595533-10 2019 Factors independently associated with reduced steroid excess in Crohn"s disease included maintenance with anti-TNF agents (OR 0.61 [95% CI 0.24-0.95]), treatment in a centre with a multi-disciplinary team (OR 0.54 [95% CI 0.20-0.86]) and treatment at an intervention centre (OR 0.72 [95% CI 0.46-0.97]). Steroids 46-53 tumor necrosis factor Homo sapiens 111-114 31997099-7 2020 Finally, recent data have shed light on the increased risk of particular types of lymphoma in adolescent on thiopurines, whereas biologic therapies, in particular, anti-TNF, now are positioned as a preferred and effective steroid-sparing agents in moderate to severe IBD. Steroids 222-229 tumor necrosis factor Homo sapiens 169-172 32801271-1 2020 A 45-year-old man with steroid-dependent ulcerative pancolitis was hospitalized with frequent diarrhea, abdominal pain and distension 3 months after induction of golimumab, a tumor necrosis factor-alpha antagonist. Steroids 23-30 tumor necrosis factor Homo sapiens 175-202 31955619-1 2020 Background: This study was to assess the clinical efficacy of epidural injections with tumor necrosis factor-alpha (TNF-alpha) inhibitor in patients with chronic radicular pain caused by lumbar spinal stenosis (LSS).Methods: In a randomized controlled trial (RCT), patients diagnosed with mild-to-moderate LSS underwent epidural intervention with three different drugs and were allocated to TNF-alpha inhibitor group (Group A), steroid group (Group B) and lidocaine-only group (Group C). Steroids 428-435 tumor necrosis factor Homo sapiens 116-125 32209197-16 2020 Conclusion: In combination with corticosteroids and immunosuppressants, anti-TNF alpha mAbs are effective and well-tolerated in severe/refractory vasculo-BD, with a favorable steroid -sparing effect and rare postoperative complications. Steroids 39-46 tumor necrosis factor Homo sapiens 77-86 32116074-3 2022 Monotherapy of thrombolytics cannot achieve satisfactory results because of concomitant inflammation.Objective: This pilot study aimed to determine the efficacy of an anti-TNF-alpha agent in patients with refractory livedoid vasculopathy.Methods: We studied five patients with livedoid vasculopathy who were resistant to steroids, antiplatelets, or danazol therapy, and were treated with etanercept 25-50 mg once a week for 12 consecutive weeks. Steroids 321-329 tumor necrosis factor Homo sapiens 172-181 31902928-5 2020 Regarding neutrophilic airway inflammation in steroid-resistant asthma, IL-17 derived from Th17 cells and IL-8 and tumor necrosis factor-alpha derived mainly from macrophages were reported to be involved in the pathogenesis. Steroids 46-53 tumor necrosis factor Homo sapiens 115-142 31500631-1 2019 BACKGROUND: In adult patients with arthritis, use of the tumor necrosis factor (TNF) inhibitor etanercept (ETN) is often associated with a reduction in the utilization of co-medications, particularly steroids. Steroids 200-208 tumor necrosis factor Homo sapiens 57-78 31500631-1 2019 BACKGROUND: In adult patients with arthritis, use of the tumor necrosis factor (TNF) inhibitor etanercept (ETN) is often associated with a reduction in the utilization of co-medications, particularly steroids. Steroids 200-208 tumor necrosis factor Homo sapiens 80-83 30748107-13 2019 Expression of TNF-alpha, IL-2, IL-4, IL-5, and IL-13 mRNA in the NPs treated by steroid, AZA, and 6-MP were significantly lower than those of the control (p < 0.001 for all). Steroids 80-87 tumor necrosis factor Homo sapiens 14-23 31424716-3 2019 When a temporal association between increasing his infliximab dose and the global progression of his disease was identified, he was ultimately diagnosed with a TNF-alpha inhibitor-induced psoriasis flare.Despite the patient"s long-standing history of psoriasis, a plausible psoriasis rebound reaction after systemic steroids was not strongly considered in light of his histopathology. Steroids 316-324 tumor necrosis factor Homo sapiens 160-169 31122819-5 2019 Indeed, anti-TNF-alpha therapy has been used to treat steroid-refractory GVHD. Steroids 54-61 tumor necrosis factor Homo sapiens 13-22 31089818-7 2019 RESULTS: After achievement of remission by full-dose steroids, there were significant differences of TNF-alpha between the two groups after 1-, 3- and 5-month follow-up (p < 0.001, 0.003, and 0.001, respectively). Steroids 53-61 tumor necrosis factor Homo sapiens 101-110 31439050-15 2019 CONCLUSIONS: Concurrent treatment with anti-TNFalpha and ICI appears to be safe, facilitates steroid tapering, and prevents irEC. Steroids 93-100 tumor necrosis factor Homo sapiens 44-52 30294905-0 2019 Alteration of serum and tissue tumor necrosis factor alpha levels: A possible mechanism of action of oral pulse steroids in the treatment of alopecia areata. Steroids 112-120 tumor necrosis factor Homo sapiens 31-58 30294905-2 2019 OBJECTIVE: To study the effect of oral pulse steroids on both serum and tissue levels of TNF-alpha in AA patients. Steroids 45-53 tumor necrosis factor Homo sapiens 89-98 30294905-8 2019 CONCLUSION: TNF-alpha plays an important role in the evolution of AA lesions, and alteration in both serum and tissue levels of TNF-alpha could be considered one of the important mechanisms of action of systemic oral pulse steroids in the treatment of AA. Steroids 223-231 tumor necrosis factor Homo sapiens 128-137 30719968-10 2019 CONCLUSIONS: Monoclonal TNF-alpha inhibitors induce a remarkable decrease in the recurrence of AU during a long-term follow-up period and lead to a significant steroid sparing effect along with stabilisation of visual acuity. Steroids 160-167 tumor necrosis factor Homo sapiens 24-33 28372498-9 2019 Patients who regained organ function recovery had significantly higher TNF-alpha production capacity on day 6 ( P = .01), which persisted after adjustment for age, Acute Physiology and Chronic Health Evaluation III score, and steroid administration ( P = .03). Steroids 226-233 tumor necrosis factor Homo sapiens 71-80 30826963-13 2019 Steroid therapy (oral or intravenously) is often efficient, but one-fourth of patients need rescue therapy with anti-TNF. Steroids 0-7 tumor necrosis factor Homo sapiens 117-120 30753845-8 2019 In PBMCs, exposure to these steroids resulted in the increase of mRNA and secreted protein levels of IL-1beta, TNFalpha, and IL-6 cytokines, as well as in the increase of INFgamma mRNA level, decrease of IL-2 mRNA level, increase of TGFbeta mRNA level, and decrease of IL-4 mRNA and IL-10 secreted protein levels. Steroids 28-36 tumor necrosis factor Homo sapiens 111-119 30606261-0 2019 Involvement of tumor necrosis factor alpha in steroid-associated osteonecrosis of the femoral head: friend or foe? Steroids 46-53 tumor necrosis factor Homo sapiens 15-42 30625342-6 2019 Gonadal steroid hormones differentially influenced the Hp expression in LPS-induced WHB, where the addition of Estrogen increased Hp expression, with suppression of TNFalpha, in both genders. Steroids 8-15 tumor necrosis factor Homo sapiens 165-173 30287909-1 2019 The aim of this case-control study was to evaluate whether 47 single-nucleotide polymorphisms (SNPs) in steroid hormone-related genes are associated with the risk of RA and anti-TNF drug response. Steroids 104-119 tumor necrosis factor Homo sapiens 178-181 30991399-7 2019 RESULTS: OZOILE and steroid topical treatment produced a similar reduction of TNF-alpha and IL-1beta mRNA levels in foreskins from patients with LS when compared to untreated patients (p < 0.001). Steroids 20-27 tumor necrosis factor Homo sapiens 78-87 30562409-7 2018 Anti-tumour necrosis factor (TNF) drugs block a critical cytokine in the inflammatory signalling process, and have emerged as effective steroid-sparing immunomodulatory agents in a wide range of non-ocular conditions. Steroids 136-143 tumor necrosis factor Homo sapiens 0-27 30562409-7 2018 Anti-tumour necrosis factor (TNF) drugs block a critical cytokine in the inflammatory signalling process, and have emerged as effective steroid-sparing immunomodulatory agents in a wide range of non-ocular conditions. Steroids 136-143 tumor necrosis factor Homo sapiens 29-32 29961771-13 2018 After adjusting for disease severity, steroid use, age, IBD type, and duration and concomitant 6-mercaptopurine use, anti-TNFalpha treatment was associated with a higher risk of overall maternal complications (adjusted Odds Ratio (aOR) = 1.49; 95% confidence interval (CI): 1.31-1.67) and infections (aOR = 1.31; 95% CI: 1.16-1.47). Steroids 38-45 tumor necrosis factor Homo sapiens 122-130 30322965-4 2018 Steroids such as dexamethasone greatly enhanced TNF-alpha-induced moLC differentiation and blocked DC-SIGN expression. Steroids 0-8 tumor necrosis factor Homo sapiens 48-57 29382512-7 2018 RESULTS: The addition of steroids to the perfusate solution reduced the generation of proinflammatory cytokines (interleukin-6, -8, -1beta, and tumor necrosis factor-alpha) and the development of myocardial edema during EVHP (percentage of weight gain: control = 26% +- 7% versus steroid = 16% +- 10%, p = 0.049). Steroids 25-33 tumor necrosis factor Homo sapiens 113-171 30036148-9 2018 Due to a potential inflammatory mechanism of this acute PAH in the setting of IP, TNF-alpha blockers and steroids were associated. Steroids 105-113 tumor necrosis factor Homo sapiens 82-91 29746256-3 2018 Glucocorticoids (GCs), which are steroids that bind and activate the glucocorticoid receptor (GR), are able to protect animals and humans against acute TNF-induced inflammatory symptoms. Steroids 33-41 tumor necrosis factor Homo sapiens 152-155 30069732-6 2018 Patients with steroid- and methotrexate-refractory AOSD can now benefit from efficient and well-tolerated biologic agents such as IL-1, IL-6, and tumor necrosis factor-alpha antagonists. Steroids 14-21 tumor necrosis factor Homo sapiens 146-173 30042265-12 2018 Some patients are resistant to steroid therapy, in which case infliximab, anti-TNF-a antibody, is recommended. Steroids 31-38 tumor necrosis factor Homo sapiens 79-84 29382512-7 2018 RESULTS: The addition of steroids to the perfusate solution reduced the generation of proinflammatory cytokines (interleukin-6, -8, -1beta, and tumor necrosis factor-alpha) and the development of myocardial edema during EVHP (percentage of weight gain: control = 26% +- 7% versus steroid = 16% +- 10%, p = 0.049). Steroids 25-32 tumor necrosis factor Homo sapiens 113-171 28803697-2 2018 Polymorphisms of cytokines genes including tumor necrosis factor alpha (TNF-alpha)may influence susceptibility to NS as well as different patients" steroid responses. Steroids 148-155 tumor necrosis factor Homo sapiens 43-70 29684967-4 2018 Anti-TNF-alpha agent have progressively been introduced earlier in treatment algorithms for UC in order to minimize steroid exposure and dependence and to maximize disease control and quality of life. Steroids 116-123 tumor necrosis factor Homo sapiens 5-14 29455252-14 2018 CONCLUSIONS: Treatment of pediatric uveitis with anti-TNF-alpha agents may improve outcome while providing steroid-sparing effect, when conventional immunosuppression fails. Steroids 107-114 tumor necrosis factor Homo sapiens 54-63 29548010-2 2018 Anti-tumor necrosis factor (anti-TNF) antibodies are superior to conventional therapies to achieve sustained remission without steroids and mucosal healing. Steroids 127-135 tumor necrosis factor Homo sapiens 33-36 29593377-10 2018 Cytotoxic immunosuppressive agents for refractory chronic ocular disease, as well as biologic anti-TNFalpha therapies, have advanced the management of chronic disease and should be considered corticosteroid-sparing strategies before the onset of significant steroid-induced morbidity. Steroids 199-206 tumor necrosis factor Homo sapiens 99-107 28803697-2 2018 Polymorphisms of cytokines genes including tumor necrosis factor alpha (TNF-alpha)may influence susceptibility to NS as well as different patients" steroid responses. Steroids 148-155 tumor necrosis factor Homo sapiens 72-81 28803697-8 2018 RESULTS: Serum TNF-alpha levels were significantly higher in NS patients than in controls and in steroid resistant NS (SRNS) than in steroid sensitive NS (SSNS) (P<0.001 for each). Steroids 97-104 tumor necrosis factor Homo sapiens 15-24 28803697-8 2018 RESULTS: Serum TNF-alpha levels were significantly higher in NS patients than in controls and in steroid resistant NS (SRNS) than in steroid sensitive NS (SSNS) (P<0.001 for each). Steroids 133-140 tumor necrosis factor Homo sapiens 15-24 28803697-11 2018 The risk of resistance to steroid therapy was significantly high in NS carrying TNF-alpha-238GA genotype and A allele, TNF-alpha-308, AA genotypes and A allele, and TNF-alpha-863CA, AA genotypes and A allele. Steroids 26-33 tumor necrosis factor Homo sapiens 80-89 28803697-11 2018 The risk of resistance to steroid therapy was significantly high in NS carrying TNF-alpha-238GA genotype and A allele, TNF-alpha-308, AA genotypes and A allele, and TNF-alpha-863CA, AA genotypes and A allele. Steroids 26-33 tumor necrosis factor Homo sapiens 119-128 28803697-11 2018 The risk of resistance to steroid therapy was significantly high in NS carrying TNF-alpha-238GA genotype and A allele, TNF-alpha-308, AA genotypes and A allele, and TNF-alpha-863CA, AA genotypes and A allele. Steroids 26-33 tumor necrosis factor Homo sapiens 119-128 28803697-12 2018 The TNF-alpha GCG (-308/-863/-238) haplotype has protective roles against NS and steroid resistance. Steroids 81-88 tumor necrosis factor Homo sapiens 4-13 28803697-14 2018 Additionally the risk of steroid resistance was significantly high in TNF-alpha AAA haplotype"s NS carrier (OR (95%CI): 2.2 (1.19-4.36), P=0.01). Steroids 25-32 tumor necrosis factor Homo sapiens 70-79 28803697-17 2018 CONCLUSION: This study reported, for the first time, that TNF-alpha promoter gene polymorphisms and/or haplotypes are risk factors of NS and resistance to steroid among Egyptian children. Steroids 155-162 tumor necrosis factor Homo sapiens 58-67 29190601-10 2017 CONCLUSIONS: IL-6-G174C and TNFalpha-G308A polymorphisms may affect susceptibility to idiopathic nephrotic syndrome and might affect steroid response in INS patients. Steroids 133-140 tumor necrosis factor Homo sapiens 28-36 29184006-8 2017 This is the first report showing a possible role of anti-TNFalpha in pain management in CED with unsatisfactory response to steroids. Steroids 124-132 tumor necrosis factor Homo sapiens 57-65 30783041-9 2018 Esophageal stenosis despite medical treatment requires endoscopic dilation, while the use of thiopurines or anti-TNF drugs may be considered in refractory or steroid-dependent EGID (other than EoE). Steroids 158-165 tumor necrosis factor Homo sapiens 113-116 28643285-13 2017 In the case of anti-TNF-induced lesions, topical steroids are usually sufficient and discontinuation of anti-TNF is seldom warranted. Steroids 49-57 tumor necrosis factor Homo sapiens 20-23 28902728-9 2017 CONCLUSIONS: A change in FDG activity at FDG PET/CT performed prior to the second induction dose of anti-TNF therapy has the potential to predict clinical response and steroid-free remission in patients with Crohn disease. Steroids 168-175 tumor necrosis factor Homo sapiens 105-108 28119748-12 2017 The inhibitory effects of the two steroid drugs were also observed in the production of total mucin, MUC2 and MUC5AC proteins, and TNF-alpha. Steroids 34-41 tumor necrosis factor Homo sapiens 131-140 28457111-8 2017 Mean baseline serum TNFalpha level was significantly higher in the steroid-resistant nephrotic syndrome patients than the controls (6.13 pg/ml vs. 4.36 pg/ml, P = 0.0483). Steroids 67-74 tumor necrosis factor Homo sapiens 20-28 28457111-9 2017 Mean post-treatment TNFalpha level was significantly higher in the steroid-resistant than in the steroid-sensitive nephrotic syndrome patients (5.67 pg/ml vs. 2.14 pg/ml, P = 0.001). Steroids 67-74 tumor necrosis factor Homo sapiens 20-28 28457111-9 2017 Mean post-treatment TNFalpha level was significantly higher in the steroid-resistant than in the steroid-sensitive nephrotic syndrome patients (5.67 pg/ml vs. 2.14 pg/ml, P = 0.001). Steroids 97-104 tumor necrosis factor Homo sapiens 20-28 28457111-10 2017 In the steroid-resistant nephrotic syndrome patients, mean serum TNFalpha levels were similar before and after treatment. Steroids 7-14 tumor necrosis factor Homo sapiens 65-73 27766929-7 2017 Biologic agents like anti-tumor necrosis factor antibodies are being used as second line treatment in those patients dependent on steroids or in cases of refractory sarcoidosis. Steroids 130-138 tumor necrosis factor Homo sapiens 26-47 28967957-12 2017 Low mucosal TNFalpha concentrations were associated with steroid sensitivity. Steroids 57-64 tumor necrosis factor Homo sapiens 12-20 28475384-7 2017 Biologic agents targeting TNF remain important for steroid-sparing therapy in moderate-to-severe UC and CD. Steroids 51-58 tumor necrosis factor Homo sapiens 26-29 28264814-7 2017 In the dose-response analysis, higher steroid dose was associated with an increased risk of serious infections during pregnancy (coefficient for each unit increase in average prednisone equivalent mg daily dose=0.019, P=0.02).Conclusions Risk of serious infections is similar among pregnant women with systemic inflammatory conditions using steroids, non-biologics, and TNF inhibitors. Steroids 38-45 tumor necrosis factor Homo sapiens 370-373 27250593-0 2016 Letter: anti-TNF in steroid-dependent ulcerative colitis - are the available data enough? Steroids 20-27 tumor necrosis factor Homo sapiens 13-16 27957272-0 2016 The effect of diode laser and topical steroid on serum level of TNF-alpha in oral lichen planus patients. Steroids 38-45 tumor necrosis factor Homo sapiens 64-73 27957272-9 2016 CONCLUSIONS: Topical steroids reduce pain, reticular, atrophic, erosive RAE score and TNF-alpha serum level more than laser treatment. Steroids 21-29 tumor necrosis factor Homo sapiens 86-95 26979943-0 2016 Effect of IGF-I and TNF-alpha on intensification of steroid pathways in women with PCOS phenotypes are not identical. Steroids 52-59 tumor necrosis factor Homo sapiens 20-29 27075461-15 2016 The corticosteroid therapy was found associated with higher PWV, (p < 0.05), while there was no difference between vascular parameters and use of non-steroid therapies (methotrexate (MTX), anti-TNF alfa agents). Steroids 11-18 tumor necrosis factor Homo sapiens 197-200 26923897-6 2016 The presented case was diagnosed with CD and successfully treated with anti-TNF (tumor necrosis factor) due to steroid refractory. Steroids 111-118 tumor necrosis factor Homo sapiens 76-79 26668517-1 2015 We present the case of a 53-year-old woman with long-standing ulcerative colitis and severe, steroid-dependent disease course unresponsive to treatment with azathioprine, methotrexate, anti-TNF antibodies (infliximab, adalimumab) and tacrolimus, who refused colectomy as a therapeutic option. Steroids 93-100 tumor necrosis factor Homo sapiens 190-193 27403384-0 2016 Investigating the Impacts of Preoperative Steroid Treatment on Tumor Necrosis Factor-Alpha and Duration of Extubation Time underwent Ventricular Septal Defect Surgery. Steroids 42-49 tumor necrosis factor Homo sapiens 63-90 27403384-5 2016 AIMS: This research was to investigate the effects of pre-operative steroid use on inflammatory mediator TNF-alpha and on time to extubation postoperatively in ventricular septal defect patients undergoing cardiopulmonary bypass surgery. Steroids 68-75 tumor necrosis factor Homo sapiens 105-114 27403384-17 2016 CONCLUSION: There is a strong indication that preoperative steroid treatment reduced the TNF-alpha level together with shortens duration of postoperative intubation and positively contributes to extubation in ventricular septal defect patients operated in cardiac surgery with cardiopulmonary bypass. Steroids 59-66 tumor necrosis factor Homo sapiens 89-98 27099725-2 2016 Severe AP could be considered a further indication, instead of a relative restriction, to anti-TNFalpha in steroid-dependent IBD patients needing therapy with this class of drugs. Steroids 107-114 tumor necrosis factor Homo sapiens 95-103 26392121-3 2015 Previously, we showed the role of TNF-alpha in steroid-sensitive and IL-1beta in steroid-resistant immune-mediated hearing loss. Steroids 47-54 tumor necrosis factor Homo sapiens 34-43 26483672-2 2015 CASE PRESENTATION: A 39-year-old woman treated with MTX and a TNF inhibitor for rheumatoid arthritis and uveitis had steroid-resistant vitreous opacity. Steroids 117-124 tumor necrosis factor Homo sapiens 62-65 26346875-7 2015 New anti-TNF use (1.4%) was associated with younger age, absence of Medicaid coverage, hospitalisation, and higher preceding use of burst (IRR=2.35, CI 1.59 to 3.47) and maintenance steroids (IRR=2.40, CI 1.05 to 5.48). Steroids 182-190 tumor necrosis factor Homo sapiens 9-12 26346875-8 2015 Among anti-TNF users, we observed high rates of concurrent maintenance steroid use (19%). Steroids 71-78 tumor necrosis factor Homo sapiens 11-14 26112052-10 2015 However, steroid treatment significantly decreased pro-inflammatory cytokines IL-1beta, IL-8, TNF and IFN-gamma at the time of organ procurement. Steroids 9-16 tumor necrosis factor Homo sapiens 94-97 25037120-0 2015 Steroid treatment can inhibit nuclear localization of members of the NF-kappaB pathway in human disc cells stimulated with TNF-alpha. Steroids 0-7 tumor necrosis factor Homo sapiens 123-132 25037120-1 2015 Steroid applications are able to repress inflammatory activity in various conditions, including herniation of the nucleus pulposus (HNP), by inhibiting tumour necrosis factor (TNF)-alpha, but the effects of long-term use are unknown. Steroids 0-7 tumor necrosis factor Homo sapiens 152-186 26557831-5 2015 RESULTS: In steroid-refractory UC, early intensive therapy using anti-tumor necrosis factor (TNF) antibodies or the calcineurin inhibitors cyclosporine and tacrolimus is indicated in any case to prevent progression to a toxic megacolon and/or to avoid proctocolectomy. Steroids 12-19 tumor necrosis factor Homo sapiens 70-91 25694859-0 2015 Drug free remission after steroid-dependent disappearance of lymphoproliferative disorder in rheumatoid arthritis patient treated with TNF-alpha blockade: case study. Steroids 26-33 tumor necrosis factor Homo sapiens 135-144 25892889-6 2015 Furthermore, use of anti-TNF agents is usually reserved for those cases that prove to be refractory to steroids. Steroids 103-111 tumor necrosis factor Homo sapiens 25-28 25131534-16 2015 Fifty percent of patients with anti-TNF-associated DILI required steroid therapy, but most did not need long-term treatment. Steroids 65-72 tumor necrosis factor Homo sapiens 36-39 26045843-0 2015 Combined effect of tnf-alpha polymorphisms and hypoxia on steroid-induced osteonecrosis of femoral head. Steroids 58-65 tumor necrosis factor Homo sapiens 19-28 26045843-2 2015 And the polymorphisms of TNF-alpha were presented as risk factors for steroid-induced osteonecrosis of the femoral head (SONFH). Steroids 70-77 tumor necrosis factor Homo sapiens 25-34 25729557-7 2015 Tumor necrosis factor (TNF) alpha inhibitors have been proven to be highly effective in the treatment of IBD patients which are steroid-dependent or refractory to conventional therapy and in patients with associated articular manifestations. Steroids 128-135 tumor necrosis factor Homo sapiens 0-33 26125144-0 2015 Anti-tumor necrosis factor monoclonal antibody for steroid-dependent TB-IRIS in AIDS. Steroids 51-58 tumor necrosis factor Homo sapiens 5-26 24475168-8 2014 TNF-alpha blockers demonstrated clinical benefit as compared to placebo control as evidenced by an increased frequency of clinical remission (p<0.00001), steroid-free remission (p = 0.01), endoscopic remission (p<0.00001) and a decrease in frequency of colectomy (p = 0.03). Steroids 157-164 tumor necrosis factor Homo sapiens 0-9 25617625-1 2015 UNLABELLED: The purpose of the study was to determine the effect of ginseng-based steroid Rg1 on TNF-alpha and IL-10 gene expression in human skeletal muscle against exercise challenge, as well as on its ergogenic outcomes. Steroids 82-89 tumor necrosis factor Homo sapiens 97-106 25348881-10 2015 Anti-TNF-alpha treatment was used in three of the GI partial obstruction cases: two with complete relief and one with partial response that was supplemented with steroids. Steroids 162-170 tumor necrosis factor Homo sapiens 5-14 25101334-1 2014 Antitumour necrosis factor (anti-TNF) therapy has been a major advance in the treatment of inflammatory bowel disease (IBD) by improving rates of mucosal healing, steroid-free remission, and decreasing rates of hospitalization and surgery. Steroids 163-170 tumor necrosis factor Homo sapiens 33-36 24978425-3 2014 As the pathogenesis of TED is thought to involve the upregulation of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), it has been postulated that anti-TNF agents may be used as steroid-sparing agents in the treatment of TED. Steroids 206-213 tumor necrosis factor Homo sapiens 106-133 24978425-3 2014 As the pathogenesis of TED is thought to involve the upregulation of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), it has been postulated that anti-TNF agents may be used as steroid-sparing agents in the treatment of TED. Steroids 206-213 tumor necrosis factor Homo sapiens 135-144 24709278-2 2014 METHODS: We conducted a systematic literature review between January 2000 and May 2013 to investigate the efficacy of a second anti-TNFalpha agent in the treatment of ACU in children (<=16 years) refractory to a first course of a single anti-TNFalpha treatment, topical and/or systemic steroid therapy and at least one DMARD. Steroids 289-296 tumor necrosis factor Homo sapiens 132-140 24517287-14 2014 Based on other reported GPPP cases, TNF-alpha antagonists are used as rescue therapy in GPPP refractory to steroid and cyclosporine therapy, but careful consideration of the advantages and disadvantages is warranted before using them. Steroids 107-114 tumor necrosis factor Homo sapiens 36-45 24625845-0 2014 Inflammation: TNF snuffs out steroids. Steroids 29-37 tumor necrosis factor Homo sapiens 14-17 24235078-17 2014 TNF-alpha inhibitors are useful in case of steroid-resistant sarcoidosis or in patients who develop severe steroid toxicity. Steroids 43-50 tumor necrosis factor Homo sapiens 0-9 24235078-17 2014 TNF-alpha inhibitors are useful in case of steroid-resistant sarcoidosis or in patients who develop severe steroid toxicity. Steroids 107-114 tumor necrosis factor Homo sapiens 0-9 24653848-6 2014 We report a rare case of steroid resistant Crohn"s disease associated with multivisceral sarcoidosis, treated successfully by an anti-TNF alpha agent, infliximab. Steroids 25-32 tumor necrosis factor Homo sapiens 134-143 24601700-8 2014 Patients with steroid-refractory aGvHD received a different second-line therapies (antithymocyte globulin, anti-TNFalpha antibody, anti CD52 antibody) with response rate 45 % (CR - 18 %, PR - 27 %). Steroids 14-21 tumor necrosis factor Homo sapiens 112-120 24225487-2 2014 RECENT FINDINGS: Multiple case series and observational studies support the use of anti-tumor necrosis factor (TNF) medications, in particular infliximab, in patients who relapse upon tapering steroids and/or adding nonbiologic immunosuppressive agents. Steroids 193-201 tumor necrosis factor Homo sapiens 83-109 24225487-2 2014 RECENT FINDINGS: Multiple case series and observational studies support the use of anti-tumor necrosis factor (TNF) medications, in particular infliximab, in patients who relapse upon tapering steroids and/or adding nonbiologic immunosuppressive agents. Steroids 193-201 tumor necrosis factor Homo sapiens 111-114 23357593-7 2013 Following withdrawal of anti-TNF agents and a course of steroids, the clinical picture resolved. Steroids 56-64 tumor necrosis factor Homo sapiens 29-32 23574282-4 2013 In patients with more severe disease, although anti-TNF agents are more powerful and act more rapidly, there is a subset of patients with moderate-to-severe IBD without important anatomical damage who may achieve a prolonged steroid-free clinical and anatomical remission on azathioprine monotherapy. Steroids 225-232 tumor necrosis factor Homo sapiens 52-55 24105393-9 2013 Older steroid-responsive patients were less likely to start an anti-TNF agent during the first year of follow-up than younger patients (7% versus 31%, P = 0.006), but there was no difference in 1-year colectomy rates (27% versus 28%, P = 0.63). Steroids 6-13 tumor necrosis factor Homo sapiens 68-71 23901289-10 2013 CONCLUSION: TNF antagonists allowed significant steroid sparing and were well tolerated, but do not seem to be effective against sarcoidosis joint involvement. Steroids 48-55 tumor necrosis factor Homo sapiens 12-15 23333920-8 2013 Our results demonstrated that IL-27 induced and synergized with TNF-alpha to up-regulate CXCL10 mRNA and protein concentrations in a steroid-insensitive manner. Steroids 133-140 tumor necrosis factor Homo sapiens 64-73 24471301-15 2013 According to available data, it seems that early intensive therapy with anti-TNF drugs as monotherapy or in combination with immunosuppressive drugs in this group of patients increases possibility of induction of remission, mucosal healing and maintenance of steroid-free remission. Steroids 259-266 tumor necrosis factor Homo sapiens 77-80 24471301-16 2013 Candidates for anti-TNF therapy are also patients who did not respond to conventional treatment, patients with moderate or severe disease who are intolerant to steroids, patients in whom we expect severe adverse effects from steroid treatment, patients who do not accept steroid treatment and patients with frequent relapses and need for steroids. Steroids 225-232 tumor necrosis factor Homo sapiens 20-23 24030227-2 2013 It has also been demonstrated that anti-TNF are effective in steroid-dependent and steroid-refractory CD and UC. Steroids 61-68 tumor necrosis factor Homo sapiens 40-43 23354348-1 2013 Infliximab is a chimeric IgG1 monoclonal antibody to tumor necrosis factor (TNF)-a used in the treatment of steroid refractory or dependent Crohn"s disease (CD). Steroids 108-115 tumor necrosis factor Homo sapiens 53-74 23354348-1 2013 Infliximab is a chimeric IgG1 monoclonal antibody to tumor necrosis factor (TNF)-a used in the treatment of steroid refractory or dependent Crohn"s disease (CD). Steroids 108-115 tumor necrosis factor Homo sapiens 76-79 23539523-8 2013 Larger case studies are needed to confirm the efficacy of TNF-alpha inhibition in steroid refractory CMUSE. Steroids 82-89 tumor necrosis factor Homo sapiens 58-67 24030227-2 2013 It has also been demonstrated that anti-TNF are effective in steroid-dependent and steroid-refractory CD and UC. Steroids 83-90 tumor necrosis factor Homo sapiens 40-43 24030227-7 2013 Anti-TNF therapies have been shown superior to immunosuppressants and combination therapy superior to anti-TNF monotherapy in inducing steroid-free remission and mucosal healing. Steroids 135-142 tumor necrosis factor Homo sapiens 5-8 23051721-5 2012 RESULTS: Treatment of steroid-resistant Crohn"s disease is based on the introduction of immunomodulators such as azathioprine, 6-mercaptopurine or methotrexate, the anti-TNF drugs infliximab, adalimumab and certolizumab pegol. Steroids 22-29 tumor necrosis factor Homo sapiens 170-173 23526476-0 2013 Monoclonal Anti-TNF-alpha Antibodies for Severe Steroid-Dependent Asthma: A Case Series. Steroids 48-55 tumor necrosis factor Homo sapiens 16-25 23526476-11 2013 CONCLUSION: This case series suggests that anti-TNF-alpha drugs may improve the condition of a subgroup of patients with severe steroid-refractory asthma, with a favourable risk-benefit profile for most, considering asthma severity, occurrence of life-threatening exacerbations and complications of long-term oral steroids. Steroids 128-135 tumor necrosis factor Homo sapiens 48-57 23526476-11 2013 CONCLUSION: This case series suggests that anti-TNF-alpha drugs may improve the condition of a subgroup of patients with severe steroid-refractory asthma, with a favourable risk-benefit profile for most, considering asthma severity, occurrence of life-threatening exacerbations and complications of long-term oral steroids. Steroids 314-322 tumor necrosis factor Homo sapiens 48-57 23165380-1 2012 OBJECTIVES: To characterize levels of tumor necrosis factor (TNF; formerly known as tumor necrosis factor alpha), a well-established proinflammatory cytokine, in patients with immune-mediated sensorineural hearing loss (IM-SNHL) and to determine the role of this cytokine in identifying steroid-responsive hearing loss. Steroids 287-294 tumor necrosis factor Homo sapiens 38-59 23165380-1 2012 OBJECTIVES: To characterize levels of tumor necrosis factor (TNF; formerly known as tumor necrosis factor alpha), a well-established proinflammatory cytokine, in patients with immune-mediated sensorineural hearing loss (IM-SNHL) and to determine the role of this cytokine in identifying steroid-responsive hearing loss. Steroids 287-294 tumor necrosis factor Homo sapiens 61-64 23165380-1 2012 OBJECTIVES: To characterize levels of tumor necrosis factor (TNF; formerly known as tumor necrosis factor alpha), a well-established proinflammatory cytokine, in patients with immune-mediated sensorineural hearing loss (IM-SNHL) and to determine the role of this cytokine in identifying steroid-responsive hearing loss. Steroids 287-294 tumor necrosis factor Homo sapiens 84-111 23165380-10 2012 RESULTS: Steroid nonresponders had the highest mean baseline plasma levels of TNF compared with steroid responders and control subjects (27.6, 24.1, and 14.4 pg/mL, respectively) (P = .03). Steroids 9-16 tumor necrosis factor Homo sapiens 78-81 22504554-9 2012 Western blot analysis demonstrated that the expression of phosphorylated endothelial nitric oxide synthase (eNOS) increased, whereas that of inducible nitric oxide synthase (iNOS) decreased following the 96-h steroid treatment of TNF-alpha-stimulated HCAECs. Steroids 209-216 tumor necrosis factor Homo sapiens 230-239 22508292-6 2013 The anti-TNF cohort was significantly younger at diagnosis and at the time of initiation of anti-TNF or steroid therapy. Steroids 104-111 tumor necrosis factor Homo sapiens 9-12 22796281-7 2012 CONCLUSIONS: Anti-TNF therapy is associated with a small but significant risk of SI that is associated with the concomitant use of steroids, advanced age at the start of anti-TNF treatment, and the type of anti-TNF agent. Steroids 131-139 tumor necrosis factor Homo sapiens 18-21 23153702-7 2012 However, the treatment with both steroids decreased the secretion of TNF-alpha, IL-18 and TGF-beta1 by EEC in the presence of ESC. Steroids 33-41 tumor necrosis factor Homo sapiens 69-78 22876034-5 2012 Different randomized trials assessed the efficacy of anti-TNF treatment not only to induce, but also to maintain, steroid-free remission. Steroids 114-121 tumor necrosis factor Homo sapiens 58-61 22735878-5 2012 However, infliximab, the chimeric monoclonal antibody to tumor necrosis factor-a, is now considered as a primary treatment because of the disease"s relatively high rate of steroid resistance. Steroids 172-179 tumor necrosis factor Homo sapiens 57-80 22588657-3 2012 Steroids, immunosuppressants such as azathioprine, 6-mercaptopurine, methotraxate or ciclosporine, as well as biologicals, which act as TNF-alpha antagonists, are commonly used for maintenance therapy and treatment of acute exacerbations of IBD. Steroids 0-8 tumor necrosis factor Homo sapiens 176-185 22515220-6 2012 There was a clear chronologic relationship with, and clinical remission upon withdrawal or steroid suppression of the anti-TNF-alpha agents. Steroids 91-98 tumor necrosis factor Homo sapiens 123-132 22284606-4 2012 The efficacy of immunosuppressive drugs like azathioprine methotrexate or anti-tumor necrosis factor antibodies appears to be too low to reduce the use of steroids. Steroids 155-163 tumor necrosis factor Homo sapiens 79-100 21988215-12 2011 Anti-TNF therapy is indicated in patients intolerant or not responding to steroids and immunosuppressors and in fistulizing Crohn"s disease. Steroids 74-82 tumor necrosis factor Homo sapiens 5-8 21644041-2 2011 Steroid-resistant disease can be treated with immunosuppressive drugs, antimalarial therapies and recently with anti-TNFalpha agents. Steroids 0-7 tumor necrosis factor Homo sapiens 117-125 21789495-10 2011 Future research is needed to position the available anti-TNF agents and combined immunosuppressive therapy in the treatment of UC to achieve and maintain steroid free remission. Steroids 154-161 tumor necrosis factor Homo sapiens 57-60 21972387-6 2011 Asthma control was achieved with inhaled steroids, allowing anti-TNF-alpha treatment to continue. Steroids 41-49 tumor necrosis factor Homo sapiens 65-74 21210752-6 2011 Steroid sparing agents include antimetabolites such as methotrexate, azathioprine and mycophenolate mofetil; calcineurin inhibitors which include cyclosporine, tacrolimus; alkylating agents which include cyclophosphamide and chlorambucil; and biologics which include the TNF-alpha inhibitors infliximab, adalimumab and etanercept and daclizumab, IFN-alpha(2a) and rituximab. Steroids 0-7 tumor necrosis factor Homo sapiens 271-280 21683309-5 2011 This case report suggests the effectiveness of adalimumab as first anti-TNFalpha in case of steroid-dependent/resistant gastrointestinal BD. Steroids 92-99 tumor necrosis factor Homo sapiens 72-80 20843756-5 2011 The following items have been chosen: definitions of active, inactive, steroid dependent and resistant disease; measures of activity; anti-tumor necrosis factor alpha therapy use in active steroid dependent and refractory luminal Crohn"s Disease, in fistulising Crohn"s Disease, in steroid dependent and resistant active Ulcerative Colitis; risk of cancer; risk of infections during anti-tumor necrosis factor alpha therapy; special situations. Steroids 189-196 tumor necrosis factor Homo sapiens 139-166 21751503-9 2011 There is increasing evidence that early intervention with immunosuppressives or biologic agents aimed at tumor necrosis factor-alpha usually has rapid and prolonged benefits, including steroid sparing, reductions in hospitalizations and, reductions in the need for surgery. Steroids 185-192 tumor necrosis factor Homo sapiens 105-132 20843756-5 2011 The following items have been chosen: definitions of active, inactive, steroid dependent and resistant disease; measures of activity; anti-tumor necrosis factor alpha therapy use in active steroid dependent and refractory luminal Crohn"s Disease, in fistulising Crohn"s Disease, in steroid dependent and resistant active Ulcerative Colitis; risk of cancer; risk of infections during anti-tumor necrosis factor alpha therapy; special situations. Steroids 189-196 tumor necrosis factor Homo sapiens 139-166 20497138-0 2010 Systematic review: steroid withdrawal in anti-TNF-treated patients with inflammatory bowel disease. Steroids 19-26 tumor necrosis factor Homo sapiens 46-49 20736834-6 2010 In addition to the concomitant and alternative use of immunosuppressive agents to steroid therapy, disease remission in refractory neuro-ophthalmic sarcoidosis with tumor necrosis factor alpha inhibitors has also been reported. Steroids 82-89 tumor necrosis factor Homo sapiens 165-192 20833730-3 2010 IFNgamma and TNFalpha synergistically induce CXCL10 release from human ASM cells in a steroid-insensitive manner, via an as yet undefined mechanism. Steroids 86-93 tumor necrosis factor Homo sapiens 13-21 21591983-8 2011 TNF-alpha (-308) AG phenotype was detected to be significantly higher in steroid-refractory and splenectomized cases at the end of the first year than in the steroid-responsive (complete response (CR) and remission (R)) cases (OR: 4.137, 95% CI: 1.156-14.807, p < 0.05). Steroids 73-80 tumor necrosis factor Homo sapiens 0-9 21591983-8 2011 TNF-alpha (-308) AG phenotype was detected to be significantly higher in steroid-refractory and splenectomized cases at the end of the first year than in the steroid-responsive (complete response (CR) and remission (R)) cases (OR: 4.137, 95% CI: 1.156-14.807, p < 0.05). Steroids 158-165 tumor necrosis factor Homo sapiens 0-9 21591983-11 2011 With these findings, it was found that TNF-alpha/AG, TGF-beta 1/TT, IFN-gamma/TT, MBL/BB, and IL-1RA A1/A2 genotypes were detected as the genes of susceptibility to ITP, while TNF-alpha/AG, IFN-gamma/AA, and MBL/AB genotypes might be important in response to steroid treatment. Steroids 259-266 tumor necrosis factor Homo sapiens 39-48 21386777-0 2010 Steroid-induced inflammatory neuropathy in a patient on tumor necrosis factor-alpha antagonist therapy. Steroids 0-7 tumor necrosis factor Homo sapiens 56-83 21386777-1 2010 We describe a patient on the tumor necrosis factor-alpha antagonist, adalimumab, for 2 years for rheumatoid arthitis, who developed a rapidly progressive inflammatory neuropathy shortly after starting oral steroids. Steroids 206-214 tumor necrosis factor Homo sapiens 29-56 20833730-4 2010 We report that TNFalpha activates the classical NF-kappaB (nuclear factor kappaB) pathway, whereas IFNgamma activates JAK2/STAT-1alpha and that inhibition of the JAK/STAT pathway is more effective in abrogating CXCL10 release than the steroid fluticasone. Steroids 235-242 tumor necrosis factor Homo sapiens 15-23 20833730-8 2010 Our results provide evidence that synergism between TNFalpha and IFNgamma lies at the level of coactivator recruitment in human ASM and suggest that inhibition of JAK/STAT signaling may be of therapeutic benefit in steroid-resistant airway disease. Steroids 215-222 tumor necrosis factor Homo sapiens 52-60 20497138-2 2010 AIM: To conduct a systematic review to establish figures for steroid withdrawal in anti-TNF treated inflammatory bowel disease-patients. Steroids 61-68 tumor necrosis factor Homo sapiens 88-91 20497138-4 2010 We selected English-language publications that addressed the effect of anti-TNF on steroid withdrawal. Steroids 83-90 tumor necrosis factor Homo sapiens 76-79 20175769-1 2010 BACKGROUND: The calcineurin inhibitor tacrolimus and the anti-TNF-antibody infliximab are established options in steroid-refractory ulcerative colitis (UC). Steroids 113-120 tumor necrosis factor Homo sapiens 62-65 21086936-4 2010 Failure of previous treatment and steroid dependency were the main reasons for initiating anti-TNF-alpha therapy. Steroids 34-41 tumor necrosis factor Homo sapiens 95-104 20439544-2 2010 In contrast, glucocorticoids (GCs) are steroid hormones that suppress inflammation, at least in part by regulating the expression and action of TNF. Steroids 39-55 tumor necrosis factor Homo sapiens 144-147 20140224-0 2010 Gene expression profiling and network analysis reveals lipid and steroid metabolism to be the most favored by TNFalpha in HepG2 cells. Steroids 65-72 tumor necrosis factor Homo sapiens 110-118 20140224-6 2010 CONCLUSIONS: TNFalpha alters the transcriptome profiling within HepG2 cells with an interesting catalog of genes being affected and those involved in lipid and steroid metabolism to be the most favored. Steroids 160-167 tumor necrosis factor Homo sapiens 13-21 19147181-8 2010 Following withdrawal of anti-TNFalpha agents and a brief course of steroids, the clinical picture resolved. Steroids 67-75 tumor necrosis factor Homo sapiens 29-37 20120429-6 2010 This report will discuss the possible mechanism of action of the addition of TNF-alpha inhibitors as a steroid-sparing agent in these patients. Steroids 103-110 tumor necrosis factor Homo sapiens 77-86 20137155-5 2010 Many of these agents, such as mycophenolate mofetil, anti-tumor necrosis factor antibodies, and anti-interleukin-2Ralpha-chain antibodies, have demonstrated promising activity in steroid-refractory aGVHD. Steroids 179-186 tumor necrosis factor Homo sapiens 58-79 20926883-15 2010 Clinical practice should change such that combination therapy with an anti-TNF agent and azathioprine replace azathioprine in patients failing first line therapy with mesalamine and/or steroids. Steroids 185-193 tumor necrosis factor Homo sapiens 75-78 20025597-10 2009 An overall long lasting remission of less than 30% with scheduled administration of TNF-alpha blockers in patients with steroid dependent or refractory CD seems to be lifelike and alternative therapeutic options are warranted. Steroids 120-127 tumor necrosis factor Homo sapiens 84-93 19896079-1 2009 Anti-Tumor Necrosis Factor Alpha (TNF-alpha) therapy with infliximab has shown to be effective for patients with steroid-refractory acute graft-versus-host disease (aGVHD). Steroids 113-120 tumor necrosis factor Homo sapiens 5-32 19896079-1 2009 Anti-Tumor Necrosis Factor Alpha (TNF-alpha) therapy with infliximab has shown to be effective for patients with steroid-refractory acute graft-versus-host disease (aGVHD). Steroids 113-120 tumor necrosis factor Homo sapiens 34-43 19604433-11 2009 In one patient in whom the steroid dosage was increased due to poor response to anti-TNF-alpha therapy, brainstem infarction occurred four months later. Steroids 27-34 tumor necrosis factor Homo sapiens 85-94 19542427-6 2009 Production of IL-1alpha, IL-10, IL-17, IFN-gamma, G-CSF, GM-CSF, TNF-alpha, and IFN-inducible protein 10 (IP-10) correlated significantly with in vitro steroid sensitivity; however, only IL-2 and TNF-alpha reduced steroid sensitivity when added exogenously. Steroids 152-159 tumor necrosis factor Homo sapiens 65-74 19533547-2 2009 Our aim was to assess the properties of the monoclonal TNF-alpha antibody infliximab in a patient with high-dose steroid refractory CS. Steroids 113-120 tumor necrosis factor Homo sapiens 55-64 19326415-6 2009 Although anti-tumor necrosis factor alpha therapy has been widely used for the treatment of steroid-resistant acute graft-versus-host disease in the hematopoietic stem cell transplant setting, there previously have been no reported cases of its use in liver transplantation. Steroids 92-99 tumor necrosis factor Homo sapiens 14-41 18932199-7 2009 Several TNF-R components were influenced by LH and/or steroid ablation; notably, steroid ablation reduced (P < 0.05) luteal TNF-alpha, but not TNF-beta, mRNA levels, which was prevented by progestin treatment. Steroids 81-88 tumor necrosis factor Homo sapiens 127-136 19027157-6 2009 Regulation of the TNF/TNFR system by steroid hormones also suggests a role in uterine function including menstrual cycle-dependent destruction and regeneration of endometrial tissue. Steroids 37-53 tumor necrosis factor Homo sapiens 18-21 19436689-10 2009 CONCLUSIONS: EBC TNF-alpha level was low in patients receiving systemic steroid and antibiotic therapy for AECOPD. Steroids 72-79 tumor necrosis factor Homo sapiens 17-26 21686765-1 2009 This report describes the development of lymphoedema in a patient with rheumatoid arthritis (RA) who was treated with tumour necrosis factor alpha (TNFalpha) inhibitors.The patient was a 62-year-old woman with a long-standing history of RA that had been uncontrolled with steroids and methotrexate. Steroids 272-280 tumor necrosis factor Homo sapiens 148-156 18775652-4 2008 At admission in the responder subgroup, incubation with both steroids under basal conditions resulted in an increase of TNF-alpha levels, which decreased after treatment. Steroids 61-69 tumor necrosis factor Homo sapiens 120-129 18775652-5 2008 After stimulation with phytohemagglutinin, an enhancement of TNF-alpha suppression by steroids was detectable after successful antidepressive treatment. Steroids 86-94 tumor necrosis factor Homo sapiens 61-70 19008611-12 2008 The GG genotype of IL-6 -G174C, TT genotype of IL-4 -C590T, and AA genotype of TNF-alpha -G308A cytokine gene polymorphisms may be causative factors for nonresponsiveness towards steroid therapy among INS children. Steroids 179-186 tumor necrosis factor Homo sapiens 79-88 19008611-11 2008 TNF-alpha revealed a strong association at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46), as well as at allelic level (P = 0.0433, OR = 2.251, 95% CI = 1.09-4.66), demonstrating that it may be considered one of the genetic risk factors affecting the steroid response in INS patients. Steroids 267-274 tumor necrosis factor Homo sapiens 0-9 16850114-11 2007 Steroid-dependent or refractory cases may respond to other immunosuppressants including anti-TNF-alpha agents. Steroids 0-7 tumor necrosis factor Homo sapiens 93-102 17947510-1 2008 We have previously shown that long-term treatment of airway smooth muscle (ASM) cells with a combination of TNF-alpha and IFN-gamma impaired steroid anti-inflammatory action through the up-regulation of glucocorticoid receptor beta isoform (GRbeta) (Mol Pharmacol 2006;69:588-596). Steroids 141-148 tumor necrosis factor Homo sapiens 108-117 17947510-2 2008 We here found that steroid actions could also be suppressed by short-term exposure of ASM cells to TNF-alpha and IFN-gamma (6 h) as shown by the abrogated glucocorticoid responsive element (GRE)-dependent gene transcription; surprisingly, neither GRalpha nuclear translocation nor GRbeta expression was affected by cytokine mixture. Steroids 19-26 tumor necrosis factor Homo sapiens 99-108 17894921-3 2007 Biologic therapies, such as the anti-TNF agent infliximab, offer promise but are not without controversy; despite many positive reports, steroid-refractory patients are less likely than other individuals to respond to infliximab. Steroids 137-144 tumor necrosis factor Homo sapiens 37-40 18541197-1 2008 Infliximab, a chimeric monoclonal antibody (mAb) against tumor necrosis factor (TNF)-alpha, has shown activity against steroid refractory acute graft-versus-host disease (aGVHD). Steroids 119-126 tumor necrosis factor Homo sapiens 57-90 18042798-3 2008 Because tumor necrosis factor-alpha (TNFalpha) is an important effector of experimental GVHD, we treated patients with new-onset GVHD with steroids plus the TNFalpha inhibitor etanercept on a previously reported pilot trial (n = 20) and a phase 2 trial (n = 41). Steroids 139-147 tumor necrosis factor Homo sapiens 37-45 16944071-4 2007 There are few reports of treatment of refractory or steroid-dependent TA with tumor necrosis factor alpha (TNF-alpha) inhibitors including infliximab and etanercept. Steroids 52-59 tumor necrosis factor Homo sapiens 78-105 16944071-4 2007 There are few reports of treatment of refractory or steroid-dependent TA with tumor necrosis factor alpha (TNF-alpha) inhibitors including infliximab and etanercept. Steroids 52-59 tumor necrosis factor Homo sapiens 107-116 18239400-3 2007 Anti-TNF agents represent choice alternatives for patients who do not respond to steroids or in whom steroids are contraindicated. Steroids 101-109 tumor necrosis factor Homo sapiens 5-8 17560419-7 2007 Recent small studies with anti-tumor necrosis factor (TNF) agents are promising for most extra-intestinal manifestations of Crohn"s disease, and may permit more steroid-sparing disease control in the future. Steroids 161-168 tumor necrosis factor Homo sapiens 26-52 17560419-7 2007 Recent small studies with anti-tumor necrosis factor (TNF) agents are promising for most extra-intestinal manifestations of Crohn"s disease, and may permit more steroid-sparing disease control in the future. Steroids 161-168 tumor necrosis factor Homo sapiens 54-57 17202177-11 2007 However, clinical responses may not be due to direct effects of DMARDs on LILR expression but due to partial inhibition of LIRA2-mediated TNF-alpha production by steroids leading to suppression of inflammation. Steroids 162-170 tumor necrosis factor Homo sapiens 138-147 17261090-0 2007 Steroid-resistant sarcoidosis: is antagonism of TNF-alpha the answer? Steroids 0-7 tumor necrosis factor Homo sapiens 48-57 17234454-3 2007 The aim of this study was to evaluate whether there was any relation between serum TNF-a levels and the response to ECP in patients with steroid refractory of extensive chronic GvHD. Steroids 137-144 tumor necrosis factor Homo sapiens 83-88 17582178-7 2007 The levels of TNFa were suppressed by use of steroids. Steroids 45-53 tumor necrosis factor Homo sapiens 14-18 17206641-0 2007 Predictive value of mucosal TNF-alpha transcripts in steroid-refractory Crohn"s disease patients receiving intensive immunosuppressive therapy. Steroids 53-60 tumor necrosis factor Homo sapiens 28-37 17038555-6 2007 However, when the steroid production data were normalized by the cell number, TNF-alpha increased the basal production of cortisol, androstenedione, DHEA, DHEAS, and aldosterone (137, 121, 165, 73, and 28%, respectively), and the 8-bromo-cAMP-induced production of cortisol, DHEAS, and aldosterone (122, 121, and 256%, respectively). Steroids 18-25 tumor necrosis factor Homo sapiens 78-87 17117445-14 2006 CONCLUSIONS: In a pragmatic setting, anti-TNF therapy led to reduced need for steroid injections and other DMARDs, as well as reductions in use of several hospital resources. Steroids 78-85 tumor necrosis factor Homo sapiens 42-45 17909718-10 2007 Four hours after surgery, LPS-induced TNF-alpha secretion was significantly reduced in the steroid group, but it increased rapidly during the following days. Steroids 91-98 tumor necrosis factor Homo sapiens 38-47 16539822-5 2006 More specifically, we propose that anti-TNF-alphaagents be considered in active PsA resistant to non-steroidal anti-inflammatory drugs, to at least two local steroid injections and at least 2 conventional disease-modifying anti-rheumatic agents (in cases of oligo/monoarthritis and/or enthesitis), and to at least two conventional disease-modifying anti-rheumatic agents (in patients with peripheral joints synovitis). Steroids 101-108 tumor necrosis factor Homo sapiens 40-43 16699531-0 2006 Combination antithymocyte globulin and soluble TNFalpha inhibitor (etanercept) +/- mycophenolate mofetil for treatment of steroid refractory acute graft-versus-host disease. Steroids 122-129 tumor necrosis factor Homo sapiens 47-55 16517575-7 2006 Sputum cells from COPD patients (both steroid free and steroid treated) produced significantly less TNFalpha than cells from healthy non-smoking subjects (p=0.017 and p=0.001, respectively). Steroids 38-45 tumor necrosis factor Homo sapiens 100-108 16517575-7 2006 Sputum cells from COPD patients (both steroid free and steroid treated) produced significantly less TNFalpha than cells from healthy non-smoking subjects (p=0.017 and p=0.001, respectively). Steroids 55-62 tumor necrosis factor Homo sapiens 100-108 16710025-13 2006 Four other patients with steroid-refractory enterocolitis appeared to respond promptly to tumor necrosis factor alpha blockade with infliximab. Steroids 25-32 tumor necrosis factor Homo sapiens 90-117 16549165-18 2006 The daily dose of steroid (mg/d) and A allele frequency for TNF-alpha -238 G/A genotype were significant predictors of HOMA index in linear regression analysis. Steroids 18-25 tumor necrosis factor Homo sapiens 60-69 16620022-7 2006 Molecular biological techniques have revealed, that many of the established conventional antiinflammatory drugs such as salicylic acids, steroids or immunuosuppressants act at the same molecules that are the target for modern biologicals, i.e., the cytokine TNF or the transcription factor NFkappaB. Steroids 137-145 tumor necrosis factor Homo sapiens 258-261 16830299-1 2006 Infliximab is a monoclonal antibody that targets TNF-alpha and has been shown to be effective for the management of steroid-dependent or refractory Crohn"s disease. Steroids 116-123 tumor necrosis factor Homo sapiens 49-58 16291871-5 2006 We also found that TNFalpha and IFNgamma impaired GC responsiveness by inhibiting steroid induced both 1) GRalpha-DNA binding activity and 2) GC-responsive element-(GRE)-dependent gene transcription. Steroids 82-89 tumor necrosis factor Homo sapiens 19-27 16988499-10 2006 RESULTS: Local administration of the TNF-alpha blocker allowed methylprednisolone to be tapered off without loss of hearing function in 4/5 steroid-dependent patients. Steroids 140-147 tumor necrosis factor Homo sapiens 37-46 16988499-14 2006 CONCLUSIONS: The results of this pilot trial demonstrate that in patients with AIED, transtympanic delivery of the TNF-alpha blocker infliximab once weekly for 4 weeks allowed steroids to be tapered off, resulted in hearing improvement and reduced disease relapses. Steroids 176-184 tumor necrosis factor Homo sapiens 115-124 16255837-10 2006 CONCLUSIONS: These findings suggest that cutaneous GR function is abnormal in antidepressant-resistant depression, that circulating TNF-alpha may play a significant role in this abnormality and that the efficacy of topical steroids in antidepressant-resistant depressives is reduced. Steroids 223-231 tumor necrosis factor Homo sapiens 132-141 16479743-3 2005 Aim of our study is to test anti-TNF alpha treatment as a steroid sparing tool in PMR patients affected by DM or osteoporosis. Steroids 58-65 tumor necrosis factor Homo sapiens 33-42 16393329-0 2005 Chlamydia pneumoniae infection enhances cellular proliferation and reduces steroid responsiveness of human peripheral blood mononuclear cells via a tumor necrosis factor-alpha-dependent pathway. Steroids 75-82 tumor necrosis factor Homo sapiens 148-175 15489577-2 2004 The antibody to tumor necrosis factor alpha, infliximab, has shown to be effective in the treatment of steroid-refractory ulcerative colitis in pilot studies. Steroids 103-110 tumor necrosis factor Homo sapiens 16-43 15808446-2 2005 Topical steroid phobia is rampant in many countries, a real advantage for the entry on the market of topical immunomodulators (TIMs), which inhibit both antigen specific and non-specific T cell activation in the skin, by blockade of gene transcription of proinflammatory cytokines such as IL2 and TNF alpha. Steroids 8-15 tumor necrosis factor Homo sapiens 297-306 16128605-8 2005 TNFalpha is known to be a contributing factor in kidney allograft rejection, and may have value in predicting the onset of steroid-resistant acute rejection after liver transplantation. Steroids 123-130 tumor necrosis factor Homo sapiens 0-8 15231721-0 2004 Tumor necrosis factor-alpha suppresses the expression of steroid receptor coactivator-1 and -2: a possible mechanism contributing to changes in steroid hormone responsiveness. Steroids 144-159 tumor necrosis factor Homo sapiens 0-27 15638237-2 2004 Preliminary data suggest a benefit of anti-tumor necrosis factor alpha (Infliximab) therapy in patients with steroid refractory UC. Steroids 109-116 tumor necrosis factor Homo sapiens 43-70 15231721-4 2004 To assess TNF-alpha effects on steroid hormone-mediated transcriptional activity, UtSMC were transfected with progesterone receptor B (PR-B) and a model PRE2-luciferase reporter construct. Steroids 31-46 tumor necrosis factor Homo sapiens 10-19 15231721-8 2004 In conclusion, TNF-alpha impairs progesterone-stimulated PR-B-mediated transactivation, and these effects appear to be due, in part, to reduced expression of SRC-1 and -2, which is a novel mechanism by which inflammation can functionally block steroid hormone action. Steroids 244-259 tumor necrosis factor Homo sapiens 15-24 14740444-5 2003 Thus, available steroid pre-hormones are rapidly converted to proinflammatory estrogens in the synovial tissue in the presence of inflammatory cytokines (i.e. TNF alpha, IL-1, IL-6). Steroids 16-23 tumor necrosis factor Homo sapiens 159-168 15208591-10 2004 However, cells from this subset of steroid-insensitive subjects were still capable of inhibiting TNF-alpha-induced histone acetylation. Steroids 35-42 tumor necrosis factor Homo sapiens 97-106 15379214-5 2004 The anti-inflammatory steroid dexamethasone (DEX) inhibited mPGES-1 mRNA and protein expression as well as PGE2 production induced by IL-1beta or TNFalpha. Steroids 22-29 tumor necrosis factor Homo sapiens 146-154 14978174-15 2004 CONCLUSION: TNFalpha blockade with infliximab was effective at inducing remission in 88% of patients with antibody-associated systemic vasculitis and permitted reduction in steroid doses. Steroids 173-180 tumor necrosis factor Homo sapiens 12-20 15306588-2 2004 Recently, tumour necrosis factor alpha (TNF-alpha) antibodies were recognised as effective in steroid refractory CD. Steroids 94-101 tumor necrosis factor Homo sapiens 40-49 15242697-3 2004 Steroids modulate some plasma cytokines (decreasing TNFalpha, IL-8, IL-6 and increasing IL-10), whereas ability to reduce plasma and urinary TNFsr-2 and IL-1ra and peri-operative renal injury is unknown. Steroids 0-8 tumor necrosis factor Homo sapiens 52-60 15485092-5 2004 Thus, available steroid prehormones are rapidly converted to proinflammatory estrogens in the synovial tissue in the presence of inflammatory cytokines (i.e., TNFalpha, IL-1, IL-6). Steroids 16-23 tumor necrosis factor Homo sapiens 159-167 12938167-1 2003 We have investigated the effects of sex steroids, estradiol (E2), and testosterone (T) on the synthesis of tumor necrosis factor alpha (TNF-alpha) and interleukin-10 (IL-10) in phorbol-myristate-acetate (PMA)-differentiated human monoblastic U937 cells. Steroids 40-48 tumor necrosis factor Homo sapiens 107-134 12707837-6 2003 By using ROC curve, TNF-alpha production greater or equal to a cut-off point of 50 pg/ml could be used to predict resistance to steroid therapy (predictability 93.2%). Steroids 128-135 tumor necrosis factor Homo sapiens 20-29 12707837-9 2003 TNF-alpha levels in PBMC culture could be used to predict the pathological type of PNS and the response of these patients to steroid therapy. Steroids 125-132 tumor necrosis factor Homo sapiens 0-9 15040702-4 2003 Thalidomide (TH) and systemic steroids (S), both TNFa production inhibitors, are the two current effective drugs for the management of ENL. Steroids 30-38 tumor necrosis factor Homo sapiens 49-53 12794059-5 2003 We have demonstrated this in four types of cross-talk mechanisms on different cells in which steroids have major roles: (1) The tumor necrosis factor (TNF)-glucocorticoid receptor (GR) transcriptional interaction in cellular targets of TNF-induced cytotoxicity. Steroids 93-101 tumor necrosis factor Homo sapiens 151-154 12794059-5 2003 We have demonstrated this in four types of cross-talk mechanisms on different cells in which steroids have major roles: (1) The tumor necrosis factor (TNF)-glucocorticoid receptor (GR) transcriptional interaction in cellular targets of TNF-induced cytotoxicity. Steroids 93-101 tumor necrosis factor Homo sapiens 236-239 12537056-5 2003 We here report a rare case of extra-intestinal Crohn"s disease resistant to steroid therapy, which was successfully treated with infliximab, a chimeric antibody directed against TNF-alpha that is the only registered agent for the treatment of Crohn"s disease. Steroids 76-83 tumor necrosis factor Homo sapiens 178-187 12370131-3 2002 In this study, we investigated the influence of various steroid hormones on the IL-1beta (50 U/mL)/TNF-alpha (50 U/mL) stimulated human dermal microvascular endothelial cell line (HMEC-1) and human umbilical vein endothelial cells (HUVEC). Steroids 56-63 tumor necrosis factor Homo sapiens 99-108 12541166-5 2003 The recombinant monoclonal anti-TNF-antibody Infliximab (Remicade) has been approved for the treatment of steroid refractory and steroid dependent Crohn"s disease in Germany since 9/2000 and the efficacy of Infliximab is well documented. Steroids 106-113 tumor necrosis factor Homo sapiens 32-35 12541166-5 2003 The recombinant monoclonal anti-TNF-antibody Infliximab (Remicade) has been approved for the treatment of steroid refractory and steroid dependent Crohn"s disease in Germany since 9/2000 and the efficacy of Infliximab is well documented. Steroids 129-136 tumor necrosis factor Homo sapiens 32-35 12146528-8 2002 Both estrogen and progesterone inhibited the apoptosis of U937 cells triggered by exogenous TNF-a CONCLUSIONS: Female steroid hormones may have dual effects on the pathogenesis of pyogenic granuloma in pregnancy. Steroids 118-134 tumor necrosis factor Homo sapiens 92-97 12108176-13 2002 Controlled studies of new biological treatments like cytokine inhibitors (anti-TNF-alpha, anti-interferon gamma) could demonstrate a clear sparing effect in steroids, a goal not yet achieved by the use of current DMARDs, including MTX. Steroids 157-165 tumor necrosis factor Homo sapiens 79-88 29539023-9 2002 Both estrogen and progesterone inhibited the apoptosis of U937 cells triggered by exogenous TNF-alpha Conclusions: Female steroid hormones may have dual effects on the pathogenesis of pyogenic granuloma in pregnancy. Steroids 122-138 tumor necrosis factor Homo sapiens 92-101 11380043-6 2001 Controlled trials of the investigational anti-TNF-alpha agent CDP-571 show benefit for induction of clinical improvement and steroid-sparing, but further investigation is needed. Steroids 125-132 tumor necrosis factor Homo sapiens 46-55 11985524-3 2002 Median levels of IFN-gamma and TNF-alpha in T1R patients fell during treatment with steroids; however, TNF-alpha levels increased as the steroid dose was reduced. Steroids 84-92 tumor necrosis factor Homo sapiens 31-40 11985524-3 2002 Median levels of IFN-gamma and TNF-alpha in T1R patients fell during treatment with steroids; however, TNF-alpha levels increased as the steroid dose was reduced. Steroids 84-91 tumor necrosis factor Homo sapiens 31-40 11985524-4 2002 Median IL-10 levels increased throughout the steroid treatment period and were associated strongly with TNF-alpha levels. Steroids 45-52 tumor necrosis factor Homo sapiens 104-113 12144121-6 2002 RESULTS: TNF-alpha and IL-6 serum concentrations significantly decreased after steroid therapy administration. Steroids 79-86 tumor necrosis factor Homo sapiens 9-18 12144121-10 2002 Symptom regression following steroid therapy administration went along with significant decrease of cytokines levels, confirming that TNF-alpha and IL-6 play a role in the pathogenesis of this reaction. Steroids 29-36 tumor necrosis factor Homo sapiens 134-143 11920401-0 2002 Inadequately low serum levels of steroid hormones in relation to interleukin-6 and tumor necrosis factor in untreated patients with early rheumatoid arthritis and reactive arthritis. Steroids 33-49 tumor necrosis factor Homo sapiens 83-104 11677207-1 2001 BACKGROUND & AIMS: Treatment with a chimeric anti-tumor necrosis factor (TNF) antibody (infliximab) has been shown to be highly efficient for patients with steroid-refractory Crohn"s disease (CD). Steroids 160-167 tumor necrosis factor Homo sapiens 49-75 11677207-1 2001 BACKGROUND & AIMS: Treatment with a chimeric anti-tumor necrosis factor (TNF) antibody (infliximab) has been shown to be highly efficient for patients with steroid-refractory Crohn"s disease (CD). Steroids 160-167 tumor necrosis factor Homo sapiens 77-80 11720326-0 2001 Anti-TNF therapies have eliminated the need for steroids in pediatric Crohn"s disease: pro. Steroids 48-56 tumor necrosis factor Homo sapiens 5-8 11720327-0 2001 Anti-TNF therapies have eliminated the need for steroids in pediatric Crohn"s disease: con. Steroids 48-56 tumor necrosis factor Homo sapiens 5-8 11937893-1 2001 Anti-TNF Therapies Have Eliminated the Need for Steroids in Pediatric Crohn"s Disease. Steroids 48-56 tumor necrosis factor Homo sapiens 5-8 11690703-9 2001 On steroids, sICAM-1 in hepatic vein and TNFalpha in both vascular beds decreased. Steroids 3-11 tumor necrosis factor Homo sapiens 41-49 11690703-12 2001 CONCLUSIONS: In severe AH under steroids, the short term histological improvement was associated with a decrease in circulating TNFalpha, a decrease in ICAM-1 expression, and correlated to hepatic vein sICAM-1 changes. Steroids 32-40 tumor necrosis factor Homo sapiens 128-136 11575456-10 2001 In conclusion, in ulcerative colitis, eosinophils are attracted to the intestinal tissue by chemotactic factors, of which IL-5 and TNF-alpha may be the most prominent steroid-sensitive ones. Steroids 167-174 tumor necrosis factor Homo sapiens 131-140 11563881-1 2001 The tumour necrosis factor-alpha (TNF-alpha) neutralizing antibody, Infliximab (Ifx), reduces disease activity in patients with active steroid-dependent or fistulizing Crohn"s disease. Steroids 135-142 tumor necrosis factor Homo sapiens 34-43 10843762-1 2000 The synthetic steroid cholesterylphosphoserine (CPHS) inhibited the secretion of TNF-alpha in lipopolysaccharide-challenged human monocytes. Steroids 14-21 tumor necrosis factor Homo sapiens 81-90 11122142-2 2000 The steroids dexamethasone (Dex) and 1,25(OH)(2) D(3) both render U937 leukaemic cells resistant to TNF-induced apoptosis. Steroids 4-12 tumor necrosis factor Homo sapiens 100-103 11147702-6 2000 There was a marked decrease in TNF levels in rejecting patients in response to treatment with steroids. Steroids 94-102 tumor necrosis factor Homo sapiens 31-34 11009092-0 2000 Sex steroids induce apoptosis of CD8+CD4+ double-positive thymocytes via TNF-alpha. Steroids 4-12 tumor necrosis factor Homo sapiens 73-82 11009092-3 2000 Here we show that a typical sex steroid, testosterone, specifically targets CD8+CD4+ double-positive (DP) thymocytes for apoptosis via TNF-alpha. Steroids 32-39 tumor necrosis factor Homo sapiens 135-144 11009092-6 2000 Thus, TNF-alpha is the critical mediator of sex steroid-induced apoptosis in thymocytes, and its manipulation should provide a point of intervention to modulate T cell production in sex hormone disorders. Steroids 48-55 tumor necrosis factor Homo sapiens 6-15 10932075-0 2000 Topical steroid treatment of allergic rhinitis decreases nasal fluid TH2 cytokines, eosinophils, eosinophil cationic protein, and IgE but has no significant effect on IFN-gamma, IL-1beta, TNF-alpha, or neutrophils. Steroids 8-15 tumor necrosis factor Homo sapiens 188-197 10873156-4 2000 TNF-alpha (10 ng/ml)-induced IL-8 release was markedly inhibited by the steroids dexamethasone (Dex) (0.1 to 10 microM) and fluticasone (Flut) (0.01 to 1 microM) but unaffected by Salbu, Salme, FSK, or 8-Br-cAMP. Steroids 72-80 tumor necrosis factor Homo sapiens 0-9 11149914-8 2001 The combined use of beta2-agonists, rolipram, and steroids abolished TNF-alpha-induced eotaxin release. Steroids 50-58 tumor necrosis factor Homo sapiens 69-78 10843762-6 2000 The inhibition of TNF-alpha secretion by CPHS may contribute to the immunosuppressive activity of this steroid. Steroids 103-110 tumor necrosis factor Homo sapiens 18-27 10961356-2 2000 Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. Steroids 126-134 tumor necrosis factor Homo sapiens 62-71 10897669-8 2000 Steroid also dosage-dependently suppressed TNF production of lymphocytes after 24 hours of incubation while IL-10 production increased. Steroids 0-7 tumor necrosis factor Homo sapiens 43-46 10606965-15 2000 The carriage of allele 2 may favour steroid-dependent disease and to a lesser extent fistulizing and colonic disease, possibly secondary to a more intense TNF-alpha-driven inflammatory reaction at the mucosal level. Steroids 36-43 tumor necrosis factor Homo sapiens 155-164 10888707-0 2000 The adrenal steroid status in relation to inflammatory cytokines (interleukin-6 and tumour necrosis factor) in polymyalgia rheumatica. Steroids 12-19 tumor necrosis factor Homo sapiens 84-106 10719713-10 2000 Infliximab, an anti-TNF-alpha antibody, is a potent therapy for fistulising Crohn"s disease or steroid-refractory disease. Steroids 95-102 tumor necrosis factor Homo sapiens 20-29 8671447-11 1996 The effects of steroids on TNF-alpha production were less marked than that of IL-1, with values increasing or decreasing to a maximum of three times the basal value. Steroids 15-23 tumor necrosis factor Homo sapiens 27-36 10612095-7 1999 There was a decrease of TNF-alpha, sTNF-RI and total lesion area in MRI after steroid therapy, but the differences did not reach statistical significance. Steroids 78-85 tumor necrosis factor Homo sapiens 24-33 9630160-7 1998 In contrast, mRNA expression of two inflammatory cytokines, TNFalpha and IFNgamma, decreased following steroid therapy. Steroids 103-110 tumor necrosis factor Homo sapiens 60-68 9704146-6 1998 The clinical effectiveness of anti-TNF-alpha antibodies and of IL-10 has been demonstrated in steroid-refractory Crohn"s disease patients. Steroids 94-101 tumor necrosis factor Homo sapiens 35-44 10411704-7 1999 RESULTS: The recipient TNF-alpha high producer genotype and IL-10 high producer genotype were significantly associated with multiple REs (>/=2) in human leukocyte antigen (HLA)-DR mismatched transplants (P = 0.0047 and P = 0.045, respectively), whereas only the TNF-alpha high producer genotype was associated with steroid-resistant REs (P = 0.025). Steroids 318-325 tumor necrosis factor Homo sapiens 23-32 8892643-7 1996 Therefore, although both types of cytokines were processed by Golgi, only TNF-alpha and the inducible component of TGF-beta production were protein kinase C or steroid-regulated processes. Steroids 160-167 tumor necrosis factor Homo sapiens 74-83 7638240-3 1995 The functions of TNF may be determined in part by differential expression of the two species of TNF receptors, both of which seem to be regulated by female sex steroid hormones. Steroids 160-176 tumor necrosis factor Homo sapiens 17-20 8636308-9 1996 TNF is produced in macrophages, but above all in 17 alpha-hydroxylase-positive cells (steroid-producing cells) in the zona reticularis and medulla. Steroids 86-93 tumor necrosis factor Homo sapiens 0-3 8572786-13 1996 CONCLUSIONS: Earlier steroid administration in the immunosuppressive protocol for HTx or HLTx may be preferable to reduce the inflammatory response to cardiopulmonary bypass, as reflected by a lower production of tumor necrosis factor alpha and IL-8, and a greater release of IL-10. Steroids 21-28 tumor necrosis factor Homo sapiens 213-240 7638240-3 1995 The functions of TNF may be determined in part by differential expression of the two species of TNF receptors, both of which seem to be regulated by female sex steroid hormones. Steroids 160-176 tumor necrosis factor Homo sapiens 96-99 8963748-10 1995 Steroid hormones and cytokines (interleukin-1 alpha, -beta, tumor necrosis factor, interferon-gamma) have a major regulatory influence on protein secretion, including the secretion of immunoglobulin into the saliva. Steroids 0-16 tumor necrosis factor Homo sapiens 32-81 1499722-1 1992 Glucocorticoid steroids provide considerable protection against the systemic toxicity of tumor necrosis factor-alpha (TNF-alpha, cachexin). Steroids 15-23 tumor necrosis factor Homo sapiens 89-116 7649354-6 1995 Tumor necrosis factor-alpha (TNF) dependent increase IL-1 beta mRNA levels were additive to the effects of the steroids. Steroids 111-119 tumor necrosis factor Homo sapiens 0-27 7569052-6 1995 The main targets for the proliferative effects of IL-2 and TNF alpha in this culture system during the first 48 h are leukocytes rather than steroid-producing cells. Steroids 141-148 tumor necrosis factor Homo sapiens 59-68 8036608-4 1993 Resistant to therapy patients with active rheumatic process kept for a long period on steroids exhibited TNF alpha concentrations less than 50 pg/ml. Steroids 86-94 tumor necrosis factor Homo sapiens 105-114 1450407-5 1992 This potentiation was steroid-specific for 1,25-(OH)2D3 because dexamethasone inhibited TNF-alpha mRNA. Steroids 22-29 tumor necrosis factor Homo sapiens 88-97 7529028-7 1995 The phospholipase A2 inhibitor primaquine (30 microM) had no effect on the inhibitory responses to TNF alpha, whereas the anti-inflammatory steroid dexamethasone (1 microM) prevented TNF alpha inhibition of mitogenic responses. Steroids 140-147 tumor necrosis factor Homo sapiens 183-192 7529028-8 1995 Thus, concentrations of TNF alpha, within the range detected in bronchoalveolar lavage fluid from asthmatics, suppress mitogenic responses by a mechanism that is sensitive to inhibition by anti-inflammatory steroids, but does not appear to involve established targets for modulation by steroids, including arachidonic acid metabolism or induction of nitric oxide synthase. Steroids 207-215 tumor necrosis factor Homo sapiens 24-33 7529028-8 1995 Thus, concentrations of TNF alpha, within the range detected in bronchoalveolar lavage fluid from asthmatics, suppress mitogenic responses by a mechanism that is sensitive to inhibition by anti-inflammatory steroids, but does not appear to involve established targets for modulation by steroids, including arachidonic acid metabolism or induction of nitric oxide synthase. Steroids 286-294 tumor necrosis factor Homo sapiens 24-33 7733621-5 1995 rIL-2 induced TNF-alpha release was significantly higher in patients who had received prior rIL-2 immunotherapy, while steroids resulted in a significant suppression of TNF-alpha release. Steroids 119-127 tumor necrosis factor Homo sapiens 169-178 8008306-0 1994 Modulation of human granulosa cell steroid production in vitro by tumor necrosis factor alpha: implications of white blood cells in culture. Steroids 35-42 tumor necrosis factor Homo sapiens 66-93 1396331-3 1992 Macrophage products, interleukin-1 (IL-1) and tumor necrosis factor alpha stimulate and/or inhibit steroid production in cultures of Leydig cells. Steroids 99-106 tumor necrosis factor Homo sapiens 46-73 1426318-0 1992 Ovarian steroids modulate human monocyte tumor necrosis factor alpha messenger ribonucleic acid levels in cultured human peripheral monocytes. Steroids 8-16 tumor necrosis factor Homo sapiens 41-68 1426318-1 1992 OBJECTIVE: To determine whether tumor necrosis factor alpha (TNF-alpha) messenger ribonucleic acid (mRNA) levels in human peripheral monocytes are regulated by ovarian steroids. Steroids 168-176 tumor necrosis factor Homo sapiens 32-59 1426318-1 1992 OBJECTIVE: To determine whether tumor necrosis factor alpha (TNF-alpha) messenger ribonucleic acid (mRNA) levels in human peripheral monocytes are regulated by ovarian steroids. Steroids 168-176 tumor necrosis factor Homo sapiens 61-70 1426318-6 1992 Physiological levels of progesterone (P) and estradiol (E2) modulate TNF-alpha mRNA from peripheral blood monocytes with an apparent inverse relationship between steroid concentration and TNF-alpha message. Steroids 162-169 tumor necrosis factor Homo sapiens 188-197 1499722-1 1992 Glucocorticoid steroids provide considerable protection against the systemic toxicity of tumor necrosis factor-alpha (TNF-alpha, cachexin). Steroids 15-23 tumor necrosis factor Homo sapiens 118-127 1499722-2 1992 In animal experiments RU 38486 (mifepristone), a steroid antagonist, increased the synthesis of TNF and sensitized the animals to the cytotoxic action of TNF. Steroids 49-56 tumor necrosis factor Homo sapiens 154-157 2242421-9 1990 They further suggest that the altered spectrum and reduced severity of IL-2 side effects observed in patients receiving dexamethasone may be attributable in part to the suppressive effect of steroids on IL-2-induced TNF synthesis. Steroids 191-199 tumor necrosis factor Homo sapiens 216-219 1345871-6 1992 In patients with inactive disease, either as a result of surgery or treatment with steroids, the concentration of stool TNF alpha fell to those of controls. Steroids 83-91 tumor necrosis factor Homo sapiens 120-129 1702707-9 1991 These results show that TNF-alpha suppresses the synthesis of cortisol and shifts the steroid secretory pattern towards androgen production at least partly by suppressing the accumulation of mRNAs for adrenal cytochrome P450 oxidases. Steroids 86-93 tumor necrosis factor Homo sapiens 24-33 1802490-4 1991 In addition, in connection with steroid treatment in the high disease activity group, TNF alpha was significantly increased in plasma from RA patients with high disease activity compared with those of low disease activity (p = 0.0009). Steroids 32-39 tumor necrosis factor Homo sapiens 86-95 1802490-5 1991 Furthermore, TNF alpha decreased significantly in relation to steroid medication, parallel to clinical improvement (p = 0.016). Steroids 62-69 tumor necrosis factor Homo sapiens 13-22 1910217-6 1991 These results suggest that the serial determination of sCD8 and TNF serum levels could provide valuable predictive information as to steroid-resistant aGVHD responsiveness to anti-IL-2R treatment. Steroids 133-140 tumor necrosis factor Homo sapiens 64-67 33764319-3 2021 We aimed to evaluate the association between TNFalpha -308G > A polymorphism with Idiopathic Nephrotic Syndrome and its effect on the response to steroid therapy. Steroids 146-153 tumor necrosis factor Homo sapiens 45-53 1964798-4 1990 Two steroid hormones, glucocorticoid and 1,25-dihydroxyvitamin D3, block the cytotoxicity of TNF. Steroids 4-11 tumor necrosis factor Homo sapiens 93-96 2155834-4 1990 Results show that TNF-alpha effectively suppresses the production of cortisol and shifts the steroid synthesis towards androgen production. Steroids 93-100 tumor necrosis factor Homo sapiens 18-27 35589630-3 2022 In steroid-refractory patients, immunosuppressants (ISs) have been used as second-line agents, and tumor necrosis factor-alpha (TNF-alpha) inhibitors as third-line agents. Steroids 3-10 tumor necrosis factor Homo sapiens 128-137 35296124-13 2022 Discontinuation of tumor necrosis factor antagonists (anti-TNF-alpha) resulted in resolution of the symptoms with no recurrence in the first case, but there was evidence of recurrence in the other 2 cases, where one was managed with rituximab and the second one improved with pulse steroid therapy. Steroids 282-289 tumor necrosis factor Homo sapiens 59-68 35105497-10 2022 Psoriasis patients who used non-steroidal anti-inflammatory drugs or topical steroids had significantly lower GI, PD >= 4 mm (%), and saliva IL-1beta and TNF-alpha levels. Steroids 77-85 tumor necrosis factor Homo sapiens 154-163 34157324-6 2021 In vitro studies, steroid resistance model was induced by the TNF-alpha and IFN-gamma. Steroids 18-25 tumor necrosis factor Homo sapiens 62-71 34157324-14 2021 The combination of TNF-alpha and IFN-gamma could conspicuously increase the GRbeta expression and reduce GRalpha/GRbeta, and induce steroid resistance in podocytes. Steroids 132-139 tumor necrosis factor Homo sapiens 19-28 34157324-17 2021 The combination of TNF-alpha and IFN-gamma induce podocytes can establish steroid resistance model in vitro. Steroids 74-81 tumor necrosis factor Homo sapiens 19-28 34210671-11 2021 TNF- inhibitors (HR=3.346; 95% CI 1.277-8.763), NSAID use (HR=2.558; 95% CI 1.383 to 4.729), lupus erythematosus (HR=5.251; 95% CI 1.478 to 18.659) and Hispanic race (HR=3.198; 95% CI 1.022 to 10.005) were significantly positively associated with steroid sparing resolution. Steroids 248-255 tumor necrosis factor Homo sapiens 0-3 34206410-2 2021 The aim of this report was to describe a rare steroid-dependent form of leukocytoclastic vasculitis induced by an anti-TNF-alpha agent in a young woman with ulcerative colitis. Steroids 46-53 tumor necrosis factor Homo sapiens 119-128 34103339-0 2021 TNF-alpha inhibitors used as steroid-sparing maintenance monotherapy in parenchymal CNS sarcoidosis. Steroids 29-36 tumor necrosis factor Homo sapiens 0-9 34103339-1 2021 OBJECTIVE: To assess the efficacy of tumour necrosis factor-alpha (TNF-alpha) inhibitors used as steroid-sparing monotherapy in central nervous system (CNS) parenchymal sarcoidosis. Steroids 97-104 tumor necrosis factor Homo sapiens 67-76 34103339-2 2021 METHODS: The French Multiple Sclerosis and Neuroinflammation Centers retrospectively identified patients with definite or probable CNS sarcoidosis treated with TNF-alpha inhibitors as steroid-sparing monotherapy. Steroids 184-191 tumor necrosis factor Homo sapiens 160-169 34103339-9 2021 The mean (SD) minimum dose of steroids was 31.5 (33) mg before TNF-alpha inhibitor initiation and 6.5 (5.5) mg after (p=0.001). Steroids 30-38 tumor necrosis factor Homo sapiens 63-72 34103339-12 2021 CONCLUSION: TNF-alpha inhibitors can greatly reduce steroids dosing in patients with CNS parenchymal sarcoidosis, even refractory. Steroids 52-60 tumor necrosis factor Homo sapiens 12-21 35622932-7 2022 CONCLUSION: Uncontrolled FOM in childhood may result in permanent extraocular eye muscle damage, while TNF-alpha blockade provides an excellent steroid-sparing effect. Steroids 144-151 tumor necrosis factor Homo sapiens 103-112 35224020-2 2022 Available treatments and treatment strategies, particularly anti-TNF, allow healing intestinal lesions and maintaining steroid-free remission in a subset of patients. Steroids 119-126 tumor necrosis factor Homo sapiens 65-68