Malignancy

2013 ◽  
pp. 172-176
Author(s):  
Jennifer Hamilton ◽  
Clive Kelly
Keyword(s):  
Rheumatic Disease ◽  
Evidence Base ◽  
Necrosis Factor Alpha ◽  
Relative Risks ◽  
Underlying Malignancy ◽  
Clinical Presentations ◽  
Increased Risk ◽  
Risk Of Malignancy ◽  
Musculoskeletal Manifestations ◽  
Factor Alpha

This chapter addresses the links between malignancy and rheumatic disease. It begins with a summary of rheumatological conditions associated with an increased risk of malignancy, and describes and discusses specific neoplasms associated with each rheumatic disorder. The present knowledge base is summarized in tabular form, describing the relative risks of different malignancies for each relevant rheumatic disease. The diseases featured include rheumatoid arthritis, primary Sjögren’s syndrome, scleroderma, dermatomyositis and systemic lupus. The next section reviews the drugs used in present rheumatological practice known to be associated with malignancy, describing the specific established risks linked to each of the following agents: azathioprine, cyclophosphamide, ciclosporin, anti-tumour necrosis factor alpha (TNFα‎‎) agents, and mycophenolate mofetil. The evidence base and strength of these associations are summarized. Finally we describe the musculoskeletal manifestations that arise as a consequence of underlying malignancy, considering bone pain, polymyalgia, arthropathy, and vasculitis as clinical presentations or complications of underlying neoplasia. This section also includes descriptions of less common rheumatic disorders that may also be associated with cancer, including erythema nodosum, Sweet’s syndrome, and pyoderma gangrenosum.

scholarly journals Reintroduction of immunosuppressive medications in pediatric rheumatology patients with histoplasmosis: a case series

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Rachel A. Brown ◽  
Fatima Barbar-Smiley ◽  
Cagri Yildirim-Toruner ◽  
Monica I. Ardura ◽  
Stacy P. Ardoin ◽  
...  
Keyword(s):  
Rheumatic Disease ◽  
Lupus Erythematosus ◽  
Histoplasma Capsulatum ◽  
Case Series ◽  
Organ Damage ◽  
Necrosis Factor Alpha ◽  
Pulmonary Histoplasmosis ◽  
Immunosuppressive Medications ◽  
Biologic Dmard ◽  
Factor Alpha

Abstract Background Children with rheumatic diseases (cRD) receiving immunosuppressive medications (IM) are at a higher risk for acquiring potentially lethal pathogens, including Histoplasma capsulatum (histoplasmosis), a fungal infection that can lead to prolonged hospitalization, organ damage, and death. Withholding IM during serious infections is recommended yet poses risk of rheumatic disease flares. Conversely, reinitiating IM increases risk for infection recurrence. Tumor necrosis factor alpha inhibitor (TNFai) biologic therapy carries the highest risk for histoplasmosis infection after epidemiological exposure, so other IM are preferred during active histoplasmosis infection. There is limited guidance as to when and how IM can be reinitiated in cRD with histoplasmosis. This case series chronicles resumption of IM, including non-TNFai biologics, disease-modifying anti-rheumatic drugs (DMARDs), and corticosteroids, following histoplasmosis among cRD. Case presentation We examine clinical characteristics and outcomes of 9 patients with disseminated or pulmonary histoplasmosis and underlying rheumatic disease [juvenile idiopathic arthritis (JIA), childhood-onset systemic lupus erythematosus (cSLE), and mixed connective tissue disease (MCTD)] after reintroduction of IM. All DMARDs and biologics were halted at histoplasmosis diagnosis, except hydroxychloroquine (HCQ), and patients began antifungals. Following IM discontinuation, all patients required systemic or intra-articular steroids during histoplasmosis treatment, with 4/9 showing Cushingoid features. Four patients began new IM regimens [2 abatacept (ABA), 1 HCQ, and 1 methotrexate (MTX)] while still positive for histoplasmosis, with 3/4 (ABA, MTX, HCQ) later clearing their histoplasmosis and 1 (ABA) showing decreasing antigenemia. Collectively, 8/9 patients initiated or continued DMARDs and/or non-TNFai biologic use (5 ABA, 1 tocilizumab, 1 ustekinumab, 3 MTX, 4 HCQ, 1 leflunomide). No fatalities, exacerbations, or recurrences of histoplasmosis occurred during follow-up (median 33 months). Conclusions In our cohort of cRD, histoplasmosis course following reintroduction of non-TNFai IM was favorable, but additional studies are needed to evaluate optimal IM management during acute histoplasmosis and recovery. In this case series, non-TNFai biologic, DMARD, and steroid treatments did not appear to cause histoplasmosis recurrence. Adverse events from corticosteroid use were common. Further research is needed to implement guidelines for optimal use of non-TNFai (like ABA), DMARDs, and corticosteroids in cRD following histoplasmosis presentation.

scholarly journals Protective Effects of Methotrexate against Proatherosclerotic Cytokines: A Review of the Evidence

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Arduino A. Mangoni ◽  
Angelo Zinellu ◽  
Salvatore Sotgia ◽  
Ciriaco Carru ◽  
Matteo Piga ◽  
...  
Keyword(s):  
Rheumatic Disease ◽  
Vascular Inflammation ◽  
Interleukin 1 ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Disease States ◽  
Autoimmune Rheumatic Disease ◽  
Cardiovascular Morbidity And Mortality ◽  
Increased Risk ◽  
Meta Analyses

There is good epidemiological evidence that patients with autoimmune rheumatic disease states, particularly rheumatoid arthritis, have an increased risk of cardiovascular morbidity and mortality when compared to the general population. The presence of a chronic systemic proinflammatory state in this patient group disrupts the structural and functional integrity of the endothelium and the arterial wall, favouring the onset and progression of atherosclerosis. A significant role in the detrimental effects of inflammation on endothelial function and vascular homeostasis is played by specific proatherosclerotic cytokines such as tumour necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6). Recent systematic reviews and meta-analyses have shown that treatment with methotrexate, a first-line disease-modifying antirheumatic drug (DMARD), is associated with a significant reduction in atherosclerosis-mediated cardiovascular events, such as myocardial infarction and stroke, and mortality, when compared to other DMARDs. This suggests that methotrexate might exert specific protective effects against vascular inflammation and atherosclerosis in the context of autoimmune rheumatic disease. This review discusses the available evidence regarding the potential antiatherosclerotic effects of methotrexate through the inhibition of TNF-α, IL-1, and IL-6 and provides suggestions for future experimental and human studies addressing this issue.

scholarly journals -308G/A polymorphism of tumor necrosis factor alpha (TNF-α) gene and metabolic syndrome susceptibility: a meta-analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dong Wang ◽  
Liqun He ◽  
Xiaotian Zhang
Keyword(s):  
Metabolic Syndrome ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Dominant Model ◽  
Necrosis Factor Alpha ◽  
Increased Risk ◽  
Tnf Α ◽  
Factor Alpha ◽  
Allele Model ◽  
Necrosis Factor

AbstractMany studies tried to assess the relationship between -308G/A polymorphism of tumor necrosis factor alpha (TNF-α) gene and risk of metabolic syndrome (MS), but their results were contradictory. This meta-analysis aimed to precisely evaluate this association. A systematic literature search was performed in Pubmed database and WanFang Med Online, STATA software 14.0 was used for the meta-analysis. Eleven independent studies containing 3277 cases and 3312 controls were included in our meta-analysis. In overall analysis, significant association was found between -308G/A polymorphism of TNF-α and MS in both allele model (OR 1.47, 95% CI 1.09–1.98, P 0.013) and dominant model (OR 1.77, 95% CI 1.21–2.58, P 0.003). In the subgroup analysis, the A allele was associated with increased risk of MS in Asia group (allele model: OR 1.82 95% CI 1.31–2.53, P < 0.001; dominant model: OR 2.30, 95% CI 1.64–3.21 P < 0.001; homozygous model: OR 2.29, 95% CI 1.31–4.01, P 0.004), and decreased risk of MS in Europe group (dominant model: OR 0.83, 95% CI 0.70–0.99, P < 0.001; recessive model: OR 0.51, 95% CI 0.28–0.92, P 0.025; homozygous model: OR 0.49 95% CI 0.27–0.89, P 0.02). The A allele also appeared to linked to increased risk of MS in CDS group and IDF groups. No significant association was observed in NCEPATPIII group. Our results suggested that -308G/A of TNF-α gene was a risk factor for MS, but it may played different roles in different ethnics, further studies with larger sample size and more other ethnics should be performed to confirm our conclusions.

The correlation analysis of tumor necrosis factor-alpha-308G/A polymorphism and venous thromboembolism risk: A meta-analysis

2016 ◽  
Vol 31 (9) ◽  
pp. 625-631 ◽  
Author(s):  
Quangen Gao ◽  
Peijin Zhang ◽  
Wei Wang ◽  
He Ma ◽  
Yue Tong ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Genetic Models ◽  
Necrosis Factor Alpha ◽  
Increased Risk ◽  
Factor Alpha ◽  
Necrosis Factor

Objective Venous thromboembolism is a common complex disorder, being the resultant of gene–gene and gene–environment interactions. Tumor necrosis factor-alpha is a proinflammatory cytokine which has been implicated in venous thromboembolism risk. A promoter 308G/A polymorphism in the tumor necrosis factor-alpha gene has been suggested to modulate the risk for venous thromboembolism. However, the published findings remain inconsistent. Methods In this study, we conducted a meta-analysis of all available data regarding this issue. Eligible studies were identified through search of Pubmed, EBSCO Medline, Web of Science, and China National Knowledge Infrastructure (CNKI, Chinese) databases up to June 2014. Pooled Odd ratios (ORs) with 95% confidence intervals were applied to estimating the strength of the genetic association in the random-effects model or fixed-effects model. Results A total of 10 studies involving 1999 venous thromboembolism cases and 2166 controls were included in this meta-analysis to evaluate the association between tumor necrosis factor-alpha-308G/A polymorphism and venous thromboembolism risk. Overall, no significantly increased risk venous thromboembolism was observed in all comparison models when all studies were pooled into the meta-analysis. However, in stratified analyses by ethnicity, there was a pronounced association with venous thromboembolism risk among West Asians in three genetic models (A vs. G: OR = 1.82, 95%CI = 1.13–2.94; GA vs. GG: OR = 1.82, 95%CI = 1.08–3.06; AA/GA vs. GG: OR = 1.88, 95%CI = 1.12–3.16). When stratifying by source of controls, no significant result was detected in all genetic models. Conclusion This meta-analysis demonstrates that tumor necrosis factor-alpha 308G/A polymorphism may contribute to susceptibility to venous thromboembolism among West Asians. Studies are needed to ascertain these findings in larger samples and different racial groups.

scholarly journals Death of a 29-Year-Old Male from Undifferentiated Sepsis

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Kathryn A. Trebuss ◽  
Samantha Buttemer ◽  
Jeffrey S. Wilkinson ◽  
Josie Xu ◽  
John P. Rossiter ◽  
...  
Keyword(s):  
Improve Patient Safety ◽  
Necrosis Factor Alpha ◽  
Safety Measures ◽  
Root Cause ◽  
Increased Risk ◽  
Factor Alpha ◽  
Definition Of ◽  
Disseminated Disease ◽  
Improve Patient ◽  
Necrosis Factor

Tumour necrosis factor alpha inhibitors, such as infliximab, and other biologic agents are associated with increased risk of opportunistic infection, including tuberculosis. Tuberculosis infections associated with infliximab tend to present atypically and can be difficult to diagnose, as they are more likely to manifest as extrapulmonary or disseminated disease. The authors report a case involving a 29-year-old male patient who died following 16 days of treatment for undifferentiated sepsis and who was found on autopsy to have widespread disseminated tuberculosis. Prior to the onset of illness, the patient had received infliximab for the treatment of Crohn’s disease. Following discussion of the case, the authors review the definition of adverse events, provide a root cause analysis of the cognitive errors and breakdowns in the health care system that contributed to the reported outcome, and identify opportunities to address these breakdowns and improve patient safety measures for future cases.

scholarly journals Atherosclerosis and Rheumatoid Arthritis: More Than a Simple Association

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Lorenzo Cavagna ◽  
Nicola Boffini ◽  
Giovanni Cagnotto ◽  
Flora Inverardi ◽  
Vittorio Grosso ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Primary Role ◽  
Cvd Risk ◽  
Necrosis Factor Alpha ◽  
Increased Risk ◽  
Starting Point ◽  
Autoimmune Processes ◽  
Oxidative Processes ◽  
Factor Alpha ◽  
Necrosis Factor

In the last decades a large amount of evidence linked rheumatoid arthritis (RA) to atherosclerosis. In fact, RA patients have an increased risk of cardiovascular events that is not fully explained by other classic cardiovascular risk factors. RA and atherosclerosis may share several common pathomechanisms and inflammation undoubtedly plays a primary role. The proinflammatory cytokines such as tumor necrosis factor alpha and interleukin-6, involved in the pathogenesis of RA, are also independently predictive of subsequent cardiovascular disease (CVD). In RA, inflammation alters HDL constituents and the concentration of LDL and HDL, thus facilitating atherosclerosis and CVD events. On the other hand, also the increase of oxidative processes, frequently observed in RA, induces atherosclerosis. Interestingly, some genetic polymorphisms associated with RA occurrence enhance atherosclerosis, however, other polymorphisms associated with RA susceptibility do not increase CVD risk. Several other mechanisms may influence atherosclerotic processes in RA. Moreover, atherosclerosis may be directly mediated also by underlying autoimmune processes, and indirectly by the occurrence of metabolic syndrome and impaired physical activity. Finally, the effects of RA therapies on cardiovascular system in general and on atherosclerosis in particular are really wide and different. However, the starting point of every RA treatment is that disease control, or better remission, is the best way we have for the reduction of CVD occurrence.

Vaccination in immunocompromised children

2013 ◽  
pp. 721-724
Author(s):  
Marloes Heijstek ◽  
Mario Abinun ◽  
Nico Wulffraat
Keyword(s):  
Disease Activity ◽  
Immunosuppressive Treatment ◽  
Immunosuppressive Drugs ◽  
High Dose ◽  
Necrosis Factor Alpha ◽  
Live Attenuated Vaccines ◽  
European League Against Rheumatism ◽  
Increased Risk ◽  
Immunosuppressed Patients ◽  
Factor Alpha

Can immunocompromised children be safely and effectively vaccinated? This chapter discusses the recommendations from the European League Against Rheumatism (EULAR) for the immunization of immunocompromised patients. Patients with rheumatic or autoinflammatory diseases treated with high-dose glucocorticoids, high-dose disease-modifying antirheumatic drugs (DMARDs), or biologicals are considered immunocompromised. Safe and effective vaccination is crucial in these patients, given their increased risk of infection. Safe vaccination implies that vaccination has no effect on disease activity and has only mild adverse effects. Effective vaccination denotes that patients are protected against infections after immunization. Particularly in severely immunosuppressed patients, concerns arise on the safety of (live-attenuated) vaccines and on the detrimental effect of immunosuppressive treatment on the immunogenicity of vaccines. Overall, vaccinations do not increase disease activity and do not cause severe adverse events. It is recommended to withhold live-attenuated vaccines in patients on high-dose immunosuppressive drugs and biologicals, but booster vaccinations can be considered when essential. Generally, immunogenicity of vaccines is good with some exceptions: responses are reduced in patients on high-dose glucocorticoids and rituximab; methotrexate reduces responses to (pneumococcal) polysaccharide vaccines; and tumour necrosis factor alpha (TNFα‎‎) may lower vaccine-induced antibody concentrations and may cause accelerated waning of immunity. Offering vaccination before immunosuppressive drugs and/or measuring antibodies after immunization is recommended.

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