Successful tumor necrosis factor α blockade treatment in therapy‐resistant sarcoidosis

Ulbricht, Kai; Stoll, Matthias; Bierwirth, Janine; Witte, Torsten; Schmidt, Reinhold

doi:10.1002/art.11357

Cited by 80 publications

(37 citation statements)

References 5 publications

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“…The results of our study are in line with other case series demonstrating efficacy of infliximab in 64-100% of sarcoidosis patients treated [12,30,31]. In the present study, uveitis demonstrated the best response rate (74%), followed by RFI (57%) and SFN (54%).…”

Section: Discussionsupporting

confidence: 92%

“…In the present study, uveitis demonstrated the best response rate (74%), followed by RFI (57%) and SFN (54%). These response rates are in line with previous research [11,23,29,31,32]. It is probable that the higher response rate for uveitis is influenced by the shorter time between diagnosis and initiating TNF inhibitors (4.5¡4.3 years for uveitis, compared with 6.3¡5.6 years for SFN and 6.8¡5.6 years for RFI; p50.05).…”

Section: Discussionsupporting

confidence: 90%

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Association of the TNF-α G-308A polymorphism with TNF-inhibitor response in sarcoidosis

et al. 2014

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Responsiveness to tumour necrosis factor (TNF) inhibitors has been associated with the TNF-a G-308A polymorphism in rheumatoid arthritis. The aim of this study was to examine the association between the presence of this polymorphism and the response to TNF inhibitors in patients with refractory sarcoidosis.Patients (n5111) who started TNF-inhibitor treatment (76 infliximab, 35 adalimumab) were followed for at least 1 year. The main symptoms in these patients were fatigue (n5100, 90.1%), small fibre neuropathy (n591, 82.0%), pulmonary involvement (n569, 62.2%), and/or uveitis (n531, 27.9%). Patients were additionally genotyped for the presence of the TNF-a G-308A polymorphism. Treatment response was assessed using clinical outcome measures and questionnaires.Three-quarters (n583, 74.8%) of the patients responded well. Of the patients without the variant A-allele 93.6% (73 out of 78, p,0.001) improved, while 30.3% (10 out of 33) of variant A-allele carriers responded favourably to TNF inhibitors. For patients with the GG-genotype, the probability of improving compared with remaining stable or deteriorating was three times higher (risk ratio 3.09, 95% CI 1. 84-5.20).Sarcoidosis patients without the TNF-a -308A variant allele (GG-genotype) had a three-fold higher response to TNF inhibitors (adalimumab or infliximab). Further research is needed to evaluate the value of genotyping for the TNF-a G-308A polymorphism in order to tailor TNF-inhibitor treatment. @ERSpublications TNF-a G-308A polymorphism predicts TNF-inhibitor response in refractory sarcoidosis: a step to personalised medicine?

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 90%

Association of the TNF-α G-308A polymorphism with TNF-inhibitor response in sarcoidosis

et al. 2014

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“…The choice of agent therefore depends on other factors, including individual symptoms, patients' convenience, access to treatment and patients' preferences [7]. But TNFalpha inhibition has also been associated with induction or worsening of various autoimmune diseases, such as systemic lupus, vasculitis, interstitial lung disease, psoriasis, and the granulomatosis Crohn's disease and also sarcoidosis.…”

Section: Discussionmentioning

confidence: 98%

Using TNF-alpha antagonist Adalimumab for treatment for multisystem sarcoidosis: a case study

et al. 2011

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We report the usage of the TNF-alpha antagonist adalimumab in patients with progressive multisystem sarcoidosis. Three patients with multisystem sarcoidosis (MSS) were treated with adalimumab for 12 months. All three patients were quickly responded to adalimumab and experienced a nearly complete regression of the symptoms that lead to an intensive immunosuppression. However, some accompanying symptoms of sarcoidosis, such as splenomegalia, did not respond. One patient suffered 18 months later a new unspecified abdominal lymphadenopathy. TNF-alpha antagonists can be helpful agents in the treatment for MSS. However, the experience with TNF-alpha antagonists in patients with sarcoidosis is still limited. Multicenter trials and a comparison of the different agents are needed to validate the safety and efficacy in these patients. Optimal dosage, duration of therapy and long-term toxicity of anti-TNF therapy in patients with refractory sarcoidosis are yet to be determined in prospective trials.

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“…[83][84][85][86][87][88][89][90] Table 7 summarizes the use of infl iximab for lung disease, including four RCTs for lung disease 86,89,91,92 and 11 case series of infl iximab in which additional information regarding toxicity is provided. 85,[93][94][95][96][97][98][99][100][101][102] Also included in Table 8 are several studies in nonpulmonary disease that provide specifi c information regarding toxicity of the drug. 10,76, 3.1.3.1 Toxicity-Detailed reviews of the side effect profi le have been published.…”

Section: Infl Iximabmentioning

confidence: 99%

Monitoring of Nonsteroidal Immunosuppressive Drugs in Patients With Lung Disease and Lung Transplant Recipients

Baughman

Meyer

Nathanson

et al. 2012

Chest

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Objectives: Immunosuppressive pharmacologic agents prescribed to patients with diffuse interstitial and infl ammatory lung disease and lung transplant recipients are associated with potential risks for adverse reactions. Strategies for minimizing such risks include administering these drugs according to established, safe protocols; monitoring to detect manifestations of toxicity; and patient education. Hence, an evidence-based guideline for physicians can improve safety and optimize the likelihood of a successful outcome. To maximize the likelihood that these agents will be used safely, the American College of Chest Physicians established a committee to examine the clinical evidence for the administration and monitoring of immunosuppressive drugs (with the exception of corticosteroids) to identify associated toxicities associated with each drug and appropriate protocols for monitoring these agents. Methods: Committee members developed and refi ned a series of questions about toxicities of immunosuppressives and current approaches to administration and monitoring. A systematic review was carried out by the American College of Chest Physicians. Committee members were supplied with this information and created this evidence-based guideline. Conclusions: It is hoped that these guidelines will improve patient safety when immunosuppressive drugs are given to lung transplant recipients and to patients with diffuse interstitial lung disease. CHEST 2012; 142(5):e1S-e111SAbbreviations: ACCP 5 American College of Chest Physicians; ALT 5 alanine aminotransferase; ATG 5 antithymocyte globulin; CHF 5 congestive heart failure; CMV 5 cytomegalovirus; CNI 5 calcineurin inhibitor; COI 5 confl ict of interest; CsA 5 cyclosporin A; FDA 5 US Food and Drug Administration; HBV 5 hepatitis B virus; HMG-CoA 5 b -hydroxy-bmethylglutaryl-coenzyme A; HSP 5 Health and Science Policy Committee; IL2RA 5 IL-2 receptor a ; ILD 5 interstitial lung disease; IPF 5 idiopathic pulmonary fi brosis; ITP 5 idiopathic thrombocytopenia purpura; LAM 5 lymphangioleiomyomatosis; MESNA 5 sodium 2-sulfonylethanesufonate; MPA 5 mycophenolic acid; mTOR 5 mammalian target of rapamycin; PTLD 5 posttransplant lymphoproliferative disease; RCT 5 randomized controlled trial; SIRS 5 systemic infl ammatory response syndrome; TNF 5 tumor necrosis factor; TPMT 5 thiopurine methyltransferase

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Successful tumor necrosis factor α blockade treatment in therapy‐resistant sarcoidosis

Cited by 80 publications

References 5 publications

Association of the TNF-α G-308A polymorphism with TNF-inhibitor response in sarcoidosis

Association of the TNF-α G-308A polymorphism with TNF-inhibitor response in sarcoidosis

Using TNF-alpha antagonist Adalimumab for treatment for multisystem sarcoidosis: a case study

Monitoring of Nonsteroidal Immunosuppressive Drugs in Patients With Lung Disease and Lung Transplant Recipients

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