Worsening of Vitiligo and Onset of New Psoriasiform Dermatitis following Treatment with Infliximab

2011 ◽  
Vol 15 (5) ◽  
pp. 280-284 ◽  
Author(s):  
Khalid M. AlGhamdi ◽  
Huma Khurrum ◽  
Ammar Rikabi
Keyword(s):  
Tumor Necrosis ◽  
Interface Reaction ◽  
Inflammatory Dermatosis ◽  
Immune Mediated ◽  
Tnf Α ◽  
History Of ◽  
Laboratory Investigations ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

Background: Vitiligo is a depigmentation disorder caused by melanocyte destruction that possibly results from an autoimmune mechanism. Psoriasis is an immune-mediated, chronic, inflammatory dermatosis. Although tumor necrosis factor α antagonists (anti-TNF-α), such as infliximab, are effective in treating psoriasis, many cases reported in the literature indicate that psoriasis might also be induced by treatment with infliximab. Some studies also suggest that TNF-α antagonists might be an effective treatment for vitiligo because the disorder is characterized by increased levels of TNF-α, indicating that it might play a role in the pathogenesis of this disease. Objective: We report a case of psoriasiform dermatitis with vacuolar interface reaction that occurred after infliximab therapy in a patient with vitiligo. Method: A 17-year-old male patient with vitiligo vulgaris was treated with an intravenous infusion of 5 mg/kg of infliximab at 0, 2, and 6 weeks and then once every 6 weeks over a span of 6 months. The patient was monitored both clinically and with laboratory investigations. He had no personal or family history of psoriasis. He tolerated the treatment well, without side effects. However, he developed a biopsy-proven psoriasiform lesion for the first time 4 months after he completed his sixth dose of infliximab. His vitiligo also worsened. Conclusion: This case report shows that infliximab given for vitiligo did not improve the disorder and that the vitiligo actually progressed. Moreover, psoriasiform lesions developed after this therapy. Further studies are needed to identify the effects of infliximab in patients with vitiligo.

Effectiveness of tumor necrosis factor α inhibitors and their concentration and immunogenicity: features in various immune-mediated diseases

2021 ◽  
pp. 47-52
Author(s):  
T. Yu. Nuriakhmetova ◽  
I. Kh. Valeeva ◽  
Ya. O. Shevnina ◽  
N. A. Cheremina ◽  
E. V. Sukhorukova ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Certolizumab Pegol ◽  
Low Concentration ◽  
Immune Mediated ◽  
Tnf Α ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Factor Α ◽  
Necrosis Factor

Aim. To compare the concentration and immunogenicity of TNF-α inhibitors (TNFi) and their relationship with efficacy in patients with rheumatic diseases (RD) and inflammatory bowel diseases (IBD).Materials and methods. The study included 104 patients with RD (48.1%) and IBD (51.9%) who received infliximab (INF, 30.8%), adalimumab (ADA, 38.5%) and certolizumab pegol (CZP, 30.8%). We assessed the efficacy of the drug, trough concentration of TNFi and the level of antibodies. In 30 patients, the concentration of TNFi and the level of antibodies were assessed twice with an interval of 15 [13; 17] months.Results. TNF-α inhibitors were effective in 77 (74%) patients. In the group of IBD and RD, the incidence of inefficiency was 33.3% and 18.0%, the ineffectiveness of CZP was found only in IBD group (p = 0.024). A low concentration of TNFi was detected at the first visit in 29 (53.7%) patients with IBD and 24 (48.0%) with RD, at the second visit in 4 (36.4%) patients with IBD and 9 (47.4%) with RD. In all patients with RD who did not respond to IFN and CZP, the subtherapeutic concentration was determined (p = 0.047), in the IBD group – only in 64.3% cases (p > 0.050). At the first visit, antibodies to TNFi were found in 24 (23.1%) patients, at the second visit in 7 (23.3%) exclusively in the RD group (p = 0.019), in 5 of them repeatedly. The formation of Ab was associated with 27.8% of cases of escape of the effect of TNF-α in IBD and 22.2% of cases of ineffectiveness in RD (p > 0.050).Conclusions. The incidence of TNF-α efficacy did not differ between RD and IBD, CZP ineffectiveness was observed exclusively in patients with IBD. In patients with RD, a significant relationship was found between ineffectiveness and low concentration of TNFi. The frequency of Ab formation did not differ between the groups of diseases.

scholarly journals Serum PR3-ANCA Is a Predictor of Primary Nonresponse to Anti-TNF-α Agents in Patients with Ulcerative Colitis

2021 ◽  
pp. 1-6
Author(s):  
Atsushi Yoshida ◽  
Katsuyoshi Matsuoka ◽  
Fumiaki Ueno ◽  
Toshio Morizane ◽  
Yutaka Endo ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Odds Ratio ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Study Data ◽  
Mayo Score ◽  
Tnf Α ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

<b><i>Background:</i></b> Anti-tumor necrosis factor-α (TNF-α) agents are effective for moderately to severely active ulcerative colitis (UC). Nonetheless, a proportion of patients fail to respond to these agents as therapy for induction of remission. Recent studies indicated that perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) may predict response to anti-TNF-α agents in UC patients. However, whether PR3-ANCA can predict primary nonresponse (PNR) to anti-TNF-α agents has not yet been evaluated. The aim of this study was to examine whether PR3-ANCA can predict PNR to anti-TNF-α in UC patients. <b><i>Methods:</i></b> This was a single-center retrospective study. Data were extracted from 50 patients with UC who had measurements of PR3-ANCA and received anti-TNF-α agents for the first time as induction therapy. The primary endpoint of this study was a proportion of patients with PNR stratified by PR3-ANCA positivity. PNR to anti-TNF-α agents was defined as failure to achieve reduction in partial Mayo score by 2 or more points and change to other therapeutics within 6 weeks. <b><i>Results:</i></b> Fourteen (28%) of the 50 patients were PR3-ANCA positive. Seventeen (34%) of the 50 patients demonstrated PNR. Eleven (78.6%) of the 14 PR3-ANCA-positive patients demonstrated PNR, while 6 (16.7%) of the 36 PR3-ANCA-negative patients demonstrated PNR. Multivariate analysis demonstrated that PR3-ANCA positivity was associated with PNR to anti-TNF-α agents (odds ratio 19.29, 95% CI: 3.30–172.67; <i>p</i> = 0.002). <b><i>Conclusion:</i></b> PR3-ANCA positivity can predict PNR to anti-TNF-α agents in UC patients.

scholarly journals Tuberculosis Presenting as an Inflammatory Pseudotumor of the Sciatic Nerve in a Rheumatoid Arthritis Patient Taking Etanercept

2021 ◽  
pp. jrheum.210540
Author(s):  
Bruno Miguel Fernandes ◽  
José Miguel Pereira ◽  
Pedro Rodrigues Pereira ◽  
Miguel Bernardes
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis ◽  
Disease Activity Score ◽  
Latent Infection ◽  
Left Knee ◽  
Active Tuberculosis ◽  
Tnf Α ◽  
History Of ◽  
Factor Α ◽  
Necrosis Factor

Active tuberculosis (TB) in patients treated with anti–tumor necrosis factor-α (TNF-α) agents usually results from the reactivation of a latent infection.1,2 A 46-year-old woman with rheumatoid arthritis in Disease Activity Score in 28 joints remission who was taking etanercept (ETN) was admitted in our hospital due to a 4-month history of progressive hypoesthesia and paresthesia, initially on her left foot and later with extension up to the left knee.

scholarly journals Acute Erythroderma in a Patient Receiving TNF-α-Blocking Therapy for Hidradenitis Suppurativa

2018 ◽  
Vol 10 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Farida Benhadou ◽  
Guillaume Hellgren ◽  
Fabienne Willaert ◽  
Véronique del Marmol
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Hidradenitis Suppurativa ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Adalimumab Therapy ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) normally binds to TNF-α receptors, leading to the inflammatory response of autoimmune diseases. Adalimumab is a TNF-inhibiting, anti-inflammatory, biological medication which binds to TNF-α, thus reducing this inflammatory response. The use of TNF-α-inhibiting medication, such as adalimumab, being the first FDA-approved treatment for hidradenitis suppurativa, has drastically changed the management of dermatological diseases. One rarely reported manifestation that occurs as a side effect associated with the use of TNF-α-blocking agents is erythroderma. This study, for the first time, reports the case of a patient suffering from hidradenitis suppurativa with concomitant psoriasis, who developed a severe and acute erythrodermic rash after the start of adalimumab therapy.

scholarly journals Anti-allergic Inflammatory Triterpenoids Isolated from the Spikes of Prunella Vulgaris

2016 ◽  
Vol 11 (1) ◽  
pp. 1934578X1601100 ◽  
Author(s):  
Hyun Gyu Choi ◽  
Tae Hoon Kim ◽  
Sang-Hyun Kim ◽  
Jeong Ah Kim
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inhibitory Effect ◽  
Prunella Vulgaris ◽  
Tnf Α ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Twelve known triterpenoids (1–12) and two steroids (13 and 14) have been isolated from the spike of the plant Prunella vulgaris. Among them, 2α,3α,23-trihydroxyursa-12,20(30)-dien-28-oic acid (10) was isolated for the first time from this plant. All isolates were evaluated for their inhibitory effect on the gene expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and release of histamine in human mast cells. β-Amyrin (5), 10, and euscaphic acid (12) showed suppression of histamine release with percentage inhibitions of 46.7, 57.9, and 54.2%, respectively. In addition, 5 and 10 showed strong inhibition of TNF-α and IL-6 in the test for pro-inflammatory cytokines. Our results suggest that compounds 5 and 10 largely contribute to the anti-allergic inflammatory effect of P. vulgaris.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor Necrosis Factor-α Production-Enhancing Properties of Novel Adamantylalkylthio Derivatives of Some Heterocyclic Compounds

2005 ◽  
Vol 60 (4) ◽  
pp. 471-475 ◽  
Author(s):  
Barbara Orzeszko ◽  
Tomasz Świtaj ◽  
Anna B. Jakubowska-Mućka ◽  
Witold Lasek ◽  
Andrzej Orzeszko ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heterocyclic Compounds ◽  
Tumor Necrosis ◽  
The Novel ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Factor Α ◽  
Derivatives Of ◽  
Necrosis Factor

Certain adamantylated heterocycles were previously shown to enhance the secretion of tumor necrosis factor alpha (TNF-α) by murine melanoma cells that have been transduced with the gene for human TNF-α and constitutively expressed this cytokine. The stimulatory potency of those compounds depended, among other factors, on the structure of the linker between the adamantyl residue and the heterocyclic core. In the present study, a series of (1-adamantyl)alkylsulfanyl derivatives of heterocyclic compounds was prepared by alkylation of the corresponding thioheterocyles. Of the novel adamantylalkylthio compounds tested in the aforementioned cell line, 2-(2-adamantan-1-ylethylsulfanyl)- 4-methyl-pyrimidine was found to be the most active

scholarly journals Tumor necrosis factor α Inhibition for Alzheimer’s Disease

2017 ◽  
Vol 9 ◽  
pp. 117957351770927 ◽  
Author(s):  
Rudy Chang ◽  
Kei-Lwun Yee ◽  
Rachita K Sumbria
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Short Review ◽  
Tnf Α ◽  
Factor Α ◽  
Ad Therapy ◽  
Necrosis Factor

Tumor necrosis factor α (TNF-α) plays a central role in the pathophysiology of Alzheimer’s disease (AD). Food and Drug Administration–approved biologic TNF-α inhibitors are thus a potential treatment for AD, but they do not cross the blood-brain barrier. In this short review, we discuss the involvement of TNF-α in AD, challenges associated with the development of existing biologic TNF-α inhibitors for AD, and potential therapeutic strategies for targeting TNF-α for AD therapy.

Tumor necrosis factor-α-associated lysosomal permeabilization is cathepsin B dependent

2002 ◽  
Vol 283 (4) ◽  
pp. G947-G956 ◽  
Author(s):  
Nathan W. Werneburg ◽  
M. Eugenia Guicciardi ◽  
Steven F. Bronk ◽  
Gregory J. Gores
Keyword(s):  
Tumor Necrosis Factor ◽  
Cathepsin B ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Fluorescent Protein ◽  
Tnf Α ◽  
Calcein Release ◽  
Green Fluorescent ◽  
Factor Α ◽  
Necrosis Factor

Cathepsin B (Cat B) is released from lysososomes during tumor necrosis factor-α (TNF-α) cytotoxic signaling in hepatocytes and contributes to cell death. Sphingosine has recently been implicated in lysosomal permeabilization and is increased in the liver by TNF-α. Thus the aims of this study were to examine the mechanisms involved in TNF-α-associated lysosomal permeabilization, especially the role of sphingosine. Confocal microscopy demonstrated Cat B-green fluorescent protein and LysoTracker Red were both released from lysosomes after treatment of McNtcp.24 cells with TNF-α/actinomycin D, a finding compatible with lysosomal destabilization. In contrast, endosomes labeled with Texas Red dextran remained intact, suggesting lysosomes were specifically targeted for permeabilization. LysoTracker Red was released from lysosomes in hepatocytes treated with TNF-α or sphingosine in Cat B(+/+) but not Cat B(−/−) hepatocytes, as assessed by a fluorescence-based assay. With the use of a calcein release assay in isolated lysosomes, sphingosine permeabilized liver lysosomes isolated from Cat B(+/+) but not Cat B(−/−) liver. C6ceramide did not permeabilize lysosomes. In conclusion, these data implicate a sphingosine-Cat B interaction inducing lysosomal destabilization during TNF-α cytotoxic signaling.

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