scholarly journals Treatment with Tumor Necrosis Factor-α Inhibitors, History of Allergy, and Hypercalcemia Are Risk Factors of Immune Reconstitution Inflammatory Syndrome in HIV-Negative Pulmonary Tuberculosis Patients

2019 ◽  
Vol 9 (1) ◽  
pp. 96
Author(s):  
Yoshimasa Hachisu ◽  
Yasuhiko Koga ◽  
Shu Kasama ◽  
Kyoichi Kaira ◽  
Masakiyo Yatomi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Multivariate Analysis ◽  
Immune Reconstitution ◽  
Tumor Necrosis ◽  
Hiv Patients ◽  
Tnf Α ◽  
History Of ◽  
Inflammatory Syndrome ◽  
Necrosis Factor ◽  
Inhibitor Treatment

Immune reconstitution inflammatory syndrome (IRIS) is an immune reaction that occurs along with the recovery of the patient’s immunity. Tuberculosis-related IRIS (TB-IRIS) upon tumor necrosis factor (TNF)-α inhibitor treatment has been reported in non-human immunodeficiency virus (HIV) patients. However, the importance of biological treatment, as a risk factor of IRIS, has not yet been established. In this study, we examined TB-IRIS in non-HIV patients to explore the role of TNF-α inhibitor treatment. Out of 188 patients with pulmonary TB, seven patients had IRIS. We examined univariate logistic and multivariate analysis to elucidate risk factors of TB-IRIS. Univariate analysis indicated that usage of immunosuppressive drugs, TNF-α inhibitors, and history of food or drug allergy were significantly related with TB-IRIS. On initial treatment, the values of serological markers such as serum albumin and serum calcium were significantly related with TB-IRIS. There was a higher mortality rate in patients with TB-IRIS. Furthermore, multivariate analysis revealed that usage of TNF-α inhibitors, history of allergy, and serum hypercalcemia were related to TB-IRIS. Usage of TNF-α inhibitors, history of allergy, and serum hypercalcemia may be independent predictors of TB-IRIS in non-HIV patients. Since higher mortality has been reported for TB-IRIS, we should pay attention to TB patients with these risk factors.

scholarly journals High Levels of TNF-α and TIM-3 as a Biomarker of Immune Reconstitution Inflammatory Syndrome in People with HIV Infection

Life ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 527
Author(s):  
Lucero A. Ramon-Luing ◽  
Ranferi Ocaña-Guzman ◽  
Norma A. Téllez-Navarrete ◽  
Mario Preciado-García ◽  
Dámaris P. Romero-Rodríguez ◽  
...  
Keyword(s):  
Immune Reconstitution Inflammatory Syndrome ◽  
Immune Reconstitution ◽  
Control Group ◽  
Hiv Patients ◽  
Art Initiation ◽  
Tnf Α ◽  
Ifn Γ ◽  
Α Level ◽  
Inflammatory Syndrome

Immune reconstitution inflammatory syndrome (IRIS) is an exacerbated immune response that can occur to HIV+ patients after initiating antiretroviral therapy (ART). IRIS pathogenesis is unclear, but dysfunctional and exhausted cells have been reported in IRIS patients, and the TIM-3/Gal-9 axis has been associated with chronic phases of viral infection. This study aimed to evaluate the soluble levels of TIM-3 and Gal-9 and their relationship with IRIS development. TIM-3, Gal-9, TNF-α, IFN-γ, IL-6, TNFR1, TNFR2, E-cadherin, ADAM10, and ADAM17 were measured to search for IRIS-associated biomarkers in plasma samples from 0-, 4-, 8-, 12-, and 24-weeks after ART initiation of 61 HIV+ patients (15 patients developed IRIS, and 46 did not). We found that patients who developed IRIS had higher levels of TIM-3 [median 4806, IQR: 3206–6182] at the time of the IRIS events, compared to any other follow-up time evaluated in these patients or compared with a control group of patients who did not develop IRIS. Similarly, IRIS patients had a higher TNF-α level [median 10.89, IQR: 8.36–12.34] at IRIS events than any other follow-up time evaluated. Other molecules related to the TIM-3 and TNF-α pathway (Gal-9, IL-6, IFN-γ, TNFR1, TNFR2, ADAM-10, and ADAM-17) did not change during the IRIS events. In conclusion, our data suggest that a high level of soluble TIM-3 and TNF-α could be used as an IRIS biomarker.

Tuberculosis (TB)-associated immune reconstitution inflammatory syndrome in TB-HIV co-infected patients in Malaysia: prevalence, risk factors, and treatment outcomes

Sexual Health ◽  
2014 ◽  
Vol 11 (6) ◽  
pp. 532 ◽  
Author(s):  
Hong Yien Tan ◽  
Yean Kong Yong ◽  
Sin How Lim ◽  
Sasheela Ponnampalavanar ◽  
Sharifah F. S. Omar ◽  
...  
Keyword(s):  
Risk Factors ◽  
T Cell ◽  
Treatment Outcomes ◽  
Immune Reconstitution Inflammatory Syndrome ◽  
Immune Reconstitution ◽  
Cd4 T Cell ◽  
Cell Recovery ◽  
Hiv Patients ◽  
Pathogen Load ◽  
Inflammatory Syndrome

Background Tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) is an important early complication of antiretroviral therapy (ART) in countries with high rates of endemic TB, but data from South-East Asia are incomplete. Identification of prevalence, risk factors and treatment outcomes of TB-IRIS in Malaysia was sought. Methods: A 3-year retrospective study was conducted among TB-HIV co-infected patients treated at the University of Malaya Medical Centre. Simple and adjusted logistic regressions were used to identify the predictors for TB-IRIS while Cox regression was used to assess the influence of TB-IRIS on long-term CD4 T-cell recovery. Results: One hundred and fifty-three TB-HIV patients were enrolled, of whom 106 had received both anti-TB treatment (ATT) and ART. The median (IQR) baseline CD4 T-cell count was 52 cells μL–1 (13–130 cells μL–1). Nine of 96 patients (9.4%) developed paradoxical TB-IRIS and eight developed unmasking TB-IRIS, at a median (IQR) time of 27 (12–64) and 19 (14–65) days, respectively. In adjusted logistic regression analysis, only disseminated TB was predictive of TB-IRIS [OR: 10.7 (95% CI: 1.2–94.3), P = 0.032]. Mortality rates were similar for TB-IRIS (n = 1, 5.9%) and non-TB-IRIS (n = 5, 5.7%) patients and CD4 T-cell recovery post-ART was not different between the two groups (P = 0.363). Conclusion: Disseminated TB was a strong independent predictor of TB-IRIS in Malaysian HIV-TB patients after commencing ART. This finding underscores the role of a high pathogen load in the pathogenesis of TB-IRIS; so interventions that reduce pathogen load before ART may benefit HIV patients with disseminated TB.

Association of Genetic Polymorphisms in DC-SIGN, Toll-Like Receptor 3, and Tumor Necrosis Factor α Genes and the Lewis-Negative Phenotype With Chikungunya Infection and Disease in Nicaragua

2020 ◽  
Author(s):  
Filemón Bucardo ◽  
Yaoska Reyes ◽  
Marlen Morales ◽  
Rafaela Briceño ◽  
Fredman González ◽  
...  
Keyword(s):  
Risk Factors ◽  
Tumor Necrosis Factor ◽  
Joint Pain ◽  
Tumor Necrosis ◽  
Intercellular Adhesion Molecule ◽  
Toll Like Receptor ◽  
Odds Ratios ◽  
Tnf Α ◽  
Necrosis Factor ◽  
Negative Phenotype

Abstract Background Chikungunya infections range from subclinical infection to debilitating arthralgia and to chronic inflammatory rheumatism. Tumor necrosis factor (TNF) α, DC-SIGN (dendritic cell–specific intercellular adhesion molecule 3–grabbing nonintegrin), Toll-like receptor (TLR) 3, and blood groups have been directly or indirectly implicated in the susceptibility and pathogenesis of chikungunya. Methods To test the hypothesis that polymorphisms in genes coding for these molecules determine clinical outcomes of chikungunya infection, a retrospective case-control study was performed in León, Nicaragua. The study included 132 case patients and 132 controls, matched for age, sex and neighborhood. Case patients had clinical symptoms of chikungunya, which was diagnosed by means of polymerase chain reaction. Controls were individuals not reporting abrupt presentation of clinical chikungunya-like symptoms. Polymorphisms were identified by TaqMan single-nucleotide polymorphism genotyping assays. Results After adjustment for sociodemographic risk factors, chikungunya disease was associated with polymorphism in DC-SIGN and TLR3 genes (odds ratios, 5.2 and 3.3, respectively), and TNF-α with reduced persistent joint pain (0.24). Persistent joint pain was also associated with age, female sex and other comorbid conditions. Most interestingly, the Lewis-negative phenotype was strongly associated with both symptomatic chikungunya and immunoglobulin G seropositivity (odds ratios, 2.7, and 3.3, respectively). Conclusion This study identified polymorphisms in DC-SIGN, TLR3, and TNF-α genes as well as Lewis-negative phenotype as risk factors for chikungunya infection and disease progression.

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.

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.

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