RESUMO

The abnormal biological activity of cytokines and their imbalance are implicated in developing rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Cytokine levels were measured in RA and SLE patients and compared to healthy controls using the Wilcoxon rank sum test and Kruskal-Wallis test. The relationship between cytokine levels and blood and clinical parameters was assessed using Spearman's correlation test. Compared to healthy controls, both RA and SLE patients exhibited elevated levels of GM-CSF, CX3CL1, IFN-α2, IL-12p70, IL-17A, TNF-α, IL-1ß, and IFN-γ, which is evidence of their shared inflammatory signature. IL-2 levels were elevated exclusively in RA patients, while MCP-1 and IL-10 were uniquely increased in SLE patients. Notably, TNF-α showed the most significant increase in SLE patients. IL-4 was elevated in SLE patients with nephritis, correlating with IL-6, IL-10, sCD40L, and IL-8, suggesting B cell involvement in lupus nephritis. The negative correlation between CX3CL1 and TNF-α with HDL in RA and SLE respectively, highlights the potential association of these inflammatory markers with cardiovascular risk. These findings underscore the complex cytokine interplay in RA and SLE. CX3CL1 emerges as a potential therapeutic target for RA, while TNF-α and IL-4 show promise as therapeutic targets for SLE.

Assuntos

Artrite Reumatoide , Citocinas , Lúpus Eritematoso Sistêmico , Humanos , Artrite Reumatoide/sangue , Lúpus Eritematoso Sistêmico/sangue , Feminino , Citocinas/sangue , Masculino , Adulto , Pessoa de Meia-Idade , Biomarcadores/sangue , Estudos de Casos e Controles , Idoso

RESUMO

Introduction: Tuberculosis is an infectious disease that can be prevented and cured, but it is still associated with high morbidity and mortality rates. Disseminated tuberculosis, although rare, can occur in individuals with underlying pathologies that affect the immune system. Currently, there are limited reports on disseminated tuberculosis in individuals with congenital disorders. Clinical case: We present a case of a patient with a history of ß thalassemia who was admitted to the emergency department with symptoms of abdominal pain and constitutional symptoms. The final diagnosis was disseminated tuberculosis. This case is of particular interest due to its atypical presentation, the initial suspicion of malignancy, and the extensive involvement of the disease despite the patient's absence of immunosuppression history. Conclusions: Disseminated tuberculosis in immunocompetent patients is a rare presentation associated with poor outcomes. The history of ß thalassemia may be a risk factor to consider based on the metabolic pathways involved in the pathophysiology of both diseases.

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Introducción: la tuberculosis es una enfermedad infecciosa prevenible y curable asociada a una alta morbimortalidad, la presentación de tuberculosis diseminada es poco frecuente y está asociada a patologías que comprometen el sistema inmunitario. En la actualidad hay pocos informes sobre tuberculosis diseminada y trastornos congénitos subyacentes. Caso clínico: paciente con antecedente de talasemia ß que ingresó al servicio de urgencias por dolor abdominal y síntomas constitucionales con diagnóstico final de tuberculosis diseminada. Es un caso de especial interés debido a la presentación atípica, la sospecha diagnóstica inicial de malignidad y el amplio compromiso de la enfermedad a pesar de que el paciente no tenía antecedentes de inmunosupresión. Conclusiones: la tuberculosis diseminada en el paciente inmunocompetente es una presentación poco frecuente asociada a desenlaces adversos. El antecedente de talasemia ß podría ser un factor de riesgo para tener en cuenta con base en las vías metabólicas involucradas en la fisiopatología de ambas enfermedades.

RESUMO

La Artritis Reumatoide (AR) es una enfermedad autoinmune frecuente, caracterizada por inflamación crónica en las articulaciones que puede progresar a la destrucción ósea. Aunque la fisiopatología de la AR no es clara, se ha visto que las células T y las células B desempeñan un importante papel en la misma. Estudios con Rituximab (RTX), un fármaco que elimina las células B CD20+, han contribuido a esclarecer y destacar la participación de las células B en la AR. Las células B pueden contribuir a la autoinmunidad de manera dependiente de la producción de los anticuerpos e independiente de esta producción. Esta última función puede ser debida al papel de las células B como presentadoras de antígeno para las células T y productoras de citocinas y quimiocinas. Para contribuir a entender este último mecanismo, se revisaron los artículos donde se evidenciaron los efectos del tratamiento con RTX sobre la citocinas y quimiocinas circulantes en pacientes con AR. Se encontró que la mayoría de las citocinas estudiadas disminuyeron sus niveles en circulación luego del tratamiento con RTX. La IL-10 y la IL-6 se vieron consistentemente disminuidas en los pacientes que respondieron al tratamiento y podrían ser marcadores del tratamiento con Rituximab.

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Summary Rheumatoid Arthritis (RA) is a common autoimmune disease characterized by chronic inflammation in the joints that can progress to bone destruction. Although the pathophysiology of RA is unclear, T cells and B cells are though to be involved. Rituximab (RTX), a drug that eliminates CD20 + B cells, has helped to clarify and highlight the role of B cells in RA. B cells can contribute to autoimmunity by mechanisms dependent on the production of antibodies and independent of this production. The latter may depend on the role of B cells as antigen-presenting cells for T cells and their capacity to produce cytokines and chemokines. To contribute to our understanding of this mechanism, studies that evaluated levels of circulating cytokines and chemokines in patients with RA after treatment with RTX were reviewed. Most cytokines studied decreased their levels in circulation after treatment with RTX. IL-10 and IL-6 consistently were decreased in patients responding to treatment and maybe markers of Rituximab treatment.

Assuntos

Humanos

RESUMO

ABSTRACT The physiological mechanism in systemic lupus erythematosus is not yet fully elucidated. It is currently known that it is a multifactorial autoimmune disease which includes genetic, environmental and immune factors. Over the years it has been reported that cytokines play a predominant role during the course of the disease. In this review some findings reported in recent years were reviewed and the most important cytokines in SLE were considered; and we analyzed how the levels of each cytokine have been found in patients and how each of them can contribute to the proposed mechanisms and the relationship with the disease, as well as their possible effects on the triggering and control of systemic lupus erythematosus. The aimed of this article is to provide a focused review of the current knowledge of cytokines in SLE.

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RESUMEN Los mecanismos fisiopatológicos en el lupus eritematoso sistémico (LES) aún no están completamente elucidados. Actualmente se sabe que es una enfermedad autoinmune multifactorial que comprende factores genéticos, ambientales e inmunes. A lo largo de los años se ha reportado que las citocinas tienen un papel preponderante durante el curso de la enfermedad. En esta revisión, algunos hallazgos reportados durante los últimos años fueron revisados para algunas de las citocinas más importantes descritas en el lupus, se analizó cómo se han encontrado los niveles de cada citocina en los pacientes y cómo cada una de ellas puede contribuir a los mecanismos propuestos, también se abordó su relación con la enfermedad, así como sus posibles efectos en el desencadenamiento y control del LES. El propósito de este artículo es brindar una revisión focalizada en el conocimiento actual de las citocinas en el LES.