ABSTRACT
Introducción: La fascitis necrotizante es un cuadro muy grave causado por una infección bacteriana de la piel y de tejidos blandos subcutáneos, cuya evolución es hacia la destrucción y necrosis de los tejidos en un corto espacio de tiempo; el lupus eritematoso sistémico es una enfermedad autoinmune de causa desconocida que quienes la padecen tienen una mayor probabilidad de contraer infecciones debido al mal funcionamiento del sistema inmunológico y/o los efectos secundarios causados por los medicamentos. Objetivo: Observar la importancia de un tratamiento rápido y eficaz de la fascitis necrotizante en un paciente con lupus eritematoso sistémico y esteatohepatitis no alcohólica. Presentación de caso: Se presentó el caso clínico de un paciente de 30 años con diagnóstico de lupus eritematoso sistémico que desarrolló de forma concomitante de fascitis necrotizante y esteatohepatitis no alcohólica. A pesar de un tratamiento adecuado, el paciente fue agresivo. Tuvo una estadía hospitalaria de 83 días, con una evolución desfavorable que conllevó a la muerte(AU)
Introduction: Necrotizing fasciitis is a very serious condition caused by a bacterial infection of the skin and subcutaneous soft tissues, whose evolution is towards the destruction and necrosis of the tissues in a short space of time; Systemic lupus erythematosus is an autoimmune disease of unknown cause that sufferers are more likely to contract infections due to poor immune system function and/or side effects caused by medications. Objective: To observe the importance of rapid and effective treatment of necrotizing fasciitis in a patient with systemic lupus erythematosus and non-alcoholic steatohepatitis. Case report: We report the clinical case of a 30-year-old patient diagnosed with systemic lupus erythematosus who concomitantly developed necrotizing fasciitis and nonalcoholic steatohepatitis. Despite adequate treatment, the patient was aggressive. The patient had a hospital stay of 83 days, with an unfavorable evolution that led to his death(AU)
Subject(s)
Humans , Male , Adult , Fasciitis, Necrotizing/mortality , Non-alcoholic Fatty Liver Disease/complications , Lupus Erythematosus, Systemic/etiologyABSTRACT
O lúpus eritematoso sistêmico é uma doença crônica, complexa e multifatorial que apresenta manifestações em vários órgãos. O seu acometimento ocorre 10 vezes mais no sexo feminino do que no masculino. É uma doença com uma clínica variada e com graus variados de gravidade, causando fadiga, manifestações cutâneas, como rash malar, fotossensibilidade, queda de cabelo e manifestações musculoesqueléticas, como artralgia, mialgia e atrite. Podem ocorrer flares (crises), que se caracterizam por aumento mensurável na atividade da doença. No climatério, no período da pré-menopausa, o lúpus eritematoso sistêmico ocorre com mais frequência, podendo ocorrer também na pós-menopausa. Algumas doenças são mais frequentes na fase do climatério, e a presença do lúpus pode influenciar na sua evolução, como a doença cardiovascular, osteoporose e tromboembolismo venoso. A terapia hormonal oral determina aumento do risco de tromboembolismo venoso no climatério, e na paciente com lúpus eritematoso sistêmico há aumento dos riscos de flares e de trombose. Em vista disso, a terapia hormonal é recomendada apenas para pacientes com lúpus eritematoso sistêmico estável ou inativo, sem história de síndrome antifosfolípides e com anticorpos antifosfolípides negativa, devendo-se dar preferência para a terapia estrogênica transdérmica, em menor dose e de uso contínuo. Na paciente com lúpus eritematoso sistêmico ativo ou com história de síndrome antifosfolípides ou com anticorpos antifosfolípides positiva, recomenda-se a terapia não hormonal, como os antidepressivos. (AU)
Systemic lupus erythematosus is a chronic, complex, multifactorial disease that manifests in several organs. Its involvement occurs 10 times more in females than in males. It is a disease with a varied clinic and varying degrees of severity, causing fatigue, skin manifestations such as malar rash, photosensitivity, hair loss and musculoskeletal manifestations such as arthralgia, myalgia and arthritis. Flare may occur, which are characterized by measurable increase in disease activity. In the climacteric, in the premenopausal period, systemic lupus erythematosus occurs more frequently, and may also occur in the postmenopausal period. Some diseases are more frequent in the Climacteric phase and the presence of lupus can influence its evolution, such as cardiovascular disease, osteoporosis and venous thromboembolism. Oral hormone therapy determines an increased risk of venous thromboembolism in the climacteric and in patients with systemic lupus erythematosus there is an increased risk of flares and thrombosis. In view of this, hormone therapy is only recommended for patients with stable or inactive systemic lupus erythematosus, without a history of antiphospholipid syndrome and with antiphospholipid antibodies, giving preference to transdermal estrogen therapy, at a lower dose and for continuous use. In patients with active systemic lupus erythematosus or with a history of antiphospholipid syndrome or positive antiphospholipid antibodies, non-hormonal therapy, such as antidepressants, is recommended. (AU)
Subject(s)
Humans , Female , Adult , Middle Aged , Lupus Erythematosus, Systemic/etiology , Lupus Erythematosus, Systemic/therapy , Osteoporosis/etiology , Thromboembolism/etiology , Cardiovascular Diseases/etiology , Antiphospholipid Syndrome/complications , Hormones/administration & dosage , Hormones/therapeutic useABSTRACT
Systemic lupus erythematosus (SLE) is a complex chronic autoimmune disease characterized by tissue damage and widespread inflammation in response to environmental challenges. Deposition of immune complexes in kidneys glomeruli are associated with lupus nephritis, determining SLE diagnosis. Periodontitis is a chronic inflammatory disease characterized by clinical attachment and bone loss, caused by a microbial challenge - host response interaction. Deposition of immune complex at gingival tissues is a common finding in the course of the disease. Considering that, the primary aim of this study is to investigate the deposition of immune complexes at gingival tissues of SLE patients compared to systemically healthy ones, correlating it to periodontal and systemic parameters. Twenty-five women diagnosed with SLE (SLE+) and 25 age-matched systemically healthy (SLE-) women were included in the study. Detailed information on overall patient's health were obtained from file records. Participants were screened for probing depth (PD), clinical attachment loss (CAL), gingival recession (REC), full-mouth bleeding score (FMBS) and plaque scores (FMPS). Bone loss was determined at panoramic X-ray images as the distance from cementenamel junction to alveolar crest (CEJ-AC). Gingival biopsies were obtained from the first 15 patients submitted to surgical periodontal therapy of each group, and were analyzed by optical microscopy and direct immunofluorescence to investigate the deposition of antigen-antibody complexes. Eleven (44%) patients were diagnosed with active SLE (SLE-A) and 14 (56%) with inactive SLE (LES-I). Mean PD, CAL and FMBS were significantly lower in SLE+ than SLE-(p < 0.05; Mann Whitney). The chronic use of low doses of immunosuppressants was associated with lower prevalence of CAL >3 mm. Immunofluorescence staining of markers of lupus nephritis and/or proteinuria was significantly increased in SLE+ compared to SLE-, even in the presence of periodontitis. These findings suggest that immunomodulatory drugs in SLE improves periodontal parameters. The greater deposition of antigen-antibody complexes in the gingival tissues of patients diagnosed with SLE may be a marker of disease activity, possibly complementing their diagnosis.
Subject(s)
Antigen-Antibody Complex/immunology , Disease Susceptibility , Gingiva/immunology , Lupus Erythematosus, Systemic/etiology , Periodontitis/etiology , Adult , Antigen-Antibody Complex/metabolism , Biomarkers , Comorbidity , Disease Management , Female , Fluorescent Antibody Technique , Humans , Immunohistochemistry , Lupus Erythematosus, Systemic/diagnosis , Lupus Erythematosus, Systemic/epidemiology , Lupus Erythematosus, Systemic/metabolism , Male , Middle Aged , Periodontitis/diagnosis , Periodontitis/epidemiology , Periodontitis/metabolism , Risk Factors , Severity of Illness Index , Young AdultABSTRACT
Subacute cutaneous lupus erythematosus (SCLE) is a subtype of cutaneous lupus erythematosus that can be triggered by endogenous or exogenous factors. Among the exogenous factors are some medications, drugs, tobacco, infections, and vaccines. In this context, the benefits of vaccination are questioned because although it is important to prevent infections in immunosuppressed patients a theoretical risk of developing systemic lupus erythematosus (SLE) remains in these patients. This report presents a case of a previously healthy female patient who developed SCLE after measles vaccination and progressed to SLE and thereby suggests a possible trigger of the disease.
Subject(s)
Lupus Erythematosus, Cutaneous/diagnosis , Lupus Erythematosus, Cutaneous/immunology , Lupus Erythematosus, Systemic/immunology , Measles/immunology , Vaccination/adverse effects , Antirheumatic Agents/administration & dosage , Antirheumatic Agents/therapeutic use , Drug Therapy, Combination , Female , Folic Acid/administration & dosage , Folic Acid/therapeutic use , Follow-Up Studies , Glucocorticoids/administration & dosage , Glucocorticoids/therapeutic use , Humans , Hydroxychloroquine/administration & dosage , Hydroxychloroquine/therapeutic use , Lupus Erythematosus, Cutaneous/etiology , Lupus Erythematosus, Systemic/diagnosis , Lupus Erythematosus, Systemic/etiology , Measles/prevention & control , Methotrexate/administration & dosage , Methotrexate/therapeutic use , Middle Aged , Prednisone/administration & dosage , Prednisone/therapeutic use , Vitamin B Complex/administration & dosage , Vitamin B Complex/therapeutic useABSTRACT
Systemic lupus erythematosus (SLE) is an autoimmune and multisystemic chronic inflammatory disease that can affect various organs, including skin, joints, kidneys, lungs and the nervous system. Infectious agents have long been implicated in the pathogenesis of SLE. The new viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has shown that, in genetically predisposed patients could trigger the presentation or exacerbation of the autoimmune disease. We herein report a case of a 45-year-old man who presented respiratory symptoms, bilateral pleural effusion, ascites, splenomegaly, severe thrombocytopenia and renal failure with proteinuria and hematuria. SARS-CoV-2 PCR confirmed the COVID-19 diagnosis. We diagnosed the patient with SLE based on the clinical manifestations and positive immunological markers (2019 European League Against Rheumatism/American College of Rheumatology, score of 18). Glucocorticoid pulses were administered to the patient, which improved renal function. However, thrombocytopenia was also refractory to IV immunoglobulin and rituximab, so the patient underwent splenectomy. Through a systematic search of the medical literature, we retrieved two cases with newly onset SLE and five cases with previous SLE diagnosis that showed activity of the disease due to SARS-CoV-2 infection. We herein present a systemic review of these cases and discuss the clinical manifestations that could help to the diagnosis of this clinical condition.
Subject(s)
COVID-19/complications , Lupus Erythematosus, Systemic/etiology , SARS-CoV-2 , Autoimmunity , Glucocorticoids/therapeutic use , Humans , Lupus Erythematosus, Systemic/diagnosis , Lupus Erythematosus, Systemic/drug therapy , Male , Middle AgedABSTRACT
Systemic lupus erythematosus (SLE) is a complex chronic autoimmune disease characterized by tissue damage and widespread inflammation in response to environmental challenges. Deposition of immune complexes in kidneys glomeruli are associated with lupus nephritis, determining SLE diagnosis. Periodontitis is a chronic inflammatory disease characterized by clinical attachment and bone loss, caused by a microbial challenge host response interaction. Deposition of immune complex at gingival tissues is a common finding in the course of the disease. Considering that, the primary aim of this study is to investigate the deposition of immune complexes at gingival tissues of SLE patients compared to systemically healthy ones, correlating it to periodontal and systemic parameters. Twenty-five women diagnosed with SLE (SLE+) and 25 age-matched systemically healthy (SLE) women were included in the study. Detailed information on overall patient's health were obtained from file records. Participants were screened for probing depth (PD), clinical attachment loss (CAL), gingival recession (REC), full-mouth bleeding score (FMBS) and plaque scores (FMPS). Bone loss was determined at panoramic X-ray images as the distance from cementenamel junction to alveolar crest (CEJ-AC). Gingival biopsies were obtained from the first 15 patients submitted to surgical periodontal therapy of each group, and were analyzed by optical microscopy and direct immunofluorescence to investigate the deposition of antigen-antibody complexes. Eleven (44%) patients were diagnosed with active SLE (SLE-A) and 14 (56%) with inactive SLE (LES-I). Mean PD, CAL and FMBS were significantly lower in SLE+ than SLE(p < 0.05; Mann Whitney). The chronic use of low doses of immunosuppressants was associated with lower prevalence of CAL >3 mm. Immunofluorescence staining of markers of lupus nephritis and/or proteinuria was significantly increased in SLE+ compared to SLE, even in the presence of periodontitis. These findings suggest that immunomodulatory drugs in SLE improves periodontal parameters. The greater deposition of antigen-antibody complexes in the gingival tissues of patients diagnosed with SLE may be a marker of disease activity, possibly complementing their diagnosis.
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Young Adult , Gingiva/immunology , Lupus Erythematosus, Systemic/etiology , Antigen-Antibody Complex/immunology , Periodontitis/etiology , Disease SusceptibilityABSTRACT
Background: Systemic lupus erythematosus (SLE) is a potentially fatal complex autoimmune disease, that is characterized by widespread inflammation manifesting tissue damage and comorbidities across the human body including heart, blood vessels, joints, skin, liver, kidneys, and periodontal tissues. The etiology of SLE is partially attributed to a deregulated inflammatory response to microbial dysbiosis and environmental changes. In the mouth, periodontal environment provides an optimal niche for local and systemic inflammation. Our aim was to evaluate the reciprocal impact of periodontal subgingival microbiome on SLE systemic inflammation. Methods: Ninety-one female subjects were recruited, including healthy (n = 31), SLE-inactive (n = 29), and SLE-active (n = 31). Patients were screened for probing depth, bleeding on probing, clinical attachment level, and classified according to CDC/AAP criteria with or without periodontal dysbiosis. Serum inflammatory cytokines were measured by human cytokine panel and a targeted pathogenic subgingival biofilm panel was examined by DNA-DNA checkerboard from subgingival plaque samples. Results: The results showed significant upregulation of serum proinflammatory cytokines in individuals with SLE when compared to controls. Stratification of subject's into SLE-inactive (I) and SLE-active (A) phenotypes or periodontitis and non-periodontitis groups provided new insights into SLE pathophysiology. Ten proinflammatory cytokines were upregulated in serum of SLE-I only and one in SLE-A only. Four molecules overlapped in SLE-A and SLE-I. Anti-inflammatory cytokines included IL-4 IL-10, which were upregulated in SLE-I sera (but not SLE-A), controlling clinical phenotypes. Out of 24 significant differential oral microbial abundances found in SLE, 14 unique subgingival bacteria profiles were found to be elevated in SLE. The most severe oral pathogens (Treponema denticola and Tannerella forsythia) showed increase abundances on SLE-A periodontal sites when compared to SLE-I and healthy controls. Inflammation as measured by cytokine-microbial correlations showed that periodontal pathogens dominating the environment increased proinflammatory cytokines systemically. Conclusions: Altogether, low-grade systemic inflammation that influenced SLE disease activity and severity was correlated to dysbiotic changes of the oral microbiota present in periodontal diseases.
Subject(s)
Disease Susceptibility , Host-Pathogen Interactions , Lupus Erythematosus, Systemic/etiology , Microbiota , Periodontitis/etiology , Adult , Aged , Aged, 80 and over , Autoimmunity , Computational Biology/methods , Cytokines/metabolism , Female , Humans , Inflammation Mediators/metabolism , Lupus Erythematosus, Systemic/metabolism , Male , Metagenome , Metagenomics/methods , Microbiota/immunology , Middle Aged , Periodontitis/metabolism , PhylogenyABSTRACT
Systemic lupus erythematosus (SLE) is associated with a high burden of cardiovascular disease (CVD), which is in part imputed to classical vascular risk factors such as hypertension. Hypertension is frequent among patients with SLE and studies show it is more prevalent in SLE patients than in people without SLE. Despite the high frequency of hypertension in SLE patients, the pathophysiological mechanisms underlying the development of hypertension remain poorly understood. 24-h ambulatory blood pressure monitoring has emerged as a valuable tool in determining blood pressure (BP) in SLE patients in whom hypertension has been associated with damage accrual, stroke and cognitive dysfunction. Although prevalent, current guidelines neglect the specific management of hypertension in SLE patients in their recommendations. This review discusses the mechanisms that may lead to hypertension and the literature evaluating hypertension screening and management in SLE patients.
Subject(s)
Hypertension/complications , Lupus Erythematosus, Systemic/etiology , Lupus Erythematosus, Systemic/pathology , Humans , Prognosis , Risk FactorsABSTRACT
Introducción: El lupus eritematoso sistémico es una enfermedad autoinmune, inflamatoria y sistémica, de causa desconocida, que puede afectar al aparato estomatognático. Objetivo: Describir las manifestaciones bucomaxilofaciales en pacientes con lupus eritematoso sistémico. Métodos: Se realizó un estudio observacional, descriptivo, de serie de casos, de 25 pacientes con diagnóstico de la enfermedad, ingresados en el Servicio de Reumatología del Hospital Provincial Docente Clinicoquirúrgico Saturnino Lora Torres de Santiago de Cuba, durante el 2017. Resultados: Entre las lesiones intrabucales resultaron más frecuentes las periodontopatías, con 68,0 por ciento, y de las extrabucales, el eritema, con 40,0 por ciento. De igual forma, 10 pacientes presentaron alteración en la articulación temporomandibular, lo que representó 40,0 por ciento Conclusiones: Se pudo identificar una gran afectación en el complejo bucal a causa del lupus eritematoso sistémico. Al respecto, los estomatólogos desempeñan un importante papel en la detección de sus manifestaciones clínicas.
Introduction: The systemic erythematous lupus is an autoinmune, inflammatory and systemic disease, of unknown cause which can affect the stomatognatic aparatus. Objective: To describe the oral maxilofacial manifestations in patients with systemic erithematous lupus. Methods: An observational, series of cases descriptive study of 25 patients with diagnosis of the disease, admitted in the Rheumatology Service of Saturnino Lora Torres Teaching Provincial Clinical-Surgical Hospital in Santiago de Cuba was carried out during 2017. Results: Among the intraoral lesions there were the periodontopathies as the most frequent, with 68.0 percent, and of the extraoral lesions, the eritema, with 40.0 percent Likewise, 10 patients presented changes in the temporomandibular joint, what represented a 40.0 percent. Conclusions: A great damage could be identified in the oral complex because of the systemic erythematous lupus. In this respect, stomatologists plays an important role in the detection of its clinical manifestations.
Subject(s)
Humans , Male , Female , Oral Manifestations , Lupus Erythematosus, Systemic/etiology , Autoimmune Diseases , Tooth Diseases , Temporomandibular Joint DisordersABSTRACT
OBJECTIVE: The objective of this study is to evaluate the influence of exposure to air pollutants and inhalable environmental elements during pregnancy and after birth until childhood-onset systemic lupus erythematosus(cSLE) diagnosis. METHODS: This case-control study comprised 30 cSLE patients and 86 healthy controls living in the Sao Paulo metropolitan area. A structured and reliable questionnaire (kappa index for test-retest was 0.78) assessed demographic data, gestational and perinatal-related-factors, and exposure to inhalable elements during pregnancy and after birth (occupational exposure to inhalable particles and/or volatile vapor, and/or tobacco, as well as, the presence of industrial activities or gas stations near the home/work/daycare/school). Tropospheric pollutants included: particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3) and carbon monoxide (CO). RESULTS: The median current age was similar between cSLE patients and healthy controls [16.0 (5-21) versus 15.0 (4-21) years, p = .32], likewise the frequency of female gender (87% versus 78%, p = .43). The frequencies of prematurity (30% versus 6%, p = .001), maternal occupational exposure during pregnancy (59% versus 12%, p < .001), exposure to volatile vapor (48% versus 8%, p < .001) and fetal smoking (maternal and/or secondhand) (37% versus 19%, p = .008) were significantly higher in cSLE patients compared with controls. In a multivariate analysis regarding the gestation period, maternal occupational exposure (OR 13.5, 95% CI 2.5-72.4, p = .002), fetal smoking (OR 8.6, 95%CI 1.6-47, p = .013) and prematurity (OR 15.8, 95%CI 1.9-135.3, p = .012) remained risk factors for cSLE development. Furthermore, exposure to secondhand smoking during pregnancy and after birth (OR 9.1, 95%CI 1.8-42.1, p = .002) was also a risk factor for cSLE development. CONCLUSIONS: Prematurity and environmental factors were risk factors for developing cSLE.
Subject(s)
Air Pollutants/adverse effects , Infant, Premature , Lupus Erythematosus, Systemic/etiology , Maternal Exposure/adverse effects , Particulate Matter/adverse effects , Adult , Carbon Monoxide/adverse effects , Case-Control Studies , Child , Female , Humans , Infant, Newborn , Male , Pregnancy , Risk Factors , Smoking/adverse effectsABSTRACT
Toll-like receptors (TLRs) participate in the innate immune response and trigger the immune responses of the body. Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown aetiology, characterized by an excessive autoimmune response in the body affecting the connective tissues. The disease is possibly triggered by both environmental aetiological factors and pathological organic processes such as exposure to sunlight, chronic infectious processes and genetic factors. Conversely, periodontal disease is an infectious disease caused by microorganisms in the oral cavity, resulting in a chronic inflammatory process which continuously stimulates the immune response, thus causing damage to the periodontal tissues. The expression of both TLR-2 and TLR-4 receptors are increased in both SLE and periodontal disease. Periodontitis might trigger excessive activation of immune response occurring in SLE by maintaining a high expression of TLRs, leading in turn to the acceleration of the onset and progression of autoimmune reactions. In addition, periodontal treatment is able to reduce the expression of these receptors and therefore the symptoms of SLE. Here we discuss the possible interaction between SLE and periodontitis, and suggest further studies evaluating common features in both factors that could explored, due to morbidity and mortality of SLE and the high incidence of periodontal infections around the world.
Subject(s)
Lupus Erythematosus, Systemic/immunology , Periodontitis/immunology , Toll-Like Receptor 2/immunology , Toll-Like Receptor 4/immunology , Animals , Humans , Lupus Erythematosus, Systemic/etiology , Lupus Erythematosus, Systemic/physiopathology , Periodontitis/etiology , Periodontitis/physiopathology , Toll-Like Receptor 2/genetics , Toll-Like Receptor 4/geneticsABSTRACT
This was a case study in which 3 patients with autoimmune/auto-inflammatory syndrome induced by adjuvants (ASIA) after quadrivalent human papillomavirus vaccination (HPV) were evaluated and described. All the patients were women. Diagnosis consisted of HLA-B27 enthesitis related arthritis, rheumatoid arthritis and systemic lupus erythematous, respectively. Our results highlight the risk of developing ASIA after HPV vaccination and may serve to increase the awareness of such a complication. Factors that are predictive of developing autoimmune diseases should be examined at the population level in order to establish preventive measures in at-risk individuals for whom healthcare should be personalized and participatory.
Subject(s)
Adjuvants, Immunologic/adverse effects , Arthritis, Juvenile , Arthritis, Rheumatoid , Lupus Erythematosus, Systemic , Papillomavirus Infections/prevention & control , Papillomavirus Vaccines/adverse effects , Uterine Cervical Neoplasms/prevention & control , Adjuvants, Immunologic/administration & dosage , Adolescent , Antirheumatic Agents/administration & dosage , Arthritis, Juvenile/etiology , Arthritis, Juvenile/immunology , Arthritis, Juvenile/physiopathology , Arthritis, Juvenile/therapy , Arthritis, Rheumatoid/drug therapy , Arthritis, Rheumatoid/etiology , Arthritis, Rheumatoid/immunology , Arthritis, Rheumatoid/physiopathology , Autoantibodies/blood , Female , Glucocorticoids/administration & dosage , HLA-B27 Antigen/blood , Humans , Lupus Erythematosus, Systemic/drug therapy , Lupus Erythematosus, Systemic/etiology , Lupus Erythematosus, Systemic/immunology , Lupus Erythematosus, Systemic/physiopathology , Papillomavirus Vaccines/administration & dosage , Treatment Outcome , Young AdultABSTRACT
By the late nineteenth century an international controversy arose referred to the probable existence of certain diseases such as leprosy, syphilis and lupus in pre-Columbian America. Led by the American physician Albert Sidney Ashmead (1850-1911), it brought together scholars from Europe and the Americas. In this context, certain types of Peruvian archaeological pottery and "mummies", along with series of photographs illustrating the effects of these diseases in contemporary patients, met a prominent role as comparative evidence. In this article we analyze how this type of collections were used as evidence in the debates about pathologies of the past, an issue that from a historical standpoint have received considerably little attention.
Subject(s)
Archaeology/history , Mummies/history , Photography/history , History, 19th Century , Leprosy/history , Leprosy/microbiology , Lupus Erythematosus, Cutaneous/etiology , Lupus Erythematosus, Cutaneous/history , Lupus Erythematosus, Systemic/etiology , Lupus Erythematosus, Systemic/history , Mummies/pathology , Peru , Syphilis/history , Syphilis/microbiologyABSTRACT
Introdução: O Lúpus Eritematoso Sistêmico (LES) é uma doença autoimune multissistêmica de etiologia complexa que envolve fatores ambientais, genéticos e hormonais. É caracterizada pela produção de autoanticorpos e mediadores inflamatórios, ativação e proliferação de células T autorreativas e perda da autotolerância imunológica. Em pacientes com LES, a expressão do receptor primário de ativação CD69 é aumentada e a de células T supressoras/reguladoras (Treg) CD4+CD25+FoxP3+ é reduzida. O CD69 é essencial para ativação de células T CD4 autorreativas enquanto que as células Treg são importantes na manutenção da autotolerância. Desta forma, células T tem um papel central na patogênese do LES, mas os mecanismos implicados na falência da autotolerância ainda não são elucidados, destacando a importância de estudos em modelos experimentais da doença, como o de LES-induzido por pristane. Objetivo: Quantificar células T CD4+CD69+ ativadas e Treg CD4+CD25+FoxP3+ no sangue, baço e LP de camundongos Balb/c LESinduzido por pristane no sentido de avaliar a falência de autotolerância neste modelo. Métodos: Analisamos 84 camundongos Balb/c fêmeas: 52 receberam por via intraperitoneal uma dose única de 0,5 ml de pristane e 32 a mesma dose de salina. Amostras de sangue, baço e LP dos camundongos eutanasiados foram coletadas 90, 120, 180 e 300 (T90, T120, T180 e T300) dias após a inoculação de pristane ou salina. Células mononucleares do sangue periférico (CMSP), do LP (CMLP) e esplenócitos foram obtidos por lise das hemácias seguida de lavagens com RPMI medium 1640 e centrifugação, e posteriormente criopreservadas até a avaliação por citometria de fluxo usando o aparelho Guava EasyCyteTM HT (Millipore). Para esta etapa, as células foram descongeladas, lavadas com RPMI medium 1640 e incubadas com anticorpos monoclonais dirigidos contra CD3, CD4, CD25, CD28, CD69, CTLA-4, FoxP3, CD14 e Ly6C (BD PharmingenTM). Os resultados foram expressos como média ± DP e teste de...
Introduction: Systemic Lupus Erythematosus (SLE) is multisystemic autoimmune disease with complex etiology that involves environmental, genetic and hormonal factors. Is characterized by auto-antibodies and inflammatory mediators production, autoreactive T cells activation and proliferation and loss of immunogenic autotolerance. In patients with SLE, expression of CD69 activation primary receptor is increased and the CD4+CD25+FoxP3+ suppressor/regulatory T cell (Treg) is reduced. CD69 is essential for activation of autoreactive CD4 T cells while Treg cells are important in autotolerance maintenance. In this way, T cells have a central role in the pathogenesis of SLE however, the mechanisms implied in the autotolerance failure are still not elucidated, highlighting the importance of studies in this disease's experimental models, such as pristane-induced SLE. Objective: Quantify activated CD4+CD69+ T cells and CD4+CD25+FoxP3+ Treg in blood, spleen and peritoneal lavage (PL) of Balb/c mice with pristane-induced SLE in order to evaluate autotolerance failure in this model. Methods: 84 female Balb/c mice were analyzed: 52 received a single intraperitoneal 0,5 ml dose of pristane and 32 the same dose of saline. Euthanized mice samples of blood, spleen and peritoneal lavage were collected 90, 120, 180 and 300 (T90, T120, T180 and T300) days after inoculation of pristane or saline. Mononuclear cells from peripheral blood (PBMC), PL (PLMC) and splenocytes were obtained by lysis of erythrocytes followed by washings with RPMI medium 1640 and centrifugation, subsequently criopreserved until evaluation by flow cytometry using the appliance GuavaEasyCyteTM HT (Millipore). For this step, cells were unfrozen, washed with RPMI medium 1640 and incubated with monoclonal antibodies against CD3, CD4, CD25, CD28, CD69, CTLA-4, FoxP3, CD14 and Ly6C (BD PharmingenTM). The results were expressed as mean ± SD and Mann-Whitney 11 test was used for statistical analysis, being considered...
Subject(s)
Animals , Female , Mice , Alkanes , Autoimmune Diseases , Lupus Erythematosus, Systemic/etiology , Mice , T-Lymphocytes, RegulatoryABSTRACT
INTRODUCTION: Nowadays it is described a high prevalence of hypovitaminosis D in Systemic Lupus Erythematosus (SLE), which is associated with some clinical manifestations and increased inflammatory activity. OBJECTIVE: To evaluate the association between vitamin D insufficiency with SLE and inflammatory markers. METHODS: Cross-sectional study, in which have been evaluated 45 SLE patients and 24 controls without the disease. Levels of 25-hydroxyvitamin D [25(OH) D] less than 30 ng/mL were considered inadequate. Disease activity was assessed by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). High sensitivity C reactive protein (hsCRP) and interleukin-6 (IL-6) were evaluated for verification of the inflammatory status. For assessment of renal involvement, analysis of abnormal elements and urinay sediment (AES), quantitative hematuria and pyuria, proteinuria and creatinine clearance in 24-hour urine and serum anti-double stranded DNA were performed. RESULTS: The prevalence of 25(OH)D insufficiency was 55% in SLE patients and 8% in the controls participants (p = 0.001). The median of 25(OH)D was lower in patients than in controls. Patients with insufficient 25(OH)D had higher levels of IL-6 and higher prevalence of hematuria in the AES. There was no correlation between vitamin D and SLEDAI or lupus nephritis. CONCLUSION: In our study, vitamin D deficiency was more prevalent in patients with SLE and was associated with higher levels of IL-6 and hematuria.
Subject(s)
Inflammation/etiology , Lupus Erythematosus, Systemic/etiology , Vitamin D Deficiency/complications , Adolescent , Adult , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Prevalence , Vitamin D Deficiency/epidemiology , Young AdultABSTRACT
Paciente do sexo feminino, 24 anos, diagnosticada há seis anos com lúpus eritematoso sistêmico, apresentou dispneia aos médios esforços após quadro depré-eclampsia e edema agudo de pulmão. Foi realizada ecocardiografia que revelou trombo intracavitário no VEe discinesia, necessitando de internação para anticoagulação. A cintilografia tomográfica de perfusão miocárdica com 99mTc-sestamibi revelou defeitos de perfusão miocárdica compatíveis com área de isquemia estimada em 12 %. Discutem-se neste relato os aspectos clínicos das complicações cardiovasculares do lúpus eritematoso sistêmico.
Female patient, 24 years old, diagnosed six years ago with systemic lupus erythematosus, presented dyspnea on moderate exertion after preeclampsia and acute lung edema. Echocardiography disclosed an intracavitary thrombus in the LV with dyskinesia,requiring hospitalization for anticoagulation. Myocardial perfusion SPECT showed 99Tcm-sestamibi myocardial perfusion defects compatible with an area of ischemia estimated at 12%. This report discusses clinical aspects of cardiovascular complications resulting from systemic lúpus erythematous.
Subject(s)
Humans , Female , Young Adult , Myocardial Ischemia/physiopathology , Lupus Erythematosus, Systemic/etiology , Women , Radionuclide Imaging/methods , Chronic Disease , Risk Factors , Acute Coronary Syndrome/diagnosisABSTRACT
PURPOSE OF REVIEW: To provide an update on infections in systemic lupus erythematosus (SLE) and Sjögren's syndrome, particularly addressing their role as triggers of autoimmunity, their impact on mortality, the main microorganisms, the approaches to differential diagnosis with disease flares and recommendations for vaccination. RECENT FINDINGS: New mechanisms for autoimmunity triggered by Epstein-Barr virus and human commensal microbiota have been described. The increased risk for tuberculosis was recently demonstrated for the first time in Sjögren's syndrome. C-reactive protein was reported to be a more sensitive and specific marker for bacterial infections in SLE than procalcitonin and phagocyte-specific S100A8/A9 protein. Inactivated vaccines are well tolerated and efficacy was demonstrated for influenza vaccine. Immunogenicity is generally reduced but adequate in SLE. Prednisone or immunosuppressants are associated with decreased vaccine serological response, whereas hydroxicloroquine seems to improve vaccine immunogenicity. Other infection-preventive measures for these diseases include antimalarials and prophylaxis for tuberculosis or Pneumocystis jirovecii. SUMMARY: Advances in the role of infectious agents as triggers for SLE and Sjögren's syndrome have provided new insights into disease development. Knowledge on vaccine immunogenicity, safety and efficacy has improved with evidence of a generally reduced but adequate response for inactivated vaccines in SLE. Other preventive measures comprise infection prophylaxis and antimalarials.