RESUMO
RESUMEN Introducción: Las mordeduras de serpiente continúan siendo un problema de salud pública, especialmente en países tropicales como Colombia. Objetivo: Caracterizar los casos de accidente ofídico atendidos en un nuevo centro de asesoría toxicológica de Medellín, Colombia. Metodología: Se realizó un estudio descriptivo, retrospectivo, revisando la base de datos donde se registra la información relacionada con la asesoría brindada por dicho centro desde el 1 de enero hasta el 31 de diciembre de 2016. Resultados: Se registraron 117 casos de accidente ofídico, de los cuales 93 (79%) eran hombres y 24 (21%) mujeres, con una mediana de edad de 32 años (rango: 2 a 82 años). El seguimiento de los casos pudo lograse en 55 de los 117 accidentes (47%), y se describieron complicaciones en 18 de los 55 (33%) pacientes. La complicación descrita con mayor frecuencia fue brote maculopapular pruriginoso asociado con la administración del suero, sin que se identificaran diferencias entre las distintas marcas de suero antiofídico utilizado. Se documentó la muerte de un paciente (0,85%). El género Bothrops produjo la mayoría de los accidentes. Discusión: Los datos obtenidos coinciden con la bibliografía publicada.
ABSTRACT Introduction: Snakebites continue to be a public health problem, especially in tropical countries like Colombia. Objetive: To characterize the snakebite cases attended by a new poison center in Medellin, Colombia. Methodology: A descriptive, retrospective study was carried out, reviewing the information of the Center's database from January 1st to December 31st, 2016. Results: There were 117 cases of ophidian accidents, affecting 93 men (79%) and 24 women (21%), with a median age of 32 years (range: 2 to 82 years). The follow-up of the cases could be done in 55 of the 117 accidents (47%), and complications were described in 18 of those 55 (33%) patients. The most commonly reported complication was a pruritic maculopapular rash that was associated to serum administration, without differences between the several brands of anti-ophidian serum used. The death of one patient (0.85%) was documented. The genus Bothrops caused most of the accidents. Discussion: Our results agree with previously published data.
Assuntos
Humanos , Mordeduras de Serpentes , Doença do Soro , Toxicologia , Colômbia , Animais PeçonhentosRESUMO
La enfermedad del suero constituye un síndrome clínico causado por la formación de complejos inmunes que generan una reacción de hipersensibilidad, con manifestaciones clínicas típicas de erupción cutánea, artritis, y fiebre que inician de 1 a 3 semanas después de la administración de un fármaco y suelen desaparecer al cabo de varios días de interrumpir la administración del agente causal, pudiendo persistir durante intervalos mayores, especialmente cuando son fármacos de acción prolongada o retardada. Se describe el caso de una paciente con síndrome de Sjõgren primario que presentó enfermedad del suero secundaria al uso de rituximab.
Serum sickness is a clinical syndrome caused by the formation of immune complexes that generate a hypersensitivity reaction. Typical manifestations are rashes, arthritis, and fever beginning within3 weeks after administration of a drug and usually disappear several days after the suppression of the causative agent, although theymight persist for longer periods, especially with long-acting drugs. We describe the case of a female patient with primary Sjogren'ssyndrome who presented secondary serum sickness after usingrituximab.
Assuntos
Doença do Soro , Síndrome de SjogrenRESUMO
La enfermedad del suero es una enfermedad alérgica rara que se produce por la administración de material antigénico exógeno. Históricamente causada por suero heterólogo; corresponde a una reacción de hipersensibilidad tipo III mediada por depósitos de complejos inmunes circulantes en los pequeños vasos sanguíneos, la cual induce la activación del complemento y subsecuente inflamación. Las características clínicas son fiebre, erupción cutánea, artralgias y linfadenopatías, pudiendo llegar a producir glomerulonefritis o compromiso de otro órgano. Presentamos el caso de un paciente que desarrolló enfermedad del suero posterior a la administración de suero antiofídico.
Serum sickness is a rare allergic disease, produced by the administration of exogenous antigenic material. Historically caused by heterologous serum, it corresponds to a type III hypersensitivity reaction mediated by deposits of circulating immune complexes in small blood vessels, which induces complement activation and subsequent inflammation. Clinical features are fever, rash, arthralgia and lymphadenopathy; this pathology may lead to glomerulonephritis or other organ involvement. We report a patient who developed serum sickness after antivenom administration.
Assuntos
Humanos , Masculino , Pessoa de Meia-Idade , Doença do Soro , Doenças do Complexo Imune , SoroRESUMO
Serum sickness is an immune-complex-mediated illness that frequently occurs in patients after polyclonal antibody therapy (thymoglobulin). Although serum sickness has been described secondary to thymoglobulin therapy in adults, there are no reports in children on thymoglobulin-induced acute renal failure. We report a case of serum sickness in a 10-year-old girl who was treated for severe aplastic anemia using rabbit antithymocyte globulin (ATG). Eleven days after being started on antithymocyte globulin treatment, she developed fever, gross hematuria, arthralgia, rash, and acute renal failure. Laboratory results showed decreased complement levels, hypergammaglobulinemia, serum creatinine of 4.8 mg/dL (0.6 mg/dL at baseline), and blood urea nitrogen of 79 mg/dL (28 mg/dL at baseline). Peritoneal dialysis was required for 14 days. The patient's symptoms resolved after 13 days on treatment with a short course of high-dose steroids for 3 days, followed by a prednisolone taper. Early recognition and accurate diagnosis is the key for managing thymoglobulin-induced serum sickness, as treatment is highly effective at achieving good outcomes.
Assuntos
Injúria Renal Aguda/complicações , Anemia Aplástica/tratamento farmacológico , Soro Antilinfocitário/uso terapêutico , Doença do Soro/complicações , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/tratamento farmacológico , Anemia Aplástica/diagnóstico , Animais , Criança , Feminino , Humanos , Coelhos , Doença do Soro/diagnóstico , Doença do Soro/tratamento farmacológico , Esteroides/uso terapêutico , Resultado do TratamentoRESUMO
Bovine serum albumin (BSA) injected into the rabbits induces acute immune complex glomerulonephritis. Since albumin is filtered and reabsorbed in the tubules, we investigated whether tubulointerstitial cells participate in the pathogenesis of this experimental condition. For this purpose, we induced immune-complex nephritis in 45 rabbits with the injection of 125I-BSA and urinary BSA excretion, glomerular and tubulointerstitial BSA accumulation, lymphocyte infiltration, proliferative activity and MHC class II antigens were examined 2, 4-5 and 6-8 days after immunization. Proteinuria developed day 6-8. BSA was found in urine from day 2 (mean +/- SE; 1089 +/- 339 micro g/24 h) and peaked on day 4 after immunization (2249 +/- 1106). BSA content (cpm/g tissue) in tubulointerstitium (TI) and glomeruli were similar at day 2 (457 +/- 45 and 407 +/- 75, respectively), but afterward increased significantly in TI, reaching a peak level on day 5 (1026 +/- 406) while remained unchanged in glomeruli (388 +/- 95). At the same time, preceding the onset of proteinuria, maximal intensity of the lymphocyte infiltration, proliferative activity and MHC class II antigen expression in tubular cells, monocytes/macrophages and interstitial cells were observed. Our study shows that antigen is excreted in the urine and concentrated in TI in association with overexpression of MHC class II molecules and lymphocyte infiltration. These findings occur prior to the development of proteinuria and suggest that the tubulointerstitial cells play a critical role in the pathogenesis of this model.
Assuntos
Antígenos/análise , Túbulos Renais/imunologia , Doença do Soro/imunologia , Animais , Antígenos/urina , Antígenos de Histocompatibilidade Classe II/análise , Antígenos de Histocompatibilidade Classe II/urina , Radioisótopos do Iodo , Glomérulos Renais/química , Glomérulos Renais/imunologia , Túbulos Renais/química , Linfócitos/imunologia , Proteinúria , Coelhos , Soroalbumina Bovina/administração & dosagem , Soroalbumina Bovina/análise , Fatores de TempoAssuntos
Criança , Humanos , Eritema Multiforme/diagnóstico , Eritema Multiforme/etiologia , Toxidermias/diagnóstico , Toxidermias/etiologia , Toxidermias/terapia , Síndrome de Stevens-Johnson/diagnóstico , Síndrome de Stevens-Johnson/etiologia , Urticária/diagnóstico , Urticária/etiologia , Diagnóstico Diferencial , Hipersensibilidade a Drogas , Transtornos de Fotossensibilidade , Doença do Soro , Síndrome de Stevens-JohnsonAssuntos
Anafilaxia/fisiopatologia , Anafilaxia/genética , Anafilaxia/imunologia , Anafilaxia/reabilitação , Anafilaxia/terapia , Conjuntivite/fisiopatologia , Conjuntivite/imunologia , Conjuntivite/reabilitação , Conjuntivite/terapia , Doença do Soro/diagnóstico , Doença do Soro/fisiopatologia , Doença do Soro/genética , Doença do Soro/imunologia , Doença do Soro/reabilitação , Doença do Soro/terapiaRESUMO
Exantema es una erupción de la piel con lesiones de distinto tipo, configuración y disposición. El diagnóstico diferencial para pacientes febriles con exantema es extenso. Las posibles causas son enfermedades infecciosas, drogas, enfermedades dermatológicas, inmunológicas y/o neoplásicas. Una historia detallada y un examen físico cuidadoso pueden ser esenciales para hacer un diagnóstico correcto. La historia debe incluir el sitio de comienzo, porcentaje y dirección de extensión, presencia o ausencia de prurito y relación temporal con la fiebre. En este artículo se revisarán diagnósticos no infecciosos de exantemas febriles
Assuntos
Humanos , Exantema , Febre , Artrite Juvenil , Dermatite Alérgica de Contato/complicações , Dermatite Esfoliativa , Dermatomiosite , Exantema , Doença Enxerto-Hospedeiro , Hipersensibilidade , Lúpus Eritematoso Cutâneo/complicações , Psoríase , Doença do Soro , Síndrome de Sézary/complicações , Síndrome de Stevens-Johnson/complicações , Síndrome de Stevens-Johnson/induzido quimicamente , Síndrome de Sweet/complicações , Síndrome Hipereosinofílica/complicações , Síndrome de Linfonodos Mucocutâneos/complicações , Doença de Still de Início Tardio , Queimadura Solar , VasculiteRESUMO
Treatment with cyclosporin A (CsA) improves proteinuria and reduces renal cellular infiltration in chronic serum sickness (CSS). We examined if these effects were associated with a reduced renal expression of CD54 and its ligands, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and MHC class II molecules. We studied two groups of rats in which CSS was induced by daily injections of ovalbumin (OVA): a group treated with CsA (OVA.CsA group, n = 11) and a group that received no treatment (OVA.CSS group, n = 11). An additional group of five rats (control group) received only phosphate buffer. Immunostaining techniques were used to follow CSS and to study the expression of CD54, CD18, CD11b/c, IFN-gamma, TNF-alpha and MHC class molecules. Proteinuria (mg/24 h) was reduced from 248.2 +/- 73.1 (OVA.CCS group) to 14.5 +/- 13.1 with CsA treatment (P < 0.0001). The renal expression of CD54 and its ligands (CD18 and CD11b/c) was reduced by 50% to 75%. Correspondingly, there was a 60% to 85% reduction in the number of infiltrating leucocytes. The number of cells expressing TNF-alpha, IFN-gamma and MHC II molecules was also reduced. CsA reduces expression of CD54 and its ligands. This effect is associated with a reduction of cellular infiltration, IFN-gamma, TNF-alpha-producing cells and with MHC II expression in the kidney. These findings suggest that expression of adhesion molecules plays a critical role in CSS and underline the importance of cellular immunity in this experimental model.
Assuntos
Ciclosporina/uso terapêutico , Regulação da Expressão Gênica/efeitos dos fármacos , Imunossupressores/uso terapêutico , Molécula 1 de Adesão Intercelular/biossíntese , Rim/metabolismo , Nefrite/tratamento farmacológico , Doença do Soro/tratamento farmacológico , Animais , Moléculas de Adesão Celular/biossíntese , Moléculas de Adesão Celular/genética , Quimiotaxia de Leucócito , Doença Crônica , Creatinina/sangue , Ciclosporina/farmacologia , Modelos Animais de Doenças , Antígenos de Histocompatibilidade/biossíntese , Antígenos de Histocompatibilidade/genética , Doenças do Complexo Imune/tratamento farmacológico , Doenças do Complexo Imune/etiologia , Imunização , Imunossupressores/farmacologia , Molécula 1 de Adesão Intercelular/genética , Interferon gama/biossíntese , Interferon gama/genética , Glomérulos Renais/imunologia , Glomérulos Renais/patologia , Masculino , Microscopia de Fluorescência , Nefrite/etiologia , Nefrite/imunologia , Ovalbumina/imunologia , Proteinúria/tratamento farmacológico , Proteinúria/etiologia , Ratos , Ratos Sprague-Dawley , Doença do Soro/imunologia , Doença do Soro/metabolismo , Linfócitos T/efeitos dos fármacos , Linfócitos T/imunologia , Fator de Necrose Tumoral alfa/biossíntese , Fator de Necrose Tumoral alfa/genéticaRESUMO
Peripheral blood leukocytes infiltrate the kidney in chronic serum sickness (CSS). We therefore studied the expression of CD54 and its ligands CD18 and CD11b/c in CSS in 10 rats with CSS, 6 rats immunized similarly who did not developed proteinuria (no-CSS group), and 10 normal rats (control group). Intense (6 to 35 times more than controls) leukocyte infiltration was observed in CSS. The CSS group over-expressed CD54 in glomeruli and interstitium in association with increments in CD18- and CD11b/c-positive cells ranging 2.5 to 7 times the number found in controls. 75% of infiltrating leukocytes expressed CD18 and 87% expressed CD11b/c. The non-CSS group had leukocyte infiltration and expression of adhesion molecules similar to control group. Adherence of CD43-positive cells to renal tissues was 4 times higher in renal tissue from CSS rats than to normal kidney. Pretreatment with corresponding Mabs reduced adherence by half. We concluded that over-expression of CD54 and its ligands CD18 and CD11b/c in infiltrating leukocytes occur in CSS. Binding experiments suggest the functional relevance of these molecules.
Assuntos
Moléculas de Adesão Celular/metabolismo , Doença do Soro/imunologia , Animais , Anticorpos Monoclonais , Antígenos CD18/metabolismo , Adesão Celular , Doença Crônica , Modelos Animais de Doenças , Integrina alfaXbeta2/metabolismo , Molécula 1 de Adesão Intercelular/metabolismo , Rim/imunologia , Glomérulos Renais/imunologia , Leucócitos/imunologia , Antígeno de Macrófago 1/metabolismo , Masculino , Ratos , Ratos Sprague-Dawley , Doença do Soro/etiologiaRESUMO
Os modelos experimentais de glomerulonefrite da doença do soro crônica têm sido importantes ao longo das últimas décadas para estudar o comportamento das glomerulopatias por imunecomplexos, auxiliando na compreensão de doenças primária dos rins como a glomerulopatia de lesões mínimas / glomerulosclerose focal e glomerulonefrite membranosa, assim como de afecções secundárias, como no lúpus eritematoso sistêmico e na própria doença do soro. A maioria dos modelos estudados recentemente têm empregado proteínas com carga modificada e se ativeram às comparações entre proteínas nativas e suas versões cationizadas ou anionizadas ao extremo. O presente trabalho empregou soroalbumina bovina (BSA) modificada pela carbamilação (cBSA) com perfil aniônico (PL 5,2 6,5) para, através de inoculações endovenosas diárias por duas semanas, induzir glomerulonefrite em um grupo de ratos Wistar previamente imunizados com BSA nativa (nBSA) e adjuvante completo de Freund (ACF) (grupo nc: n=32). Dois grupos controle foram imunizados de forma idêntica e foram inoculados posteriormente com nBSA (grupo nn: n=15) ou salina (grupo ns: n=15). Um quarto grupo recebeu inoculação subcutânea com salina +ACF e posteriormente salina endovenosa (grupo SS: n=5). A proteinúria foi medida a níveis basal, após a imunização, uma e duas semanas após o início da indução. A pesquisa de macrófagos foi negativa em todos os grupos. O modelo apresentou um padrão clínico e histológico intermediário entre a glomerulosclerose focal e a glomerulonefrite membranosa, se comportando de forma similar a doença provocada em camundongos com gamaglobulina bovina catiônica, sugerindoque outras alterações físico-químicas na molécula além da carga possam ter papel tão ou mais importante
Assuntos
Animais , Glomerulonefrite/induzido quimicamente , Glomerulonefrite/etiologia , Glomerulonefrite/imunologia , Glomerulonefrite/patologia , Doença do Soro/imunologia , Complexo Antígeno-Anticorpo , Ratos WistarRESUMO
Al hablar de los aspectos relacionados a la patología del complemento, se hace relación a las deficiencias congénitas, descritas para todos los componentes aislados, pero destacando la mayor frecuencia de la deficiencia congénita de C2. También se menciona la asociación de enfermedades por autoinmunidad con el déficit de los componentes de la vía clásica (C1, C4 y C2), la infección severa y recurrente con el déficit de C3, el angioedema hereditario y deficiencia de C1INH, según sea el sector bloqueado o afectado. Entre los defectos adquiridos se mencionan la relación con diversos grupos de enfermedades como las colageno-vasculares (enfermedad del suero, lupus eritematoso sistémico y artritis reumatoide). En la patología renal se revisa su responsabilidad en las glomerulonefritis agudas, lupus, glomerulonefritis membranoproliferativa y síndrome nefrótico. Finalmente, se menciona la participación del complemento en ciertas hemopatías: anemias y trombocitopenias inmunes y la hemoglobinuria paroxística nocturna
Assuntos
Humanos , Proteínas do Sistema Complemento/deficiência , Doença Aguda , Anemia Hemolítica Autoimune/imunologia , Artrite Reumatoide/imunologia , Proteínas do Sistema Complemento/genética , Proteínas do Sistema Complemento/imunologia , Glomerulonefrite Membranoproliferativa/imunologia , Glomerulonefrite/imunologia , Hemoglobinúria Paroxística/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Púrpura Trombocitopênica Idiopática/imunologia , Doença do Soro/imunologia , Inquéritos e QuestionáriosRESUMO
Al hablar de los aspectos relacionados a la patología del complemento, se hace relación a las deficiencias congénitas, descritas para todos los componentes aislados, pero destacando la mayor frecuencia de la deficiencia congénita de C2. También se menciona la asociación de enfermedades por autoinmunidad con el déficit de los componentes de la vía clásica (C1, C4 y C2), la infección severa y recurrente con el déficit de C3, el angioedema hereditario y deficiencia de C1INH, según sea el sector bloqueado o afectado. Entre los defectos adquiridos se mencionan la relación con diversos grupos de enfermedades como las colageno-vasculares (enfermedad del suero, lupus eritematoso sistémico y artritis reumatoide). En la patología renal se revisa su responsabilidad en las glomerulonefritis agudas, lupus, glomerulonefritis membranoproliferativa y síndrome nefrótico. Finalmente, se menciona la participación del complemento en ciertas hemopatías: anemias y trombocitopenias inmunes y la hemoglobinuria paroxística nocturna (AU)
Assuntos
Humanos , Proteínas do Sistema Complemento/deficiência , Proteínas do Sistema Complemento/genética , Proteínas do Sistema Complemento/imunologia , Doença do Soro/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Artrite Reumatoide/imunologia , Anemia Hemolítica Autoimune/imunologia , Púrpura Trombocitopênica Idiopática/imunologia , Glomerulonefrite Membranoproliferativa/imunologia , Hemoglobinúria Paroxística/imunologia , Glomerulonefrite/imunologia , Doença Aguda , Inquéritos e QuestionáriosRESUMO
Because hypercellularity is an important feature in acute serum sickness (AcSS), we quantified glomerular proliferation with immunoperoxidase staining using anti-proliferating cell nuclear antigen (PCNA Mab) and studied its relationship with lymphocyte infiltration (M108 Mab). AcSS was induced in 31 New Zealand White rabbits; group A (n = 14), with proteinuria, sacrificed 6-8 days after immunization; group B (n = 10), without proteinuria, sacrificed 6-7 days after immunization; group C (n = 7), sacrificed prior to development of AcSS. Four normal rabbits were included as controls. Intraglomerular proliferation (PCNA-positive cells/glomerular cross section) was increased in group A (12.2 +/- SEM, 1.84) but not in groups B (0.93 +/- 0.17) and C (0.37 +/- 0.05), which were similar to controls (0.66 +/- 0.06). Lymphocyte infiltration (lymphs/glomerular cross section) increased with time and was more prominent in rabbits with proteinuria (1.9 +/- 0.21, P < 0.001 vs controls). Lymphocyte infiltration was correlated with proliferative activity (Spearman correlation, r = 0.67, P < 0.0001). There was correlation between the severity of glomerular deposition of IgG and C3 and glomerular proliferation and proteinuria. These studies demonstrate a chronological association between lymphocyte infiltration and proliferative activity in AcSS.
Assuntos
Glomérulos Renais/patologia , Doença do Soro/patologia , Doença do Soro/fisiopatologia , Linfócitos T/patologia , Doença Aguda , Animais , Complexo Antígeno-Anticorpo/metabolismo , Divisão Celular/fisiologia , Glomérulos Renais/imunologia , Antígeno Nuclear de Célula em Proliferação/análise , Proteinúria/patologia , Proteinúria/fisiopatologia , CoelhosRESUMO
In an effort to explain the increased incidence of serum sickness-like reactions (SSLR) in patients receiving cefaclor, we used an in vitro murine microsomal system as a surrogate for in vivo hepatic drug biotransformation. Lymphocytes from three groups of subjects were exposed to a nonselective mixture of cefaclor metabolites. After an 18-hour incubation of lymphocytes with these metabolites, cells were examined for viability by trypan blue exclusion. The subject groups consisted of patients with a previous history of SSLR after cefaclor therapy (n = 19), patients who experienced adverse reactions to cefaclor suggestive of immediate hypersensitivity (n = 11), and control subjects who had previously tolerated at least two courses of cefaclor therapy without adverse effect (n = 9). Additionally, immediate family members of six subjects with cefaclor-associated SSLR were studied. Lymphocyte killing was 100% greater than baseline (i.e., a non-drug-containing control) in subjects with SSLR compared with those with immediate hypersensitivity reactions (4% cell death above baseline; p < 0.001) and nonaffected control subjects (6% cell death above baseline; p < 0.001). Family studies were consistent with a pattern of maternal inheritance; five of six mothers who had not received cefaclor had a positive (i.e., > or = 35% cell death above baseline) in vitro cytotoxic response. Other studies confirmed the requirement for biotransformation of the parent drug to elicit cell death, demonstrated specificity of the reaction to cefaclor, illustrated a lack of cross-reactivity to cephalexin in subjects with SSLR to cefaclor, and verified the reproducibility of the reaction over time in an affected subject. Our findings indicate that cefaclor associated SSLR may be a unique adverse drug reaction that requires biotransformation of the parent drug and may result from inherited defects in the metabolism of reactive intermediates. Furthermore, this condition can be retrospectively confirmed with an in vitro lymphocyte-based cytotoxicity assay.
Assuntos
Acetaminofen/efeitos adversos , Cefaclor/efeitos adversos , Cefalexina/efeitos adversos , Linfócitos/efeitos dos fármacos , Microssomos Hepáticos/efeitos dos fármacos , Doença do Soro/induzido quimicamente , Acetaminofen/farmacocinética , Adolescente , Adulto , Biotransformação , Cefaclor/farmacocinética , Morte Celular/efeitos dos fármacos , Cefalexina/farmacocinética , Criança , Pré-Escolar , Testes Imunológicos de Citotoxicidade , Feminino , Humanos , Lactente , Linfócitos/imunologia , Linfócitos/patologia , Masculino , Microssomos Hepáticos/metabolismo , Reprodutibilidade dos Testes , Sensibilidade e Especificidade , Doença do Soro/sangue , Doença do Soro/imunologia , Doença do Soro/patologiaRESUMO
Four patients had serum sickness-like reactions during treatment with cefprozil, a new cephalosporin. Two patients had had previous mild reactions associated with cephalosporin therapy. It remains uncertain whether cefprozil-associated serum sickness-like reaction represents a unique or a class-related adverse drug reaction.
Assuntos
Cefalosporinas/efeitos adversos , Doença do Soro/induzido quimicamente , Adulto , Bronquite/tratamento farmacológico , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Otite Média/tratamento farmacológico , Sinusite/tratamento farmacológico , CefprozilRESUMO
One week after treatment with intravenously administered immune globulin and aspirin, a child with Kawasaki disease had persistent fever and an increase in coronary artery diameter to greater than 3 mm. Two additional doses of immune globulin were given intravenously. Rapid hemolysis occurred, followed by disseminated intravascular coagulation and serum sickness. Clinicians should be aware that immune globulin preparations contain antibodies to blood-type antigens that may cause significant hemolysis and disseminated intravascular coagulation.
Assuntos
Coagulação Intravascular Disseminada/etiologia , Hemólise/imunologia , Imunoglobulinas Intravenosas/efeitos adversos , Síndrome de Linfonodos Mucocutâneos/terapia , Doença do Soro/etiologia , Sistema ABO de Grupos Sanguíneos/imunologia , Aspirina/uso terapêutico , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Lactente , MasculinoRESUMO
Monocytes have been demonstrated to play an important role in acute serum sickness (AcSS) nephritis. Because accumulation of monocytes within the glomeruli could be the result of local lymphokine production, we studied migration inhibition factor (MIF) activity in supernatants from glomerular cultures, analyzed its temporal relationship with monocyte and lymphocyte accumulation, and tested the effect of anti-T lymphocyte monoclonal antibody on local MIF production. AcSS was induced in 12 rabbits, and one additional rabbit had antigen elimination without proteinuria. Single nephrectomy was performed at the time of antigen elimination in all animals; the remaining kidney was removed four days (4 rabbits) or 14 days afterwards (5 rabbits). In glomerular cross sections (gcs), lymphocytes were identified using monoclonal antibody M108, and monocytes by nonspecific esterase stain (ES). MIF activity was determined in supernatants of cultures of isolated glomeruli by the agarose microdroplet method. Peak of MIF activity (84.3 +/- 2.6%, SEM) was observed the first day of proteinuria in association with peak of lymphocyte infiltration (1.15 +/- 0.1 lymphocytes/gcs) and monocyte infiltration (2.4 +/- 0.3 mean ES score/gcs). MIF activity diminished by day 4 (66.0 +/- 6.3%) and reached control levels by day 14 (12.8 +/- 3.2%). There was a significant correlation between lymphocyte infiltration and MIF activity (r = 0.776, P less than 0.0001) as well as between MIF activity and monocyte accumulation (r = 0.858, P less than 0.0001). In five additional rabbits with AcSS, glomeruli were isolated, treated successively with M108 and normal rabbit serum, and supernatants harvested from 24-hour cultures were tested for MIF activity.(ABSTRACT TRUNCATED AT 250 WORDS)