ABSTRACT
OBJECTIVE: To evaluate the role of parvovirus B19 (B19), varicella zoster virus (VZV), and human herpes virus 6 (HHV-6) in the aetiopathology of giant cell arteritis (GCA). METHODS: Temporal artery biopsy specimens from 57 patients with GCA and 56 controls were investigated. DNA was obtained by biopsy, and quantitative real time polymerase chain reaction assay performed to establish the prevalence and viral load of B19, VZV, and HHV-6. Amplification of the human beta-globin gene was used as internal positive control. RESULTS: (a) B19 was detected in 31/57 (54%) patients (median viral load 45.2 (25th-75th centiles 0-180.2) copies/microg DNA) v 21/56 (38%) controls (median viral load 0 (0-66.7) copies/microg of DNA; p = 0.07 for DNA prevalence, p = 0.007 for viral load. Among 31 B19 positive samples, 21 (68%) patients with biopsy proven GCA had >10(2) B19 copies/microg of DNA v 5/21 (24%) controls; p = 0.001. (b) No significant difference was found for VZV (p = 0.94 for DNA prevalence; p = 0.76 for viral load) and HHV-6 (p = 0.89 for DNA prevalence; p = 0.64 for viral load) in the GCA group compared with controls. CONCLUSION: B19 may have a role in the aetiopathology of GCA, particularly in those patients with high viral load; no evidence was found for VZV and HHV-6.
Subject(s)
Giant Cell Arteritis/virology , Herpesvirus 3, Human/isolation & purification , Herpesvirus 6, Human/isolation & purification , Parvoviridae Infections/complications , Parvovirus B19, Human/isolation & purification , Aged , Aged, 80 and over , DNA, Viral/analysis , Female , Herpes Zoster/complications , Humans , Male , Middle Aged , Polymerase Chain Reaction/methods , Roseolovirus Infections/complications , Viral LoadABSTRACT
OBJECTIVE: To describe the incidence and characteristics of the infection caused by Mycobacterium tuberculosis in patients with autoimmune diseases. PATIENTS AND METHODS: Searching in the database of the department at our institution, all new cases of tuberculosis from 1991 to 2000 were identified in patients with autoimmune diseases; the total follow-up time was calculated as the difference between first and last visits. Time with immunosuppressive drug therapy was obtained for patients with rheumatoid arthritis from a database oriented to the longitudinal follow-up of these patients. The incidence density was calculated as the quotient between the absolute frequency of cases and the sum of individual periods at risk for each subgroup. RESULTS: Fifteen cases of tuberculosis were identified from 3,634 risk patients followed for an accumulated period of 9,795 years (overall incidence 153 per 100,000 patients-year). Fourteen patients were receiving disease-modifying drugs and eleven were receiving corticosteroids at diagnosis. The location of tuberculosis infection was the lung for 33.3% of cases. The incidence by drugs in patients with rheumatoid arthritis was 143 per 100,000 patients-year with methotrexate, 2,703 per 100,000 patients-year with azathioprin, 7,692 per 1,000 patients-year with cyclophosphamide, and 4,878 per 100,000 patients-year for anti-TNFalpha. CONCLUSIONS: Compared with the general population, the incidence density of tuberculosis is increasing in our population, with a higher frequency of extrapulmonary involvement. The incidence density is variable among patients with rheumatoid arthritis depending upon the used drugs.
Subject(s)
Autoimmune Diseases/epidemiology , Mycobacterium tuberculosis/isolation & purification , Rheumatic Diseases/epidemiology , Tuberculosis/epidemiology , Adult , Aged , Antitubercular Agents/therapeutic use , Autoimmune Diseases/drug therapy , Female , Humans , Immunosuppressive Agents/adverse effects , Incidence , Male , Middle Aged , Rheumatic Diseases/drug therapy , Tuberculosis/drug therapyABSTRACT
Objetivo. Describir la incidencia y las características de la infección por Mycobacterium tuberculosis en pacientes con enfermedades autoinmunes.Pacientes y métodos. Se identificaron los casos nuevos de tuberculosis desde 1991 a 2000 en pacientes con enfermedad autoinmune a partir de la base de datos del servicio; se calculó el tiempo total de seguimiento como la diferencia entre la primera y la última visita. El tiempo de tratamiento con fármacos inmunosupresores se obtuvo en pacientes con artritis reumatoide de una base de datos orientada al seguimiento longitudinal de estos pacientes. Se calculó la densidad de incidencia como el cociente entre la frecuencia absoluta de casos y la suma de los períodos individuales de riesgo en cada subgrupo. Resultados. Se identificaron 15 casos de tuberculosis en 3.634 pacientes en riesgo seguidos durante un período acumulado de 9.795 años (incidencia global: 153 por 100.000 pacientes-año).Catorce pacientes estaban recibiendo fármacos modificadores de la enfermedad y once corticosteroides en el momento del diagnóstico. La localización de la infección tuberculosa fue pulmonar en el 33,3 por ciento de los casos. La incidencia por fármacos en pacientes con artritis reumatoide fue de 143 por 100.000 pacientes-año con metotrexato, 2.703 por 100.000 pacientes-año con azatioprina, 7.692 por 1.000 pacientes-año con ciclofosfamida y 4.878 por 100.000 pacientes-año con anti-TNF . Conclusiones. La densidad de incidencia de tuberculosis está aumentada en nuestra población comparado con la de la población general, existiendo una mayor frecuencia de afectación extrapulmonar. La densidad de incidencia es variable en pacientes con artritis reumatoide en función de los fármacos utilizados (AU)
Subject(s)
Middle Aged , Adult , Aged , Male , Female , Humans , Tuberculosis , Incidence , Mycobacterium tuberculosis , Rheumatic Diseases , Antitubercular Agents , Autoimmune Diseases , Immunosuppressive AgentsABSTRACT
OBJECTIVE: To determine whether anti-TNF alpha (infliximab) treatment affects B cell activation in patients with rheumatoid arthritis (RA) METHODS: B cell activation was analyzed in fifteen anti-TNF-treated RA patients. CD23 expression was used as a B cell activation marker and was studied before and after three months of infliximab treatment. PBMC were stimulated with anti-CD3 mAb during 18 h and were separated by rosseting into E+ and E-cells. B cells were assessed in E-population by double staining with CD19 and CD23. ELISA assays were used to assess both soluble TNF alpha and circulant immune complexes (CIC) containing TNF alpha. We also used B cells from tonsils to establish the relationship between B cell activation and TNF alpha CIC. RESULTS: The proportion of B cells expressing CD23 was higher before infliximab exposure than after treatment (48.3 +/- 16.7 versus 29.5 +/- 12.5, p = 0.007). T-B cell interactions were assessed by means of blocking antibodies to CD154, CD40, CD69, and CD18; these interactions were not specially affected by infliximab treatment. We could demonstrate CIC containing TNF alpha after infliximab treatment, these CIC, similarly to others IgG-containing immune complexes, were capable to downregulate CD23 on B cells. CONCLUSIONS: Infliximab treatment in RA downregulates CD23 expression on T-cell activated B cells. This downregulation is connected with the presence of CIC containing TNF alpha. Presumably, the Fc gamma RIIb1 endows IgG-containing immune complexes, as TNF alpha-anti-TNF alpha, with the capacity to regulate B cells and inflammatory cells.
