UIC - Unidade de Imunologia Clínica
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Browsing UIC - Unidade de Imunologia Clínica by Author "Almeida, I."
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- Anti-Ro52 Antibodies and Interstitial Lung Disease in ConnectiveTissue Diseases Excluding SclerodermaPublication . Ferreira, J.; Almeida, I.; Marinho, A.; Cerveira, C.; Vasconcelos, C.The presence of anti-Ro52 antibodies has been reported in a wide variety of autoimmune diseases, particularly in myositis, scleroderma, and autoimmune liver diseases. Clinical significance of anti-Ro52 antibodies remains controversial, and studies are lacking for clarifying the association of anti-Ro52 with interstitial lung disease (ILD) in connective tissue diseases (CTD). Objectives. To determine if anti-Ro52 antibodies are associated with ILD in CTD other than scleroderma. Methods. Singlecenter, retrospective study based on immunoblotting panel analysis and patients clinical records. Results. In our connective tissue disease cohort, 162 patients had immunoblotting panels with anti-Ro52 reactivity analysis, 41 (25,3%) had inclusion criteria. Among the 41 selected sera, 85.4% (n = 35) had anti-Ro52 reactivity. The prevalence of ILD in the positive anti-Ro52 antibodies was 71.4% (n = 25), and 16.7% (n = 1) in the negative anti-Ro52 group (P = 0.018). Overall sensitivity (96.2%), specificity (83.3%), positive (71.4%) and negative (83.3%) predictive values of anti-Ro52 antibodies to determine ILD in CTD is detailed in this study. Conclusion. Ro52 autoantibodies are associated with ILD in CTD excluding scleroderma. We suggest that the presence of anti-Ro52 reactivity in CTD should increase the clinician curiosity for the search of ILD.
- Are Anti-Ro52 Antibodies Associated with Pulmonary Involvement in Scleroderma?Publication . Ferreira, J.; Almeida, I.; Marinho, A.; Cerveira, C.; Vasconcelos, C.Abstract Introduction: The presence of anti-Ro52 antibodies has been reported in a wide variety of autoimmune diseases, particularly in myositis, scleroderma and autoimmune liver diseases. Clinical significance of anti-Ro52 antibodies remains controversial. Studies are lacking in clarifying the association of anti-Ro52 with pulmonary involvement in scleroderma. Objectives: To determine if anti-Ro52 antibodies are associated with pulmonary involvement (interstitial, indirect pulmonary hypertension, or both) in scleroderma. Methods: Single center, retrospective study based on immunoblotting panel analysis and patients clinical records. Pulmonary manifestations were sub-grouped in: 1) interstitial (alveolitis and/or fibrosis), 2) pulmonary artery systolic pressure (PASP) ≥40 mmHg plus interstitial pulmonary disease, and 3) isolated PASP≥40 mmHg (purely vascular). Results: Our scleroderma cohort included 200 patients, of which 137 had immunoblotting panels with anti-Ro52 reactivity analysis. The search was conducted between January 2010 and July 2011. The frequency of pulmonary manifestations in patients with positive anti-Ro52 antibodies was 67.7% (n=31), and 60% (n=24) in the negative anti-Ro52 group, showing no significant differences between groups (p=0.621). Still no significant differences were found when pulmonary manifestations were evaluated according to the subgroups (p=0.525). Sensitivity, specificity, positive and negative predictive values of anti-Ro52 reactivity for determining pulmonary involvement in scleroderma were low. Conclusion: No association was found between positive anti-Ro52 antibodies and pulmonary involvement in scleroderma.
- Autologous stem cell transplantation in a patient with severe systemic sclerosisPublication . Vaz, C.; Almeida, I.; Guedes, M.; Rosário, C.; Branca, R.; Campilho, F.; Roncon, S.; Vasconcelos, C.; Campos, A.Systemic Sclerosis (SSc) is a chronic disease of the connective tissue, whose pathogenesis involves abnormalities of the immunological system. It has a variable course and there is a subgroup of patients with rapidly progressive disease or unresponsive to conventional treatment. Thesepatients can benefit from intensive immunosuppression and autologous hematopoietic stem cell transplant. Clinical case: 19-year-old (y.o.) woman diagnosed with SSc at the age of 13 y.o. with cutaneous, vascular and articular involvement with initial response to me thotrexate. Three years later the disease progressed with severe digestive involvement (dysphagia, delayed gastric emptying and weight loss) needing gastrostomy for nutritional support. She was treated with cyclophosphamide without improvement. In May 2012 she had an autologous transplant with myeloablative regimen (BEAM): carmustine 300 mg/m2 x1day; etoposide 120 mg/kg x4days; cytarabine 120 mg/kg 12/12:h x4days; melphalan 140 mg/m2 x1day. A year and a half after transplantation she is asymptomatic, without any signs or symptoms of the disease, feeds by mouth and the gastric emptying study is normal. Currently she is free of medication.
- From Clinical Presentation to the Outcome: the Natural History of PML in a Portuguese Population of HIV Infected PatientsPublication . Nery, F.; França, M.; Almeida, I.; Vasconcelos, c.Background Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system, associated with immunosuppression states. As there are only some non-published documents concerning PML in HIV infected patients in Portugal, we pretend to characterize natural history of PML infection in a population of HIV patients. Methods We retrospectively reviewed, from 1992 to 2009, PML cases in a population of 724 HIV infected patients followed in our institution. Clinical, biological, imagery features and outcomes were characterized. Results Twenty-five (3.45%) patients were identified as having PML. The mean time between HIV and PML diagnosis was 20.4 months. PML was the presentation of HIV infection in 40% of the patients, and 92% had CD4 T cell count lower than 200/mm3. Paresis was the most common clinical presentation. No specific characteristics were found in cerebrospinal fluid and JCV DNA was positive in 3 of 7 patients. MRI revealed characteristic findings. Combined antiretroviral therapy was started or changed in 96% of the patients. Neurological condition got worse in 12 patients. From the 14 deaths, 5 were directly attributed to PML progression. Follow-up was lost in 8 patients. Conclusions PML was the presentation of HIV infection in more than 1/3 of patients, frequently associated with advanced immunocompromise. MRI sensitivity to PML is high, and JCV DNA determination in CSF was not revealed to be sensible. PML diagnosis should be taken into account in HIV patients presenting any neurological symptoms, and HIV infection should be suspected when radiological findings suggest PML lesions even in previously healthy individuals.
- HIV-2 integrase polymorphisms and longitudinal genotypic analysis of HIV-2 infected patients failing a raltegravir-containing regimenPublication . Cavaco-Silva, J.; Abecasis, A.; Miranda, A.; Poças, J.; Narciso, J.; Águas, M.; Maltez, F.; Almeida, I.; Germano, I.; Diniz, A.; Gonçalves, M.; Gomes, P.; Cunha, C.; Camacho, R.To characterize the HIV-2 integrase gene polymorphisms and the pathways to resistance of HIV-2 patients failing a raltegravir-containing regimen, we studied 63 integrase strand transfer inhibitors (INSTI)-naïve patients, and 10 heavily pretreated patients exhibiting virological failure while receiving a salvage raltegravir-containing regimen. All patients were infected by HIV-2 group A. 61.4% of the integrase residues were conserved, including the catalytic motif residues. No INSTI-major resistance mutations were detected in the virus population from naïve patients, but two amino acids that are secondary resistance mutations to INSTIs in HIV-1 were observed. The 10 raltegravir-experienced patients exhibited resistance mutations via three main genetic pathways: N155H, Q148R, and eventually E92Q - T97A. The 155 pathway was preferentially used (7/10 patients). Other mutations associated to raltegravir resistance in HIV-1 were also observed in our HIV-2 population (V151I and D232N), along with several novel mutations previously unreported. Data retrieved from this study should help build a more robust HIV-2-specific algorithm for the genotypic interpretation of raltegravir resistance, and contribute to improve the clinical monitoring of HIV-2-infected patients.
- LINFOPENIA T CD4 NO LUPUS ERITEMATOSO SISTÉMICOPublication . Ferreira, S.; Vasconcelos, J.; Marinho, A.; Farinha, F.; Almeida, I.; Correia, J.; Barbosa, P.; Mendonça, T.; Vasconcelos, C.Abstract: Background: Systemic Lupus Erythematosus (SLE) is an inflammatory chronic disease characterized by the presence of autoantibodies, immunocomplex production and organ injury. Several alterations of the immune system have been described, namely of CD4 T cells, with particular focus on regulatory subgroup. Objective: Quantify peripheral CD4 T cells in a population of patients with SLE and correlate it with lupus activity, affected organs, therapeutics and infections. Methods: Retrospective study involving all SLE patients seen in the clinical immunology outpatient clinic of the Hospital Geral Santo António, Porto that has done some peripheral blood flow cytometry study. Results: Twenty-nine patients have been evaluated, 16 were taking glucocorticoids and six immunossupressors. The mean SLEDAI at the study time was nine and the ECLAM was three. Thirty-one percent of the patients had leukopenia, 76% lymphocytopenia and the same number CD4 depletion. Fifty-five percent of the patients had CD4 levels lower than 500/mm3, 31% lower than 200/mm3. All patients with SLEDAI ?20 and ECLAM ?4 had CD4 counts inferior to 500/mm3 and all patients with inactive disease had CD4 superior to 500/mm3. There have been three opportunistic infections: cryptococcal meningitis, pulmonary aspergilosis, Pneumocystis jirovecii pneumonia, all in patients with CD4 counts lower than 500/mm3. Conclusion: Decreased CD4 T cells counts have been very common in this study population. There is an inverse relation between CD4 cells counts and disease activity. Opportunistic infections occurred in patients with severe CD4 depletion. Keywords: Systemic Lupus Erythematosus; CD4 T Lymphocytes; Lymphocytopenia; SLE Activity; Opportunistic infections
- A nossa regra de ouro na doença de Behçet: tratar a manifestação clínicaPublication . Ferrão, C.; Almeida, I.; Marinho, A.; Vasconcelos, C.; Correia, J.A Doença de Behçet (DB) é uma vasculite sistémica que pode ser definida na fronteira entre a doença autoimune e autoinflamatória. A sua etiopatogenia ainda não é completamente conhecida, embora saibamos que contribuem factores genéticos (Antigénios de Histocompatibilidade/ HLA, por exemplo) e ambienciais (maior prevalência em zonas específicas do globo). Há células implicadas no processo patológico (neutrófilos, macrófagos, linfócitos T reguladores) e outros componentes (factor de necrose tumoral/ TNF, interleucinas) do sistema imune. As formas clínicas da DB são muito variadas, quer na gravidade, quer nos órgãos atingidos: Behçet Mucocutâneo, Behçet Ocular, Vasculobehçet, Neurobehçet, Behçet Intestinal, Behçet Cardíaco. Independentemente dos mecanismos imuno-inflamatórios subjacentes às diversas apresentações clínicas, a terapêutica tem de ser adaptada a cada uma delas. A nossa série de DB, coligida ao longo de 20 anos, é representativa de todo o espectro clínico de DB e consideramos útil fazer uma resenha atual da terapêutica indicada, caldeando os dados da literatura, com a nossa experiência.
- Raynaud and digital ulcers in patients with juvenile systemic sclerosis: ambulatory iloprost protocol. A single center experiencePublication . Guedes, M.; Zilhão, C.; Almeida, I.; Silva, I:
- The Protective Role of HLA-DRB1(∗)13 in Autoimmune DiseasesPublication . Bettencourt, A.; Carvalho, C.; Leal, B.; Brás, S.; Lopes, D.; Martins da Silva, A.; Santos, E.; Torres, T.; Almeida, I.; Farinha, F.; Barbosa, P.; Marinho, A.; Selores, M.; Correia, J.; Vasconcelos, C.; Costa, P.; da Silva, B.Autoimmune diseases (AIDs) are characterized by a multifactorial aetiology and a complex genetic background, with the MHC region playing a major role. We genotyped for HLA-DRB1 locus 1228 patients with AIDs-213 with Systemic Lupus Erythematosus (SLE), 166 with Psoriasis or Psoriatic Arthritis (Ps + PsA), 153 with Rheumatoid Arthritis (RA), 67 with Systemic Sclerosis (SSc), 536 with Multiple Sclerosis (MS), and 93 with Myasthenia Gravis (MG) and 282 unrelated controls. We confirmed previously established associations of HLA-DRB1(∗)15 (OR = 2.17) and HLA-DRB1(∗)03 (OR = 1.81) alleles with MS, HLA-DRB1(∗)03 with SLE (OR = 2.49), HLA-DRB1(∗)01 (OR = 1.79) and HLA-DRB1(∗)04 (OR = 2.81) with RA, HLA-DRB1(∗)07 with Ps + PsA (OR = 1.79), HLA-DRB1(∗)01 (OR = 2.28) and HLA-DRB1(∗)08 (OR = 3.01) with SSc, and HLA-DRB1(∗)03 with MG (OR = 2.98). We further observed a consistent negative association of HLA-DRB1(∗)13 allele with SLE, Ps + PsA, RA, and SSc (18.3%, 19.3%, 16.3%, and 11.9%, resp., versus 29.8% in controls). HLA-DRB1(∗)13 frequency in the AIDs group was 20.0% (OR = 0.58). Although different alleles were associated with particular AIDs, the same allele, HLA-DRB1(∗)13, was underrepresented in all of the six diseases analysed. This observation suggests that this allele may confer protection for AIDs, particularly for systemic and rheumatic disease. The protective effect of HLA-DRB1(∗)13 could be explained by a more proficient antigen presentation by these molecules, favouring efficient clonal deletion during thymic selection.