Browsing by Author "Martins, AR"
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- Chronic Urticaria in the Real-Life Clinical Practice Setting in Portugal: Baseline Results from the Non-Interventional Multicentre AWARE StudyPublication . Costa, C; Rosmaninho, I; Guilherme, A; Ferreira, J; Antunes, J; Pina, A; Prates, S; Gaspar-Marques, J; Azevedo, F; Cunha, AP; Brito, C; Massa, A; Sousa, JT; Velho, GC; Raposo, I; Pinto, GM; Sousa, Vi; Martins, ARThere is a paucity of information regarding chronic urticaria patients' care in a real-world setting. The objective of this study was to report and evaluate the baseline characteristics of Portuguese chronic urticaria patients refractory to H1-antihistamines included in the AWARE study. MATERIAL AND METHODS: This is a non-interventional cohort study. Adult patients with a diagnosis of chronic urticaria with symptoms for at least two months, refractory to H1-antihistamines, consulting one of the 10 participating urticaria centers throughout Portugal have been included in the study. Baseline sociodemographic data, medical history, clinical parameters, medication, weekly urticaria activity score, and dermatology quality of life index have been collected. RESULTS: Seventy six patients were included, of which 76.3% were women. The majority of patients had a diagnosis of chronic spontaneous urticaria (88.2%) and 39.5% had angioedema. Around 91.0% of patients were medicated with non-sedative H1-antihistamines and 35.4% with a third line therapy. Median dermatology quality of life index was 5.0 and median weekly urticaria activity score was 13.0. DISCUSSION: The baseline results suggest that patients with chronic urticaria refractory to H1-antihistamines are being under-treated in the real-world setting. CONCLUSION: The AWARE study demonstrates the real impact of chronic urticaria on Portuguese patients refractory to H1-antihistamines treatment, and 30% report a very large or extremely large deleterious effect on their quality of life. The follow-up of these patients will allow evaluating strategies aimed at optimizing disease control.
- Mineral and Bone Disease (MBD) on a Kidney Transplant PatientPublication . Birne, R; Adragão, T; Ferreira, A; Dickson, J; Silva, R; Casqueiro, A; Oliveira, R; Martins, AR; Torres, J; Matias, P; Branco, P; Jorge, C; Weigert, A; Bruges, M; Machado, DA 50-year-old post-menopausal recipient of a kidney allograft with bone pain, osteoporosis, persistent hypercalcaemia and elevated parathormone (PTH) levels, despite a satisfactory graft function, was treated with bisphosphonates and cinacalcet starting, respectively, 5 and 6 months after renal transplantation (RT). Sixteen months after treatment, there was improvement of bone mineral density (BMD) measured by dualenergy X-ray absorptiometry (DEXA). A bone biopsy was taken, unveiling a surprising and worrisome result. Post-RT bone disease is different from classic CKD-MBD and should be managed distinctly, including, in some difficult cases, an invasive evaluation through the performance of a bone biopsy, as suggested in the KDIGO guidelines.
- Primary Malignant Peritoneal Mesothelioma Associated with Renal Cell Carcinoma. A Concise Review Based on a Clinical Case Baseada num Caso ClínicoPublication . Murinello, A; Carvalho, A; Figueiredo, AM; Damásio, H; Murillo, MJ; Nunes, G; Baptista, M; Martins, ARO Mesotelioma peritoneal maligno é um tumor maligno relacionado frequentemente com exposição prolongada a fibras de amianto, de mau prognóstico, de diagnóstico geralmente tardio, face à pouca expressão clínica na fase inicial da doença. Como o mesotelioma evolui geralmente só na cavidade peritoneal, doentes seleccionados poderão ter maior sobrevivência se for possível a peritonectomia extensa e quimioterapia hipertérmica intraperitoneal intraoperatória. Os autores referem a sincronicidade ainda não descrita, de mesotelioma peritoneal maligno primário e carcinoma de Grawitz. São revistos concisamente: a clínica destes tumores, síndromes paraneoplásicos (disfunção bioquímica hepática, emagrecimento extremo); etiopatogenia da acção cancerígena das fibras de amianto; mecanismos de disseminação intraperitoneal; avaliação tomodensitométrica; importância da imunohistoquímica no diagnóstico histopatológico; estadiamento; importância do tratamento multidisciplinar destes tumores.
- Two Separate Effects Contribute to Regulatory T Cell Defect in Systemic Lupus Erythematosus Patients and Their Unaffected RelativesPublication . Costa, N; Marques, O; Godinho, SI; Carvalho, C; Leal, B; Figueiredo, AM; Vasconcelos, C; Marinho, A; Moraes-Fontes, MF; Gomes da Costa, A; Ponte, C; Campanilho-Marques, R; Cóias, T; Martins, AR; Viana, JF; Lima, M; Martins, B; Fesel, CForkhead box P3 (FoxP3)+ regulatory T cells (Tregs ) are functionally deficient in systemic lupus erythematosus (SLE), characterized by reduced surface CD25 [the interleukin (IL)-2 receptor alpha chain]. Low-dose IL-2 therapy is a promising current approach to correct this defect. To elucidate the origins of the SLE Treg phenotype, we studied its role through developmentally defined regulatory T cell (Treg ) subsets in 45 SLE patients, 103 SLE-unaffected first-degree relatives and 61 unrelated healthy control subjects, and genetic association with the CD25-encoding IL2RA locus. We identified two separate, uncorrelated effects contributing to Treg CD25. (1) SLE patients and unaffected relatives remarkably shared CD25 reduction versus controls, particularly in the developmentally earliest CD4+ FoxP3+ CD45RO- CD31+ recent thymic emigrant Tregs . This first component effect influenced the proportions of circulating CD4+ FoxP3high CD45RO+ activated Tregs . (2) In contrast, patients and unaffected relatives differed sharply in their activated Treg CD25 state: while relatives as control subjects up-regulated CD25 strongly in these cells during differentiation from naive Tregs , SLE patients specifically failed to do so. This CD25 up-regulation depended upon IL2RA genetic variation and was related functionally to the proliferation of activated Tregs , but not to their circulating numbers. Both effects were found related to T cell IL-2 production. Our results point to (1) a heritable, intrathymic mechanism responsible for reduced CD25 on early Tregs and decreased activation capacity in an extended risk population, which can be compensated by (2) functionally independent CD25 up-regulation upon peripheral Treg activation that is selectively deficient in patients. We expect that Treg -directed therapies can be monitored more effectively when taking this distinction into account.