Browsing by Author "Martins, M"
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- Um caso de mania crónica numa doente com diagnóstico duplo de doença bipolar tipo I e perturbação delirantePublication . Martins, M; Gracias, MJ; Melo, JOs autores descrevem o caso de uma doente de 62 anos, sem antecedentes psiquiátricos pessoais ou familiares até aos 52 anos, altura em que inicia ideias delirantes de conteúdo somático e hipocondríaco em que acredita ter ficado doente com um “problema na cabeça” após um pequeno traumatismo no local de trabalho. É internada pela primeira vez dois anos depois do referido traumatismo com o diagnóstico de perturbação delirante tipo somático, tendo tido alta com o delírio enquistado e sem crítica para o estado patológico. Inicia acompanhamento em consulta externa de psiquiatria, com má adesão terapêutica em ambulatório, com novo internamento cerca de 1 ano depois, por agravamento das ideias delirantes somáticas e hipocondríacas. Cerca de 3 anos depois, começa a manifestar sintomas maniformes de gravidade crescente (ideias sobrevalorizadas de grandiosidade, aumento da energia, taquipsiquia, aumento do débito do discurso, desinibição, elação de humor e redução da necessidade de sono); posteriormente o quadro agrava-se com o aparecimento de ideias delirantes persecutórias e alucinações auditivo-verbais, situação que motiva novo internamento, com um episódio maníaco franco. É feito o diagnóstico duplo de perturbação delirante e perturbação bipolar tipo I, numa doente com funcionamento pré-mórbido hipertímico. Desde então e durante cerca de 4 anos mantém-se com quadro clínico relativamente estável caracterizado por humor tendencialmente elevado, ideias de grandiosidade, discurso prolixo e de débito aumentado, aspecto externo por vezes excêntrico e sem crítica para o estado patológico. Os autores discutem a evolução e as implicações clínicas de uma forma particular e relativamente pouco frequente da doença bipolar, a mania crónica.
- Crosstalk between genetics, gene expression and biochemical markers supports systemic iron homeostasis dysregulation in alzheimer diseasePublication . Crespo, A; Silva, B; Ferreira, C; Marquesa, L; Marcelino, E; Maruta, C; Costa, S; Timóteo, A; Vilares, A; Couto, F; Faustino, P; Correia, AP; Verdelho, A; Porto, G; Guerreiro, M; Herrero Valverde, A; Costa, C; Mendonça, A; Costa, L; Martins, M
- Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patientsPublication . Guerreiro, C; Silva, B; Crespo, A; Marques, L; Costa, S; Timóteo, A; Marcelino, E; Maruta, C; Vilares, A; Matos, M; Couto, F; Faustino, P; Verdelho, A; Guerreiro, M; Herrero Valverde, A; Costa, C; Mendonça, A; Martins, M; Costa, LAlzheimer's disease (AD) is a neurodegenerative disorder of still unknown etiology and the leading cause of dementia worldwide. Besides its main neuropathological hallmarks, a dysfunctional homeostasis of transition metals has been reported to play a pivotal role in the pathogenesis of this disease. Dysregulation of iron (Fe) metabolism in AD has been suggested, particularly at the level of cellular iron efflux. Herein, we intended to further clarify the molecular mechanisms underlying Fe homeostasis in AD. In order to achieve this goal, the expression of specific Fe metabolism-related genes directly involved in Fe regulation and export was assessed in peripheral blood mononuclear cells (PBMCs) from 73AD patients and 74 controls by quantitative PCR. The results obtained showed a significant decrease in the expression of aconitase 1 (ACO1; P=0.007); ceruloplasmin (CP; P<0.001) and amyloid-beta precursor protein (APP; P=0.006) genes in AD patients compared with healthy volunteers. These observations point out to a significant downregulation in the expression of genes associated with ferroportin-mediated cellular Fe export in PBMCs from AD patients, when compared to controls. Taken together, these findings support previous studies suggesting impairment of Fe homeostasis in AD, which may lead to cellular Fe retention and oxidative stress, a typical feature of this disease.
- Extensive Linear Scleroderma en Coup De Sabre With Exertion-Induced Hemiplegic MigrainePublication . Martins, M; Quintas, S; Coelho, J; Santos, T; Levy, AWe report the case of a 9-year-old girl with linear scleroderma en coup de sabre (LSCS) who developed progressive white matter involvement, presenting as intractable hemiplegic migraine-like attacks induced by exercise. After a period of severely aggressive course, clinical and radiological stabilization was achieved under immunosuppressant treatment. Intrathecal synthesis of IgG and lymphocytic pleocytosis provided indirect evidence of a chronic inflammatory process of the central nervous system. We discuss the possible immunopathogenic mechanisms responsible for the neurocutaneous involvement in LSCS, favouring the hypothesis of an autoimmune and inflammatory vasculopathy. The singular occurrence of hemiplegic migraine triggered by exertion add further insight to the currently unknown pathogenesis of scleroderma disorder. In addition, we highlight the importance of intensive immunosuppression approaches in selected cases, contrasting with the classic benign course of LCSC.
- Genetic and biochemical markers in patients with Alzheimer's disease support a concerted systemic iron homeostasis dysregulationPublication . Crespo, A; Silva, B; Marques, L; Marcelino, E; Maruta, C; Costa, S; Timóteo, A; Vilares, A; Couto, F; Faustino, P; Correia, AP; Verdelho, A; Porto, G; Guerreiro, M; Herrero Valverde, A; Costa, C; Mendonça, A; Costa, L; Martins, MAlzheimer's disease (AD) is the most common form of dementia in the elderly individuals, resulting from a complex interaction between environmental and genetic factors. Impaired brain iron homeostasis has been recognized as an important mechanism underlying the pathogenesis of this disease. Nevertheless, the knowledge gathered so far at the systemic level is clearly insufficient. Herein, we used an integrative approach to study iron metabolism in the periphery, at both genotypic and phenotypic levels, in a sample of 116 patients with AD and 89 healthy control subjects. To assess the potential impact of iron metabolism on the risk of developing AD, genetic analyses were performed along with the evaluation of the iron status profile in peripheral blood by biochemical and gene expression studies. The results obtained showed a significant decrease of serum iron, ferritin, and transferrin concentrations in patients compared with the control subjects. Also, a significant decrease of ferroportin (SLC40A1) and both transferrin receptors TFRC and TFR2 transcripts was found in peripheral blood mononuclear cells from patients. At the genetic level, significant associations with AD were found for single nucleotide polymorphisms in TF, TFR2, ACO1, and SLC40A1 genes. Apolipoprotein E gene, a well-known risk factor for AD, was also found significantly associated with the disease in this study. Taken together, we hypothesize that the alterations on systemic iron status observed in patients could reflect an iron homeostasis dysregulation, particularly in cellular iron efflux. The intracellular iron accumulation would lead to a rise in oxidative damage, contributing to AD pathophysiology.
- Granulomatous Cheilitis Associated With Crohn’s DiseasePublication . Oliveira, AM; Martins, M; Martins, A; Deus, JR
- Incidence of postoperative residual neuromuscular blockade in the postanaesthesia care unit: an observational multicentre study in Portugal.Publication . Esteves, S; Martins, M; Barros, F; Barros, F; Canas, M; Vitor, P; Seabra, M; Castro, M; Bastardo, ICONTEXT: Residual neuromuscular blockade still presents despite the use of intermediate duration muscle relaxants and is a risk factor for postoperative morbidity. OBJECTIVE: To determine the incidence of incomplete postoperative neuromuscular recovery from anaesthesia in a postanaesthesia care unit. DESIGN: Multicentre observational study. SETTING: Public Portuguese hospitals. PATIENTS: Adult patients scheduled for elective surgery requiring general anaesthesia with neuromuscular blocking agents. MAIN OUTCOME MEASURES: An independent anaesthesiologist measured neuromuscular transmission by the TOF-Watch SX acceleromyograph. Train-of-four ratios at least 0.9 and less than 0.9 were assessed as complete and incomplete neuromuscular recovery following general anaesthesia, respectively. RESULTS: The study population consisted of 350 patients [134 men and 216 women, mean (SD) age 54.3 (15.9) years]. Ninety-one patients had a train-of-four ratio less than 0.9 on arrival in the postanaesthesia care unit, an incidence of residual neuromuscular blockade of 26% [95% confidence interval (CI) 21 to 31%]. The most frequent neuromuscular blockers were rocuronium (44.2%) and cisatracurium (32%). A neuromuscular block reversal agent was used in 66.6% of the patients (neostigmine in 97%). The incidence of residual neuromuscular blockade in patients receiving reversal agents was 30% (95% CI 25 to 37%). There were no statistically significant differences in the occurrence of residual blockade relating to the neuromuscular blocker used, although higher percentages were observed for cisatracurium (32.4%) and vecuronium (32%) compared with atracurium (23.6%) and rocuronium (20.8%). Incomplete neuromuscular recovery was significantly more frequent among patients who had received a reversal agent (30.5 vs. 17.1%, P = 0.01). Incomplete neuromuscular recovery was more frequent in patients given propofol than in those exposed to sevoflurane (26.2 vs. 14.3%). CONCLUSION: The incidence of incomplete neuromuscular recovery of 26% confirms that it is relatively frequent in the postoperative period and calls attention to the dimension of this problem in Portugal
- Kraepelinian systematic paraphrenia as a recognizable disorderPublication . Borja-Santos, N; Trancas, B; Ferreira, B; Parente, J; Gamito, A; Almeida, S; Vieira, C; Luengo, A; Xavier, S; Klut, C; Graça, J; Ramos, J; Martins, M; Ribeiro, J; Neto, A; Palma, M; Luis, A; Cardoso, GObjectives: To demonstrate that systematic paraphrenia as defined by Kraepelin (the most consistent prototypic paraphrenia subtype) can be recognized and diagnosed. Subjects and methods: All patients admitted to a Portuguese psychiatric inpatient unit between September 2006 and October 2011, meeting the criteria for systematic paraphrenia based on Kraepelin’s definition, Munro’s operational criteria and the authors’ criteria, were evaluated by two senior psychiatrists. Results: Out of 27 evaluated patients, 16 (10 women and 6 men) were confirmed as having systematic paraphrenia, accounting for 0.83% of the total number of inpatients (1921). The mean age of onset was 34.3 years (SD = 8.9) and the mean duration of illness at observation was 19.5 years (SD = 12.3). Most (n = 13) had no family psychiatric history, were married (n = 11) before the onset of the disorder and none had previous sensorial deficit. Six were born outside of Portugal. Their academic achievements were only slightly inferior to the general population. Conclusions: Systematic paraphrenia can be recognized and diagnosed. Contrary to Kraepelin, the disorder seems to be more frequent in women. It does not seem to be associated with old age or heredity. This syndrome is internally consistent and its only similarity with schizophrenia is the positive symptoms’ dimension. It should also be distinguished from late paraphrenia.