Browsing by Author "Monteiro, M"
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- 8 de Novembro de 1895Publication . Almeida, C; Assunção, R; Madeira, P; Monteiro, M
- A Case of Bortezomib-Associated Thrombotic Microangiopathy in a Multiple Myeloma PatientPublication . Moreira Fonseca, N; Cardoso, F; Monteiro, M; Góis, M; Sousa, H; Fidalgo, T; Calado, J; Nolasco, FBortezomib is a first-generation proteasome inhibitor used in the treatment of multiple myeloma. We present a case of a 70-year-old woman with multiple myeloma, who presented thrombotic microangiopathy with multi-organ involvement thrombotic microangiopathy (ocular, cardiac, and renal) after bortezomib initiation. A kidney biopsy confirmed the diagnosis of thrombotic microangiopathy. A temporal relation between bortezomib exposure and thrombotic microangiopathy onset was seen in the absence of other concurrent medication or disease known to cause thrombotic microangiopathy, and thrombotic microangiopathy was only resolved after drug discontinuation. The exact pathophysiological mechanism remains unknown. To our knowledge, this is the second biopsy-proven published case of bortezomib-associated thrombotic microangiopathy. Since bortezomib is extensively used for treating patients with multiple myeloma, prescribing clinicians should maintain a high index of suspicion of this potentially fatal complication.
- CT-Proven Ischaemic Stroke as the First Manifestation of Occult Lung CancerPublication . Azeredo Costa, J; Rodrigues, M; Monteiro, M; Salvado, V; Dias, LCancer is associated with a higher risk of stroke, and in rare cases stroke can be the first manifestation of occult neoplasia. We present the case of a 74-year-old woman hospitalized for ischaemic stroke with multiple cerebral infarctions in several vascular territories. The exclusion of other aetiologies and the simultaneous presence of thromboembolic events in other organs raised the suspicion of a hypercoagulable state, which upon investigation revealed occult neoplasia of the lung. There was rapid deterioration, with recurrent thrombotic events despite anticoagulation, which eventually led to the patient's death. Learning points: Stroke can be the first manifestation of occult neoplasia.In the presence of cryptogenic stroke, high D-dimers, multiple brain infarctions in different vascular territories and thromboembolic events in other organs, the possibility of hidden neoplasia should be considered.Anticoagulation in disseminated intravascular coagulation is insufficient if the primary disease is not treated.
- Placas Pleurais Calcificadas por Exposição a AsbestosPublication . Rodrigues, M; Monteiro, M; Salvado, V; Gaspar, A
- O Prémio Nobel e a RadiologiaPublication . Almeida, C; Assunção, R; Madeira, P; Monteiro, M
- PROP1 Gene Analysis in Portuguese Patients with Combined Pituitary Hormone DeficiencyPublication . Lemos, MC; Gomes, L; Bastos, M; Leite, V; Limbert, E; Carvalho, D; Bacelar, C; Monteiro, M; Fonseca, F; Agapito, A; Castro, JJ; Regateiro, F; Carvalheiro, MOBJECTIVE: Mutations of the PROP1 gene lead to combined pituitary hormone deficiency (CPHD), which is characterized by a deficiency of GH, TSH, LH/FSH, PRL and, less frequently, ACTH. This study was undertaken to investigate the molecular defect in a cohort of patients with CPHD. DESIGN, PATIENTS AND MEASUREMENTS: A multicentric study involving 46 cases of CPHD (17 familial cases belonging to seven kindreds and 29 sporadic cases) selected on the basis of clinical and hormonal evidence of GH deficiency, central hypothyroidism and hypogonadotrophic hypogonadism, in the absence of an identified cause of hypopituitarism. Mutations of PROP1 were investigated by DNA sequencing. Clinical, hormonal and neuroradiological data were collected at each centre. RESULTS: PROP1 mutations were identified in all familial cases: five kindreds presented a c. 301-302delAG mutation, one kindred presented a c. 358C --> T (R120C) mutation and one presented a previously unreported initiation codon mutation, c. 2T --> C. Of the 29 sporadic cases, only two (6.9%) presented PROP1 germline mutations (c. 301-302delAG, in both). Phenotypic variability was observed among patients with the same mutations, particularly the presence and age of onset of hypocortisolism, the levels of PRL and the results of pituitary imaging. One patient presented a sellar mass that persisted into adulthood. CONCLUSIONS: This is the first report of a mutation in the initiation codon of the PROP1 gene and this further expands the spectrum of known mutations responsible for CPHD. The low mutation frequency observed in sporadic cases may be due to the involvement of other unidentified acquired or genetic causes.