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Biomedical subjects

Jose A Miranda-Filloy

Publications and source records attributed to Jose A Miranda-Filloy.

6 recordsLinked to original sources
PubMed2006

Cardiovascular disease in rheumatoid arthritis.

Epidemiological studies have disclosed an increased mortality due to cardiovascular (CV) complications in patients with rheumatoid arthritis (RA). Patients with this disease have an increased risk of left ventricular diastolic dysfunction and congestive heart failure that is unrelated to the presence of traditional atherosclerosis risk factors or ischemic heart disease. Endothelial dysfunction, an early step in the atherogenesis process, is observed in both early and long-standing actively treated patients with RA. High-resolution B-mode ultrasound studies of the common carotid artery have shown the presence of subclinical atherosclerosis, manifested by increased carotid intima-media thickness and carotid plaques, in patients with RA. Association between HLA-DRB1*04 shared epitope alleles, in particular with HLA-DRB1*0404, and endothelial dysfunction and CV mortality has also been observed in these patients. Chronic inflammation plays a pivotal role in the mechanisms associated with atherogenesis in RA. Tumor necrosis factor (TNF)-alpha is a potent proinflammatory cytokine implicated in the initiation and progression of inflammation as well as in the mechanisms associated with accelerated atherosclerosis in this disease. Anti-TNF-alpha therapy has proved to be clinically effective in patients with severe RA. Recent studies have also emphasized the positive effect of anti-TNF-alpha blockade in improving endothelial dysfunction in RA patients. However, this effect seems to be transient and in line with the persistence of chronic inflammation.

Adalimumab↗
PubMed2006

Giant cell arteritis: diagnosis and therapeutic management.

Giant cell arteritis (GCA) is the most common systemic vasculitis in the elderly in Western countries. Anemia and very high erythrocyte sedimentation rates are associated with lower incidence of severe ischemic events. Temporal artery biopsy is the gold standard in the diagnosis of GCA. A threshold size of 1 cm of post-formalin fixed segment of the temporal artery was associated with increased diagnostic yield of GCA. Other tools such as ultrasound, MRI, and fluorodeoxyglucose positron emission tomography are useful in the diagnosis of GCA. Corticosteroids are the cornerstone treatment of GCA. Studies using other drugs have yielded contradictory results.

Biopsy↗
PubMed2006

Lack of echocardiographic and Doppler abnormalities in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors.

OBJECTIVE: To assess the prevalence of echocardiographic and Doppler abnormalities in psoriatic arthritis (PsA) patients without clinically evident cardiovascular manifestations or classic atherosclerosis risk factors. METHODS: Fifty PsA patients were recruited from Hospital Xeral-Calde, Lugo, Spain. Patients seen during the period of recruitment that had classic cardiovascular risk factors or had suffered cardiovascular or cerebrovascular events were excluded. Fifty healthy matched controls were also studied. Echocardiographic and Doppler studies were performed in all cases and controls. RESULTS: In PsA patients the frequency of aortic and tricuspid (10%) and mitral regurgitation (16%) was not different from that seen in matched controls (10, 4, and 12%). Also, the pulmonary artery systolic pressure was normal in the group of PsA patients (23.4+/-3.9 mm Hg). The prevalence of diastolic dysfunction, in all cases due to impaired relaxation, was similar in PsA patients (28%) and controls (24%) (P=0.65). In addition, no significant echocardiographic and Doppler differences were observed when PsA patients with polyarticular pattern were compared with the remaining PsA patients. CONCLUSIONS: The present study shows that actively treated PsA patients without cardiovascular risk factors or clinically evident cardiovascular disease do not exhibit silent subclinical echocardiographic abnormalities.

Adult↗
PubMed2006

Giant cell arteritis and polymyalgia rheumatica: pathophysiology and management.

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common and often concurrent diseases in Western countries in individuals aged >50 years. Clinical features of GCA are mainly due to involvement of the cranial arteries. PMR is clinically characterised by pain, aching and morning stiffness involving the neck, shoulder and hip girdles. Both conditions are generally associated with elevation of erythrocyte sedimentation rate and C-reactive protein. A temporal artery biopsy is the gold standard test for the diagnosis of GCA. Some diseases may mimic PMR or present with polymyalgic symptoms. Corticosteroids are the cornerstone of the management of GCA and PMR. An initial dosage of prednisone 10-20 mg/day yields a dramatic improvement of PMR symptoms in most cases. In GCA, the initial prednisone dosage required is higher (40-60 mg/day). However, once established, visual loss, which is the most feared complication of GCA, does not usually improve following corticosteroid therapy. Some patients exhibit a chronic-relapsing course and may need low doses of corticosteroids for several years. Alternative corticosteroid-sparing therapies and some therapeutic agents aimed at restoring balanced bone cell activity in patients taking corticosteroids are potentially useful in the management of GCA and PMR.

Adrenal Cortex Hormones↗
PubMed2006

Lack of association of a functional -94ins/delATTG NFKB1 promoter polymorphism with susceptibility and clinical expression of biopsy-proven giant cell arteritis in northwest Spain.

OBJECTIVE: Giant cell arteritis (GCA) is a vasculitis preferentially involving large and middle-sized arteries in the elderly. The nuclear factor of k-light polypeptide gene enhancer in B cells (NF-kB) is a family of 5 proteins expressed in most cells that function to regulate gene transcription. NFKB1 gene plays a critical role in the coordination of the immune system by regulating the transcription of a broad variety of genes implicated in the immune response. A NFKB1 promoter polymorphism consisting of a common insertion/deletion (-94ins/delATTG) located between 2 putative key promoter regulatory elements and showing functional effects on the transcription of the NFKB1 gene has been described. Since GCA is a polygenic disease, we sought to assess the potential role of the -94ins/delATTG NFKB1 promoter polymorphism in susceptibility to GCA and to determine if this polymorphism is implicated in the clinical expression of this vasculitis. METHODS: Ninety-six patients with biopsy-proven GCA and 204 ethnically matched Caucasian controls from the Lugo region (Northwest Spain) were studied. Genotyping of the -94ins/delATTG NFKB1 promoter polymorphism was performed by fluorescent polymerase chain reaction (PCR). RESULTS: No significant differences in allele or genotype frequencies for this NFKB1 promoter polymorphism were observed between patients with GCA and controls even when patients were stratified according to gender, presence of polymyalgia rheumatica (n = 38), severe ischemic manifestations (n = 49), or other clinical manifestations of GCA. CONCLUSION: Our results do not support a role for -94ins/delATTG NFKB1 promoter polymorphism in susceptibility and clinical expression of GCA in a Northwestern Spanish population.

Aged↗