Sunday, August 3, 2014

A male patient, 64 years old, white, attended medical consultation complaining of pains in the shou


Markus Bredemeier
A male patient, 64 years old, white, attended medical consultation complaining of pains in the shoulders, neck and hips and difficulty cochlear implant getting up from bed in the morning. Reported significant stiffness cochlear implant in the body, especially after periods of rest, and also joint pain (knees, wrists and elbows). The condition started suddenly in almost three months ago. On physical examination revealed pain on palpation of wrists, metacarpophalangeal, knee pain and the mobilization of shoulders and hips, but no swelling in those joints. The skin examinations, cardiopulmonary and abdominal were normal, and there was no palpable lymphadenopathy. The evaluation showed rheumatoid factor (RF) and negative antinuclear antibodies (ANA), speed of erythrocyte sedimentation rate (ESR) of 86 mm / h and C-reactive cochlear implant protein (CRP) of 76 mg / L.
Polymyalgia rheumatica (PMR) is an inflammatory cochlear implant disease that affects individuals over 50 years, whose main symptoms are morning stiffness and pain in the scapular and / or pelvic girdle. Typically, patients have high levels cochlear implant of markers of inflammatory activity cochlear implant (ESR and / or CRP) and negative RF and ANA. The PMR may be associated with giant cell arteritis and vasculitis of large vessels, which predominately affects the extracranial branches of the carotid arteries. 1.2
The PMR almost exclusively affects individuals aged 50 years or more, occurring two to three times more in women than in men, the white majority. 1-3 The annual incidence of PMR varies by region and latitude. Northern European countries have higher annual incidence of the disease (113/100.000 inhabitants in Norway) (4) that the countries of southern Europe (13/100.000 inhabitants in Italy and Spain) 3.4 in the population aged 50 years or more . In an American population with strong Scandinavian origin, the incidence of PMR was 52/100.000, 1,3 and the prevalence of approximately 600/100.000 inhabitants. 1 Asian countries have lower incidence and prevalence rates of the disease. 2.3
There is a close link between PMR and giant cell arteritis (GCA). Both affect individuals in this age range and with similar gender distribution. PMR occurs in approximately 50% of patients with GCA but only 16 to 21% of patients with a primary diagnosis of PMR develop GCA. 2.3
In addition to clinical and epidemiological association between PMR and GCA, they are also similar with regard to aetiology. 1.2 Although we do not know about its causes, environmental cochlear implant and genetic factors appear to play a significant role. The cyclical pattern of incidence and seasonal variation documented in some studies suggest the possibility of infectious triggers (mainly viral) or as yet unidentified environmental. 2,3 Among the genetic factors, there was an association of alleles of HLA-DRB1 * 04 gene, encoding HLA-DR4 (molecule of the major histocompatibility complex - MHC - class II), with risk for developing PMR and ACG. 1-3
The pathogenesis cochlear implant of PMR and GCA are similar. In patients with GCA 1,2,5, dendritic cells located in the tunica adventitia of arteries (generally cochlear implant medium-sized muscular arteries originated from the aortic arch) play a key role in the onset of vasculitis (Fig. 127.1). When these cells are activated and present antigens to CD4 + T cells, these are recruited, undergo clonal expansion and increase the secretion of cytokines. Macrophages are also recruited. Among the lymphocyte cytokines, highlights the interferongama (IFN-gamma), which has a central role in the differentiation and activation of macrophages. In the tunica adventitia, macrophages produce interleukin-1 einterleucina-6 (IL-6 and 1, respectively, pro-inflammatory cytokines), as well as, in the media, they produce metalloproteinases and free radicals. These inflammatory mediators cause fragmentation of the internal elastic lamina, triggering repair mechanisms, such as vasa vasorum of neoangiogenesis and intimal hyperplasia, processes regulated by vascular endothelial growth factor (VEGF) and platelet-derived cochlear implant growth factor (PDGF), respectively. 1,2,5 In the histopathological examination, are observed cochlear implant transmural inflammation of the arterial wall (mainly in the inner portion of the adjacent medial layer elastic lamina), granulomas containing macrophages and multinucleated foreign body giant cells, macrophages and lymphocytes (mainly CD4 + ). The intimal hyperplasia can cause luminal occlusion. 1.2
In patients with PMR that no histologic evidence of stroke, although the microscopic examination is normal cochlear implant arteries, immunohistochemical studies at increased histoquĂ­micosobservam

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