2 research outputs found

    EARLY DIAGNOSIS OF GIANT CELL ARTERITIS ā€“ DOES IT MATTER?

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    Purpose: If untreated, giant cell arteritis can lead to blindness and stroke. The study objectives were to assess diagnostic procedures and treatment in early interventional clinic in University Clinical Centre Maribor in patients with temporal arteritis. Methods: Retrospective study (from 2012 to 2017) of patients diagnosed with temporal arteritis. We assessed epidemiological data, delay of diagnosis, and diagnostic procedures. Results were assessed with statistical methods (SPSS 22.0). The main goal was to determinate the delay in days between symptom onset and admission to the interventional rheumatology clinic and to assess the causes of delay. Results: Fift y-three GCA (66 % female) patients with mean age 76.25 (from 63 ā€“ 89 years) years were included. Mean time duration of symptoms before admission to our early interventional clinic was 33.74 (0ā€“180) days. The diagnostic procedure was completed in mean time of 2.04 days from the presentation at our interventional rheumatology clinic. Th e median time to the temporal artery biopsy (TAB) performed in 52 /53 patients was 2 days, with the median 2 days to the preliminary histological results from admission. TAB was positive in 43 (81.1%) of cases. The median time from admittance to colour Doppler sonography (CDS) of aortic arch branches was 2 days and it was positive in all 19 (35.8%) performed cases. 16 (30.2%) patients had polymyalgia rheumatica, 35 (66%) patients had visual disturbances, permanent one eye blindness occurred in 12 (22.64%) patients, and 2 (2.8%) patients experienced permanent blindness on both eyes. Seventeen patients (32.1%) were initially treated with intravenous methylprednisolone pulse. Th e mean initial dose of oral methylprednisolone was 45.55 (+/ā€“ 15.54) mg. All patients received low dose Aspirin. Conclusions: Early diagnosis and treatment of giant cell arteritis are very important as miss- or non-diagnose GCA can lead to permanent blindness of the patient. With better education and public awareness, better access and better professional education of primary care physicians, and early admission to secondary interventional clinics we might spare these patients from the devastating consequences of the GCA

    Accelerated Atherosclerosis in Rheumatoid Arthritis Patients and the Importance of Metalloproteinases and New Biochemical Markers

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    Bolniki z revmatoidnim artritisom (RA) imajo krajŔo pričakovano življenjsko dobo, glavni vzrok smrti predstavljajo srčno-žilna obolenja. Povečanega tveganja ni mogoče pojasniti zgolj s klasičnimi dejavniki tveganja (debelost, poviŔan krvni tlak, hiperlipidemija, kajenje). Vedno več je dokazov, da bi lahko kronično vnetje povečevalo tveganje za srčno žilna obolenja. V naŔi prospektivni raziskavi smo 15 let opazovali 70 bolnic z RA in 40 zdravih kontrol, brez klasičnih dejavnikov tveganja, ob vključitvi so bile vse premenopavzalne. Spremljali smo klasične dejavnike tveganja, vnetne pokazatelje (sedimentacijo, C reaktivni protein), citokine (interlevkin-6 (IL-6), tumorje nekrotizirajoči faktor alfa (TNF alfa)) in adhezijske molekule (ICAM in VCAM). Prisotnost aterosklerotičnega procesa smo ocenjevali z ultrazvočno preiskavo karotidnih arterij. Preiskovanke z RA so imele enako debelino intimo medije kot zdrave kontrole, potrdili pa smo statistično viŔje Ŕtevilo plakov pri bolnicah z RA, kot pri zdravih kontrolah. Med skupinama ni bilo razlik v primerjavi klasičnih dejavnikov tveganja, potrdili smo statistično pomembne razlike v neklasičnih dejavnikov tveganja. Rezultati podpirajo teorijo vnetja kot dejavnika tveganja za pospeŔeno aterosklerozo pri bolnicah z RA.Patients with rheumatoid arthritis (RA) have a lower life expectancy, with cardiovascular disease being the leading cause of death. The increased risk cannot be explained only by traditional risk factors (obesity, high blood pressure, hyperlipidemia, smoking). There is growing evidence that chronic inflammation may increase the risk of cardiovascular disease. In our prospective research, we followed 15 RA patients and 40 healthy controls for 15 yearsat the time of enrollment all participants were premenopausal. Traditional risk factors, inflammatory markers (sedimentation (ESR), C-reactive protein), cytokines (interleukin 6 (IL-6)), tumor necrosis factor alpha (TNF-alpha) and adhesion molecules (ICAM and VCAM) were monitored. The results of a carotid artery ultrasound scan were used to detect the presence of atherosclerotic process. Subjects with RA had the same intima-media thickness as healthy controlshowever, we found that RA patients had a statistically larger number of plaques compared to healthy controls. Although there were no differences between the groups when it came to traditional risk factors, we did find statistically significant variations in non-traditional risk factors. The findings support the theory that inflammation is a risk factor for accelerated atherosclerosis in RA patients
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