The Turkish version of ODI has good comprehensibility, internal consistency, and validity and is an adequate and useful instrument for the assessment of disability in patients with low back pain.
Heart type fatty acid binding protein (H-FABP) is a major cytoplasmic low-molecular weight protein and released into the circulation when the myocardium is injured. Previous studies have demonstrated that H-FABP is closely associated with acute coronary syndrome, hypertrophic and dilated cardiomyopathy, heart failure, stroke, obstructive sleep apnea syndrome, pulmonary embolism. The aim of this study was to investigate serum H-FABP value in the patients with metabolic syndrome (MetS). We measured serum H-FABP levels in 55 consecutive patients with MetS, and 73 age-matched control subjects by using a sandwich enzyme-linked immunosorbent assay. Serum H-FABP levels were significantly higher in patients with MetS than in control subjects 18.37 ± 13.0 and 7.9 ± 6.5 ng/ml, respectively, (P < 0.001). Serum H-FABP levels were significantly higher in patients with diabetic MetS than in without diabetic MetS, 24.0 ± 10.2 and 13.9 ± 12.6 ng/ml, respectively, (P: 0,003). There were statistically significant differences between patients without diabetic MetS and control subjects, 13.8 ± 12.6 and 7.9 ± 6.5 ng/ml, respectively, (P = 0.023). Patients with MetS have an increased risk of death from cardiovascular diseases. H-FABP seems to be a marker that will enable the detection of cardiac injury in the early asymptomatic period in patients with MetS.
Clinical and genetic findings of familial Mediterranean fever (FMF) may be variable in different populations. Environmental factors may also affect phenotypic features of FMF. In this study, we investigated demographic, clinical and mutational features of FMF patients who were treated in a single reference hospital in Turkey. Two hundred and sixty patients (169 females, 91 males, mean age 30.44 +/- 10.29 years) were included in this study. All patients were evaluated regarding MEFV gene mutations. The mean age of disease onset was 17.21 +/- 8.66 years (range 2-40 years). The mean duration between the disease onset and diagnosis was 9.39 +/- 8.92 years. Seventy percent of patients had symptoms before 20 years of age (early onset FMF). Arthritis and erysipelas like erythema (ELE) were more common, and the mean duration between the disease onset and diagnosis was longer in early onset FMF patients. The frequency of attacks per year, and disease severity score (DSS) was higher in early onset patients. Homozygote mutation of M694V was detected in 37 (20.2%) and 4 (5.2%) patients in early onset FMF and adult onset FMF groups, respectively (p < 0.05). Histological diagnosis of amyloidosis was established in 7 patients (2.7%). The age of disease onset was earlier, and arthritis and ELE were more frequent, and DSS was higher in patients with M694V/M694V mutation. In conclusion, mean delay to diagnosis in our FMF population is quite high. Early and adult onset forms may differ regarding some clinical, molecular and prognostic characteristics. Disease activity was higher in patients with homozygote mutation of M694V.
This study aimed to assess the frequency of all palpable lymph nodes during active disease and remission in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Hospital records of 100 SLE patients, 100 RA patients, 100 spondyloarthropathy patients, and 150 osteoarthritis patients, treated in our rheumatology department, were evaluated retrospectively. Overall frequencies of enlarged lymph nodes in patients with active RA and SLE were 82% and 69%, respectively. Enlarged lymph nodes associated with RA were mostly located in the axillary region, and in SLE the nodes were smaller and lymphadenopathy was more generalized compared with RA. Palpable lymph nodes disappeared in the majority of patients during remission. Lymphadenopathy was significantly less frequent in patients treated with steroids before admission. Lymph node enlargement is an important physical finding associated with RA and SLE disease activity. Atypical locations and unusually large lymph nodes should raise clinical suspicion of another underlying disease.
Background: Atrial conduction abnormalities in patients with scleroderma have not been evaluated in terms of P wave duration, P wave dispersion (Pd) and electromechanical coupling measured by tissue Doppler echocardiography. Methods: Twenty-four patients with scleroderma and 24 control subjects underwent resting electrocardiogram (ECG), M mode and tissue Doppler echocardiography. The P wave duration was calculated in all leads of the surface ECG. The difference between the maximum (Pmax) and minimum P wave duration was calculated and defined as Pd. Interatrial and intraatrial electromechanical delays were measured with tissue Doppler tissue echocardiography. Results: The left ventricular dimensions, fractional shortening, and left atrial diameter did not differ between the patients and the controls. Pd and Pmax were significantly higher in patients with scleroderma compared with controls: 51 ± 17 versus 28 ± 7 ms (p < 0.01) and 109 ± 10 versus 93 ± 6 ms (p < 0.01), respectively. There was a delay between the onset of the P wave on surface ECG and the onset of the late diastolic wave (A wave; PA) obtained by tissue Doppler echocardiography in patients with scleroderma compared with controls measured at lateral septal annulus (lateral PA; 122 ± 8 vs. 105 ± 7 ms, p = 0.001), septal mitral annulus (104 ± 11 vs. 93 ± 10 ms, p = 0.01) and tricuspid annulus (right ventricular PA; 71 ± 9 vs. 64 ± 7 ms, p = 0.05). Interatrial conduction time (lateral PA – right ventricular PA) was delayed in patients with scleroderma compared with controls (88 ± 13 vs. 76 ± 11 ms, p = 0.01). A positive correlation was detected between interatrial electromechanical delay (lateral PA – right ventricular PA) and Pd (r = 0.5, p = 0.03). Conclusion: Atrial conduction abnormalities as estimated with Pd and Pmax are significantly higher in patients with scleroderma compared with controls. There is a delay in both intraatrial and interatrial electromechanical coupling intervals in patients with scleroderma.
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