Kemal Üreten

Validation of the Turkish Version of the Oswestry Disability Index for Patients With Low Back Pain

Study Design. Validation of a translated, culturally adapted questionnaire. Objectives. To translate and culturally adapt the Turkish version of the Oswestry Disability Index (ODI) (2.0), and to validate its use for assessing disability in Turkish patients with low back pain. Summary of Background Data. The ODI is a reliable evaluation instrument for disability, but no validated Turkish version is available. Methods. A total of 95 outpatients with low back pain were assessed by the ODI. Sixty-five of these patients were observed on a second occasion. Translation/retranslation of the English version of the ODI was done blindly and independently by four different individuals, and adapted by a team. Individuals were given the ODI and other scales (Visual Analog Scale, Schober Test, and the Roland-Morris Disability Questionnaire) on their first visit and a week later. Results. Scores of the two ODIs were 27.10 (SD 16.22) on day 1 and 22.88 (SD 13.94) on day 7, with an intraclass correlation coefficient of r = 0.938 (P < 0.001). Cronbach’s alpha was 0.918 (day 1) and 0.895 (day 7) in the validation. Concurrent validity, measured by comparing ODI responses with the results of Visual Analog Scale and Schober test, was r = 0.367 (P < 0.01), r = −0.068 (P = 0.591) for day 1, and r = 0.392 (P < 0.01), r = −0.041 (P = 0.745) for day 7, respectively. Construct validity, tested by determining the correlation between the Turkish ODI and the Turkish adaptation of the Roland-Morris Disability Questionnaire, yielded r = 0.815 (P < 0.001) on day 1 and r = 0.708 (P < 0.001) on day 7. Conclusion. 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.

Frequency of Lymphadenopathy in Rheumatoid Arthritis and Systemic Lupus Erythematosus

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.

Assessment of Atrial Conduction in Patients with Scleroderma by Tissue Doppler Echocardiography and P Wave Dispersion

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.

Transverse myelitis in a patient with Behcet’s disease: favorable outcome with a combination of interferon-α

We report here on a 24-year-old patient with Behçet’s disease who had been diagnosed with acute transverse myelitis. He was successfully treated with a combination regimen of a steroids, cyclophosphamide, and interferon-α. The treatment strategy with specific emphasis on interferon-α is discussed in the light of the pertinent literature.

Angiotensin-converting enzyme gene polymorphism in Behçet’s disease

Endothelial cell activation and/or injury is a characteristic feature of Behçet’s disease (BD). The local renin–angiotensin system (RAS) in the vessel wall plays a prominent role in the endothelial control of vascular tonus and contributes to inflammatory processes. Angiotensin-converting enzyme (ACE) is the regulatory component of the RAS. In this study, we investigated the distribution of different alleles of the ACE gene in patients with BD, and the influence of the I/D polymorphism on different clinical manifestations of the disease. A cohort of 90 patients with BD were evaluated for their ACE genotype (male/female: 49/41, mean age: 36.9±10.6 years, min/max: 16–66 years). The mean duration of symptoms was 9.5±6.9 years (min/max: 1–35 years). The control population was composed of 30 healthy subjects (male/female: 15/15, mean age: 31.2±7.1 years, min/max: 20–45). The distribution of DD, ID and II genotypes of the ACE gene was 22 (24.5%), 56 (62.2%) and 12 (13.3%) for patients with BD, and 9 (30%), 16 (53.3%) and 5 (16.7%) for healthy controls, respectively. There was no significant difference between the groups (p>0.05). Similarly, there was no significant association between the ACE gene polymorphism and ocular, neurologic or vascular involvement of BD. The ACE gene polymorphism does not seem to play a role in the pathogenesis of BD. Moreover, possession of either the D or the I allele does not have an impact on the development of ocular, neurologic or vascular manifestations of the disease.

Hypokalemic periodic paralysis in Sjogren’s syndrome secondary to distal renal tubular acidosis

We report a 53-year-old Turkish female presented with progressive weakness and mild dyspnea. Laboratory results demonstrated severe hypokalemia with hyperchloremic metabolic acidosis. The urinary anion gap was positive in the presence of acidemia, thus she was diagnosed with hypokalemic paralysis from a severe distal renal tubular acidosis (RTA). Immunologic work-up showed a strongly positive ANA of 1:3,200 and positive antibodies to SSA and SSB. Schirmer’s test was abnormal. Autoimmune and other tests revealed Sjögren syndrome as the underlying cause of the distal renal tubular acidosis. Renal involvement in Sjogren’s syndrome (SS) is not uncommon and may precede sicca complaints. The pathology in most cases is a tubulointerstitial nephritis causing among other things, distal RTA, and, rarely, hypokalemic paralysis. Treatment consists of potassium repletion, alkali therapy, and corticosteroids. Primary SS could be a differential in women with acute weakness and hypokalemia.

Assessment of aortic wall stiffness in patients with Familial Mediterranean Fever

INTRODUCTION To evaluate aortic wall stiffness and its relation between the aortic stiffness and the left ventricular function in patients with Familial Mediterranean Fever (FMF). METHODS The study population was composed of 31 patients with FMF in attack-free period (12 men, 19 women; mean age: 36+/-7 years) and 27 healthy subjects (10 men, 17 women; mean age: 34+/-7 years) who had volunteered to participate. Aortic stiffness indices, aortic strain and distensibility, were calculated from the aortic diameters measured by echocardiography and blood pressure obtained by sphygmomanometry. RESULTS There were significant differences between the control and the patient group in aortic strain (mean (SD), 7.23+/-2.14 versus 4.91+/-1.66%, p=0.01) and distensibility (4.02+/-1.42 versus 2.84+/-1.46, 10(-6)cm(2)dyn(-1), p=0.001). Although there was no correlation between the aortic stiffness parameters and the left ventricular function parameters, there were significant negative correlations between the disease duration and aortic strain index (r=-0.29, p<0.001), and between the disease duration and distensibility (r=-0.32, p<0.001). CONCLUSION Aortic stiffness measurements were found abnormal in patients with FMF. We have also demonstrated that there were significant correlations between aortic stiffness parameters and disease duration.

Decreased Protein Z Concentrations Complicating the Hypercoagulable State of Behqet's Disease

Protein Z is a vitamin-K-dependent plasma protein that serves as a cofactor for the inhibition of factor Xa. Although the precise physiologic function of protein Z is still unknown, abnornal plasma protein Z concentrations have been associated with a number of thrombotic disease states. There is the evidence of universal activation of the hemostatic system in Behqets disease (BD), which represents a hypercoagulable/prothrombotic state. Circulating protein Z levels in patients with BD were evaluated. Plasma protein Z concentrations were assayed in 24 patients with BD (male/female: 13/11, mean age 35.4 years) and in 24 healthy controls (males/females: 14/10, mean age 59.8 years). The disease duration was 10.6 years (range, 1-30 years). None of the subjects in either group had received anticoagulants within 3 weeks before the study, and none of them had liver dysfunction. Patients complicated with vascular disease were also excluded from the study. Mean plasma concentrations of protein Z were 141 ng/mL (range, 56.8-257) in healthy controls and 107.8 ng/mL (range, 21.2-202) in BD patients (p<0.05). There was a positive correlation between the disease duration and protein Z levels in the study group (p<0.05, r=0.448). Alterations of protein Z concentrations could complicate the pathobiology of the prothrombotic state of BD. Furthermore, the tendency of increment in the protein Z with the passage of time may reflect the diminution of the disease activity.

Osteopoikilosis in a patient with rheumatoid arthritis complicated with dry eyes

Osteopoikilosis is an uncommon sclerosing bone dysplasia of unknown etiology. It is usually detected as a coincidental finding at radiographic examination. Mild joint pain and swelling may be seen in 15–20% of cases. Osteopoikilosis is rarely associated with rheumatoid arthritis. In this case report a young man with osteopoikilosis who was diagnosed as having rheumatoid arthritis complicated with dry eyes is presented. Although patients with osteopoikilosis may have articular symptoms, those patients should be carefully examined for a possible association with a rheumatic condition.

Severe Arterial Thrombophilia Associated With a Homozygous MTHFR Gene Mutation (A1298C) in a Young Man With Klinefelter Syndrome

Klinefelter syndrome (KS) is the most common sex chromosome disorder in men. It may be associated with an increased risk for venous thrombosis and thromboembolism, which is partially explained by hypofibrinolysis due to androgen deficiency. Additional genetic or acquired thrombophilic states have been shown in KS patients complicated with venous thrombosis as isolated case reports. Arterial thrombotic events had not been previously reported in KS. In this study, a young man with KS who developed acute arterial thrombosis during testosterone replacement therapy is presented. He was homozygous for the A1298C mutation of the methylenetetrahydrofolate reductase (MTHFR) gene.