ABSTRACT
PURPOSE: The Western Ontario Shoulder Instability Index (WOSI) is the most commonly used patient-reported outcome measure to record the quality of life in patients with shoulder instability. The current study aimed to translate the WOSI into the Persian language and evaluate its psychometric properties. METHODS: The translation procedure of the WOSI was performed according to a standard guideline. A total of 52 patients were included in the study and responded to the Persian WOSI, Oxford shoulder score (OSS), Oxford shoulder instability score (OSIS), and disabilities of arm, shoulder and hand (DASH). A sub-group of 41 patients responded for the second time to the Persian WOSI after an interval of 1-2 weeks. The internal consistency, test-retest reliability using intraclass correlation coefficient (ICC), measurement error, minimal detectable change (MDC), and floor and ceiling effect were analyzed. The hypothesis testing method was used to assess construct validity by calculating Pearson correlation coefficient between WOSI and DASH, OSS, and OSIS. RESULTS: Cronbach's alpha value was 0.93, showing strong internal consistency. Test-retest reliability was good to excellent (ICC = 0.90). There was no floor and ceiling effect. The standard error of measurement and MDC were 8.30% and 23.03%, respectively. Regarding construct validity, 83.3% of the results agreed with hypotheses. High correlations were observed between WOSI and DASH, OSS and OSIS (0.746, 0.759 and 0.643, respectively) indicating excellent validity for the Persian WOSI. CONCLUSION: The current study results demonstrated that the Persian WOSI is a valid and reliable instrument and can be used in the clinic and research for Persian-speaking patients with shoulder instability.
Subject(s)
Joint Instability , Shoulder Joint , Humans , Shoulder , Cross-Cultural Comparison , Joint Instability/diagnosis , Ontario , Quality of Life , Reproducibility of Results , LanguageABSTRACT
Background: Activated protein C (APC) inactivates factor V (FV) by cleavage of its heavy chain at Arg306, Arg506, Arg679, and Lys994. Mutational changes, which abolish APC cleavage sites, may predispose thrombosis by altering the inactivation process of FV. FV Leiden (FVL) (Arg506Glu) has been demonstrated as a strong risk factor for thrombosis. In the current study, we have studied whether mutations in the cleavage sites of FV for APC, not due to FVL, would have a role in presenting APC resistance (APCR) and initiation of a cerebral thrombotic event. Methods: A group of 22 patients with a history of cerebral venous thrombosis (CVT), who were not carriers of FVL enrolled in the study. The patients who had conditions associated with acquired APCR were excluded from the study. APCR test was performed on the remaining 16 patients, which showed APCR in 4 plasma samples. DNA sequencing was performed on four exons of FV of APCR patients, encoding Arg306, Arg506, Arg679, and Lys994. Results: Mutations were not found within nucleotides encoding the cleavage sites; neither was found within their close upstream and downstream sequences. Conclusion: Our results show that polymorphisms affecting cleavage sites of FV other than Arg506Glu it would be less likely to be the basis for APCR and its increased thrombosis susceptibility. In addition, it emphasizes on the importance of screening for APCR in the patients diagnosed with CVT.
ABSTRACT
BACKGROUND: Factor V G1691A (FV Leiden), FII GA20210, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations are the most common genetic risk factors for thromboembolism in the Western countries. However, there is rare data in Iran about cerebral venous and sinus thrombosis (CVST) patients. The aim of this study was to evaluate the frequency of common genetic thrombophilic factors in CVST patients. MATERIALS AND METHODS: Forty consequently CVST patients from two University Hospital in Isfahan University of Medical Sciences aged more than 15 years from January 2009 to January 2011 were recruited. In parallel, 51 healthy subjects with the same age and race from similar population selected as controls. FV Leiden, FII GA20210, MTHFR C677T, and FV Cambridge gene mutations by polymerase chain reaction technique were evaluated in case and control groups. RESULTS: FV Leiden, FII GA20210, and FV Cambridge gene mutations had very low prevalence in both case (5%, 2%, 0%) and control (2.5%, 0%, 0%) and were not found any significant difference between groups. MTHFR C677T mutations was in 22 (55%) of patients in case group and 18 (35.5%) of control group (P = 0.09). CONCLUSION: This study showed that the prevalence of FV Leiden, FII GA20210, and FV Cambridge were low. Laboratory investigations of these mutations as a routine test for all patients with CVST may not be cost benefit.
ABSTRACT
BACKGROUND: Different risk factors have been suggested for ischemic stroke in young adults. In a group of these patients despite of extensive diagnostic work-up, the primary cause remains unknown. Coagulation tendency is accounted as a possible cause in these patients. Previous studies on factor V Leiden (FVL) as the main cause of inherited thrombophilia for clarifying the role of FVL in stroke have resulted in controversial findings. The current study investigates the role of this factor in ischemic stroke among Iranians. MATERIALS AND METHODS: This case-control study was performed between September 2007 and December 2008 in Isfahan, Iran. The case group comprised of 22 patients of which 15 were males and 7 were females with age range of ≤50 years, diagnosed as ischemic stroke without classic risk factors and the control group consisted of 54 healthy young adults. After filling consent form, venous blood samples were obtained and sent to the laboratory for genetic examination. RESULTS: No FVL mutation was found in the case group. There was one carrier of the mutation as heterozygous in the control group (relative frequency = 1.85%). CONCLUSIONS: Based on our study, FVL might not be considered as an independent risk factor for ischemic stroke in Iranian individuals who are not suffering from other risk factors of ischemic stroke.
