Objectives: This study aims to investigate the relationship between subclinical carotid atherosclerosis and vitamin D deficiency in Egyptian ankylosing spondylitis (AS) patients and their impact on disease activity. Patients and methods: This cross-sectional study included 40 AS patients (36 males, 4 females; mean age 45.9±8.4 years; range 33 to 55 years) diagnosed according to the 1984 modified New York criteria with equal number of healthy controls (26 males, 14 females; mean age 48.4±7.8 years; range 31 to 55 years). Patients' histories were taken and clinical examinations were performed. Disease activity was assessed with Bath AS metrology index (BASMI), Bath AS disease activity index (BASDAI), and Bath AS functional index (BASFI) scores. Laboratory evaluation included lipid profile and 25-hydroxyvitamin D [25(OH)D] was determined by enzyme-linked immunosorbent assay. Bilateral carotid intima-media thickness (CIMT) was measured by a high-resolution ultrasound with linear 7-12 MHz transducer. Average of CIMT of right and left common carotid arteries was used. Results: Statistically significant differences were found between patients and controls in terms of CIMT (p<0.001), 25(OH)D3 (p<0.001) and triglycerides (p=0.02). A significant positive correlation was present between CIMT and disease duration (r=0.74), disease activity scores [BASFI (r=0.60), BASMI (r=0.49), BASDAI (r=0.65)] and lipid profile except for high-density lipoprotein (HDL) that had a negative correlation (r=-0.52). A significant negative correlation was present between 25(OH)D3 levels and CIMT (r=-0.38) and lipid profile except for HDL having a positive correlation (r=0.40). Conclusion: Prevalence of subclinical carotid atherosclerosis in AS patients compared to the healthy population was associated with high disease activity and functional limitations. In AS patients, 25(OH)D3 deficiency is a risk factor for accelerated atherosclerosis.
Background: Brain atrophy measurement is now a cornerstone in basic neuro-imaging science. While assessment of white matter atrophy by visual inspection is subjective, volumetric approaches are time-consuming and not often feasible. Bi-caudate ratio represents a linear surrogate parameter of brain volume that can be derived from standard imaging sequences. This study highlights the value of the bi-caudate ratio (BCR) as a MRI marker of white matter atrophy in patients with multiple sclerosis and ischemic leukoencephalopathy and set a cut-off value to differentiate between patients with white matter atrophy and normal subjects. Results: A total of 115 patients (54 males and 61 females) diagnosed with white matter leukoencephalopathy (MS in 51 patients and ischemic leukoencephalopathy in 64 patients) were included. Another group of 60 subjects with a normal white matter signal was recruited as a control group. BCR for the patient group ranged from 0.13 to 0.27 (mean (± SD) = 0.16 ± 0.02), while for the control group, it ranged from 0.05 mm to 0.13 (mean (± SD) = 0.09 ± 0.01). The difference between the two groups was statistically significant (P value < 0.001). A cut-off value of 0.13 was used to differentiate between the BCR in both patients and control groups with sensitivity, specificity, and accuracy of 99.2%, 100%, and 99%, respectively. The difference in BCR for patients diagnosed with MS and ischemic leukoencephalopathy was also statistically significant (P value < 0.001). Conclusion: The bi-caudate ratio represents a linear measurement of subcortical atrophy that can be useful as a surrogate marker of global supra-tentorial white matter atrophy instead of the usually performed visual and therefore subjective assessment. It is an easily obtained measure that can be performed without complex time-consuming volumetric studies. Our findings also revealed that the BCR is higher in patients with ischemic leukoencephalopathy than in patients with MS.
Background Osteoarthritis (OA) of the knee joint is a common cause of chronic disability in older adults. During the past 10 years, the infrapatellar fat pad (IPFP) has emerged as a new player in the pathogenesis of knee OA. Its exact role in the pathogenesis of knee OA remains uncertain. While many studies focused on the detrimental effect of the chemical mediators released by IPFP and their role in the accentuation of the development of OA, only few studies elucidated the beneficial effect of IPFP maximal area as a local shock absorber protecting the adjacent articular structures from progressive damage. The aim of this study was to evaluate the relation between the IPFP maximal area and the prevalence of OA manifestations. We also studied the relation between the subcutaneous (SC) fat thicknesses on the medial aspect of the knee as a surrogate marker of body obesity and the IPFP area. Results A total of 216 knee scans for 188 adult patients (64 males and 124 females) who met the inclusion criteria were examined. They were between 45 and 66 years (mean 52.5 years). The mean IPFP area for all patients was 6.9 cm2 (± 1.6 SD) (ranged from 4.5 to 11 cm2). After adjustment for potential confounders, there was a significant negative association between IPFP area and radiographic manifestations of OA (osteophites, joint space narrowing, and grade of OA) (P value < 0.001 for each), as well as MRI manifestations of OA (cartilage defects and subchondral bone marrow lesions) (P value < 0.001 and < 0.003, respectively). There was a negative but non-significant association between IPFP area and SC fat thickness. Conclusion In our study, we found supportive evidence that IPFP maximal area is associated with fewer osteoarthritic knee changes and less cartilage damage, suggesting that it plays a protective role against the development and progression of OA. Further large-scale clinical studies are awaited to confirm the obtained results. Based on our findings, it would be recommended to avoid IPFP resection during surgery in order to maintain its protective effect.
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