Multiple sclerosis versus cerebral small vessel disease in MRI: a practical approach using qualitative and quantitative signal intensity differences in white matter lesions.

BACKGROUND: Multiple sclerosis (MS) and cerebral small vessel disease (CSVD) are relatively common radiological entities that occasionally necessitate differential diagnosis. PURPOSE: To investigate the differences in magnetic resonance imaging (MRI) signal intensity (SI) between MS and CSVD related white matter lesions. MATERIAL AND METHODS: On 1.5-T and 3-T MRI scanners, 50 patients with MS (380 lesions) and 50 patients with CSVD (395 lesions) were retrospectively evaluated. Visual inspection was used to conduct qualitative analysis on diffusion-weighted imaging (DWI)_b1000 to determine relative signal intensity. The thalamus served as the reference for quantitative analysis based on SI ratio (SIR). The statistical analysis utilized univariable and multivariable methods. There were analyses of patient and lesion datasets. On a dataset restricted by age (30-50 years), additional evaluations, including unsupervised fuzzy c-means clustering, were performed. RESULTS: Using both quantitative and qualitative features, the optimal model achieved a 100% accuracy, sensitivity, and specificity with an area under the curve (AUC) of 1 in patient-wise analysis. With an AUC of 0.984, the best model achieved a 94% accuracy, sensitivity, and specificity when using only quantitative features. The model's accuracy, sensitivity, and specificity were 91.9%, 84.6%, and 95.8%, respectively, when using the age-restricted dataset. Independent predictors were T2_SIR_max (optimal cutoff=2.1) and DWI_b1000_SIR_mean (optimal cutoff=1.1). Clustering also performed well with an accuracy, sensitivity, and specificity of 86.5%, 70.6%, and 100%, respectively, in the age-restricted dataset. CONCLUSION: SI characteristics derived from DWI_b1000 and T2-weighted-based MRI demonstrate excellent performance in differentiating white matter lesions caused by MS and CSVD.

Investigation of anti-galectin-8 levels in patients with multiple sclerosis: A consort-clinical study.

BACKGROUND: Galectins are a family of endogenous mammalian lectins involved in pathogen recognition, killing, and facilitating the entry of microbial pathogens and parasites into the host. They are the intermediators that decipher glycan-containing information about the host immune cells and microbial structures to modulate signaling events that cause cellular proliferation, chemotaxis, cytokine secretion, and cell-to-cell communication. They have subgroups that take place in different roles in the immune system. The effect of galectin-8 on multiple sclerosis disease (MS) has been studied in the literature, but the results seemed unclear. In this study, we aimed to determine anti-galectin-8 (anti-Gal-8) levels in MS and their potential use as biomarkers. METHODS: In this experimental study, 45 MS patients diagnosed according to McDonald criteria were included in the patient group. The healthy control group contained 45 people without MS diagnosis and any risk factors. Demographic data, height, weight, body mass index, blood glucose, thyroid-stimulating hormone, alanine transaminase, aspartate transaminase, creatinine, low-density lipoprotein, anti-Gal-8 levels, the prevalence of hypertension, diabetes mellitus and coronary artery disease were recorded. In addition, the expanded disability status scale and disease duration were evaluated in the patient group. Data were presented as mean ±â€…standard deviations. RESULTS: The mean blood anti-galectin-8 value of the patient group was 4.84 ±â€…4.53 ng/mL, while it was 4.67 ±â€…3.40 ng/mL in the control group, and the difference in these values was found statistically insignificant (P > .05). Moreover, body mass index, glucose, alanine transaminase, aspartate transaminase, thyroid-stimulating hormone, and low-density lipoprotein levels were also statistically insignificant (P > .05). CONCLUSION: This study examined anti-Gal-8 levels in MS patients. The relationship between MS and galectin-8 and anti-Gal-8 levels in patients needs further clarification. As a result, the study's results could help elucidate the pathogenesis of MS and give more evidence for diagnosis.

Comparison of Serum Mitochondrial Open Reading Frame of the 12S rRNA-c (MOTS-c) Levels in Patients With Multiple Sclerosis and Healthy Controls.

Background Multiple sclerosis (MS) is a major global problem, and as its pathogenesis is understood more clearly, therapeutic options expand accordingly. The mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) is a novel mitochondria-derived protein acting on metabolic homeostasis. In this study, we aimed to investigate the role of serum MOTS-c in the pathophysiology of the disease in MS patients and to discuss the mechanism of MOTS-c. Methodology In total, 43 patients diagnosed with relapsing-remitting MS and 41 healthy controls were enrolled in the study. MOTS-c, fasting blood glucose, insulin, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), lipid panel, and body mass index levels were assessed. Results The participants' MOTS-c levels remained significantly lower than that of the control group, while their fasting blood glucose and HOMA-IR values were higher. The multivariate logistic regression analysis established that increased MOTS-c levels could be a protective factor against the development of MS disease. The area under the receiver operating characteristic curve for MOTS-c was calculated as 0.782 (95% confidence interval = 0.684-0.879, p = 0.0001). Conclusions This study is the first to scrutinize MOTS-c levels in MS patients. We tried to provide clinical evidence that MOTS-c could act as a highly discriminative biomarker between MS patients and control groups, which may hold great promise for future therapeutic options.

Investigation of blood leptin and adropin levels in patients with multiple sclerosis: A CONSORT-clinical study.

BACKGROUND: The effects of adipokines have been investigated in multiple sclerosis (MS) in the literature. Results are uncertain, and subgroups like adropin have not been previously studied. We primarily aimed to determine leptin and adropin levels in MS and their potential use as a biomarker. METHODS: This study was an experimental research. While 44 MS patients diagnosed according to McDonald criteria were included in the patient group, 40 people without MS diagnosis and risk factors took part in the control group. Demographic data, height, weight, body mass index, blood glucose, thyroid-stimulating hormone, alanine transaminase, aspartate transaminase, creatinine, low-density lipoprotein, leptin, adropin levels, presence of hypertension, diabetes mellitus, coronary artery disease were recorded. Expanded disability status scale and disease duration were also evaluated in the patient group. Our data were presented as mean ±â€Šstandard deviations. RESULTS: The mean blood leptin value of the patient group (6.12 ±â€Š5.34 ng/mL) was significantly lower than the value of the control group (13.02 ±â€Š8.25 ng/mL) (P < .001). The patient group had a mean adropin level of 504.12 ±â€Š311.17 ng/mL, which was significantly lower than that of the control group (747.0 ±â€Š309.42 ng/mL) (P < .001). Statistically insignificant differences were found between their body mass index, glucose, alanine transaminase, aspartate transaminase, thyroid-stimulating hormone, low-density lipoprotein levels (P > .001). CONCLUSION: This is the first study that has evaluated adropin levels in patients with MS. The relationship between MS and leptin levels is still unclear. Therefore, our study might be helpful to elucidate MS pathogenesis and provide supportive criteria for diagnosis.