Against common belief, syncope can occur in sitting as well as in supine position. Emotional triggers were commoner in patients with syncope in supine and sitting positions while prodromal symptoms and circumstances were similar for all positions. Syncope should be considered in body positions other than standing.
In this cohort the percentage of new remission rates per year steadily declined after the first year. Ocular myasthenia had lesser clinical worsening episodes and high chance of complete stable remission. Generalized disease had less chance drug free remission. The risk of episodes of worsening persisted at a steady rate over a period of time, being maximum in the first year. The risk of exacerbations was unpredictable and could occur after prolonged clinical quiescence, often was related to reduction of immunosuppression. The disease course did not differ significantly in the juvenile and adult age-groups. There was a strong case for permanent immunomodulation in MG.
Objective: Alzheimer's disease (AD) is characterised by progressive cognitive decline due to neurodegeneration. Over activation of the hypothalamic–pituitary–adrenal axis, oxidative stress and inflammation potentially damage the neuronal system, affecting cognition. Aim: This study aimed to assess the relationship between serum cortisol, Interleukin-6 (IL-6) and homocysteine (Hcy) levels in AD. Methods: Case-Control observational study consisting of 71 patients with AD and 70 healthy controls above 60 years of age. Serum samples were analysed for cortisol, IL-6 and Hcy levels using chemiluminescence immunoassay (Immulite 1000) technique. Cognitive functions were measured using the Mini-Mental State Examination (MMSE) Score. AD subjects were categorised based on the modified Kuppuswamy socioeconomic status scale. Statistical evaluation was conducted using SPSS Statistics software. Group data were analysed using a two-tailed Student's t-test, analysis of variance (ANOVA), the Mann–Whitney U test and Pearson's correlation test. Results: Serum cortisol, IL-6 and Hcy levels were significantly increased (p < 0.01) in AD (cortisol: 19.69 ± 8.96 ug/dl; IL-6: 10.27 ± 2.76 pg/ml; Hcy: 23.29 ± 3.81 μmol/l), as compared with the controls (cortisol: 13.37 ± 5.59 ug/dl; IL-6: 3.37 ± 0.79 pg/ml; Hcy: 8.25 ± 2.36 μmol/l). MMSE scores in AD were negatively correlated with cortisol, IL-6 and Hcy levels. Conclusions: Serum cortisol, IL-6 and Hcy levels are independent biomarkers for AD progression. Hypercortisolaemia, hyperhomocysteinemia and inflammation play important roles in AD-related cognitive dysfunction and are interlinked.
Aims: The aim of this study was to investigate thyroid status in Alzheimer’s Disease (AD) patients and its response to donepezil and vitamin B12 supplement therapy for 6 months. Design: Case-Control Observational study. Place and Duration: Department of Biochemistry, GGMC & Sir J. J. Group of Hospitals, Mumbai, India between March 2017 and July 2019. Methodology: Case-Control study comprised of 71 AD patients and 70 healthy controls above 60 years of age. Blood serum samples were analyzed for thyroid hormones levels by the chemiluminescence method. AD patients were treated with donepezil (5 mg/day) and vitamin B12 supplement (1.5 mg/day) and thyroid profile was observed at intervals of 3 and 6 months. Statistical evaluation was done by using IMB SPSS statistics version 25. Results: Serum levels of thyroid hormones were low in euthyroid AD patients when compared with controls at the baseline level [T3 (120.64 ± 20.64 vs 127.8 ± 17.29), T4 (7.71 ± 2.34 vs 7.54 ± 1.85), FT3 (1.2 ± 0.13 vs 2.26 ± 0.63) and FT4 (0.79 ± 0.08 vs 1.29 ± 0.27)] except TSH which was increased in AD [TSH (2.71 ± 1.19 vs 2.34 ± 0.65)]. During follow-ups at 3 and 6 months, there was a slight decrease in TSH levels in response to the therapy. Conclusion: The AD patients were euthyroid with low T3, FT3 and FT4 serum levels and high TSH serum levels. Thyroid hormones might play a role as markers for disease progression. Donepezil and vitamin B12 therapy could not benefit restore the normal thyroid functioning in a period of 6 months. Further longitudinal research with larger cohort might help in elucidating thyroid dysfunction in AD and develop novel therapeutic strategies.
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