-
Clinical and Experimental Rheumatology Jun 2022Studies report that autoimmune thyroid disease and elevated levels of thyroid autoantibodies are associated with fibromyalgia and widespread chronic pain. The aim of... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVES
Studies report that autoimmune thyroid disease and elevated levels of thyroid autoantibodies are associated with fibromyalgia and widespread chronic pain. The aim of this meta-analysis was to investigate the relationship between fibromyalgia and thyroid autoimmunity. Clinical symptoms and depression associated with fibromyalgia were also investigated in relation to the presence of thyroid autoantibodies.
METHODS
A literature search was conducted on PubMed and Embase for studies published between January, 1980 and February, 2020 on thyroid autoimmunity in fibromyalgia patients. Two reviewers independently screened and assessed the quality of the articles. Meta-analysis was performed to analyse the difference in frequency of thyroid autoantibody positivity between fibromyalgia patients and healthy controls. Clinical symptoms and depression were also analysed according to the presence of thyroid autoantibodies.
RESULTS
Data from 10 original studies were included in the systematic review, and 5 case-control studies that satisfied the selection criteria were subjected to meta-analysis. Thyroid autoantibody positivity was more common in fibromyalgia patients compared to healthy controls (thyroid peroxidase antibody: OR 3.41, 95% CI 1.97-5.90; thyroglobulin antibody: OR 2.23, 95% CI 1.23-4.01). The frequency of postmenopausal status was significantly higher in fibromyalgia patients with thyroid autoantibodies (OR 1.95, 95% CI 1.23-3.08). However, the severity of disease (pain and fatigue level, fibromyalgia impact questionnaire score, and disease duration) and prevalence of depression did not show a statistically significant difference according to thyroid autoantibody positivity.
CONCLUSIONS
Thyroid autoimmunity should be considered in fibromyalgia patients. The percentage of women in menopause was higher in thyroid autoantibody positive fibromyalgia patients.
Topics: Autoantibodies; Autoimmunity; Causality; Female; Fibromyalgia; Humans; Thyroid Gland
PubMed: 34369360
DOI: 10.55563/clinexprheumatol/y3gfva -
Environmental Pollution (Barking, Essex... Nov 2018Biomarkers of antioxidant and biotransformation systems are commonly used to assess polycyclic aromatic hydrocarbons (PAHs) pollution in fish. Despite their extensive... (Meta-Analysis)
Meta-Analysis Review
Biomarkers of antioxidant and biotransformation systems are commonly used to assess polycyclic aromatic hydrocarbons (PAHs) pollution in fish. Despite their extensive application of biomarkers, contradictory results are vastly reported in the literature, even for the same species in similar contamination scenarios. This study aims to verify response patterns of biomarkers in fish exposed to PAHs. Through systematic reviews and meta-analyses, we were able to evaluate: (i) overall magnitude of PAHs effects on biotransformation and oxidative stress biomarkers; (ii) patterns of response among experimental approaches (laboratory, field and active biomonitoring), environment (marine and freshwater) and fish habitat (pelagic, demersal, etc.); (iii) effects of exposure route, time and concentration of PAHs; and (iv) which biomarkers respond best to PAHs exposure. Overall, biomarker responses were significantly affected by PAHs exposure. The activities of ethoxyresorufin-O-deethylase (EROD), glutathione S-transferase (GST), superoxide dismutase (SOD), glutathione peroxidase (GPx) and levels of oxidized glutathione (GSSG) and lipid peroxide (LPO) significantly increased in fish exposed to PAHs, whereas catalase (CAT) and glutathione reductase (GR) activities and levels of reduced glutathione (GSH) were not affected. Amongst responsive biomarkers, EROD and GST activities significantly differed among approaches and between marine and freshwater environments, but were not affected by fish habitat. GSSG levels were higher in fish from laboratory bioassays compared to the field, but did not differ between environments nor habitats. Exposure route played a major role only for GST and GPx responses. Finally, increasing PAHs concentration and exposure time had a significant effect on all assessed biomarkers, except for CAT. We conclude that EROD and GST are robust biomarkers to assess PAHs effects in fish. Contrarily, CAT is an inadequate biomarker of PAHs exposure since no significant response was observed. Our study also highlighted some research gaps in PAHs contamination studies, such as a clear lack of active biomonitoring experiments.
Topics: Animals; Antioxidants; Biomarkers; Biotransformation; Catalase; Cytochrome P-450 CYP1A1; Environmental Monitoring; Fishes; Fresh Water; Glutathione; Glutathione Peroxidase; Glutathione Transferase; Oxidative Stress; Polycyclic Aromatic Hydrocarbons; Superoxide Dismutase; Water Pollutants, Chemical
PubMed: 30005257
DOI: 10.1016/j.envpol.2018.07.004 -
Nutrients Aug 2022Elevated levels of oxidative stress could cause and aggravate Alzheimer's disease (AD). Selenium (Se) is a trace element with antioxidant and anti-inflammatory activity... (Meta-Analysis)
Meta-Analysis Review
Elevated levels of oxidative stress could cause and aggravate Alzheimer's disease (AD). Selenium (Se) is a trace element with antioxidant and anti-inflammatory activity with neuroprotective effects. To evaluate the effects of Se supplementation in patients with AD or mild cognitive impairment (MCI) through a systematic review and meta-analysis, data were searched and collected from four electronic databases, including clinical trial studies published until December 2020, following the PRISMA guidelines. Statistical analysis was performed by RevMan, and the risk of bias was assessed using the Rob 2 tool. A total of 1350 scientific papers were collected, and following evaluation 11 papers were included in the systematic review and 6 of these were used in the meta-analysis. Studies that evaluated only Se supplementation observed an improvement in Se levels, glutathione peroxidase (GPX) activity, and in some cognitive tests in MCI patients; similarly, improvement in Se levels and mini-mental score was also observed in AD patients. Regarding supplementation of Se plus other nutrients, improvement in cognitive tests was observed in both AD and MCI patients. Therefore, Se supplementation is a good alternative for patients with AD and MCI for improving Se levels and GPX activity. More detailed studies are required to further evaluate the effects of Se on the cognitive deficit and oxidative stress associated with AD and MCI.
Topics: Alzheimer Disease; Antioxidants; Cognition Disorders; Cognitive Dysfunction; Dietary Supplements; Humans; Selenium
PubMed: 35956381
DOI: 10.3390/nu14153205 -
Heliyon Jun 2023(MO), has been studied extensively, and has numerous medicinal and socioeconomic benefits. Emerging research has investigated the efficacy of MO extract and/or its... (Review)
Review
(MO), has been studied extensively, and has numerous medicinal and socioeconomic benefits. Emerging research has investigated the efficacy of MO extract and/or its phytochemical derivatives against ischemic stroke . To date, no studies comprehensively reviewing the effects of MO extract and/or its phytochemical derivatives against ischemic stroke have been published. A systematic review and meta-analysis was conducted to assess the effects of MO extract and/or its phytochemical derivatives against focal ischemic stroke, modeled . Compared with control groups, significant reduction in infarct volume and malondialdehyde levels, and signficant increase in antioxidant enzymes superoxide dismutase, glutathione peroxidase and catalase. The primary mechanism of action of MO extract and its phytochemical derivatives which confers neuroprotection is reduction in oxidative stress by increasing antioxidant enzymes. On the whole, the present systematic review critically assessed evidence which demonstrated that MO extract may confer protective effect on experimental ischemic stroke. Although effect size may have been overestimated due to the limited number of included studies, small sample sizes and possible publication bias, results generated in this meta-analysis dmeonstrate that MO extract may be a promising neuroprotective agent against human ischemic stroke.
PubMed: 37303567
DOI: 10.1016/j.heliyon.2023.e16622 -
European Journal of Dermatology : EJD Dec 2018Vitiligo is associated with (autoimmune) thyroid disease. However, confounding factors, including type and onset of vitiligo, require elucidation. We conducted a... (Meta-Analysis)
Meta-Analysis
Vitiligo is associated with (autoimmune) thyroid disease. However, confounding factors, including type and onset of vitiligo, require elucidation. We conducted a meta-analysis to identify vitiligo patients with increased risk of (autoimmune) thyroid disease. Studies were identified based on searches in PubMed, MEDLINE, Embase, and the Cochrane Library from inception of these databases to August 31st, 2017. Odds ratios (ORs) for the prevalence of (autoimmune) thyroid disease and thyroid antibodies in vitiligo patients were pooled, and subgroup analysis was performed. Thirty-seven studies with 78,714 vitiligo patients met the inclusion criteria. The prevalence of thyroid disease (TD) (OR: 3.932; 95% CI: 2.230-6.933), autoimmune TD (OR: 5.879; 95% CI: 2.682-12.885), anti-thyroperoxidase (TPO) antibody (OR: 3.838; 95% CI: 2.968-4.963), and anti-thyroglobulin antibody (OR: 3.513; 95% CI: 2.346-5.260) was significantly higher in vitiligo patients than in controls. Notably, the prevalence of TD and anti-TPO antibody was significantly higher in patients with non-segmental vitiligo, compared to those with segmental vitiligo. In contrast, the prevalence of TD was significantly lower in early-, compared to the late-onset vitiligo group (OR: 0.333; 95% CI: 0.244-0.453). Physicians should be aware of the increased risk of (autoimmune) thyroid disease in vitiligo patients. We recommend routine screening for anti-thyroid antibodies in vitiligo patients.
Topics: Autoantibodies; Humans; Iodide Peroxidase; Prevalence; Thyroglobulin; Thyroid Diseases; Thyroiditis, Autoimmune; Vitiligo
PubMed: 30698146
DOI: 10.1684/ejd.2018.3449 -
Archives of Gynecology and Obstetrics Jun 2024We aimed to perform a systematic review and meta-analysis addressing the efficacy of levothyroxine therapy in pregnant women with subclinical hypothyroidism considering... (Meta-Analysis)
Meta-Analysis Review
PURPOSE
We aimed to perform a systematic review and meta-analysis addressing the efficacy of levothyroxine therapy in pregnant women with subclinical hypothyroidism considering most recent evidence and subgroups of interest for clinical practice.
METHODS
PubMed, Embase, and Cochrane Central were searched from inception for randomized controlled trials (RCTs) comparing levothyroxine with placebo or no intervention in pregnant women with subclinical hypothyroidism. We used a random-effects model and conducted subgroup analyses based on thyroid peroxidase antibody status, thyroid stimulating hormone levels, fertility treatment, and recurrent miscarriage.
RESULTS
We included 11 RCTs comprising 2,749 pregnant women with subclinical hypothyroidism. Patients treated with levothyroxine (1,439; 52.3%) had significantly lower risk of pregnancy loss (risk ratio 0.69; 95% confidence interval 0.52-0.91; p < 0.01; 6 studies). However, there was no significant association between levothyroxine and live birth (risk ratio 1.01; 95% confidence interval 0.99-1.03; p = 0.29; 8 studies). No statistically significant interaction was observed across subgroups (p > 0.05).
CONCLUSION
Levothyroxine replacement therapy for subclinical hypothyroidism during pregnancy may decrease pregnancy loss when early prescribed. Nevertheless, further investigation is needed in patients with thyroid stimulating hormone above four milliunits per liter, especially when associated with recurrent miscarriage or infertility.
Topics: Humans; Pregnancy; Female; Hypothyroidism; Thyroxine; Pregnancy Complications; Randomized Controlled Trials as Topic; Thyrotropin; Abortion, Habitual
PubMed: 38676741
DOI: 10.1007/s00404-024-07512-3 -
Annals of Palliative Medicine Apr 2021This investigation systematically evaluated the selenium levels and the effects of selenium supplementation in patients with autoimmune thyroid disease (AITD). (Meta-Analysis)
Meta-Analysis
BACKGROUND
This investigation systematically evaluated the selenium levels and the effects of selenium supplementation in patients with autoimmune thyroid disease (AITD).
METHODS
Randomized controlled trials (RCTs) related to selenium supplementation in patients with AITD were selected from the PubMed, Medline, Web of Sciences, Embase, Cochrane Library, and Spring databases. All related literature published between January 2000 and November 2020 were included. The RCT bias risk assessment was conducted according to the Cochrane Handbook 5.0.2. The Review Manager 5.3 software was applied for meta-analysis of the included literature.
RESULTS
A total of 17 articles meeting the requirements were selected, including a total of 1,911 subjects. Meta-analysis results showed that the serum free triiodothyronine (FT3) levels in patients was greatly reduced after selenium supplementation compared to placebo treatment (MD =-0.40; 95% confidential interval (CI): -0.70--0.10; Z=2.61; P=0.009). Serum free thyroxine (FT4) levels and anti-thyroid peroxidase antibody (TPOAb) levels were also significantly reduced (MD = -0.76; 95% CI: -1.58--0.07; Z=1.79; P=0.07), and anti-thyroid peroxidase antibody (TPOAb) level was decreased observably (MD =-150.25; 95% CI: -04.06--96.43; Z=5.47; P<0.00001). The thyroid stimulating hormone (TSH) levels (MD =0.06; 95% CI: -0.53-0.66; Z=0.21; P=0.83) and anti-thyroglobulin antibody (TGAb) levels (MD =17.19; 95% CI: -254.86-289.25; Z=0.12; P=0.90) were not significantly different between the experimental group and the control group.
CONCLUSIONS
Selenium-containing drugs were effective in treating AITD patients, and greatly reduced the levels of FT3, FT4, and TPOAb in AITD patients. These results suggested that selenium level had a great effect on AITD and selenium supplementation showed a very important effect on AITD.
Topics: Hashimoto Disease; Humans; Pharmaceutical Preparations; Selenium; Thyroid Hormones
PubMed: 33894732
DOI: 10.21037/apm-21-449 -
Frontiers in Pharmacology 2023Liver injury is a severe liver lesion caused by various etiologies and is one of the main areas of medical research. C.A. Meyer has traditionally been used as medicine... (Review)
Review
Liver injury is a severe liver lesion caused by various etiologies and is one of the main areas of medical research. C.A. Meyer has traditionally been used as medicine to treat diseases and regulate body functions. Ginsenosides are the main active components of ginseng, and their effects on liver injury have been extensively reported. Preclinical studies meeting the inclusion criteria were retrieved from PubMed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), and Wan Fang Data Knowledge Service Platforms. The Stata 17.0 was used to perform the meta-analysis, meta-regression, and subgroup analysis. This meta-analysis included ginsenosides Rb1, Rg1, Rg3, and compound K (CK), in 43 articles. The overall results showed that multiple ginsenosides significantly reduced alanine aminotransferase (ALT) and aspartate aminotransferase (AST), affected oxidative stress-related indicators, such as superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GSH-Px), and catalase (CAT), and reduced levels of inflammatory factor, such as factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6). Additionally, there was a large amount of heterogeneity in the meta-analysis results. Our predefined subgroup analysis shows that the animal species, the type of liver injury model, the duration of treatment, and the administration route may be the sources of some of the heterogeneity. In a word, ginsenosides have good efficacy against liver injury, and their potential mechanisms of action target antioxidant, anti-inflammatory and apoptotic-related pathways. However, the overall methodological quality of our current included studies was low, and more high-quality studies are needed to confirm their effects and mechanisms further.
PubMed: 37251340
DOI: 10.3389/fphar.2023.1184774 -
Phytotherapy Research : PTR Sep 2023The present study aimed to assess the effect of propolis supplementation on oxidative status, a key contributor to the etiology of many chronic diseases. A systematic... (Meta-Analysis)
Meta-Analysis Review
The present study aimed to assess the effect of propolis supplementation on oxidative status, a key contributor to the etiology of many chronic diseases. A systematic search of multiple databases, including Web of Science, SCOPUS, Embase, PubMed, and Google Scholar, was conducted from inception to October 2022 to identify articles examining the effect of propolis on glutathione (GSH), glutathione peroxidase (GPX), total antioxidant capacity (TAC), superoxide dismutase (SOD), and malondialdehyde (MDA) levels. The quality of the included studies was evaluated using the Cochrane Collaboration tool. A total of nine studies were included in the final analysis, and a random-effects model was used to pool the estimated effects. Results showed that propolis supplementation significantly increased the levels of GSH (SMD = 3.16; 95% CI: 1.15, 5.18; I = 97.2%), GPX (SMD = 0.56; 95% CI: 0.07, 1.05; p = 0.025; I = 62.3%), and TAC (SMD = 3.26; 95% CI: 0.89, 5.62; I = 97.8%, p < 0.001). However, the effect of propolis on SOD was not significant (SMD = 0.05; 95% CI: -0.25, 0.34; I = 0.0%). Although the MDA concentration was not significantly decreased overall (SMD = -0.85, 95% CI: -1.70, 0.09; I = 93.3%), a significant decrease in MDA levels was observed at doses ≥1000 mg/day (SMD = -1.90; 95% CI: -2.97, -0.82; I = 86.4) and supplementation durations of less than 11 weeks (SMD = -1.56; 95% CI: -2.60, -0.51; I = 90.4). These results suggest that propolis is a safe supplement with a beneficial effect on GSH, GPX, and TAC levels and may be an effective adjunctive therapy for diseases where oxidative stress is a key factor in the etiology. However, further high-quality studies are necessary to make more precise and comprehensive recommendations given the limited number of studies, clinical diversity, and other limitations.
Topics: Antioxidants; Propolis; Dietary Supplements; Oxidative Stress; Superoxide Dismutase; Glutathione Peroxidase; Biomarkers
PubMed: 37317592
DOI: 10.1002/ptr.7899 -
Brain, Behavior, and Immunity Jan 2022Bile acids, mainly ursodeoxycholic acid (UDCA) and its conjugated species glycoursodeoxycholic acid (GUDCA) and tauroursodeoxycholic acid (TUDCA) have long been known to... (Review)
Review
From dried bear bile to molecular investigation: A systematic review of the effect of bile acids on cell apoptosis, oxidative stress and inflammation in the brain, across pre-clinical models of neurological, neurodegenerative and neuropsychiatric disorders.
Bile acids, mainly ursodeoxycholic acid (UDCA) and its conjugated species glycoursodeoxycholic acid (GUDCA) and tauroursodeoxycholic acid (TUDCA) have long been known to have anti-apoptotic, anti-oxidant and anti-inflammatory properties. Due to their beneficial actions, recent studies have started to investigate the effect of UDCA, GUDCA, TUDCA on the same mechanisms in pre-clinical models of neurological, neurodegenerative and neuropsychiatric disorders, where increased cell apoptosis, oxidative stress and inflammation in the brain are often observed. A total of thirty-five pre-clinical studies were identified through PubMed/Medline, Web of Science, Embase, PsychInfo, and CINAHL databases, investigating the role of the UDCA, GUDCA and TUDCA in the regulation of brain apoptosis, oxidative stress and inflammation, in pre-clinical models of neurological, neurodegenerative and neuropsychiatric disorders. Findings show that UDCA reduces apoptosis, reactive oxygen species (ROS) and tumour necrosis factor (TNF)-α production in neurodegenerative models, and reduces nitric oxide (NO) and interleukin (IL)-1β production in neuropsychiatric models; GUDCA decreases lactate dehydrogenase, TNF-α and IL-1β production in neurological models, and also reduces cytochrome c peroxidase production in neurodegenerative models; TUDCA decreases apoptosis in neurological models, reduces ROS and IL-1β production in neurodegenerative models, and decreases apoptosis and TNF-α production, and increases glutathione production in neuropsychiatric models. In addition, findings suggest that all the three bile acids would be equally beneficial in models of Huntington's disease, whereas UDCA and TUDCA would be more beneficial in models of Parkinson's disease and Alzheimer's disease, while GUDCA in models of bilirubin encephalopathy and TUDCA in models of depression. Overall, this review confirms the therapeutic potential of UDCA, GUDCA and TUDCA in neurological, neurodegenerative and neuropsychiatric disorders, proposing bile acids as potential alternative therapeutic approaches for patients suffering from these disorders.
Topics: Animals; Apoptosis; Bile; Bile Acids and Salts; Brain; Humans; Inflammation; Oxidative Stress; Ursidae
PubMed: 34601012
DOI: 10.1016/j.bbi.2021.09.021