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Association between COVID-19 and Male Fertility: Systematic Review and Meta-Analysis of Observational Studies.
Wang, S, Zhang, A, Pan, Y, Liu, L, Niu, S, Zhang, F, Liu, X
The world journal of men's health. 2023;41(2):311-329
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Several studies have been published documenting possible relationships between Covid-19 and male infertility, but it remains unclear whether Covid-19 affects sperm quality and sex hormones. This meta-analysis and systematic review of observational studies aimed to determine any relationship between Covid-19 infection and male fertility. The results showed that Covid-19 decreased sperm count, sperm concentration, motility, but had no effect on semen volume, immotility, normal morphology or nonprogressive sperm motility. Infection also affected some hormone levels and that effects on hormones were dependent on age of infection onset. Covid-19 infection with or without fever also differentially affected outcomes with those with fever having reduced sperm concentration and progressive sperm motility, which was not seen in those who did not experience fever. Disease severity also affected outcomes with those with moderate Covid-19 having reduced sperm motility, which was not seen in individuals who had mild disease. It was concluded that Covid-19 infection reduced sperm quality and disrupted sex hormones. This study could be used by healthcare professionals to understand that Covid-19 infection may affect the fertility of men.
Abstract
PURPOSE Whether COVID-19 reduces male fertility remains requires further investigation. This meta-analysis and systematic review evaluated the impact of COVID-19 on male fertility. MATERIALS AND METHODS The literature in PubMed, Embase, MEDLINE, Web of Science, and Cochrane Library up to January 01, 2022 was systematically searched, and a meta-analysis was conducted to investigate the effect of COVID-19 on male fertility. Totally 17 studies with a total of 1,627 patients and 1,535 control subjects were included in our meta-analysis. RESULTS Regarding sperm quality, COVID-19 decreased the total sperm count (p=0.012), sperm concentration (p=0.001), total motility (p=0.001), progressive sperm motility (p=0.048), and viability (p=0.031). Subgroup analyses showed that different control group populations did not change the results. It was found that during the illness stage of COVID-19, semen volume decreased, and during the recovery stage of COVID-19, sperm concentration and total motility decreased <90 days. We found that sperm concentration and total motility decreased during recovery for ≥90 days. Fever because of COVID-19 significantly reduced sperm concentration and progressive sperm motility, and COVID-19 without fever ≥90 days, the sperm total motility and progressive sperm motility decreased. Regarding disease severity, the moderate type of COVID-19 significantly reduced sperm total motility, but not the mild type. Regarding sex hormones, COVID-19 increased prolactin and estradiol. Subgroup analyses showed that during the illness stage, COVID-19 decreased testosterone (T) levels and increased luteinizing hormone levels. A potential publication bias may have existed in our meta-analysis. CONCLUSIONS COVID-19 in men significantly reduced sperm quality and caused sex hormone disruption. COVID-19 had long-term effects on sperm quality, especially on sperm concentration and total motility. It is critical to conduct larger multicenter studies to determine the consequences of COVID-19 on male fertility.
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Sleep Disturbance Affects Immune Factors in Clinical Liver Cancer Patients.
Wang, Z, Wang, Y, Huang, J, Xu, J, Chen, F, Zhu, Z, Gao, L, Qin, J, Liu, B, Liang, C
Current oncology (Toronto, Ont.). 2022;29(10):7943-7952
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Many studies have shown that sleep disorders promote tumor growth and can impair immunity at the cellular level. There is however a lack of research in patients with liver cancer. The aim of this study was the asses the quality of sleep and the prevalence of disturbed sleep in patients with liver cancer and to explore whether sleep quality influences immune factors. 210 patients with liver cancer were randomly divided into 2 groups: HBV (Hepatitis B virus) cirrhosis and non-HBV cirrhosis. Their sleep quality was evaluated using a questionnaire and then the patients were divided into 2 groups according to these scores. The association between sleep disturbances and immune factors was analysed by logistic regression models. Over half the patient experienced poor sleep quality. Sleep disturbances were higher in patients with liver cancer of non-HBV cirrhosis than with that coming from the HBV virus. A rise in CD3+ T cells and a reduction in NK cells are associated with sleep disturbances in patients with non-HBV cirrhosis liver cancer. Medicines that can promote sleep and therefore improve immune function might be beneficial. Non-pharmacological sleep interventions to improve sleep quality, should be a safer choice where there are complex drug side effects.
Abstract
BACKGROUND Sleep-wake disturbance is prevalent in patients with liver cancer, but there is no direct evidence of its association and related biological mechanisms. Our study was to assess quality of sleep and to describe prevalence of sleep disturbances in patients with different etiologies of liver cancer, especially to explore whether sleep quality influences immune factors. METHODS A total of 210 patients with liver cancer from August 2015 to December 2015 were randomly divided into two groups including HBV cirrhosis and non-HBV cirrhosis. The Pittsburgh Sleep Quality Index (PSQI) was used to evaluate their sleep quality, and then 202 patients enrolled in this study were divided into two groups according to their PSQI scores: PSQI ≤ 5 and PSQI > 5. The association between sleep disturbances and immune factors was analyzed by logistic regression models. RESULTS A total of 56.9% of liver cancer patients experienced poor sleep quality (PSQI > 5). The prevalence of sleep disturbances was significantly higher in patients with liver cancer of non-hepatitis B virus (HBV) cirrhosis than with that evolving from HBV cirrhosis (66.7% vs. 50%, p = 0.018). In non-HBV cirrhosis liver cancer patients, the PSQI > 5 group had a higher percentage of CD3+ T cells (71.06 ± 11.07 vs. 63.96 ± 14.18, p = 0.014) and lower natural killer (NK) cells (14.67 ± 9.65 vs. 20.5 ± 10.77, p = 0.014) compared with patients with PSQI ≤ 5. Logistic regression further confirmed that liver cancer patients without HBV cirrhosis are more prone to experience poor sleep with increased CD3+ T cells (OR = 1.07, 95% CI = 1.01-1.13, p = 0.030) and decreased NK cells (OR = 0.92, 95% CI = 0.85-0.98, p = 0.014). Our results indicate that increased CD3+ T cells and decreased NK cells are both associated with sleep disturbances in patients with liver cancer of non-HBV cirrhosis. CONCLUSIONS Most liver cancer patients suffer from sleep disturbances, especially evolving from non-HBV cirrhosis. A rise in CD3+ T cells and a reduction in NK cells are associated with sleep disturbances in patients with liver cancer of non-HBV cirrhosis.
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Role of mitochondria, oxidative stress and the response to antioxidants in myalgic encephalomyelitis/chronic fatigue syndrome: A possible approach to SARS-CoV-2 'long-haulers'?
Wood, E, Hall, KH, Tate, W
Chronic diseases and translational medicine. 2021;7(1):14-26
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Cases of chronic fatigue have been reported following recovery from Covid-19, in what is termed ‘Long Covid’, with symptoms likened to that of sufferers from chronic fatigue syndrome (CFS) and myalgic encephalomyelitis (ME). How CFS/ME develop and treatments may help to further understand Covid-19. This review study of 111 studies aimed to identify where urgent research is required to help understand the potential of chronic fatigue therapies in Covid-19. The study first reviewed disrupted cellular energy production in ME/CFS and increased presence of damaging oxidants. Current therapies for improving cellular energy production in CFS/ME were then reviewed and Ritalin, ubiquinone and mitoquinol mesylate were heavily featured. Antioxidant therapies in CFS/ME were reviewed and observations would suggest that trials in patients with long covid are needed. It was concluded that research in cellular energy production in CFS/ME has been increasing, however remains contradictory due to a lack of a definitive diagnosis, differing disease severity and the huge differences between patients who suffer from CFS/ME. Further research is required in ME/CFS and Covid-19. This study could be used by health care professionals to understand the importance of monitoring symptoms of fatigue post Covid-19 infection and the possible use of ME/CFS treatments.
Abstract
A significant number of SARS-CoV-2 (COVID-19) pandemic patients have developed chronic symptoms lasting weeks or months which are very similar to those described for myalgic encephalomyelitis/chronic fatigue syndrome. This study reviews the current literature and understanding of the role that mitochondria, oxidative stress and antioxidants may play in the understanding of the pathophysiology and treatment of chronic fatigue. It describes what is known about the dysfunctional pathways which can develop in mitochondria and their relationship to chronic fatigue. It also reviews what is known about oxidative stress and how this can be related to the pathophysiology of fatigue, as well as examining the potential for specific therapy directed at mitochondria for the treatment of chronic fatigue in the form of antioxidants. This study identifies areas which require urgent, further research in order to fully elucidate the clinical and therapeutic potential of these approaches.
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Case report and systematic review suggest that children may experience similar long-term effects to adults after clinical COVID-19.
Ludvigsson, JF
Acta paediatrica (Oslo, Norway : 1992). 2021;110(3):914-921
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The long-term effects of COVID-19 is becoming increasingly documented in adults. Symptoms such as fatigue, headache and depression have all been reported, however data on the possible long-term effects of COVID-19 in children is scarce. The aim of this systematic review and case report was to describe the long-term effects of COVID-19 in five children and support this with other reports in the literature. The results showed that of the five case reports of long COVID, four were girls aged 9-15 years. All subjects reported symptoms lasting between 6-8 months. Most common symptoms were fatigue, difficulty breathing and heart issues. The systematic literature review did not find any publications which documented long COVID in children. It was concluded that children may experience long COVID symptoms and girls may be more susceptible. This study could be used by healthcare professionals to understand that children may also be affected by long COVID and that patients should be monitored for symptoms for at least 6-8 months.
Abstract
AIM: Persistent symptoms in adults after COVID-19 are emerging and the term long COVID is increasingly appearing in the literature. However, paediatric data are scarce. METHODS This paper contains a case report of five Swedish children and the long-term symptoms reported by their parents. It also includes a systematic literature review of the MEDLINE, EMBASE and Web of Science databases and the medRxiv/bioRxiv pre-print servers up to 2 November 2020. RESULTS The five children with potential long COVID had a median age of 12 years (range 9-15) and four were girls. They had symptoms for 6-8 months after their clinical diagnoses of COVID-19. None were hospitalised at diagnosis, but one was later admitted for peri-myocarditis. All five children had fatigue, dyspnoea, heart palpitations or chest pain, and four had headaches, difficulties concentrating, muscle weakness, dizziness and sore throats. Some had improved after 6-8 months, but they all suffered from fatigue and none had fully returned to school. The systematic review identified 179 publications and 19 of these were deemed relevant and read in detail. None contained any information on long COVID in children. CONCLUSION Children may experience similar long COVID symptoms to adults and females may be more affected.
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Persistent fatigue following SARS-CoV-2 infection is common and independent of severity of initial infection.
Townsend, L, Dyer, AH, Jones, K, Dunne, J, Mooney, A, Gaffney, F, O'Connor, L, Leavy, D, O'Brien, K, Dowds, J, et al
PloS one. 2020;15(11):e0240784
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Tiredness is a common symptom of Covid-19; however, it is unknown if this fatigue persists once recovered. This observational study of 128 recovered Covid-19 patients aimed to determine if fatigue persisted after recovery and whether severity of disease could predict fatigue. The results showed that post Covid-19 fatigue was reported in more than half of the participants and was particularly pronounced in females and in those with depression. Severity of disease did not predict fatigue. It was concluded that fatigue appears to outlast infection and fatigue was independent of disease severity. This study could be used by health care practitioners to understand that fatigue is common even after recovery from Covid-19 infection and women and sufferers of depression are the most susceptible.
Abstract
Fatigue is a common symptom in those presenting with symptomatic COVID-19 infection. However, it is unknown if COVID-19 results in persistent fatigue in those recovered from acute infection. We examined the prevalence of fatigue in individuals recovered from the acute phase of COVID-19 illness using the Chalder Fatigue Score (CFQ-11). We further examined potential predictors of fatigue following COVID-19 infection, evaluating indicators of COVID-19 severity, markers of peripheral immune activation and circulating pro-inflammatory cytokines. Of 128 participants (49.5 ± 15 years; 54% female), more than half reported persistent fatigue (67/128; 52.3%) at median of 10 weeks after initial COVID-19 symptoms. There was no association between COVID-19 severity (need for inpatient admission, supplemental oxygen or critical care) and fatigue following COVID-19. Additionally, there was no association between routine laboratory markers of inflammation and cell turnover (leukocyte, neutrophil or lymphocyte counts, neutrophil-to-lymphocyte ratio, lactate dehydrogenase, C-reactive protein) or pro-inflammatory molecules (IL-6 or sCD25) and fatigue post COVID-19. Female gender and those with a pre-existing diagnosis of depression/anxiety were over-represented in those with fatigue. Our findings demonstrate a significant burden of post-viral fatigue in individuals with previous SARS-CoV-2 infection after the acute phase of COVID-19 illness. This study highlights the importance of assessing those recovering from COVID-19 for symptoms of severe fatigue, irrespective of severity of initial illness, and may identify a group worthy of further study and early intervention.
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Immediate and long-term consequences of COVID-19 infections for the development of neurological disease.
Heneka, MT, Golenbock, D, Latz, E, Morgan, D, Brown, R
Alzheimer's research & therapy. 2020;12(1):69
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Covid-19 may cause brain dysfunction evidenced by symptoms individuals experience once they have contracted the disease. Loss of smell, taste and confusion have all been reported by patients and a number of severe cases have reported incidences of stroke. These are all of concern, as Covid-19 can severely affect the elderly who ordinarily are the most likely to suffer from brain disorders. This small review paper of 27 studies stated that there are four possible ways in which Covid-19 may affect the brain, which put Covid-19 sufferers at an increased risk of long-term brain disorders. This was supported by findings, which showed one third of Covid-19 patients leave hospital with evidence of brain dysfunction. Inflammation was heavily reviewed by the authors as a possible causal factor. It was concluded that patients who survive Covid-19 infection are at an increased risk for developing brain disorders such as Alzheimer's disease, however it was acknowledged that further studies are required. Clinicians could use this study to understand the possible need for both short-term and long-term monitoring of brain function in individuals who have survived Covid-19, especially if they are elderly.
Abstract
Increasing evidence suggests that infection with Sars-CoV-2 causes neurological deficits in a substantial proportion of affected patients. While these symptoms arise acutely during the course of infection, less is known about the possible long-term consequences for the brain. Severely affected COVID-19 cases experience high levels of proinflammatory cytokines and acute respiratory dysfunction and often require assisted ventilation. All these factors have been suggested to cause cognitive decline. Pathogenetically, this may result from direct negative effects of the immune reaction, acceleration or aggravation of pre-existing cognitive deficits, or de novo induction of a neurodegenerative disease. This article summarizes the current understanding of neurological symptoms of COVID-19 and hypothesizes that affected patients may be at higher risk of developing cognitive decline after overcoming the primary COVID-19 infection. A structured prospective evaluation should analyze the likelihood, time course, and severity of cognitive impairment following the COVID-19 pandemic.
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Danger signals and inflammaging in osteoarthritis.
Millerand, M, Berenbaum, F, Jacques, C
Clinical and experimental rheumatology. 2019;37 Suppl 120(5):48-56
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Osteoarthritis (OA) is the most common and disabling joint disease worldwide and aging is the most important risk factor for its development. It was considered a ‘wear and tear’ disease for a long time, however it is now clear that low-grade inflammation is at the root of OA. This process is called ‘inflammaging’ – the presence of low-grade inflammation and decreased efficiency of the immune system with aging. This highly technical review paper describes the reaction of the immune system to small molecules that begin to circulate after cell stress or damage in the joints (known as damage-associated molecular patterns or DAMPs), causing inflammation. The paper includes a discussion on potential medication targets, including anti-inflammatory compounds such as ginger. Nutrition Practitioners working with OA and wanting to understand the inflammatory process involved will find this paper useful.
Abstract
Osteoarthritis (OA) is the most common age-related chronic and disabling joint disease. Long considered to be a "wear and tear" disease, OA is now seen as a low-grade inflammation disease that affects all tissues of the joint, involving cartilage degradation, bone remodelling, osteophytes, and synovitis. The process, called inflammaging, is characterised by the association of low-grade inflammation, profound changes in intra-cellular mechanisms, and the decreased efficiency of the immune system with ageing. The activation of innate immunity plays a critical role in the development and progression of OA. Innate immunity, including inflammasome activation, is triggered by small endogenous molecules called alarmins or damage-associated molecular patterns (DAMPs). These molecules are released in the extracellular media after cell stress or damage, bind to pathogen-recognition receptors (PRRs), such as Toll-like receptors (TLRs) and the receptor for advanced glycation end products (RAGE), and activate the secretion of pro-inflammatory factors, leading to joint inflammation. Moreover, such sterile inflammation triggers cell senescence, characterised by a senescence-associated secretory phenotype (SASP). Understanding the substantial age-related changes of joint tissues that influence the pathogenesis of OA is critical to improving the quality of life of elderly people in the context of increased life expectancy. This review will focus on age-related sterile inflammation in OA and highlight the various innovative and promising therapies targeting the mechanisms of aging.