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Selenium, Stroke, and Infection: A Threefold Relationship; Where Do We Stand and Where Do We Go?
Liampas, A, Zis, P, Hadjigeorgiou, G, Vavougios, GD
Nutrients. 2023;(6)
Abstract
Stroke is currently the second most common cause of death worldwide and a major cause of serious long-term morbidity. Selenium is a trace element with pleotropic effects on human health. Selenium deficiency has been associated with a prothrombotic state and poor immune response, particularly during infection. Our aim was to synthesize current evidence on the tripartite interrelationship between selenium levels, stroke, and infection. Although evidence is contradictory, most studies support the association between lower serum selenium levels and stroke risk and outcomes. Conversely, limited evidence on the role of selenium supplementation in stroke indicates a potentially beneficial effect of selenium. Notably, the relationship between stroke risk and selenium levels is bimodal rather than linear, with higher levels of serum selenium linked to disturbances of glucose metabolism and high blood pressure, morbidities which are, in turn, substrates for stroke. Another such substrate is an infection, albeit forming a bidirectional relationship with both stroke and the consequences of impaired selenium metabolism. Perturbed selenium homeostasis leads to impaired immune fitness and antioxidant capacity, which both favor infection and inflammation; specific pathogens may also contend with the host for transcriptional control of the selenoproteome, adding a feed-forward loop to this described process. Broader consequences of infection such as endothelial dysfunction, hypercoagulation, and emergent cardiac dysfunction both provide stroke substrates and further feed-forward feedback to the consequences of deficient selenium metabolism. In this review, we provide a synthesis and interpretation of these outlined complex interrelationships that link selenium, stroke, and infection and attempt to decipher their potential impact on human health and disease. Selenium and the unique properties of its proteome could provide both biomarkers and treatment options in patients with stroke, infection, or both.
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The Role of Vitamin B6 in Peripheral Neuropathy: A Systematic Review.
Muhamad, R, Akrivaki, A, Papagiannopoulou, G, Zavridis, P, Zis, P
Nutrients. 2023;(13)
Abstract
INTRODUCTION Vitamin B6 is a water-soluble vitamin that is naturally present in many foods and is accessible in many dietary supplements. The three natural forms are pyridoxine, pyridoxal, and pyridoxamine. Both vitamin B6 deficiency and high B6 intake have been described as risk factors for developing peripheral neuropathy (PN). The aim of this systematic review is to characterize and comprehensively describe B6-related PN. METHOD A systematic, computer-based search was conducted using the PubMed database. Twenty articles were included in this review. RESULTS Higher vitamin B6 levels, which usually occur following the taking of nutritional supplements, may lead to the development of a predominantly, if not exclusively, sensory neuropathy of the axonal type. After pyridoxine discontinuation, such patients subjectively report improved symptoms. However, although low vitamin B6 levels can be seen in patients suffering from peripheral neuropathy of various etiologies, there is no firm evidence that low B6 levels have a direct causal relationship with PN. Many studies suggest subjective improvement of neuropathy symptoms in patients suffering from PN of various etiologies after receiving B6 supplementation; however, no data about B6 administration as a monotherapy exist, only as part of a combination treatment, usually with other vitamins. Therefore, the potential therapeutic role of B6 cannot be confirmed to date. Supplementation with vitamin B6, even as part of a nutritional multivitamin supplement, has not been proven harmful at permitted daily doses in patients who already suffer from PN. CONCLUSION Current scientific evidence supports a neurotoxic role of B6 at high levels. Although some studies suggest that low B6 is also a potential risk factor, further studies in this area are needed.
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What's New in Neuropathy?
Varrassi, G, Tamburin, S, Zis, P, Guardamagna, VA, Paladini, A, Rekatsina, M
Cureus. 2023;(9):e44952
Abstract
Neuropathic pain presents diagnostic and treatment challenges. Despite recent advances in our understanding of the diagnosis and treatment of neuropathy, much remains to be elucidated. Familiar with neuropathy is the paradox that aberrant nerve signaling causes both sensory loss and pain. Voltage-gated sodium channels play an important role in neuronal electrogenesis and communication among neurons, and their dysregulation leads to hyperexcitability and pain. While numerous validated diagnostic assessment tools are available for neuropathy, patients often experience a diagnostic delay about the cause of their neuropathy. New research is defining more specific types of neuropathy beyond peripheral and central forms. The prevalence of pain varies by type of neuropathy, with chronic idiopathic axonal polyneuropathy associated with the highest proportion of patients experiencing pain. In the majority of types, it exceeds 50%. Gluten neuropathy, a form of peripheral neuropathy, is a new diagnostic consideration. It may require electrochemical conductance testing of hands and feet to test for sudomotor dysfunction. Among those with serologically confirmed gluten sensitivity or celiac disease, gluten neuropathy is a common neurological manifestation and may be addressed at least partially by a gluten-free diet. In Greece, a new neuropathic pain registry was created in 2014 in order to help gather data from real-world neuropathic pain patients. While still in its earliest phase, this registry has already produced demographic and treatment data that suggest suboptimal prescribing and less than recommended use of interventional procedures. Awareness campaigns are underway to encourage more Greek pain clinics to participate in this important registry.
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Osmotic demyelination syndrome improving after immune-modulating treatment: Case report and literature review.
Kalampokini, S, Artemiadis, A, Zis, P, Hadjihannas, L, Parpas, G, Kyrri, A, Hadjigeorgiou, GM
Clinical neurology and neurosurgery. 2021;:106811
Abstract
BACKGROUND Osmotic demyelination syndrome (ODS), which embraces central pontine and extrapontine myelinolysis, is an uncommon neurological disorder that occurs due to plasma osmotic changes. CASE PRESENTATION We present the case of a 55-year-old man, who presented with severe hyponatremia due to repeated vomiting, antidepressant treatment and consumption of large amounts of water. Fifteen days after sodium correction, the patient showed fluctuation of vigilance, dysarthria and dysphagia, tremor, cogwheel rigidity, bilateral facial palsy, ophthalmoplegia and tetraparesis. A brain MRI scan revealed extrapontine and later on pontine myelinolysis. He received intravenous steroids and subsequently immunoglobulin. His status began to improve gradually after completion of immunoglobulin and at three month-follow-up had no neurological deficit. LITERATURE REVIEW A comprehensive literature search of all reported ODS cases that received immunoglobulin, steroids or plasmapheresis was conducted in the electronic databases PubMed and Web of science. CONCLUSIONS Improvement was seen in most cases that received immunoglobulin either during treatment or in the first days after treatment. With regard to steroids, although most cases reported improvement in the following months their effect on the outcome is unclear. Most cases treated with plasmapheresis reported favorable outcome at variable follow-up time. Immunoglobulin and steroids have immunomodulatory effects, which could contribute to promotion of myelin repair in ODS. Plasmapheresis has effects on the immune system beyond removing myelinotoxins from the circulation. More evidence is required to support their use in ODS. However, in view of the disease severity, these therapeutic choices should be considered in the clinical management of ODS.
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Treatment of Neurological Manifestations of Gluten Sensitivity and Coeliac Disease.
Zis, P, Hadjivassiliou, M
Current treatment options in neurology. 2019;(3):10
Abstract
PURPOSE OF REVIEW The aim of this paper was to overview the current literature in order to establish the available treatment options for the neurological manifestations of gluten-related disorders (serologically confirmed gluten sensitivity and coeliac disease). RECENT FINDINGS A range of debilitating neurological manifestations is increasingly being recognized in patients with gluten sensitivity with and without enteropathy even in the absence of gastrointestinal symptoms. Ataxia is the commonest neurological manifestation, followed by peripheral neuropathy. Epilepsy, headache, encephalopathy, various movement disorders, cognitive impairment, and muscle disorders have also been linked to gluten sensitivity and coeliac disease and are discussed in this review. Strict gluten-free diet is an effective first-line treatment of the neurological manifestations of gluten-related disorders. Very few patients will require additional immunosuppressive treatment usually in the form of mycophenolate.
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6.
Movement Disorders Related to Gluten Sensitivity: A Systematic Review.
Vinagre-Aragón, A, Zis, P, Grunewald, RA, Hadjivassiliou, M
Nutrients. 2018;10(8)
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Plain language summary
Gluten related disorders (GRDs) is an umbrella term for diseases triggered by gluten, including coeliac disease and gluten sensitivity. People with GRDs may experience a wide range of symptoms including digestive and nervous system issues. Movement Disorders (MDs) refers to a group of nervous system conditions that cause abnormal movements, which may be voluntary or involuntary. This literature review looked at the current research on GRDs and MDs such as epilepsy, Parkinson’s disease, restless leg syndrome and tremors. 48 papers were used for the review. Most papers looked at MDs in those diagnosed with coeliac disease, rather than other GRDs. The authors found many examples where the symptoms of MDs, including chorea, restless leg syndrome, stiff person syndrome and tics, improved on a gluten free diet. The authors concluded that gluten-related MDs may be more common than previously thought, and that following a gluten free diet can be beneficial in many cases. They recommended that gluten sensitivity and coeliac disease should be considered in patients with MDs of unknown cause.
Abstract
Gluten related disorders (GRD) represent a wide spectrum of clinical manifestations that are triggered by the ingestion of gluten. Coeliac disease (CD) or gluten sensitive enteropathy is the most widely recognised, but extra-intestinal manifestations have also been increasingly identified and reported. Such manifestations may exist in the absence of enteropathy. Gluten sensitivity (GS) is another term that has been used to include all GRD, including those where there is serological positivity for GS related antibodies in the absence of an enteropathy. Gluten ataxia (GA) is the commonest extraintestinal neurological manifestation and it has been the subject of many publications. Other movement disorders (MDs) have also been reported in the context of GS. The aim of this review was to assess the current available medical literature concerning MDs and GS with and without enteropathy. A systematic search was performed while using PubMed database. A total of 48 articles met the inclusion criteria and were included in the present review. This review highlights that the phenomenology of gluten related MDs is broader than GA and demonstrates that gluten-free diet (GFD) is beneficial in a great percentage of such cases.
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Peripheral neuropathy in idiopathic Parkinson's disease: A systematic review.
Zis, P, Grünewald, RA, Chaudhuri, RK, Hadjivassiliou, M
Journal of the neurological sciences. 2017;:204-209
Abstract
BACKGROUND Parkinson's disease (PD) has been associated with peripheral neuropathy (PN). PN has been demonstrated in some rare genetic forms of PD (e.g. PARK2 mutations) but has also been linked to levodopa exposure. OBJECTIVE The aim of this systematic review is to clarify any evidence of peripheral nervous system involvement in idiopathic PD. METHODS A systematic computer-based literature search was conducted on PubMed database. FINDINGS The pooled estimate of the prevalence of large fiber PN in PD was 16.3% (based on 1376 patients). The pooled estimate of the prevalence of biopsy-proven small fiber neuropathy was 56.9% (based on 72 patients). Large fiber PN in PD is in the majority of cases distal, symmetrical, axonal and predominantly sensory. There are, however, few reports of chronic idiopathic demyelinating polyneuropathy and very occasional cases of acute neuropathies. Although nerve conduction studies have been performed in the majority of the studies, they included only a limited number of nerves, mainly in the lower limbs. There is little evidence to support a direct link between levodopa treatment and the development of PN in idiopathic PD. In the majority of the cases PN has been linked to abnormalities in vitamin B12, methylmalonic acid or fasting homocysteine levels. Additional aetiological risk factors for PN may be responsible for any apparent link between PD and PN. CONCLUSIONS Large-scale prospective studies with long-term follow-up with detailed baseline assessments are needed in order to understand the natural history of PN in PD, both on clinical and neurophysiological parameters.