View clinical trials related to Hashimoto Disease.
Filter by:Autoimmune encephalitis are characterized by the subacute development of memory deficits, altered mental status, and psychiatric symptoms, generally in association with anti-neuronal antibodies. Two main groups of autoimmune encephalitis may be distinguished based on the location of the targeted antigen: 1) Intracellular antigens, in which the antibodies are thought not to be pathogenic, and the disorders are usually strongly associated with cancer, constituting therefore paraneoplastic neurological syndromes; 2) Synaptic proteins and surface receptors, in which the antibodies are pathogenic and the frequency of cancer is variable depending on the antibody and the demographic characteristics of the patient. Encephalitis with antibodies against N-methy-D-aspartate receptor is the most common autoimmune encephalitis, being even more frequent than infectious etiologies. It is characterized by subacute onset of memory deficits, psychiatric symptoms, speech dysfunction, seizures, movement disorders, decreased level of consciousness, dysautonomia and central hypoventilation. Nearly 50% of women with anti-NMDAR encephalitis have an ovarian teratoma, while associated tumors in elderly patients are usually carcinomas. In contrast, most cases in children and young men are non-paraneoplastic. Recently, herpes-simplex encephalitis has been described as another trigger of NMDAR encephalitis. Conversely, for the vast majority of the non-paraneoplastic autoimmune encephalitis, no acquired triggers have been described so far. In addition to acquired susceptibility, genetic predisposition may also be important in the pathogenesis of autoimmune encephalitis. The human leukocyte antigen (HLA) is the genetic factor most frequently associated with autoimmune diseases, and it has been already linked to a few autoimmune encephalitis, such as anti-leucine rich glioma inactivated 1 (LGI1), contactin-associated protein-like 2 (CASPR2), IgLON5, and glutamic acid decarboxylase 65 (GAD65) encephalitis. However, no HLA association has been reported for NMDAR encephalitis, suggesting that in this condition, and likely in others, non-HLA loci might be involved in the pathogenesis as well. Genome-wide association studies (GWAS) are useful tools to identify variants at genomic loci that are associated with complex diseases, and in particular, to detect associations between single-nucleotide polymorphisms (SNPs) and diseases. The aim of the study is to detect genetic variants in NMDAR encephalitis and other autoimmune encephalitis.
Numerous neurological disorders affecting the central and peripheral nervous system can be attributed to the immune system through multiple effector mechanisms. However, current treatments could be drastically improved by faster and more accurate diagnosis. The sample collection will benefit to patients with rare neuroimmune syndromes such as Autoimmune Encephalitis (AE) and Paraneoplastic Neurological Syndromes (PNS) leading to a better and early diagnosis, as well as treatment improvement.
To compare the efficacy and safety of NPB-01 in patients with autoimmune encephalitis refractory to steroid pulse therapy using steroid pulse therapy as a control.
The Swiss-Ped-IBrainD is a national patient registry that collects information on diagnosis, symptoms, treatment, and follow-up of pediatric patients with an inflammatory brain disease in Switzerland. It was first implemented in 2020 in the pediatric clinic of the university hospital in Bern. Further centers all over Switzerland were opened for recruitment in 2021; Aarau, Basel, Bellinzona, Chur, Geneva, Lausanne, Lucerne, St. Gallen, and Zurich. The center in Winterthur is expected to be open for recruitment by autumn 2021. The registry provides data for national and international monitoring and research. It supports research on inflammatory brain diseases in Switzerland and the exchange of knowledge between clinicians, researchers, and therapists. The registry aims to improve the treatment of children with inflammatory brain diseases and optimizing their health care and quality of life.
To evaluate the effects of exogenous selenium supplementation on autoimmune thyroiditis.
Autoimmune encephalitis (AE) are characterized by subacute onset of memory deficits, altered mental status or psychiatric symptoms, frequently associated with seizures, inflammatory cerebrospinal fluid and in cases with prominent limbic involvement, typical magnetic resonance imaging. Several autoantibodies (Abs) may be detected in AE, although its detection is not mandatory to establish a diagnosis. These Abs mainly recognize different synaptic and cell-surface proteins in the central nervous system, and are thought to be pathogenic as they alter the normal location or function of its antigens. Paraneoplastic neurological syndromes (PNS) are immune-mediated, remote complications of cancer. The clinical presentation is highly diverse, from central nervous system disorders (limbic encephalitis, cerebellar ataxia) to peripheral neuropathies and neuromuscular junction diseases. Two different kinds of Abs are associated with PNS: a first group known as onconeural Abs, which recognize intracellular antigens and are thought not to be pathogenic; and a second one whose targeted synaptic and cell-surface antigens shared with some non-paraneoplastic AE. The primary trigger of the immune response is unknown for most of AE. In addition to acquired susceptibility such as herpes simplex encephalitis, genetic predisposition may also be important in the pathogenesis of AE. Human leukocyte antigen (HLA) is the genetic factor most frequently associated with autoimmune diseases, due to its genetic complexity and key role in the adaptive immune response. Others and we already described the HLA haplotypes associated with three types different of AE: anti-leucine-rich glioma inactivated 1 (LGI1), anti-contactin-associated protein-like 2 (CASPR2), and anti-glutamic acid decarboxylase (GAD). Nevertheless, the genetic predisposition of many other AE has not been investigated yet. Cancer is considered as the trigger of the immune response that lead to PNS development, as the neural antigens recognized by the onconeural Abs are also expressed by tumor cells. Nevertheless, it is still unknown why some patients develop PNS and others do not, even if they present the same histological type of tumor, suggesting that some particular, maybe genetic, characteristics of the patients may play a role in this susceptibility. Furthermore, there is already evidence that, for those neurological diseases that may appear either as PNS or as non-paraneoplastic autoimmune disorder (i.e. Lambert-Eaton myasthenic syndrome), HLA profiles are not the same.
The objective of this study is to evaluate the effect of vitamin D supplementation on thyroid autoimmunity, thyroid function, and other metabolic and clinical variables associated with the thyroid axis in patients with Hashimoto's thyroiditis and vitamin D deficiency.
Hashimoto's disease (HT) and psoriasis (PsO) have a significant impact on patient's quality of everyday life, and early diagnosis is critical for the symptoms management and prognosis. There is evidence that HT and PsO share common metabolic pathways that relate to their pathogenesis, and are affected by dietary and lifestyle factors. Previous studies have identified potential metabolic biomarkers, although the small number of studies hamper their validation. Of note, most studies are not longitudinal thus do not capture the metabolic fluctuations in response to disease progression or dietary changes. Thus, the purpose of this study is to identify metabolic biomarkers of HT and PsO and study the role of epigenetic factors (diet and lifestyle) on the involved metabolic pathways . In addition, a comparative analysis of the disease-related quality of life (QoL) will be performed in relation to dietary changes to unravel possible links between the QoL and the associated metabolic pathways in HT and PsO.
The aim of this non randomised retrospective study is to investigate the imaging (MRI) of auto-immune encephalitis at presentation, especially in diffusion-weighted sequences. Indeed, few series describe the MRI aspect of auto-immune at their beginning. Recognize early MRI abnormalities seen in auto-immune encephalitis could help reduce the time to positive diagnosis and improve the therapeutic management.
Herpes Simplex Virus encephalitis is the most common infectious encephalitis, with an estimated annual incidence of 1 / 250,000 to 1 / 500,000 in industrialized countries. Despite a widely used antiviral treatment, the prognosis remains poor with a mortality of 5 to 20% and a considerable morbidity rate. One of the contributing factors of bad prognosis is the development of encephalitis mediated by autoantibodies, most often directed against NMDA receptors, in the weeks following viral encephalitis. The description of this pathology is recent, the pathophysiology of this process remains poorly understood, and the management of these patients is not yet codified.