The process of finding new therapeutic indications for currently used drugs, defined as ‘repurposing’, is receiving growing attention. Chloroquine and hydroxychloroquine, with an original indication to prevent or cure malaria, have been successfully used to treat several infectious (HIV, Q fever, Whipple’s disease, fungal infections), rheumatological (systemic lupus erythematosus, antiphospholipid antibody syndrome, rheumatoid arthritis, Sjogren’s syndrome), and other immunological diseases. Indeed, they have anti-inflammatory, immunomodulating, anti-infective, antithrombotic, and metabolic effects. Among the biological effects of chloroquine and hydroxychloroquine, it is important to highlight their antitumoral properties, likely due to their strong antiproliferative, antimutagenic, and inhibiting autophagy capacities. These effects make these drugs a possible option in the treatment of several tumors in association with radiotherapy and chemotherapy. Finally, the repurposing of chloroquine and hydroxychloroquine is currently being examined for neurological diseases such as neurosarcoidosis, chronic lymphocytic inflammation with pontine perivascular enhancement responsive to corticosteroids, and primary progressive multiple sclerosis. Several ongoing clinical trials have been testing these drugs in non-neoplastic and neoplastic diseases. Moreover, the well-demonstrated good tolerability of chloroquine and hydroxychloroquine make them safe even during pregnancy. Gastrointestinal and cutaneous manifestations are considered not to be serious, while retinal, neuromuscular, and cardiac toxicities are classified as serious adverse events.

/pdf/current-and-future-use-of-chloroquine-and-hydroxychloroquine-23r4kf3fld.pdf

Current and Future Use of Chloroquine and Hydroxychloroquine in Infectious, Immune, Neoplastic, and Neurological Diseases: A Mini-Review.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly spread across the globe at unprecedented speed and is showing no signs of slowing down The outbreak of coronavirus disease 2019 (COVID-19) has led to significant health burden in infected patients especially in those with underlying comorbidities The aim of this study was to evaluate the correlation between comorbidities and their role in the exacerbation of disease in COVID-19 patients leading to fatal outcomes A systematic review was conducted using data from MEDLINE, Scopus, Web of Science, and EMBASE databases published from 1 December 2019 to 15 September 2020 Fifty-three articles were included in the systematic review Of those 53 articles, 8 articles were eligible for meta-analysis Hypertension, obesity, and diabetes mellitus were identified to be the most prevalent comorbidities in COVID-19 patients Our meta-analysis showed that cancer, chronic kidney diseases, diabetes mellitus, and hypertension were independently associated with mortality in COVID-19 patients Chronic kidney disease was statistically the most prominent comorbidity leading to death However, despite having high prevalence, obesity was not associated with mortality in COVID-19 patientsIMPORTANCE COVID-19 has plagued the world since it was first identified in December 2019 Previous systematic reviews and meta-analysis were limited by various factors such as the usage of non-peer reviewed data and were also limited by the lack of clinical data on a global scale Comorbidities are frequently cited as risk factors for severe COVID-19 outcomes However, the degree to which specific comorbidities impact the disease is debatable Our study selection involves a global reach and covers all comorbidities that were reported to be involved in the exacerbation of COVID-19 leading to fatal outcomes, which allows us to identify the specific comorbidities that have higher risk in patients The study highlights COVID-19 high-risk groups However, further research should focus on the status of comorbidities and prognosis in COVID-19 patients

Comorbidities in SARS-CoV-2 Patients: a Systematic Review and Meta-Analysis.

The American Society for Apheresis (ASFA) Journal of Clinical Apheresis (JCA) Special Issue Writing Committee is charged with reviewing, updating, and categorizing indications for the evidence‐based use of therapeutic apheresis (TA) in human disease. In the Ninth Edition, the JCA Special Issue Writing Committee has incorporated systematic review and evidence‐based approaches in the grading of evidence and categorization of apheresis indications to make recommendations on the use of apheresis in a wide variety of diseases and conditions. This edition has largely maintained the general layout and concept of a fact sheet introduced in the Fourth Edition (2007). Each fact sheet succinctly summarizes the evidence for the use of TA in a specific disease or medical condition. The Ninth Edition of the JCA Special Issue comprises 91 fact sheets and 166 graded and categorized indications. This includes seven new fact sheets, nine new indications on existing fact sheets, and eight changes in the category for existing indications. The Ninth Edition of the JCA Special Issue seeks to continue to serve as a key resource that guides the utilization of TA in the treatment of human disease.

Guidelines on the Use of Therapeutic Apheresis in Clinical Practice – Evidence‐Based Approach from the Writing Committee of the American Society for Apheresis: The Ninth Special Issue

OBJECTIVE: Discover novel autoantibodies in CIDP patients. BACKGROUND: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a disorder that includes patients with variable phenotypes and different responses to treatment. Its pathogenesis is autoimmune, with probable involvement of autoantibodies. Previous reports describe antibodies against myelin and axonal proteins, but their pathogenicity is controversial. Recent studies highlight the importance of the axo-glial junction in CIDP pathogenesis. Contactin-1 (CNTN1) and contactin associated protein 1 (CASPR1) are proteins of paranodes that play an essential role in myelination. We describe the presence of antibodies against CNTN1 and CNTN1/CASPR1 complex in a small subset of CIDP patients sharing specific clinical features. DESIGN/METHODS: We designed an unbiased approach for antigen unraveling using patients9 sera for hippocampal neuron immunoprecipitation. Mass spectrometry analysis revealed CNTN1-complex proteins in the precipitate. The presence of antibodies against CNTN1 complex was confirmed by immunocytochemistry in CNTN1-transfected cells, sciatic nerve immunohistochemistry and inhibition experiments. Patients9 clinical features and response to therapy were reviewed. RESULTS: Forty-six patients were included in the study. Two patients9 sera have antibodies against CNTN1 protein. Another patient precipitated both CNTN1 and CASPR1 proteins and had antibodies against the CNTN1/CASPR1 complex. All three patients shared clinical features including late and, aggressive onset, predominantly motor involvement with early axonal damage and poor response to intravenous immunoglobulins. CNTN1 antibodies were absent in 14 healthy controls and 90 patients with other neurological diseases, including 48 patients with Guillain-Barre syndrome. CONCLUSIONS: We describe the presence of antibodies against CNTN1-complex in a small subset of CIDP patients with homogeneous clinical features and response to therapy. Those antibodies could provide a diagnostic and prognostic biomarker. Studies with similar design can help discovering other autoantibodies and defining prognostic subgroups in CIDP. This work has been accepted for publication in Annals of Neurology. Supported by: Research grants from Fondo de Investigaciones Sanitarias (FIS intrasalud) 09/1964 (PI I Illa), Luis Querol by FIS CM 09/00017 and Gisela Nogales by FIS CD10/00027. Disclosure: Dr. Illa has received personal compensation for activities with Grifols. Dr. Nogales-Gadea has nothing to disclose. Dr. Querol has nothing to disclose. Dr. Gallardo has nothing to disclose. Dr. Rojas has nothing to disclose.

Antibodies to Contactin-1 in Chronic Inflammatory Demyelinating Polyneuropathy (P01.150)

Antibodies to glutamic acid decarboxylase (GAD) have been associated with several neurological syndromes, including stiff-person syndrome, cerebellar ataxia and epilepsy. These antibodies were first described in 1988, but several controversies about GAD autoimmunity still remain. No criteria exist to establish when a neurological syndrome is pathogenically linked to GAD antibodies, often leading to the assumption that any syndrome in which these antibodies are present is immune mediated, sometimes resulting in misdiagnosis and unnecessary treatment. In this Review, we provide recommendations for assessing the association between a neurological syndrome and the presence of GAD antibodies, and we critically review the evidence on the pathogenicity of GAD antibodies. Given that stiff-person syndrome is usually autoimmune, the presence of GAD antibodies in the cerebrospinal fluid is sufficient to confirm a pathogenic link with GAD autoimmunity. However, for cerebellar ataxia, epilepsy and other syndromes with different aetiologies, we propose that confirmation of a pathogenic link with GAD autoimmunity requires demonstration of intrathecal GAD antibody synthesis. Nevertheless, the evidence that GAD antibodies are directly pathogenic is not yet convincing. Studies in animal models are needed to demonstrate whether neurological syndromes are directly caused by specific disruption of GAD function by GAD antibodies. Antibodies to glutamic acid decarboxylase (GAD) are associated with several neurological syndromes but their importance and role are controversial. In this Review, Graus et al. propose criteria for assessing the association between GAD antibodies and neurological syndromes and discuss the pathogenicity of GAD antibodies.

GAD antibodies in neurological disorders — insights and challenges

SPS: Understanding the complexity.

Neurological complications in a predominantly African American sample of COVID-19 predict worse outcomes during hospitalization.

Treatment and Management of Autoimmune Neuropathies

Despite the surge in our knowledge of Fabry’s Disease (FD) and the advancements in diagnostic tools, there is often a significant time between the onset of symptoms and diagnosis. According to the Fabry Registry, 10.5 years is the average age of symptom onset, but 28.5 years is the average age of diagnosis. As a rare disease which shares clinical manifestations with many other disorders, FD can be challenging to recognize. This is a concern because early initiation of enzyme replacement therapy has been found to be important for reduction of disease burden. In order to help clinicians identify FD in its earliest stages, in this review we describe its neurological features, diagnosis and treatment.

https://www.rarediseasesjournal.com/articles/diagnosing-and-treatment-of-fabrys-disease-from-a-neurologic-perspective.pdf

Diagnosing and treatment of Fabry's disease from a neurologic perspective

Neurological Complications of COVID19 during March 2020 at LCMC Health University Medical Center: Dataset.

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