Dear Sirs, Whether COVID-19 can trigger Guillain-Barré syndrome (GBS) is currently controversially discussed. Recent studies in this and other journals [2-4] indicate an association. However others did not find any epidemiological evidence so far [1]. In this latter study, no significant association between COVID-19 and GBS was found. In 47 patients with GBS (of those 13 patients with definite, 12 with probable, and 22 patients without COVID-19) there was no atypical pattern in incidence, clinical presentation or response to established therapies in COVID-19 associated GBS [1]. Uniquely, a higher rate of assisted ventilation requirement was observed in GBS subsequent to COVID-19 [1]. Notably, several case series already conveyed a rapid sequence and even significant overlap of COVID-19 pneumonia and GBS [4-6]. We also observed such a rapid temporal sequence in three patients consecutively treated in our department between October 2020 and January 2021: The first patient, a 76-year-old male, presented with a reduction of his general condition and dyspnoea. Thoracic CT revealed pneumonic infiltrates typical for COVID-19. PCR analysis for SARS-CoV-2 were equivocal. Four days after hospitalization, the patient showed a rapidly evolving flaccid tetraparesis with general areflexia and phrenicobulbar involvement with consecutive requirement of intensive care. Cerebrospinal fluid (CSF) showed albuminocytologic dissociation and IgM autoantibodies against sulfatide were detected in serum (Table 1). Nerve conduction studies (NCS) revealed an axonal-demyelinating sensorimotor polyradiculoneuropathy. Intravenous immunoglobulin (IVIg) led to
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated polyradiculoneuropathy leading to disability via inflammatory demyelination of peripheral nerves. Various therapeutic approaches with different mechanisms of action are established for the treatment of CIDP. Of those, corticosteroids, intravenous or subcutaneous immunoglobulin, or plasma exchange are established first-line therapies as suggested by the recently revised EAN/PNS guidelines for the management of CIDP. In special cases, immunosuppressants or rituximab may be used. Novel therapeutic approaches currently undergoing clinical studies include molecules or monoclonal antibodies interacting with Fc receptors on immune cells to alleviate immune-mediated neuronal damage. Despite various established therapies and the current development of novel therapeutics, treatment of CIDP remains challenging due to an inter-individually heterogeneous disease course and the lack of surrogate parameters to predict the risk of clinical deterioration.
Fingolimod is a an oral disease modifying drug for relapsing remitting multiple sclerosis (MS) preventing egress of B and T cells from lymph nodes. Relevant first dose adverse events include bradycardia and atrioventricular conduction slowing. Cardiac side effects of fingolimod and combinational pharmacotherapy including duloxetine and tolterodine were monitored in mice of different age using implantable ECG telemetric systems. Cardiac tissue was assessed for S1P-receptor subtype (1 and 3), and for GIRK1 expression. Fingolimod led to a significant heart rate reduction within 60 min, which returned to baseline values within 24 h. In older mice bradycardia was more pronounced compared to younger mice. Atrioventricular conduction was not affected. Older mice showed a higher S1PR3 expression in a naïve state and receptor expression was reduced after fingolimod administration. Combination with duloxetine or tolterodine alleviated fingolimod induced heart rate decrease. Our data provide preclinical evidence that negative chronotropic effects of fingolimod might be age dependent, possibly due to an altered expression and internalization of cardiac S1PR3 in older animals. This data could be relevant for future clinical monitoring and patient selection in the aging MS population. Combinational therapies of fingolimod and duloxetine or tolterodine are well tolerated and safe without an increased risk for pronounced bradycardia or arrhythmia.
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