scholarly journals AN UPDATE DATA ON THE TREATMENT OF CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY (review of literature)

Author(s):  
Roman A. Gapeshin ◽  
Evgeny R. Barantsevich ◽  
Dmitry I. Rudenko ◽  
Oksana V. Posokhina ◽  
Tima R. Stuchevskaya

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a heterogeneous immune-mediated peripheral neuropathy with progressive or relapse-remitting course. Incidence of CIDP ranged between 1 and 8.9/100 000. Recently, most frequent therapies for CIDP treatment was glucocorticosteroids, intravenous immunoglobulin and plasma exchange. In cases of ineffectiveness or lack of effectiveness, cytostatics, monoclonal antibodies and others could be used for CIDP treatment. In the article, authors presented an update data on the use of main methods for CIDP therapy, their mechanisms of action, indication for their use and advantages and disadvantages of each of them.

2015 ◽  
Vol 10 (01) ◽  
pp. 85 ◽  
Author(s):  
Antonios Kerasnoudis ◽  
Kallia Pitarokoili ◽  
Ralf Gold ◽  
Min-Suk Yoon ◽  
◽  
...  

History-taking and nerve conduction studies are fundamental for the diagnosis and assessment of the severity of acute (AIDP) or chronic inflammatory demyelinating polyneuropathy (CIDP). The diagnostic challenge of distinguishing these two immune-mediated subacute polyradiculoneuropathies remains high, as intravenous immunoglobulin and steroids exert short-term clinical improvement in the majority of the CIDP cases, whereas steroids have no effect on AIDP patients. Accordingly, the precise classification of subacute polyradiculoneuropathies significantly affects the early application of steroids in CIDP. This review aims to give a timely update on the application of clinical, electrophysiological and nerve ultrasound parameters in distinguishing subacute CIDP from AIDP.


2019 ◽  
Vol 90 (9) ◽  
pp. 981-987 ◽  
Author(s):  
Helmar Christoph Lehmann ◽  
David Burke ◽  
Satoshi Kuwabara

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated neuropathy typically characterised by symmetrical involvement, and proximal as well as distal muscle weakness (typical CIDP). However, there are several ‘atypical’ subtypes, such as multifocal acquired demyelinating sensory and motor neuropathy (Lewis-Sumner syndrome) and ‘distal acquired demyelinating symmetric neuropathy’, possibly having different immunopathogenesis and treatment responses. In the absence of diagnostic and pathogenetic biomarkers, diagnosis and treatment may be difficult, but recent progress has been made in the application of neuroimaging tools demonstrating nerve hypertrophy and in identifying subgroups of patients who harbour antibodies against nodal proteins such as neurofascin and contactin-1. Despite its relative rarity, CIDP represents a significant economic burden, mostly due to costly treatment with immunoglobulin. Recent studies have demonstrated the efficacy of subcutaneous as well as intravenous immunoglobulin as maintenance therapy, and newer immunomodulating drugs can be used in refractory cases. This review provides an overview focusing on advances over the past several years.


2021 ◽  
pp. 72-76
Author(s):  
Anna P. Patnaik ◽  
Joseph Mininni ◽  
Neil C. Porter ◽  
Nicholas A. Morris

Acute-onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) is an immune mediated neuropathy characterized by progressive weakness and sensory impairment lasting over 2 months. Guillain-Barré-Strohl syndrome (GBS) is an immune mediated polyneuropathy with a similar presentation often over less than 4 weeks. While some have argued for the existence of recurrent GBS, most classify the syndrome as a form of relapsing-remitting CIDP. However, there are cases of GBS with treatment-related fluctuations that must be distinguished from A-CIDP as patients with A-CIDP require long-term immunotherapy. In this case report, we discuss a patient with multiple relapses over 3 years, who is more likely to have A-CIDP. His ganglioside profile, which has rarely been reported in A-CIDP, included high concentrations of anti-GM1, anti-GD1a, and anti-GD1b antibodies, which may account for his severe disease course.


2021 ◽  
Vol 104 (4) ◽  
pp. 003685042110502
Author(s):  
Liu Wang ◽  
Dan Wang ◽  
Yuyi Ruan ◽  
Xionghui Chen ◽  
Wei Chen ◽  
...  

Background: Systemic lupus erythematosus is a common autoimmune disease involving multiple systems. Clinical involvement of the central and peripheral nervous systems is not unusual, but peripheral neuropathy in systemic lupus erythematosus with chronic inflammatory demyelinating polyneuropathy is uncommon. Our study aimed to illustrate the clinical features, diagnosis, and treatment of systemic lupus erythematosus combined with chronic inflammatory demyelinating polyneuropathy, and to aid in the identification of peripheral neuropathy in systemic lupus erythematosus. Methods: This article reports a case of systemic lupus erythematosus with onset in pregnancy, with chronic inflammatory demyelinating polyneuropathy as the first manifestation. We then analyze the identification of common peripheral neuropathy in systemic lupus erythematosus in detail, based on a literature review of confirmed cases of systemic lupus erythematosus combined with chronic inflammatory demyelinating polyneuropathy. Results: A 34-year-old woman presented progressive muscle weakness and muscular atrophy in the extremities during pregnancy, 3 years previously. At 4 months after onset, she had completely lost the ability to hold objects and walk, and had slight numbness in the limbs, without paresthesia. Her condition was misdiagnosed as “motor neuron disease” at the time. Three years after onset, her condition was revisited because of nephrotic syndrome, and she was diagnosed with nephrotic syndrome and peripheral nerve injury caused by systemic lupus erythematosus. After immunosuppressive treatment with corticosteroids and intravenous cyclophosphamide, her symptoms of muscle weakness were markedly improved. This article summarizes the characteristics of systemic lupus erythematosus combined with chronic inflammatory demyelinating polyneuropathy that have been reported in the literature, from the aspects of morbidity, disease progression, nerve injury, laboratory examinations, and treatment response. Conclusions: Our identification of a common peripheral neuropathy in systemic lupus erythematosus will help to improve clinicians’ understanding of various peripheral neuropathies in systemic lupus erythematosus. It will also aid in the early diagnosis and treatment of such patients, thus improving their long-term prognosis.


2012 ◽  
Vol 8 (1) ◽  
pp. 62
Author(s):  
Antonios Kerasnoudis ◽  

Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common acquired immune-mediated inflammatory disorder of the peripheral nervous system. The diagnosis is based in classic cases, on the distribution pattern of the neurological semiology and pathological changes of nerve conduction studies (NCS). However, in cases with subtle clinical presentation, an extended diagnostic workup may be needed (cerebrospinal fluid examination, laboratory tests, nerve biopsy). NCS remain fundamental for the diagnosis, follow-up and measurement of response to immunetreatment in CIDP. However, new challenges arose on how best to acquire a static and dynamic imaging of the peripheral nerves, with the aim of providing a holistic approach to the nerve impairment. According to the literature, neuromuscular ultrasound is able to detect in cases of CIDP thickened or swollen roots, peripheral nerves or brachial plexus, findings that are consistent with ongoing inflammation. This review provides a timely update on the nerve ultrasound findings of CIDP and future possibilities of neuromuscular ultrasound are also discussed.


2004 ◽  
Vol 62 (3b) ◽  
pp. 892-894 ◽  
Author(s):  
Andrés Maria Villa ◽  
Orlando Garcea ◽  
Marianna Di Egidio ◽  
Roberto Saizar ◽  
Roberto Eduardo Pedro Sica

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated neuropathy. It presents with a course of progression which may be slow and steady or step-wise or relapsing. Sensory ataxic polyneuropathy may be the only clinical manifestation of this disease. Treatment with interferon beta1a (INF beta1a) has been tried with different results in patients who were refractory to other, more conventional, immunomodulatory therapies. Here we report on a patient who had a relapsing form of pure sensory ataxic CIDP and who failed to respond to intravenous human immunoglobulin. He was put on INF beta1a for 3 years. During this period he suffered no relapses while his condition stabilized.


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