Atormac
Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 3536  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Search
 
  
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (547 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

 
  In this Article
 »  Abstract
 » Introduction
 » Methods
 » Results
 » Discussion
 » Conclusions
 »  References
 »  Article Tables

 Article Access Statistics
    Viewed2921    
    Printed106    
    Emailed1    
    PDF Downloaded129    
    Comments [Add]    
    Cited by others 3    

Recommend this journal

 


 
Table of Contents    
ORIGINAL ARTICLE
Year : 2016  |  Volume : 64  |  Issue : 1  |  Page : 45-49

Coexistence of autoimmune diseases and autoantibodies in patients with myasthenia gravis


1 Department of Neurology, Van Regional Training and Research Hospital, Van, Ankara, Turkey
2 Ankara Training and Research Hospital, Ankara, Turkey
3 Department of Ankara Training and Research Hospital, Ankara, Turkey

Date of Web Publication11-Jan-2016

Correspondence Address:
Sibel Tamer
Specialist Neurologist, Van Regional Training and Research Hospital, Van
Turkey
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.173638

Rights and Permissions

 » Abstract 

Background: In this study, we assessed 75 patients with myasthenia gravis (MG) for coexistent autoimmune diseases (ADs) and for the characteristic autoantibodies that are associated with the most relevant forms of ADs.
Methods: The demographic and clinical characteristics of the patients were recorded. In all patients, thyroid function tests, thyroid autoantibodies, and other autoantibodies were studied. The diagnosis of autoimmune thyroid disease (AITD) was made based on the clinical features, physical examination, and laboratory findings. The diagnoses of rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) were made in accordance with the revised criteria of American College of Rheumatology. The presence of other ADs were also recorded which was based on whether or not the patient already had a diagnosis of ADs; or, whether it was detected during the period of the study based on clinical findings and/or laboratory abnormalities.
Results: Thirty-nine patients (52%) had autoantibody positivity in their sera. Thyroid autoantibodies and antinuclear antibodies were the main autoantibodies detected. In twenty one of these patients, a diagnosis of AD could not be confirmed. Eighteen patients (24%) had a confirmed diagnosis of a coexisting AD. These ADs included AITD (16%), RA (4%), SLE (2.6%), and Lambert–Eaton myasthenic syndrome (1.3%). In ten patients, the diagnosis of ADs had been established before the development of MG; 8 of the patients included those who were newly diagnosed with ADs in the course of the management of MG.
Conclusions: MG has an increased frequency of coexisting ADs. Autoantibodies that are characteristic for ADs can be found in the patients without the presence of any of the clinical findings of ADs. Clinical attention towards the management of ADs is especially needed during the follow-up of patients with MG.


Keywords: Autoantibodies; autoimmune disorder; myasthenia gravis


How to cite this article:
Tamer S, Gokce Gunes HN, Gokcal E, Yoldas TK. Coexistence of autoimmune diseases and autoantibodies in patients with myasthenia gravis. Neurol India 2016;64:45-9

How to cite this URL:
Tamer S, Gokce Gunes HN, Gokcal E, Yoldas TK. Coexistence of autoimmune diseases and autoantibodies in patients with myasthenia gravis. Neurol India [serial online] 2016 [cited 2019 Aug 23];64:45-9. Available from: http://www.neurologyindia.com/text.asp?2016/64/1/45/173638



 » Introduction Top


Myasthenia gravis (MG) is a rare autoimmune disease (AD) caused by autoantibodies against neuromuscular junction proteins such as the nicotinic acetylcholine receptor (AChR), muscle specific tyrosine kinase (MuSK), and low-density lipoprotein receptor-related protein 4.[1],[2],[3] Clinically, MG is characterized by muscle weakness and rapid fatigue aggravated by exercise and relieved by rest. AChR-specific antibodies are detected in the majority (85%) of patients with MG.[1],[3] Known antibodies cannot be detected in approximately 5–10% of patients; these cases are classified as seronegative MG (SNMG). The onset of MG is influenced by age and gender in a bimodal fashion. Females less than 50 years of age are more commonly affected than are males, and males are slightly more frequently affected by late onset MG. The classification of MG takes into account the nature of the antibodies, the age at onset of the disease, the affected muscles (ocular and/or generalized), and thymic abnormalities.[1],[2],[3],[4]

Approximately 5% of the population is affected by one or more autoimmune disorders, and the prevalence is higher in female than in male patients. Patients who are affected by one autoimmune disorder have a higher risk of developing a second one. Patients with MG have an increased risk of developing other autoimmune disorders when compared with the non-MG population.[5] In patients with MG, the frequency of developing a second autoimmune disorder is in the range of 8.7–25%, with the frequency being highest in female subjects and in individuals with early-onset MG.[6] In a systematic review, autoimmune thyroid disease (AITD) was the most frequent AD associated with MG from amongst 23 associated ADs occurring in 10% of patients with MG.[7] The other common ADs associated with MG are systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).[6],[7] When multiple ADs are present simultaneously, the patient has specific immunological markers for the simultaneously present diseases. The pathogenesis for the co-occurrence of different varieties of ADs in the same patient is unclear; however, genetic, infectious, and immunological factors have been implicated, and abnormalities in both humoral and cell-mediated immunity have been described. Similar environmental triggers in a genetically susceptible individual may lead to the co-occurrence of different ADs in the same patient.

The aim of this study was to evaluate the clinical and serological features of MG associated with other ADs.


 » Methods Top


We received permission from our local Ethics Committee to conduct the present study. After obtaining informed consent, we examined 75 patients with MG (36 men and 39 women; age range, 17–81 years) who received treatment at the Dıskapı Yıldırım Beyazıt Training and Research Hospital from 2007 to 2012. To establish the diagnosis of MG, the patients included in this study underwent a neurological assessment, which included a physical examination, a Tensilon (edrophonium) test, and electrophysiological studies.

In this study, patients with MG were subdivided into two groups. Patients were classified as seropositive if an anti-acetylcholine receptor (AChR) or anti-MuSK antibody was detected; patients in whom these antibodies were absent were classified as seronegative. Age, gender, age at the onset of the disease, and the disease duration were recorded. Early-onset MG included patients in whom the disease occurred before the age of 50 years; late-onset MG included patients who developed the disease when they were 50 years of age or older. The clinical type was recorded as ocular or generalized. The severity of MG was classified using the MG Foundation of America criteria.[8] All patients were subjected to computed tomography (CT) of the mediastinum. Thirty of the 75 MG patients with thymic abnormalities (that were visualized on the CT scan) received a thymectomy. A diagnosis of thymic hyperplasia or a thymoma was established on the histological examination.

In all patients, the levels of thyroid-stimulating hormone (TSH), free triiodothyronine, free thyroxine, antithyroid peroxidase (anti-TPO) antibody, antithyroglobulin (anti-TG) antibody, and rheumatoid factor (RF) were determined. Antinuclear antibody (ANA), antidouble-stranded deoxyribonucleic acid (anti-dsDNA), and antineutrophil cytoplasmic antibodies (ANCA; c-ANCA with a cytoplasmic fluorescence pattern, and p-ANCA with a perinuclear fluorescence pattern) were examined using enzyme-linked immunosorbent assay. Anti-Ro/SSA, anti-La/SSB, anti-Jo-1, and anti-Smith (anti-SM) antibodies were investigated by immunoblotting.

The diagnosis of Hashimoto's thyroiditis (HT) and Graves' disease (GD) was made based on clinical features, physical examination, laboratory findings, and ultrasound of the thyroid. Thyroid scintigraphy and fine-needle aspiration biopsy were performed, whenever necessary. The diagnosis of RA and SLE was made according to the American College of Rheumatology criteria.[9] Lambert–Eaton myasthenic syndrome (LEMS) was diagnosed based on clinical examination and electrophysiological findings.[10] Other ADs were recorded based on whether or not the patient already had an established diagnosis of ADs; if there was a clinical suspicion of their existence; and/or the laboratory abnormalities established their coexistence.

SPSS 17.0 (IBM corporation) was used for statistical analysis. Age and disease duration were compared using Student t-test. The gender, serological status, age at onset, clinical type, and thymic status were compared using the Chi-square test. P < 0.05 was considered to indicate statistical significance.


 » Results Top


As shown in [Table 1], of the 75 patients with MG, 40 (20 men and 20 women; age range, 17–80 years) were seropositive, and 35 (16 men and 19 women; age range, 19–81 years) were seronegative. Among the 40 seropositive patients, 37 were anti-AChR-positive, and 3 were anti-MuSK-positive. The mean ages were 50 ± 18 and 48.7 ± 15 years in the seropositive and seronegative groups, respectively. The disease duration ranged from 15 days to 31 years (median interval: 5.5 years). There were no significant differences in gender, age, duration of the disease, age at onset of the disease, clinical type and severity, or thymic disorders between the seropositive and seronegative groups.
Table 1: Demographic and clinical characteristics of seropositive and seronegative patients

Click here to view


As shown in [Table 2], 18 (24%) patients had coexistent MG and ADs. Ten patients already came with an established diagnosis of ADs before the diagnosis of MG was made; whereas in 8 patients, the diagnosis of AD was made following the recognition of MG which led to the performance of ancillary investigations. Among these 18 patients, 5 (27.7%) had ocular MG, and 13 (72.3%) had generalized MG. When analyzed according to the age of onset of the disease, 13 (72.3%) patients were less than 50 years of age, and 5 (27.7%) patients were over 50 years old. Of the 18 patients, 8 had an abnormal thymus with 7 having a thymic hyperplasia, and 1 having a thymoma. Patients with MG with associated ADs were predominantly female, experienced early-onset symptoms of MG, had a higher frequency of generalized MG, and had SNMG; however, the difference was not significant (P = 0.06).
Table 2: Autoimmune diseases ın patients wıth MG

Click here to view


Twelve patients (16%) were diagnosed with AITD. Among these 12 patients, 5 had hypothyroidism, and 4 had hyperthyroidism. Three of them were euthyroid. In MG patients with AITD, 5 (41.6%) had ocular MG, and 7 (58.4%) had mild, generalized MG (classes IIA, IIB, and IIIB). Five patients had thymic hyperplasia, and one had a thymoma. MG patients with AITD were predominantly female, experienced early-onset MG symptoms, and had a higher frequency of generalized MG; however, the difference was not significant (P = 0.04). Eight had a diagnosis of AITD before the diagnosis of MG, whereas in 4 patients, the diagnosis of AITD was established on performing investigations after the recognition of MG.

Three patients with MG also had RA (4%). All cases were associated with generalized (classes IIA, IIB, and IVB) and early-onset MG. Among the 3 RA patients, 1 patient already had a clinically overt RA when the diagnosis of MG was made, whereas 2 patients were detected to be having RA after the recognition of MG. One of the 3 patients had thymic hyperplasia and a history of thymectomy.

Two patients were diagnosed with SLE (2.6%). Both patients had generalized MG (classes IIB and IIIB) and SNMG. One patient with thymic abnormalities had a history of thymectomy before entering the study. Among the 2 patients with SLE, one experienced early and the other, late onset MG symptoms. One patient already had clinically manifest SLE when the diagnosis of MG was made; the other patient was detected to be having SLE (and fulfilled the diagnostic criteria of the disease) after the onset of MG.

A total of 39 (52%) patients, 19 seropositive and 20 seronegative, were positive for autoantibodies in the sera. The detected autoantibodies included 27 anti-TPO, 17 anti-TG, 17 ANA, 6 RF, 3 anti-TSH receptor, 2 anti-dsDNA, 1 anti-Jo-1, 1 anti-Ro/SSA, and 1 anti-La/SSB. We did not detect any anti-SM or ANCA autoantibodies. The presence of autoantibodies did not differ between the seropositive and seronegative groups. The presence of autoantibodies was higher in female patients (62.5% of females vs. 40% of male patients); however, the difference was not significant (P = 0.052).

The clinical features and electrophysiological findings indicated the coexistence of MG and LEMS in 1 (1.3%) patient. The predominance of oculobulbar symptoms and a positive edrophonium test favored a diagnosis of MG. However, areflexia with facilitation after voluntary contraction is a typical finding in LEMS, and the results of the repetitive nerve stimulation test supported concomitant LEMS. Based on these findings, we believe that this patient had MG and LEMS overlap syndrome. No commercially available autoantibodies were available to detect P/Q-type voltage-gated calcium channels. The myasthenic symptoms were of early-onset and generalized, and the thymus was normal. A tumor was found in the lungs, and the patient died 1-year after the diagnosis had been made.


 » Discussion Top


Autoimmunity occurs due to an inappropriate response against tissue elements that are normally present, leading to chronic diseases characterized by the loss of immune tolerance to self-antigens.[1],[2],[3],[4] Like most ADs, MG is caused by a complex interaction among multiple genotypes of low penetrance and various environmental factors including pathogenic exposure. The latter conditions include exposure to Epstein–Barr virus,[1],[4] administration of sex hormones,[11] low vitamin D levels, and lifestyle disorders such as cigarette smoking.[12],[13],[14]

Most autoimmune disorders appear with increased frequency in patients with MG. The prevalence of ADs in patients with MG ranges from 8.7% to 25% in the literature.[7] In a systematic review of 25 studies, the frequency of ADs was 13%. However, only four of these 25 studies provided a diagnostic criteria that could detect the associated presence of ADs.[7] We included the assessment of the recommended diagnostic criteria in our study and found a 24% incidence of association of ADs with MG. This finding is consistent with the previously published studies.

The comorbidity due to autoimmunity varies between the MG subgroups. In early-onset MG, all ADs appear more frequently than expected, particularly in female patients.[6] Late-onset MG has a lower frequency of autoimmune overlap than do the other MG subgroups.[15],[16] A thymectomy per se does not seem to be influencing the development of a second autoimmune disorder.[14] However, thymectomy may induce a breakdown in self-tolerance and be a risk factor for the development of systemic autoimmune disorders, such as SLE and neuromyelitis optica (NMO), in patients with MG.[14],[17]

A systematic review of the frequency of ADs in patients with MG showed that AITD was the most common disease that coexisted with MG.[7] The incidence of AITD was 16% in our study: HT was predominant (12%) followed by GD (4%). MG combined with AITD tends to be a milder form of the disease.[14] Ocular MG has a special link to thyroid disease. The reason for the association between AITD and ocular MG is unknown, but several hypotheses may be considered. First, ocular MG and generalized MG might actually represent separate diseases with different spectra of associated conditions. Second, immunological cross-reactivity against epitopes or auto-antigens shared by the thyroid and eye muscles might be the basis for this association. A third explanation for the higher frequency of ocular MG in AITD could be that these disorders have a common genetic background.[18],[19] In our study, we showed that the clinical features of patients with MG and AITD had an early-onset, mild clinical expression, with a lower frequency of thymic abnormalities.

The coexistence of SLE and MG has rarely been reported, and most of the published studies are case reports.[17] In our study, 2 of 75 MG patients had SLE. The prevalence of SLE in our study was 2.6%. A higher prevalence of SLE in patients with MG (7.7%; 78 patients) was reported by Sthoeger et al.[20] In accordance with previous reports, the majority of patients who had combined manifestations of MG-SLE were female.[21] In our patients, the clinical manifestations of patients with SLE and MG were less severe than that encountered when either of them is present individually. Whether thymectomy precipitates SLE is still controversial;[21] however, the co-occurrence of these two diseases (i.e., patients who had SLE before the onset of MG) cannot be explained by this hypothesis. The co-occurrence of SLE and MG may be due to a common genetic predisposition as well as coexisting immunological abnormalities.[17]

In our study, 2 of the 75 MG patients had RA (4%). The previous studies have reported a prevalence of 4.2%, a figure that was similar to that seen in our study.[22] Cases where MG may occur in patients treated with penicillamine for RA have been reported in the literature.[22] None of our cases had received treatment with penicillamine. Similar to the findings observed in patients with SLE, the manifestations of RA were also classically less severe.

Due to the chronic nature of most ADs, autoantibodies may appear before clinical symptoms manifest and could provide a good predictive marker for the potential development of the disease.[1] The presence of autoantibodies was much more than that the incidence of clinically manifest ADs in our study. Thyroid autoantibodies and ANA positivity had the highest prevalence in this cohort of patients. TPO was the most frequent autoantibody encountered alone. ANA was frequently detected with other autoantibodies. The clinical characteristics of the patients did not differ according to the type of autoantibody positivity. To predict the development of the disease, prospective studies are needed that systematically follow up patients who are positive for autoantibodies until they develop clinically manifest ADs.

A rare case of coexistence of NMO and MG was documented recently.[23] McKeon et al.,[24] reported their findings on four (2%) patients of NMO with MG, and an 11% prevalence of muscle AChR antibodies in their database of 177 patients with NMO. This high prevalence suggests that the coexistence of MG and NMO might not be coincidental. Both disorders may share a common immunopathogenesis. The coexistence of MG and NMO has mainly been reported in patients who underwent a thymectomy months to years before the development of NMO. Leite et al.,[25] reported that patients with MG in association with NMO were predominantly female, had early-onset AChR-MG, had mostly mild, generalized disease, and had achieved remission in a large proportion of cases. Visual and motor symptoms caused by MG are usually easily distinguishable on clinical grounds from those caused by optic neuritis and myelitis, respectively. Our patients had no history of optic neuritis or a longitudinally extensive transverse myelitis.


 » Conclusions Top


Our study supports the concept that patients with MG have an increased frequency of coexisting ADs. Autoantibodies can also be detected even when the diagnosis of ADs is not established. The presence of autoantibodies may result in the subsequent development of ADs during the follow-up of patients with MG.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
 » References Top

1.
Berrih-Aknin S. Myasthenia gravis: Paradox versus paradigm in autoimmunity. J Autoimmun 2014;52:1-28.  Back to cited text no. 1
    
2.
Zhang B, Tzartos JS, Belimezi M, Ragheb S, Bealmear B, Lewis RA, et al. Autoantibodies to lipoprotein-related protein 4 in patients with double-seronegative myasthenia gravis. Arch Neurol 2012;69:445-51.  Back to cited text no. 2
    
3.
Gilhus NE. Autoimmune myasthenia gravis. Expert Rev Neurother 2009;9:351-8.  Back to cited text no. 3
    
4.
Berrih-Aknin S, Le Panse R. Myasthenia gravis and autoantibodies: Pathophysiology of the different subtypes. Rev Med Interne 2014;35:413-20.  Back to cited text no. 4
    
5.
Sardu C, Cocco E, Mereu A, Massa R, Cuccu A, Marrosu MG, et al. Population based study of 12 autoimmune diseases in Sardinia, Italy: Prevalence and comorbidity. PLoS One 2012;7:e32487.  Back to cited text no. 5
    
6.
Fang F, Sveinsson O, Thormar G, Granqvist M, Askling J, Lundberg IE, et al. The autoimmune spectrum of myasthenia gravis: A Swedish population-based study. J Intern Med 2015;277:594-604.  Back to cited text no. 6
    
7.
Mao ZF, Yang LX, Mo XA, Qin C, Lai YR, He NY, et al. Frequency of autoimmune diseases in myasthenia gravis: A systematic review. Int J Neurosci 2011;121:121-9.  Back to cited text no. 7
    
8.
Jaretzki A 3rd, Barohn RJ, Ernstoff RM, Kaminski HJ, Keesey JC, Penn AS, et al. Myasthenia gravis: Recommendations for clinical research standards. Task force of the medical scientific advisory board of the myasthenia gravis foundation of America. Neurology 2000;55:16-23.  Back to cited text no. 8
    
9.
Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield NF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1982;25:1271-7.  Back to cited text no. 9
    
10.
Kim JA, Lim YM, Jang EH, Kim KK. A patient with coexisting myasthenia gravis and Lambert-Eaton myasthenic syndrome. J Clin Neurol 2012;8:235-7.  Back to cited text no. 10
    
11.
Costenbader KH, Feskanich D, Stampfer MJ, Karlson EW. Reproductive and menopausal factors and risk of systemic lupus erythematosus in women. Arthritis Rheum 2007;56:1251-62.  Back to cited text no. 11
    
12.
Karlson EW, Chang SC, Cui J, Chibnik LB, Fraser PA, De Vivo I, et al. Gene-environment interaction between HLA-DRB1 shared epitope and heavy cigarette smoking in predicting incident rheumatoid arthritis. Ann Rheum Dis 2010;69:54-60.  Back to cited text no. 12
    
13.
Bach JF. The etiology of autoimmune diseases: The case of myasthenia gravis. Ann N Y Acad Sci 2012;1274:33-9.  Back to cited text no. 13
    
14.
Gilhus NE, Nacu A, Andersen JB, Owe JF. Myasthenia gravis and risks for comorbidity. Eur J Neurol 2015;22:17-23.  Back to cited text no. 14
    
15.
Toth C, McDonald D, Oger J, Brownell K. Acetylcholine receptor antibodies in myasthenia gravis are associated with greater risk of diabetes and thyroid disease. Acta Neurol Scand 2006;114:124-32.  Back to cited text no. 15
    
16.
Matsui N, Nakane S, Nakagawa Y, Kondo K, Mitsui T, Matsumoto T, et al. Increasing incidence of elderly onset patients with myasthenia gravis in a local area of Japan. J Neurol Neurosurg Psychiatry 2009;80:1168-71.  Back to cited text no. 16
    
17.
Jallouli M, Saadoun D, Eymard B, Leroux G, Haroche J, Le Thi Huong D, et al. The association of systemic lupus erythematosus and myasthenia gravis: A series of 17 cases, with a special focus on hydroxychloroquine use and a review of the literature. J Neurol 2012;259:1290-7.  Back to cited text no. 17
    
18.
Chen YL, Yeh JH, Chiu HC. Clinical features of myasthenia gravis patients with autoimmune thyroid disease in Taiwan. Acta Neurol Scand 2013;127:170-4.  Back to cited text no. 18
    
19.
Kanazawa M, Shimohata T, Tanaka K, Nishizawa M. Clinical features of patients with myasthenia gravis associated with autoimmune diseases. Eur J Neurol 2007;14:1403-4.  Back to cited text no. 19
    
20.
Sthoeger Z, Neiman A, Elbirt D, Zinger H, Magen E, Burstein R, et al. High prevalence of systemic lupus erythematosus in 78 myasthenia gravis patients: A clinical and serologic study. Am J Med Sci 2006;331:4-9.  Back to cited text no. 20
    
21.
Hrycek A. Systemic lupus erythematosus and myasthenia gravis. Pol Arch Med Wewn 2009;119:582-5.  Back to cited text no. 21
    
22.
Poulas K, Koutsouraki E, Kordas G, Kokla A, Tzartos SJ. Anti-MuSK- and anti-AChR-positive myasthenia gravis induced by d-penicillamine. J Neuroimmunol 2012;250:94-8.  Back to cited text no. 22
    
23.
Ogaki K, Hirayama T, Chijiiwa K, Fukae J, Furuya T, Noda K, et al. Anti-aquaporin-4 antibody-positive definite neuromyelitis optica in a patient with thymectomy for myasthenia gravis. Neurologist 2012;18:76-9.  Back to cited text no. 23
    
24.
McKeon A, Lennon VA, Jacob A, Matiello M, Lucchinetti CF, Kale N, et al. Coexistence of myasthenia gravis and serological markers of neurological autoimmunity in neuromyelitis optica. Muscle Nerve 2009;39:87-90.  Back to cited text no. 24
    
25.
Leite MI, Coutinho E, Lana-Peixoto M, Apostolos S, Waters P, Sato D, et al. Myasthenia gravis and neuromyelitis optica spectrum disorder: A multicenter study of 16 patients. Neurology 2012;78:1601-7.  Back to cited text no. 25
    



 
 
    Tables

  [Table 1], [Table 2]

This article has been cited by
1 The concomitant association of thyroid disorders and Myasthenia gravis
Yu-Pei Lin,Usman Iqbal,Phung-Anh Nguyen,Md.Mohaimenul Islam,Suleman Atique,Wen-Shan Jian,Yu-Chuan(Jack) Li,Chen-Ling Huang,Chung-Huei Hsu
Translational Neuroscience. 2017; 8(1)
[Pubmed] | [DOI]
2 Immunopathogenesis in Myasthenia Gravis and Neuromyelitis Optica
Zhen Wang,Yaping Yan
Frontiers in Immunology. 2017; 8
[Pubmed] | [DOI]
3 Clinical Characteristics and Predictors of Outcome for Onconeural Antibody-Associated Disorders: A Retrospective Analysis
Shaohua Liao,Ying Qian,Huaiqiang Hu,Bing Niu,Hongwei Guo,Xiaoling Wang,Shuai Miao,Chuanfen Li,Bingzhen Cao
Frontiers in Neurology. 2017; 8
[Pubmed] | [DOI]



 

Top
Print this article  Email this article
   
Online since 20th March '04
Published by Wolters Kluwer - Medknow