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Autoantibodies in Thymoma-Associated Myasthenia Gravis with Myositis Or Neuromyotonia

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Autoantibodies in Thymoma-Associated Myasthenia Gravis with Myositis Or Neuromyotonia ORIGINAL CONTRIBUTION Autoantibodies in Thymoma-Associated Myasthenia Gravis With Myositis or Neuromyotonia A˚ se Mygland, MD; Angela Vincent, MB, FRCPath; John Newsom-Davis, MD; Henry Kaminski, MD; Francesco Zorzato, MD; Mark Agius, MD; Nils E. Gilhus, MD; Johan A. Aarli, MD Background: About 50% of patients with thymoma have and 17 patients, respectively. Antibodies to RyR corre- paraneoplastic myasthenia gravis (MG). Myositis and myo- lated with the presence of myositis (P = .03); they were carditis or neuromyotonia (NMT) will also develop in some. found in all 5 patients with myositis and in only 1 pa- Patients with thymoma-associated MG produce autoan- tient with NMT, but also in 4 of 8 patients with neither tibodies to a variety of neuromuscular antigens, particu- disease. Antibodies to VGKC were found in 4 patients larly acetylcholine receptor (AChR), titin, skeletal muscle with NMT, 1 of 3 patients undergoing testing for myo- calcium release channel (ryanodine receptor [RyR]), and sitis, and 2 of 7 patients undergoing testing with neither voltage-gated potassium channels (VGKC). comorbidity. Presence of RyR antibodies correlated with high levels of titin antibodies. Objective: To examine whether neuromuscular auto- antibodies in patients with thymoma correlate with spe- Conclusions: The results appear to distinguish par- cific clinical syndromes. tially between 3 groups of patients with thymoma- associated MG: the first with RyR antibodies and myo- Methods: Serum and plasma samples from 19 patients sitis or myocarditis, the second with NMT without RyR with thymoma-associated MG, of whom 5 had myositis antibodies, and the third without RyR antibodies, myo- and 6 had NMT, underwent testing for antibodies to sitis, or NMT. Differences in the thymoma may underlie AChR, titin, RyR, and VGKC. these pathologic associations. Results: Antibodies to AChR and titin were found in 19 Arch Neurol. 2000;57:527-531 UMORS OF the thymus, es- rise to heart failure, cardiac arrhythmia, pecially lymphoepithelial and sudden death.4,5 The occurrence of thymomas, are associated myocarditis may be a reason for the in- with autoimmune pure red creased mortality of patients with thy- blood cell anemia and neu- moma-associated MG,6 and the myositis Tromuscular disorders.1 Myasthenia gravis may explain the poor clinical response (MG) is the most common, being present of these patients to nonimmunosup- in about 50% of all patients with thy- pressive treatment of their myasthenic moma at some stage.2 Myasthenia gravis symptoms. From the Departments of is a disorder with fluctuating weakness of Neuromyotonia (NMT) can also be as- Neurology, University of Bergen, 7 Bergen, Norway (Drs Mygland, skeletal muscle that is caused by autoan- sociated with thymoma. Patients with Gilhus, and Aarli), Vest-Agder tibodies to nicotinic acetylcholine recep- NMT have hyperactivity of peripheral mo- Central Hospital, Kristiansand, tors (AChR) at the neuromuscular junc- tor nerves, causing myokymia, muscle stiff- Norway (Dr Mygland), Case tion. An inflammatory myopathy of ness, muscle cramps, and sometimes muscle Western Reserve School of striated and cardiac muscle develops in hypertrophy. Some patients experience par- Medicine, Cleveland, Ohio some patients with thymoma-associated esthesias or central nervous system symp- (Dr Kaminski), and University MG. The myositis of striated muscle is toms.7 The EMG shows characteristic bursts of California–Davis (Dr Agius); characterized by proximal muscle weak- of high-frequency motor unit discharges. the Neuroscience Group, ness, elevated creatine kinase levels, and Antibodies directed against voltage-gated Institute of Molecular Medicine, a myopathic pattern on electromyogra- potassium channels (VGKC) of periph- John Radcliff Hospital, Oxford, England (Drs Vincent and phy (EMG). Results of muscle biopsies eral nerves have been detected in patients Newsom-Davis); and the show patchy inflammatory infiltrates with with NMT, with or without thymoma; the Institute of Pathology, T and B lymphocytes, plasma cells, and dis- disorder is probably caused by antibody- University of Ferrara, Ferrara, ruption of myofibrils and sarcolemmic mediated dysfunction of VGKC that nor- Italy (Dr Zorzato). structure.3 The cardiac myositis may give mally regulate nerve excitability.8 ARCH NEUROL / VOL 57, APR 2000 WWW.ARCHNEUROL.COM 527 ©2000 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/02/2021 PATIENTS AND METHODS labeled extracts of human frontal cortex,8 and values were given as picomoles per liter. The upper limit of normal was 100 pmol/L (mean + 3 SD among 6 laboratory control PATIENTS samples, 6 samples with Lambert-Eaton myasthenic syn- drome [LEMS], and 5 samples with MG without apparent Serum or plasma samples from 19 patients with thymoma NMT; none of them were positive for the presence of VGKC and combinations of MG and other neuromuscular disor- antibodies). ders were available. Ten patients were from Norway; 5 pa- Antibodies to titin were measured by means of enzyme- tients, England; 2 patients, Germany; and 2 patients, the linked immunosorbent assay using a recombinant titin an- United States. Thymomas were classified histologically ac- tigen (MGT30) as previously described.12 Results are given cording to Kirchner and Mu¨ ller-Hermelink.18 Clinical fea- as optical density (OD) values referring to the absorbance tures of the patients are shown in Table 1. Five patients of test serum samples diluted 1:200, the serum dilution giv- had MG and myositis and/or myocarditis. One of these pa- ing the best discrimination between samples with a selec- tients has been described previously as having rippling tion of positive and negative findings. The upper limit of muscle disease with electrically silent muscle cramps, in normal was OD value 60 (the mean + 3 SD among 20 se- addition to myositis and MG.19 The myositis diagnosis was rum samples from blood donors). based on clinical symptoms, elevated serum creatine ki- Antibodies to RyR were measured by means of West- nase levels, EMG findings, and results of muscle biopsy. ern blotting with purified RyR. Terminal cisternae of sar- The myocarditis diagnosis was based on cardiac symp- coplasmic reticulum from rabbit skeletal muscle were pu- toms without any other cause and typical electrocardiog- rified by means of sucrose gradient centrifugation.21 The raphy findings. The diagnosis was verified by postmortem terminal cisternae fractions were electrophoresed on so- examination in 2 of 3 patients with myocarditis. Six pa- dium dodecyl sulfate polyacrylamide gels and transblot- tients had NMT as well as MG. The NMT diagnosis was ted onto nitrocellulose. The blots were blocked for 60 min- based on clinical criteria and EMG findings.7 Eight pa- utes with 5% dry milk in phosphate-buffered saline solution; tients with MG, but no signs of other neuromuscular dis- incubated for 120 minutes with MG serum samples di- orders, were selected randomly from the serum bank of thy- luted to 1:50; incubated for 60 minutes with peroxidase- moma-associated MG at the University of Bergen, Bergen, conjugated rabbit antibodies to human IgG diluted 1:500 Norway. Serum and plasma samples were stored at −60°C (Dako, Copenhagen, Denmark); and color developed with until use. 4-chloro-1-naphtol as previously described.9 Serum samples staining the RyR protein band in the terminal cisternae frac- ANTIBODY ASSAYS tion were considered positive for anti–RyR antibodies. Each assay was performed on all the serum samples to- STATISTICS gether. Antibodies to AChR were determined by immuno- precipitation of iodine 125 (125I)-a-bungarotoxin–labeled Correlations between presence of antibodies and clinical human AChR, and values were given as nanomoles of 125I- syndromes were assessed by means of Fisher exact test. The a-bungarotoxin–binding sites precipitated per liter of se- t test was used to compare means. All analyses were per- rum as previously described.20 formed using commercially available software (SPSS 8.0 for Antibodies to VGKC were determined as previously Windows; SPSS Inc, Chicago, Ill). P,.05 was considered described by immunoprecipitation of 125I-a-dendrotoxin– significant. Patients with thymoma-associated MG produce au- RESULTS toantibodies to a variety of neuromuscular antigens in addition to the AChR and VGKC antibodies, ie, antibod- ies to the skeletal muscle calcium (Ca2+) release channel All 19 patients with thymoma-associated MG had anti- (ryanodine receptor [RyR]) of sarcoplasmic reticulum that bodies to AChR, and 17 had antibodies to titin. The ti- transmits signals from sarcolemma to contractile fila- ters of AChR and titin antibodies did not correlate sig- ments,9 and antibodies to cytoplasmic filamentous pro- nificantly with any of the clinical syndromes (Figure), teins,10,11 particularly titin,12 or neurofilaments.13 Thy- but the titer of titin antibodies was significantly higher mic epithelial cells express epitopes shared by the target in patients with RyR antibodies than in those without such antigens for some of these antibodies.14-16 It is assumed antibodies (Table 2). that autoreactive T lymphocytes are generated in the thy- Antibodies to RyR were detected in 10 patients: 5 mic tumor and that they subsequently stimulate anti- patients had myositis; 1 patient, NMT; and 4 patients, body production against various muscle antigens.17 no associated disorders (Figure). Patients with RyR an- The incidence of these antibodies in the different tibodies had significantly higher frequency of myositis clinical subgroups of thymoma-associated neurologic dis- than patients without RyR antibodies (Table 2). One of orders has not been determined previously. We mea- the patients with myositis and RyR antibodies in whom sured antibodies to AChR, VGKC, titin, and RyR in 19 VGKC antibodies were not detected also had electri- patients with thymoma-associated MG, 11 of whom had cally silent muscle cramps (patient 9, Table 1). associated myositis or NMT. The results suggest at least Antibodies to VGKC were detected in 7 of 16 pa- 3 subgroups of thymoma-associated MG with different tients with thymoma-associated MG undergoing test- spectrums of autoantibodies.
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