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Arthritis in Myasthenia Gravis

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Arthritis in Myasthenia Gravis J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.38.11.1048 on 1 November 1975. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry, 1975, 38, 1048-1055 Arthritis in myasthenia gravis J. A. AARLI1, E.-J. MILDE, AND S. THUNOLD From the Departments of Neurology and Pathology, School of Medicine, University of Bergen, and the Rheumatic Disease Unit, The Deaconesses' Hospital, Bergen, Norway SYNOPSIS Seven patients with myasthenia gravis developed clinical signs of arthropathy. In two patients, the symptoms were due to a deforming rheumatoid arthritis and the myasthenic symptoms appeared as a transitory phase during the course of the disease. Muscle antibodies of IgG class were demonstrated with sera from both patients. Autoreactivity between muscle antibodies and rheuma- toid factor was detected in one patient. Both patients died from sudden cardiac failure. Necropsy was performed in one and revealed a spotty myocardial necrosis. One patient had juvenile rheumatoid arthritis. Two patients had mild articular symptoms with indices of multivisceral disease and sero- logical findings indicating a systemic lupus erythematosus. One patient had classical ankylosing spondylitis, and one, unspecified arthropathy. guest. Protected by copyright. The concept of myasthenia gravis as a pure cate a clinical overlap (Oosterhuis and de Haas, disorder of the neuromuscular transmission has 1968). The aim of the present paper is a re- probably been an obstacle to the full delineation appraisal ofthe relationship between myasthenia of the clinical picture of this disease. Thus, care- gravis and arthritis. Seven patients are described ful clinical examination has revealed a series of and the data compared with relevant literature. signs and symptoms connected with myasthenia gravis which cannot be attributed to the defect of METHODS transmission of the neuromuscular junction (Simpson, 1960). Some patients with myasthenia Patients were selected from among those treated at gravis develop arthritis, even to a disabling the Department of Neurology for myasthenia gravis (MG). The numerals refer to corresponding nu- occurrence of coincidental degree. The myas- merals in earlier publications (Aarli and T0nder, thenia gravis and rheumatoid arthritis may indi- 1970; Aarli, 1970-1972b). The diagnosis of MG was based mainly upon the I Address for correspondence: Dr Johan A. Aarli, Department of Neurology, 5016 Haukeland sykehus, Bergen, Norway. criteria given by Schwab and Perlo (1966). Clinical (Accepted 9 June 1975.) data are presented in Table 1. http://jnnp.bmj.com/ BLE 1 CLINICAL DATA IN SEVEN PATIENTS WITH MYASTIENIA GRAVIS (MG) AND ARTHROPATHY Pctient Sex Age at onset Type ofMG* Age when first Type ofarthropathy Other diseases no. ofMG (yr) arthropathy appeared (yr) 1 CT 51 IIBA 60 Classical RA Cardiac insufficiency on September 25, 2021 by 2 31 IIBA 17 Classical RA Cardiac insufficiency 3 18 IIBA 17 Juvenile RA Iridocyclitis 4 17 IIBA 37 Probable SLE Bell's palsy 5 22 HA 23 Probable SLE 6 CT 47 I 20 Ankylosing spondylitis - 7 V 34 IIA 36 Unspecified arthropathy - * Classification according to Oosterhuis (1964). 1048 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.38.11.1048 on 1 November 1975. Downloaded from Arthritis in myasthenia gravis 1049 k;.. ^1- w_ -x FIG. 1 Case 1. Male, aged 72 years. Anteroposterior radio- graph of hands. There is narrowing with subluxations and ulnar deviation of the MCP joints. Erosive lesions in the metacarpal heads. Slight narrowing of the PIP joints and a few erosive lesions. The diagnosis of rheumatoid arthritis (RA) and of CASE REPORTS guest. Protected by copyright. systemic lupus erythematosus (SLE) followed criteria given by the American Rheumatism Asso- Myastheliia gravis and classical rheumatoid arthritis ciation (1959). CASE 1 (MG-3) A male patient, born in 1903, had no family history of neurological or rheumatic SEROLOGICAL TESTS The antiglobulin consumption disease. He was previously of good health but, at the test (AGCT) for muscle antibodies was performed as age of 51 years, noted intermittent but increasing described earlier (Aarli and T0nder, 1970). When the painless fatiguability of both legs when walking. tissue was treated with normal human serum, a small After a few months he also developed ptosis and consumption of antiglobulin serum occurred (normal diplopia. On admission to the Department of consumption). A consumption four or more times Neurology in 1957, bilateral ptosis was present which greater than normal was designated 'pathological disappeared temporarily after injection of edropho- consumption' (PC) (Aarli and T0nder, 1970). nium. There was nasal regurgitation of fluid. The Indirect haemagglutination test (IHA) for muscle speech fatigued easily. There was symmetrical antibodies was performed using tannic acid-treated muscular weakness without wasting. Tendon reflexes red cells sensitized with citric acid extract (CA were normal and there was no sensory loss. General antigen) of skeletal muscle (Aarli, 1972b). examination and examination of the joints revealed Waaler's test for rheumatoid factor (RF) and nothing pathological. Except for a moderate eleva- absorption of RF were performed as earlier (Aarli, tion of ESR (21 mm in one hour), the routine 1971b). laboratory investigations were normal. Tests for There was no RF were not performed. radiographic http://jnnp.bmj.com/ DIRECT IMMUNOFLUORESCENCE (IF) Quick frozen evidence of thymoma. He was treated with neostig- myocardial tissue was stained as described previously mine and was able to work on a dose of 225-300 mg (Thunold et al., 1973) with monospecific FITC daily, but he was severely incapacitated for several labelled rabbit antisera against human albumin, IgA, years. IgG, IgM, fibrinogen, and /l3c/1A-globulin (C3) During 1964, he experienced a remarkable obtained from Behringwerke AG, Marburg Lahn, remission of myasthenic symptoms with only a West Germany and against Clq (Thunold et al., slight left-sided ptosis on upwards gaze and a of motor on 1970). moderate reduction power repeated on September 25, 2021 by contractions of the muscles in the forearm and hand. HISTOLOGY Myocardial tissue was fixed in 10% From the same time, however, he started suffering formalin and sections were stained with haema- from pains, swelling, and stiffness in metacarpo- toxylin and eosin, Elastin van Gieson, periodic acid phalangeal (MCP) and proximal interphalangeal Schiff (PAS), and Mallory's phosphotungstic acid (PIP) joints in both hands. Gradually his arthritis (PTAH). became worse, fulfilling the criteria of definite RA. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.38.11.1048 on 1 November 1975. Downloaded from 1050 J. A. Aarli, E.-J. Milde, and S. Thunold TABLE 2 SEROLOGICAL DATA IN SEVEN PATIENTS WITH MYASTHENIA GRAVIS AND ARTHROPATHY Patient Muscle antibodies RF test ANF Thyroglobulin no. AGC IHA antibodies 1 128 N 1280/20 P N 2 128 - 340/20 N N 3 128 - N N N 4 8 - N P N 5 64 - N P N 6 16 - N N N 7 8 - N NN N = negative. P = positive. Radiographs showed typical rheumatic destruction but bilateral ptosis developed after looking upwards of finger joints (Fig. 1). From the beginning of 1972, for less than two minutes. Tongue and facial muscles he also suffered from cardiac insufficiency with were weak. increasing dyspnoea, crural oedema, and tachycardia. The clinical condition was, however, dominated Electroconversion was performed. In 1973 he was by the rheumatic disorder. There was swelling and hospitalized for acute anteroseptal cardiac infarction. symmetrical deformity of MCP and PIP joints, with He in his in January from sudden ulnar the hands and rheumatoid died home, 1975, typical deviation of guest. Protected by copyright. cardiac failure. Necropsy was not performed. affections of several other joints. Radiographs of her joints showed rheumatoid destruction. Serologicalfindings IgG antibodies to striated Subcutaneous injection of neostigmine resulted in muscle were demonstrated by the AGCT (PC= 128). full but transitory improvement of muscle strength. Antibodies to the CA antigen of skeletal muscle were She was treated with neostigmine, later pyridostig- not detected by IHA test (Table 2). Accordingly, his mine, with a satisfactory control of the myasthenic serum contained antibodies of IgG class to some symptoms. She had intermittent diplopia but no other component of striated muscle. other symptoms of muscular fatigue. His RF titre of 1 280 remained constant until There was no radiological evidence of thymic 1974, when a significant fall in titre occurred (titre enlargement in 1953 or at later examinations. 20-40). All sera were tested simultaneously. She received gold injections, was treated with When the patient's serum was absorbed with chloroquine for six years (after manifestation of homogenized human skeletal muscle sensitized with MG), but was never treated with ACTH or steroids. his own serum after prior treatment with mercapto- She died from sudden cardiac failure at the age of ethanol to destroy 19S RF, a significant reduction of 52 years. The heart was removed at a partial necrop- RF titre occurred (Aarli, 1971b). This indicates sy. It was enlarged (weight 440 g) but showed no autoreactivity between IgG muscle antibodies and signs of valvular defects or obstructing coronary RF. atheromatosis or thrombosis. There were no signs Neither LE cells nor antinuclear factors (ANF) of old or recent infarcts. However, microscopy were detected. revealed muscle and small areas hypertrophic fibres http://jnnp.bmj.com/ of fibrosis (Fig. 2a). In addition, multiple focal areas CASE 2 (MG-1) A female patient, born in 1921, of muscle cell vacuolization and necrosis were seen, had a mother with RA. The patient had polyarthritis often accompanied by a slight infiltration of lympho- from the age of 17 years with increasing and severe cytes and histiocytes (Fig. 2b, c). In the pericardium, affection of multiple joints, fulfilling the criteria of small perineural lymphocyte infiltrations were found classical RA. (Fig. 2d). There were no signs of vasculitis or rheu- At the age of 31 years, she noticed that her voice matoid granulomas. Direct IF microscopy revealed became nasal when talking.
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