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A Study on Clinical Charateristics of Idiopathic Polymyositis

Author: LiuFang
Tutor: PuChuanQiang
School: PLA Postgraduate Medical School
Course: Neurology
Keywords: Idiopathic inflammatory myositis idiopathic polymyositis season interstitial lung disease cardiac involvement relapse peripheral nerve damage antinuclear antibodies anti-Jo-1 antibody electromyograph motor unit potentials neuromyositis
CLC: R746
Type: PhD thesis
Year: 2005
Downloads: 109
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Abstract


ObjectivsTo investigate the general features of patients withidiopathicpolymyositis.And also explore the characterises of electromyography,complications, regular patterns of relapse and muscle pathology. Material and methods1. The general picture of 102 consecutive patients with IPM admitted toPLA General Hospital between 1980 and 2004 was described statistically.2. The profile of EMG in 91 IPM patients was analyzed using x~2 -test, t-test and Wilcoxon-Wallis test to reveal positive reliability in different muscles and if EGM result was effected by some factors such as course,age.3. To analysis, the clinical and auxiliary examination fearures of 41 IPM patients with cadiac involvement using t-test, rank sum test and x~2 -test to investigate its distinct characteristics.4. Analysis on the clinical symptoms and auxiliary examination results of 17 IPM patients with ILD by means oft-test, rank sum test and x~2 -test to explore its clinical and image regular patterns. And diagnostic significance of some seru autoantibodies.5. Retrospective analysis of relapses in 19 patients with IPM in respect of treatment , treatment changes, types of relapse and the seasonal occurrence of relapses wase made by using x~2 -test to investigate regular patterns of IPM relspses.6. The character of clinical symptoms, serum examation and EMG results in 8 IPM patients with peripherial nerve damage was studiedby rank sum and x~2 -test in order to reveal its probable mechanism. Results1. The mean age was 41 ± 14 years of 102 IPM patients, compromised42.2% male patients and 57.8% female patients, male:female ratio was 1:1.4. Subacute onset was most frequent, next was chronic. At presentation, 89.2% had myasthenia of limbs, accompanying in order with: neck muscle weakness, dysphagia, weight loss, respiratory muscle weakness and ophthalmoplegia. Interstitial lung disease(16.7%) and heart involement(40.2%) were the main complications. Most IPM patients’ first onset was low extremiyies weakness(36.3%), the others in order had myalgia, arthralgia, fever, neck weakness, dysphagia. 100% symptoms in IPM patients were proximal weakness, 50% o f the patients had muscle pain and 48% of the patients had muscle atrophy, 84% of the patients had absence of reflex, 58% had hypotonic muscle. Dysphagia and female predominance were more common in weight loss group than in non-weight loss group(p<0.05). Long course and less muscle pain were more frequent in muscle atrophy group than in non-amyotrophy group(p<0.05). Weight loss and respiratory muscle weakness were more common in elderly patients than in younger patients. Elevated serum creatine kinase(CK), LDH, AST and ALT were found in 70.6%, 67.6%, 58.6% and 56.8% patients respectively. The levels of CK, LDH, AST and ALT over the upper limit were 6.9-fold, 2-fold, 2.1-fold and 2.5-fold respectively. Antinuclear antibody(ANA), anti Jo-1 antibody and anti-Ro(SSA,SSB) antibody were present in 29%, 10.2% and 2.9% of the patients respectively. 91 IPM patients were performed EMG, 79.1%(72) of the patients had myogenic changes, 8.8%(8) of the patients had neurogenic changes, 12.1%(11) of the patients had norma result. Only 69 patients had muscle biopsy and of these, 42 (61%) showed features consistent with myositis, Lymphocyte invade non -necrotic fiber was seen in 10(10/42); 14(20%) showed no inflammatory cellsinfiltration; 4 (6%) was within normal limit; 3 (4%) and 6 (9%) just showed type II fiber atrophy and both type I and II fiber atrophy. During hospitial, 7 patients(2male, 5female) died of severe myocardial infarction (1 patient) , muscular paralysis (1 patient) , respiratory failure (1 patient) , multiorgan failure (1 patient) and cardia failure (3 patients) . Mean age of dead patients was 51 + 16 years, which was more above the age of survival patients.7 dead patients all have lung and cardie involvement.2. Electrophysiological data of 91 IPM patients showed that myogenic muscle lesions were detected in 72 patients, changes were within normal limits in 11 patients, and neurogenic lesions in 8 patients. The percentage of EMG abnormality was 87.9%. Spontaneous activity was observed in 52% of the muscles, mostly in biceps brachii. The reduced mean duration of simple MUPs(71%) was most frequently observed in tibialis anterior muscles and quadriceps. The MUP amplitude decreased only in 7% of the muscles. The percentage of polyphasic MUPs was 29%, most frequently in tibialis anterior muscles. The abnormal recruitment(pathologic interference pattern) as heavy contraction was in 26% of the muscles, mainly in quadriceps, and the mean values of peak voltage were decreased in 31% of the muscles, frequently observed in quadriceps. All above the index were frequently negative in abductor pollicis brevis.3. Forty-one IPM patients(40.2%) got cardiac involvement. For the group with cardiac involvement, the symptoms that older age, fever, ILD, higher values of C-reactive protein, presence of ANA were significantly more frequent(p<0.05) than those in non-cardiac involvement group(p<0. 05). The abnormalities of electrocardiogram were sinus tachycardia(31.7%), sinus arrhythmia(26.8%), auricular premature contraction (14.6%), bundle-branch block(14.6%),abnormal ST-T (17.1%), ventricular premature contraction(7.3%), atrial ventricular block(4.9%), sinus bradycardia(2.4%) and atrial fibrillation(2.4%). when performed echocardiographic check: 6 out of 8 patients was with pericardial effusion. After treatment, 43.1% of these patients recovered, 56.1% of them improved, 9.8%patients experienced deterioration and died.4. Seventeen PM patients (16.7%) developed ILD. Fever, cough and arthralgic were more commom in patients with ILD than in those with non-ILD. In the total 17 patients, ILD occure before IPM in 9 patients ( 52.9%) , ILD companied with IPM in 5 patients(29.4%) ,ILD was onset after IPM in 3 patients (17.7%) . There were three types in our group: progressive(11 patients), asymptom(4 patients), Hamman-Rich like pattern(2 patients). Additionally, for the group with ILD, higher values of erythrocyte sedimentation rate, presence of ANA(58.30%), anti-Jo-1 antibody(33.30%), were significantly more frequent. 9 patients treated with corticosteroids alone, 7 patients out of them improved , but their lung images were not changed; the symptom and image(lung CT) of 1 patient improved; 1 patient experienced ILD deterioration, and of acute respiratory failure. 8 patients with corticosteroids and immunosuppressants drugs, 7 out of them improved, but the lung images unchanged; 1 patient had no respones to treatment,and finally died of respiratory failure.5. In the 42 follow-up patients, relapses occurred in 19 patients, amongthe total 17patients were clinical relapses, 2patients were biochemical relapses. Relapse rate was 45%. Most clinical relapses occurred during late corticosteroids or/and immunosuppressants treatment withdrawal (59%) , secondly relapse during stable maintenance therapy or in the remission of no treatment(29%),relapses during initial corticosteroids withdrawal only 12%. The pattern of biochemical relapse was not concluded, as the cases observed was fewer. The other factors that may induced relapses was fatigue and infection.6. In 8IPM patients with peripherial nerve involvment, proximal muscle weakness was more severe than distal one. One patient had normal tendon reflex,others were absence of reflexes. One had sensory disturbance below knees. Two had muscle tenderness. One had dysphagia. Five had proximal muscle atrophy. The mean level of CK、 LDH、 AST, ALT were lower than that of in EMG myogenic group (p<0.05 ) .On EMG, fibrillation potentials and positive potentials were observed in 7 patients. When slightly contraction, MUP duration increased in 5 patients, MUP duration reduced in 3 patients, MUP amplitude increase in 1 patient,while reduced 1 patient. When heavily contraction, the number of MUP loss in 4 patients. Sensory nerve conduction velocity slowed in 1 patient, motor nerve conduction velocity slowed in 2 patients. Pathology of muscle and peripheral nerve: muscle fiber hypertrophy in 3 cases, atrophy in 7 cases, inflammatory cell invasion in 3 cases, muscle fiber degeneration in 4cases, necrosis in 3 cases, nuclear ingression 5 cases, muscle fiber regeneration and interstitium hyperplasia in 2 cases, perivasculitis in 3 cases.Sural nerve biopsy in 1 patient show that amyelination and myeline sheath attenuation, axonal degeneration, the loss of myelinated nerve fibers.There was norespones to corticosteroids treatment. Conclusion1. IPM had special clinical features in sex, pattern of onset, parts ofbody to be involved, complications, laboratory examination results and cause of death.

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