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PubMed1999

[Hypothyroid myopathy: a case report].

Though proximal muscle weakness is characteristic of polymyositis, other agents may also lead to proximal muscle weakness, such as drugs, endocrine diseases, or infections. Here, we report a thirty year-old female suffering from proximal weakness which initially was thought to be a case of polymyositis with high serum creatine phosphokinase level. Very low thyroid hormone levels were found as the history inquiry revealed constipation, hoarseness and cold intolerance. The muscle biopsy showed no obvious inflammation. After thyroxine therapy, her muscle weakness recovered. Up to now, hypothyroid myopathy with muscle mitochondrial abnormalities shown by electron microscopic examination has not been reported in the medical literature in Taiwan. Hypothyroid myopathy, though it is rare, may be misdiagnosed as polymyositis clinically. Therefore, it is recommended that hypothyroid myopathy should be considered in the differential diagnosis of proximal muscle weakness.

Adult↗

PubMed1988

Chronic progressive external ophthalmoplegia. II. A qualitative and quantitative electronmicroscopy study of skeletal muscles.

This study quantifies the major electron microscopic changes in limb muscle biopsies from 31 out of 34 patients with the syndrome of chronic progressive external ophthalmoplegia. Patients were divided into three clinical groups -- A) 10 sporadic cases with muscle weakness only; B) 9 familial cases with muscle weakness only; C) 15 cases with muscle weakness and one or more of the following features: pigmentary retinopathy, cerebellar ataxia, pyramidal signs and peripheral neuropathy. Electron microscopic mitochondrial abnormalities were found in all groups (8 patients from group A, 3 from group B, 14 from group C). Quantitative measurements of certain muscle fibre constituents, using a point-counting technique, revealed decreased myofibril volume-fractions and increased volume-fractions of mitochondria, glycogen and lipid in some biopsies from each group. Mitochondrial volume-fractions correlated positively with lipid content, the proportion of type 1 fibres, and the percentage of fibres with increased oxidative enzyme activity. The three groups defined clinically showed no significant differences in terms of the relative proportions of these measured constituents.

Chronic Disease↗

PubMed1992

Early predictors of poor outcome in congenital fiber-type disproportion myopathy.

We report the cases of eight children with histologic findings in the muscle of congenital fiber-type disproportion myopathy. Five had severe muscle weakness at birth; three of them died at 6 months, 18 months, and 6.5 years of age, respectively, and the other two are ventilator dependent and need total care at 2.5 and 4 years of age. The five children with severe weakness at birth had profound respiratory muscle weakness and needed assisted ventilation since early infancy. They also had severe facial and bulbar muscle weakness that required tube feeding, and four had gastrostomy. Ptosis and marked external ophthalmoparesis were also noted. Our study shows that the presence of the above constellation of signs at birth or in early infancy is a predictor of a high rate of mortality in infancy and poor developmental outcome in the survivors.

Child↗

PubMed2002

Impairment of synaptic vesicle exocytosis and recycling during neuromuscular weakness produced in mice by 2,4-dithiobiuret.

Chronic treatment of rodents with 2,4-dithiobiuret (DTB) induces a neuromuscular syndrome of flaccid muscle weakness that mimics signs seen in several human neuromuscular disorders such as congenital myasthenic syndromes, botulism, and neuroaxonal dystrophy. DTB-induced muscle weakness results from a reduction of acetylcholine (ACh) release by mechanisms that are not yet clear. The objective of this study was to determine if altered release of ACh during DTB-induced muscle weakness was due to impairments of synaptic vesicle exocytosis, endocytosis, or internal vesicular processing. We examined motor nerve terminals in the triangularis sterni muscles of DTB-treated mice at the onset of muscle weakness. Uptake of FM1-43, a fluorescent marker for endocytosis, was reduced to approximately 60% of normal after either high-frequency nerve stimulation or K(+) depolarization. Terminals ranged from those with nearly normal fluorescence ("bright terminals") to terminals that were poorly labeled ("dim terminals"). Ultrastructurally, the number of synaptic vesicles that were labeled with horseradish peroxidase (HRP) was also reduced by DTB to approximately 60%; labeling among terminals was similarly variable. A subset of DTB-treated terminals having abnormal tubulovesicular profiles in their centers did not respond to stimulation with increased uptake of HRP and may correspond to dim terminals. Two findings suggest that posttetanic "slow endocytosis" remained qualitatively normal: the rate of this type of endocytosis as measured with FM1-43 did not differ from normal, and HRP was observed in organelles associated with this pathway- coated vesicles, cisternae, as well as synaptic vesicles but not in the tubulovesicular profiles. In DTB-treated bright terminals, end-plate potential (EPP) amplitudes were decreased, and synaptic depression in response to 15-Hz stimulation was increased compared with those of untreated mice; in dim terminals, EPPs were not observed during block with D-tubocurarine. Nerve-stimulation-induced unloading of FM1-43 was slower and less complete than normal in bright terminals, did not occur in dim terminals, and was not enhanced by alpha-latrotoxin. Collectively, these results indicate that the size of the recycling vesicle pool is reduced in nerve terminals during DTB-induced muscle weakness. The mechanisms by which this reduction occurs are not certain, but accumulated evidence suggests that they may include defects in either or both exocytosis and internal vesicular processing.

Animals↗

PubMedDate not supplied

Respiratory muscle function in patients with neuromuscular disorders and cardiopulmonary diseases.

Respiratory muscle dysfunction frequently occurs in patients with neuromuscular disorders, cardiopulmonary diseases and in patients in intensive care units. Respiratory muscle weakness and/or fatigue is responsible for dyspnoea, reduced exercise tolerance, nocturnal desaturation, and prolonged weaning from mechanical ventilation. Chronic respiratory muscle weakness may also be associated with poor quality of life and increased mortality. Patients with severe respiratory muscle weakness are at increased risk of respiratory failure due to respiratory infections, electrolyte imbalance, sedation or uncontrolled inspired oxygen therapy. Although respiratory muscle weakness is often seen in clinical practice, the consequences and the precise point at which respiratory muscle fatigue occurs remain elusive. This article reviews the pathophysiology of respiratory muscle weakness and fatigue, and therapeutic interventions for enhancing respiratory muscle function in patients with neuromuscular and cardiopulmonary diseases.

Female↗

PubMed1997

Determinants of the tension-time index of inspiratory muscles in children with cystic fibrosis.

Nutritional status and chronic pulmonary hyperinflation can alter respiratory muscle function in cystic fibrosis (CF). This study investigated: 1) whether inspiratory muscle function is reduced in children with stable CF in comparison with healthy controls; and 2) the mechanisms leading to inspiratory muscle weakness, which probably predispose to respiratory muscle fatigue. We determined the tension-time index of the inspiratory muscles (TTMUS) noninvasively at rest in 16 children with mild to moderate CF (mean age, 11 +/- 2 years) and 10 healthy controls (mean age, 11 +/- 2 years). The TTMUS was determined as follows: TTMUS = TI/TTOT.PI/PIMAX, where PI is the mean inspiratory pressure estimated from the measure of mouth occlusion pressure (P0.1), PIMAX is the maximal inspiratory pressure, and TI/TOT is the duty cycle. The results showed similar nutritional status in both groups, as well as mild to moderate airway obstruction, hyperinflation, and trapped gas in the CF group. In this group only, a significant inverse relationship was found between TI/TOT and PI/PIMAX[TITTOT = 0.482 - (0.388PI/PIMAX), r = -0.53; p < 0.05]. These patients also had greater TTMUS (TTMUS = 0.087 +/- 0.030 in CF vs. 0.056 +/- 0.014 in controls, P < 0.01) that increased with decreasing lean body mass (r = -0.70, P < 0.005), with increasing percent predicted functional residual capacity (r = 0.70, P < 0.05), and increasing volumes of trapped gas (r = 0.77, P < 0.01). The multiple linear regression analysis for these factors was significant (R2 = 0.84, P < 0.01); however, the partial regression coefficient was significant only for lean body mass (r2 = 0.60, P < 0.05). Therefore, muscle mass appeared as the strongest determinant of TTMUS in CF. This study used a noninvasive method to assess the inspiratory muscle performance in children with CF. The results suggest impairment in inspiratory muscle function in these children despite good nutritional status and only mild to moderate alteration in pulmonary function tests. In addition, we were able to investigate some of the determinants of inspiratory muscle weakness, namely, muscle mass, hyperinflation, and trapped gas, and found that muscle mass played a predominant role.

Body Mass Index↗

PubMed1993

Postpolio syndrome in New Zealand: a survey of 700 polio survivors.

AIMS: To examine the experience of postpolio syndrome amongst a group of survivors of polio currently resident in New Zealand. METHODS: A sample of 700 responded to a request for volunteers to take part in a postal survey concerning their experience of polio and postpolio symptoms. RESULTS: The mean age of respondents was 59 years. Two-thirds of them were women. The year of polio infection was between 1915 and 1962 with the majority (54%) being in the 1945-56 period. Most were under 16 years of age (73%) at the time. Paralysis and weakness in limbs and back were the most common symptoms in the acute phase of the infection. Symptoms of the postpolio syndrome were reported by significant numbers. Increasing weakness in muscle functioning in one or more area was evident amongst 38% of the sample. Generalised muscle weakness was reported by 47%, increasing muscle wastage by 17%, difficulty swallowing by 16% and shortness of breath on waking by 10%. Pain in joints was reported by 60% and excessive tiredness by 48%. After controlling for age there was little evidence that the symptoms increased with years since the acute polio infection. CONCLUSIONS: The experience of postpolio symptoms was common amongst this group of polio survivors. It is estimated that there are between 3,000 and 5,000 polio survivors in New Zealand who may be suffering postpolio symptoms. The implications of this for primary and secondary health care provision are discussed.

Adult↗

PubMed1997

Juvenile dermatomyositis in north India.

OBJECTIVE: To determine the clinical profile and therapeutic response of patients with juvenile dermatomyositis (JDM). DESIGN: Hospital based descriptive follow-up study. SAMPLE: 12 patients attending the Pediatric Rheumatology and Immunology Clinic over last five years. RESULTS: The patients were aged between 3 1/2 years to 12 years with a male to female ratio of 2:1. All patients had proximal muscle weakness at presentation. Distal muscle weakness and masseter atrophy was seen in 2 patients and neck flexor weakness and pharyngeal weakness was seen in 1 case. Muscle pain, tenderness or swallowing difficulties were not observed. Classical skin manifestations of JDM were present in all except one patient. Vasculitic lesions were not noted. One patient had diffuse lipoatrophy. Two patients developed calcinosis cutis while on treatment. All patients were put on oral corticosteroids (prednisolone 2 mg/kg/day) initially which were gradually tapered while monitoring clinical response. Early initiation of steroid therapy resulted in an excellent response. Two patients who did not show significant improvement even with prolonged steroid therapy were given oral weekly methotrexate (10 mg/m2/week). CONCLUSIONS: Most of the children with JDM showed good response to steroid therapy which needs to be continued for a prolonged period. Children who do not respond to this therapy may be given oral weekly methotrexate.

Adrenal Cortex Hormones↗

PubMed1999

[A case of microscopic polyangiitis with severe cardiac and respiratory muscle involvement].

A 66-year-old female was admitted to our hospital in January, 1998, complaining of low grade fever and muscle weakness of her legs. Physical examination revealed muscle weakness of her neck (4/5) and proximal skeletal muscles of her bilateral legs (3/5-4/5). She showed proteinuria and microhematuria. Her serum levels of ureanitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, creatinekinase, aldolase and myoglobin were all within the normal ranges. Antinuclear antibodies were negative, but her serum levels of pANCA (743 EU) and C reactive protein (18.0 mg/dl) were elevated. Neuroconduction velocity of her left common peroneal nerve was decreased to 40.8 m/sec and electric myograph showed neurogenic changes. Magnetic resonance images (MRI) of her bilateral thigh depicted high signal intensity in quadriceps by T 2 weighed images, but the signals were not enhanced by gadolinium injection. Muscle and renal biopsies revealed necrotizing vasculitis of the small arteries. Crescentic glomerulonephritis was also observed by renal biopsy. These findings supported the diagnosis of microscopic PN. On 16 th admission day, she developed acute cardiac and respiratory failures due to cardiac and respiratory muscle involvements with PN, and was assisted by mechanical ventilation. She was treated with methylprednisolone pulse therapy (500 mg/day, three consecutive days) on 18 th admission day, followed by 40 mg of oral prednisolone daily. However, her symptoms deteriorated, and herserum creatinine levels increased to 2.4 mg/dl. On 24 th admission day, intravenous cyclophosphamide pulse therapy (500 mg/day) was instituted. Her cardiac wall motion on echocardiography and serum creatinine levels gradually improved, but her skeletal and respiratory muscle weakness did not improve. On 38 th admission day, she was complicated with respiratory infection by methicillin resistant Staphylococcus aures. On 62 th admission day, she died of endotoxic shock. This is the first report describing respiratory muscle involvement with PN, and the second report describing MRI findings of muscle involvement by PN. Therefore, our case provides important clinical information for the diagnosis and treatment of the disease.

Aged↗

PubMed1995

Inspiratory muscle strength is a determinant of maximum oxygen consumption in chronic heart failure.

OBJECTIVE: To investigate the significance of respiratory muscle weakness in chronic heart failure and its relation both to maximum oxygen consumption during cardiopulmonary exercise testing and to skeletal muscle (quadriceps) strength. SUBJECTS: Seven healthy men aged 54.9 (SEM 4.3) years and 20 men with chronic heart failure aged 61.4 (1.6) years (P = 0.20) with radionuclide left ventricular ejection fraction of 25.4 (3.0)%. METHODS: Mouth pressures during maximum static inspiratory effort (PImax) at functional residual capacity (FRC) and residual volume (RV) were measured in all subjects and taken as indices of inspiratory muscle strength. Similarly, mouth pressures during maximum static expiratory effort (PEmax) at FRC and total lung capacity (TLC) were taken as indices of expiratory muscle strength. Cardiopulmonary exercise testing was performed in all subjects. All controls and 15 heart failure patients also had their right quadriceps muscle strength measured. RESULTS: There was respiratory muscle weakness in heart failure patients, with reduction of PImax at FRC (59.7) (6.3) v 85.6 (9.6) cm H2O, P = 0.045), PEmax at FRC (94.8 (6.2) v 134.6 (9.1) cm H2O, P = 0.004), and PEmax at TLC (121.7 (8.5) v 160.7 (13) cm H2O, P = 0.028). PImax at RV was also reduced but this did not reach statistical significance (77.3 (6.6) v 89.3 (13) cm H2O, P = 0.44). There was also significant weakness of the right quadriceps muscle (308.5 (22) v 446.2 (28) N, P = 0.001). PImax at both FRC and RV correlated with maximum oxygen consumption (r = 0.59, P = 0.006, and r = 0.45, P = 0.048 respectively) but not PEmax. There was, however, no significant correlation between PImax and right quadriceps strength. CONCLUSIONS: Respiratory muscle weakness is seen in chronic heart failure. The results suggest that inspiratory muscles are important in determining maximum oxygen consumption and exercise tolerance in these patients. The lack of correlation between respiratory and right quadriceps muscle strength further suggests that the magnitude and time course of respiratory and locomotor muscle weakness may differ in individual patients. Treatment aimed at improving the function of the involved muscle groups may alleviate symptoms.

Adult↗

PubMed2003

Distal myasthenia gravis frequency and clinical course in a large prospective series.

OBJECTIVES: In Myasthenia gravis (MG) proximal limb, ocular and/or bulbar muscles are most commonly affected, whereas distal extremity muscles are typically spared. The aim of the current study was to assess the frequency of primarily distal MG in the Tyrol and to describe its clinical peculiarities. MATERIAL AND METHODS: Over the past 20 years 84 patients with MG have undergone follow-up at the Department of Neurology of Innsbruck University. Types of presentation, clinical course and treatment response were followed over a period of 20 years (1980-2000). RESULTS: Six of 84 MG patients showed a predominance of muscle weakness and fatigability in distal limb muscles (two at presentation, four over the later course of the illness). There was no difference between distal MG and MG with a more typical distribution of muscle weakness regarding age, gender and response to therapy. CONCLUSIONS: The case series indicates that predominantly distal presentations of otherwise typical MG are more frequent than generally assumed and should be considered in the differential diagnosis of diseases with distal limb weakness.

Adult↗

PubMed1990

[Motor neuron disease with Parkinson's disease--case report].

The patient was a 64-year-old woman who showed muscle weakness and tremor of upper extremities and gait disturbance at the age of 62 years. The symptoms progressed and she was admitted to our hospital. Neurological examination revealed muscle weakness, muscle atrophy and fasciculation bilaterally in the upper extremities. The deep tendon reflexes were reduced in the upper extremities and increased in the lower extremities, but Babinski's sign was not present. There was mild hand tremor at rest (right greater than left). Muscle rigidity was also evident. Her gait was small-stepped and her trunk was bent forward. She showed hypomimia, but no dementia was detected. She died of respiratory failure 7 months after admission. The duration of the illness was about 2 years. At autopsy, macroscopic examination showed depigmentation of the substantia nigra and locus ceruleus, and atrophy of the anterior roots of the spinal cord. Microscopic examination revealed a few senile plaques in the temporal cortex. In the substantia nigra, the number of melanin-containing cells was decreased in its central parts. A few Lewy bodies were found in some of the remaining neurons, and melanin pigment migrated into the parenchyma. In the locus ceruleus and dorsal motor nucleus of vagus, abundant Lewy bodies and mild astrocytosis were seen. A few Lewy bodies were also seen in the nucleus raphe, nucleus basalis of Meynert and hypothalamic nuclei. Severe neuronal loss of the anterior horn cells was observed in the cervical segment, and to a lesser degree, in the lumbo-sacral segments. segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗

PubMed1998

[Legionella pneumonia caused by aspiration of hot spring water after sarin exposure].

A 72-year-old man was exposed to the sarin gas attack in a Tokyo subway on March 20 th, 1995. After exposure, he noticed eye discomfort, chest tightness, headache and weakness of the lower limbs and oropharyngeal muscles. Despite these symptoms, he visited a hot spring on the same day with his family. On March 25 th, his muscle weakness progressed, and a low grade fever appeared. His muscle weakness disappeared 8 days after exposure to sarin, but respiratory failure rapidly developed, necessitating artificial ventilation within four day after hospitalization on March 28th. Chemotherapy with erythromycin, imipenem/cilastatin, and steroid pulse therapy was begu. PCR and culture of sputum collected by bronchofiberscopy were positive for Legionella pneumophila, serogroup I. His respiratory state improved, but subsequent infection with Pseudomonous aeruginosa. Enterobacter cloacae, and Candida tropicalis/glabrata caused his death 71 days after admission. Oropharyngeal muscle weakness caused by sarin-mediated cholinesterase inhibition was strongly suspected as the cause of hot spring water aspiration. Transbronchial lung biopsy revealed organizing pneumonia with fibrosis. Bronchoscopic findings included redness, edema and fragility of all visible areas of the airway, which was thought to be due to bronchitis caused by Legionellosis.

Aged↗

PubMed2006

Dok-7 mutations underlie a neuromuscular junction synaptopathy.

Congenital myasthenic syndromes (CMSs) are a group of inherited disorders of neuromuscular transmission characterized by fatigable muscle weakness. One major subgroup of patients shows a characteristic "limb girdle" pattern of muscle weakness, in which the muscles have small, simplified neuromuscular junctions but normal acetylcholine receptor and acetylcholinesterase function. We showed that recessive inheritance of mutations in Dok-7, which result in a defective structure of the neuromuscular junction, is a cause of CMS with proximal muscle weakness.

Cell Line↗

PubMed1983

Periodic paralysis with cardiac arrhythmia.

In 1963, Klein et al. first described two girls with normokalemic periodic paralysis and cardiac arrhythmia. We have observed a 15-year-old girl with cardiac arrhythmia and normokalemia but with some features of hyperkalemic, periodic paralysis. The patient showed a waddling gait and Gower's sign. She had atrophy of the proximal muscles and deep tendon reflexes were reduced. Her ECG showed bigeminy with multifocal premature ventricular contractions. At the start of an episode of muscle weakness, the serum potassium concentration rose from 3.1 to 4.4 mEq/l. Muscle weakness was not provoked by intravenous administration of 45 g glucose or of 72 g glucose followed by 10 units of regular insulin. Muscle weakness was evoked by the ingestion of 4 g potassium chloride. During the provoked muscle weakness, the ECG showed normal sinus rhythm temporarily.

Adolescent↗

PubMed2002

Skeletal muscle of mice with a mutation in slow alpha-tropomyosin is weaker at lower lengths.

Skeletal muscle function was measured in anaesthetised transgenic mice having a mutation in the TPM3 gene (slow alpha-tropomyosin), a similar mutation as found in some patients with nemaline myopathy, and was compared with control muscles. Measurements of isometric and dynamic muscle performance were done with electrical nerve stimulation at physiological temperatures. No muscle weakness was found in the transgenic muscles when performance was measured at muscle optimum length. This was true not only with full activation but also at lower activation levels, indicating that calcium sensitivity was not affected at this length. Also, fatigability was not affected in these conditions. However, isometric force of the muscles with the mutation in TPM3 was lower at lengths below optimum, with more impairment at decreasing length. As the muscles are active over a large range of different muscle lengths during daily activities, this finding may explain, at least in part, the muscle weakness experienced by patients with nemaline myopathy.

Animals↗

PubMedDate not supplied

Short-term complications and long-term results of expansive open-door laminoplasty for cervical stenotic myelopathy.

BACKGROUND CONTEXT: Laminoplasty has been reported to achieve good operative results for treatment of cervical stenotic myelopathy. However, long-term results and prognostic factors have not been well documented. Among postoperative complications, weakness of the shoulder girdle muscles has been reported as a particular complication of laminoplasty, but the cause is still poorly understood. PURPOSE: Our aim was to clarify the short-term complications and long-term operative results after unilateral open-door laminoplasty and to identify the predictors for operative outcome. STUDY DESIGN: We retrospectively reviewed short-term complications and long-term operative results associated with cervical stenotic myelopathy treated by unilateral open-door laminoplasty. PATIENT SAMPLE: There were 162 men and 42 women with an average age of 57 years who were treated by unilateral open-door laminoplasty in the two institutions. Pathogenesis of myelopathy was cervical spondylosis in 88 patients, cervical disk herniation with a narrow spinal canal in 10, and ossification of the posterior longitudinal ligament in 106. OUTCOME MEASURES: Postoperative complications and their outcomes were examined clinically in 204 patients, and causes of motor paresis were sought with postoperative computed tomography after myelography. Postoperative improvement of clinical symptoms was assessed by recovery rate calculated with the scores of the Japanese Orthopaedic Scoring System in 80 patients. METHODS: The occurrence rate of short-term postoperative complications, causes of motor paresis, and their outcomes were reviewed in 204 patients. Clinical condition was assessed with the Japanese Orthopaedic Scoring System, recovery rate was calculated with the score, and prognostic factors for outcome were studied in 80 patients who were followed up for 5 years or longer (average, 8 years; range, 5-17 years). RESULTS: Occurrence rate of complications, such as muscle weakness, deep infection, closure of opened laminae, and others, was 10.8%. Muscle weakness was observed in 7.8% of the patients. However, this rate decreased in recent years. The cause of motor paresis is not known with certainty, but it may be secondary to operative trauma, posterior shift of the spinal cord, or to displacement of the lamina in the hinge side. Recovery rate of clinical symptoms was 62.1% at the final follow-up. Rates were 63.6% for cervical spondylosis, 87.1% for cervical disk herniation, and 61.3% for ossification of the posterior longitudinal ligament. There was no significant difference between pathologies. Patient age younger than 60 years at the time of operation and less than 1 year's duration of symptoms before surgery were significantly associated with recovery rate of clinical symptoms. Recovery rate was not correlated with either preoperative function judged by the Japanese Orthopaedic Association score or spinal sagittal diameter. CONCLUSIONS: The main cause of postoperative motor paresis of upper extremities is thought to be operative trauma, resulting from such procedures as air-drill and Kerrison rongeur handling. Short-term complications may decrease with the use of nontraumatic procedures. Better operative outcomes may be achieved with careful operative procedures and early operative treatment in the patients with myelopathy.

Adolescent↗

PubMed1989

A case of Graves' disease associated with polymyositis.

A patient with Graves' disease associated with severe muscle weakness who was finally diagnosed as polymyositis by pathological examination of the muscle is reported. A 28-year-old women was incidentally found to have hyperthyroidism when she consulted a hospital for the evaluation and treatment of anemia in 1979. She was treated with methimazole for approximately a month when she stopped the medication by herself. Approximately two yr later (Nov. 4, 1981) she consulted another hospital with complaints of palpitation and muscle weakness. Diagnosis of hyperthyroidism due to Graves' disease and thyrotoxic myopathy were made, followed by the treatment with radioiodine (4 mCi of 131I). She was further treated with propylthiouracil (PTU). Four yr after the treatment, serum thyroid hormone concentration declined to the lower level than normal and serum TSH concentration increased. She was subsequently treated with synthetic I-T4. Despite the fact she became euthyroid with the treatment, muscle weakness as well as elevated concentrations of muscle enzymes were not improved. Muscle biopsy was made in July 1983, and she was diagnosed as immune polymyositis and treatment with prednisolone and cyclophosphamide in addition to PTU or I-T4, was started. With the treatment, serum LDH decreased to the normal range. However she still has muscle weakness and serum concentrations of CPK and aldolase are still in higher levels than normal range.

Adult↗