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PubMed1996

A family with an unusual myotonic and myopathic phenotype and no CTG expansion (proximal myotonic myopathy syndrome): a challenge for future molecular studies.

Myotonic dystrophy (DM) is a well-defined autosomal dominant disorder characterized by myotonia, muscle weakness, cardiac conduction defects, cataracts, and endocrine abnormalities. Recently a newly recognized disorder, similar to but distinct from DM, has been observed with multisystem findings including intermittent myotonia, proximal myopathy, and occasional cardiac conduction disturbances. This disorder has been called proximal myotonic myopathy (PROMM). No history of anticipation is present and there is no linkage to the gene locus for DM or to the loci for the muscle sodium or chloride channels. This report describes a family with a normal size of the CTG trinucleotide repeat expansion of the DM gene in which affected individuals have myotonia (intermittent, exacerbated by cold), bilateral cataracts, mild hypogonadism and mild temporal atrophy. Affected individuals also have proximal muscle weakness, facial involvement, nonspecific abnormalities on muscle biopsy, normal cardiac conduction, and no glucose intolerance. The absence of trinucleotide repeat expansion in the DM gene is consistent with this family being affected by a disorder distinct from DM, possibly a form of PROMM.

Adult↗
PubMed1988

Endocrine myopathies.

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.

Endocrine System Diseases↗
PubMed1986

Arctic trichinosis presenting as prolonged diarrhea.

We describe an outbreak of trichinosis after the consumption of raw walrus meat in 10 Inuit inhabitants of a northern community. During the presentation of the illness, diarrhea was found in all subjects and was the dominant symptom in 8 of the 10 cases. Myalgia (60%) and muscle weakness (50%) were much less prominent complaints. The diarrhea was characteristically prolonged, lasting up to 14 wk (average 5.8 wk), as opposed to comparatively short episodes of myalgia (average 5.4 days) and muscle weakness (average 4.5 days). Prolonged diarrhea with little or no muscle symptomatology in an epidemic form represents a previously unrecognized clinical presentation of trichinosis. It remains to be determined whether this new clinical presentation is related to variant biological behavior of arctic Trichinella, to previous exposure to the parasite, or to other factors.

Adult↗
PubMed2000

[Myotubular myopathy].

The myotubular myopathy is an X-linked centronuclear myopathy characterized by severe neonatal hypotonia and generalized muscle weakness which most frequently results in the premature death of the newborn infants by respiratory failure. The characteristic muscle histopathology consists in centrally positioned nuclei in most muscle fibers. In 1996, the gene responsible for the disease, MTM1, was identificated in Xq28 region. Since then, more than hundred mutations have been isolated. Genotype - phenotype correlation is complex because mutations are found along the entire coding sequence of the MTM1 gene. Most mutations are associated with very severe phenotype with death before the first year of life, however a milder phenotype has been individualized. It is important to be aware of the existence of such milder MTM phenotype because in those patients a very mild expression permit normal life into adulthood.

Cytogenetics↗
PubMed2003

The role of biochemical tests and clinical symptoms in differential diagnosis of primary aldosteronism.

BACKGROUND: Primary aldosteronism (PA) is a secondary form of hypertension resulting from the autonomous hypersecretion of aldosterone. The recognition of PA has an important impact on clinical management, since the choice of therapy is different - surgical for adenoma and medical for hyperplasia. AIM: To evaluate patients with PA in regard to clinical and biochemical factors differentiating between adenoma of adrenal cortex (APA) and idiopathic adrenal hyperplasia (IHA). METHODS: We retrospectively analysed 62 patients with PA (33 females, 29 males, mean age 49.3+/-12.5 years, range 26-78) diagnosed in the Department of Hypertension between 1990-2001. In 37 patients (mean age 47.4+/-12.1 years, 22 females, 15 males) APA was diagnosed whereas in the remaining 26 patients (mean age 52.2+/-12.6 years, 14 males, 11 females) IHA was detected. Clinical manifestation, biochemical, serum aldosterone (SA), plasma renin activity (PRA) as well as echocardiographic parameters and blood pressure (BP) levels were evaluated. Diagnostic accuracy of computed tomography (CT) and scintigraphy was also assessed. RESULTS: Mean systolic BP was significantly higher in the patients with APA. Both groups had similar mean diastolic BP. Severe hypertension, resistant to three or more medications, was found in 63.3% of all patients. Muscle weakness was reported by 39.7% of patients, polyuria - by 19%, and polydypsia - by 10.3% of patients. Patients with muscle weakness had higher mean systolic BP level and lower plasma potassium level than patients without this complaint. Symptoms suggesting cardiac arrhythmia were reported by 45% of patients. A normal potassium level was found in 25.8% of all patients. The hypokalemic patients were younger, had shorter known duration of hypertension, higher mean systolic BP level and higher SA concentration than the normokalemic patients. Supine SA levels were significantly higher in the APA group than in the IHA group (50.3+/-29.0 ng% vs 30.5+/-14.7 ng%; p<0.001). The SA/PRA ratio higher than 30:1 was found in all patients. Response to postural test with a rise in SA concentration higher than 30% was observed in 40% patients with APA and in 87.5% patients with IHA (p<0.0001). There was a strong correlation between supine and upright SA level, and systolic and diastolic BP level as well as plasma potassium level. Left ventricular hypertrophy was present in 60% of patients. The differentiation between APA and IHA was possible using CT, scintigraphy or both methods in 75%, 89.2% and 100% of patients, respectively. CONCLUSIONS: One quarter of patients with PA were normokalemic. PA should be suspected especially in patients with severe hypertension, resistant to three or more antihypertensive drugs. Changes in SA concentration during the postural tests such as CT and scintigraphy are useful for differentiation between APA and IHA.

Adult↗
PubMed2006

[Amyotrophic lateral sclerosis (ALS): evaluation of respiratory function].

Respiratory involvement is an almost constant feature of als, with a usually rapid progression leading to respiratory failure. These characteristics justify a close follow up, usually at three-month intervals. A systematic, careful clinical evaluation is essential to detect the subtle respiratory symptoms and signs related to respiratory muscle failure. Dyspnea and orthopnea are often late findings in patients with a usually severe functional impairment due to peripheral muscle weakness. Nocturnal respiratory events (obstructive sleep apnea syndrome and hypoventilation) are strongly suggested by daytime hypersomnolence and frequent morning headaches. Physical evaluation is essential to detect accessory muscle recruitment, supine abdominal paradox, and encumbrance of upper or lower airways. Vital capacity (VC) is the most classical lung function test. The major limitation of spirometry is its poor sensitivity to detect a moderate inspiratory muscle weakness. Supine VC may improve the detection of diaphragmatic involvement. Peak expiratory flow during cough (cough PEF) gives an overall evaluation of cough efficiency, values below 160 to 270 L/min suggesting poor airway clearance. Arterial blood gases are performed at first evaluation and subsequently in case of clinical signs, significant deterioration of lung function tests, or sleep desaturations. Hypercapnia is weakly related to lung function results in bulbar patients. A specific evaluation of respiratory muscle strength is mandatory, as these tests are both sensitive and highly prognostic. Possible discrepancies (particularly in bulbar patients) between Maximal inspiratory pressure (PImax) and sniff nasal inspiratory pressure (SNIP) justify to perform both measurements and to select the highest pressure. A maximal expiratory pressure (PEmax) below 45 cm H2O may indicate a compromised cough efficiency but the correlation with cough PEF may be poor. Screening nocturnal oxymetry is useful to detect sleep apneas and hypoventilation. Criteria defining significant desaturations remain however controversial. Suspicion of obstructive sleep apnea syndrome on clinical grounds or oxymetry findings should be confirmed by a conventional polysomnography.

Amyotrophic Lateral Sclerosis↗
PubMed1995

Pulmonary function abnormalities in Prader-Willi syndrome.

OBJECTIVE: To determine whether individuals with Prader-Willi syndrome (PWS) have abnormalities in pulmonary function as a result of thoracic muscle weakness. DESIGN: Testing of spirometry, flow-volume curves, lung volumes, and static respiratory pressures was performed in patients with PWS who are followed at the University of Connecticut. All tests were performed in triplicate on two or more occasions. Only reproducible tests were accepted. Established normative data were applied for all test results. RESULTS: A total of 18 male subjects (age, 17.9 +/- 10.2 years (mean +/- SD); range, 5-39 years) and 17 female subjects (age, 23.5 +/- 13.0 years; range, 5-54 years) completed the tests. Forced vital capacity and forced expiratory volume in 1 second were reduced; the forced expiratory volume in 1 second/forced vital capacity ratio was normal, total lung capacity was in the low normal range, and residual volume was elevated. Maximum inspiratory (PImax) and expiratory (PEmax) pressures were markedly reduced in 32 subjects tested. Fifteen subjects had PEmax values and 20 subjects had PImax values < 60 cm H2O, respectively. There was a linear correlation between forced expiratory volume in 1 second and both PImax and PEmax (r = 0.71; r = 0.62, respectively), and between forced vital capacity and both PEmax and PImax (r = 0.62 and r = 0.74, respectively). There was an inverse relationship between both PImax and PEmax, and residual volume (r = 0.47 and r = 0.72, respectively). CONCLUSION: Children and adults with PWS have restrictive ventilatory impairment primarily as a result of respiratory muscle weakness. Efforts to improve thoracic muscle strength may be useful in improving pulmonary function in individuals with PWS.

Adolescent↗
PubMed1992

[Ergometric and pathologic study of a family with complex I deficiency].

We studied a family with a myopathic form of complex I deficiency with regard to the clinical symptoms, usefulness of the exercise tolerance test with an ergometer for screening of mitochondrial abnormalities, pathological findings in biopsied muscles and genetics. In this family, none of the members had disorders of the central nervous system, such as convulsions, mental deterioration or stroke-like episodes. In the two affected generations, three mothers and three children had mitochondrial abnormalities. Two children were diagnosed as having complex I deficiency. One of them, an 8-year-old girl with normal psychomotor development during infancy, began to experience easy fatigability at about 3 years of age. At the age of 5 years, she experienced respiratory distress and became unconscious. Thereafter, she had similar episodic respiratory problems with lactic acidosis. Ragged-red fibers and respiratory chain enzyme defects were detected in the biopsied muscle. Another child, a 15-year-old boy with easy fatigability but no muscle weakness, had normal respiratory chain enzyme activities and a normal oxysogram: oxygen consumption showed a normal responses when malate and pyruvate were added as substrates for the isolated mitochondria. His muscle pathology revealed rare ragged-red fibers and abnormal subsarcolemmal mitochondrial aggregation. An investigation with an ergometer showed elevated serum lactate and pyruvate levels. Only one mother had muscle weakness and hyper-lactic acidemia. The other two mothers had no muscle symptoms, but abnormal results were obtained with the ergometer.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2005

Decreased isometric skeletal muscle force in critically ill patients.

QUESTION UNDER STUDY: Critically ill patients can develop muscle weakness that prolongs recovery. The aim of this study was to evaluate contractile parameters of the involuntary isometric skeletal muscle forces as measures of muscle weakness in critically ill patients. METHODS: Prospective, controlled trial performed in an intensive care unit (ICU) of a university hospital. SUBJECTS: 19 critically ill patients (diagnoses: intracranial bleeding n = 9; sepsis n = 6; others n = 4), who were ventilated and completely immobilised for one week. 20 healthy volunteers served as controls. We measured peak torques (PT), contraction times, half-relaxation times, peak rates of torque development and decay and torque latencies of the ankle dorsiflexors of the foot after peroneal nerve stimulation. RESULTS: Patients (median Acute Physiology and Chronic Health Evaluation II score 21) had reduced PTs, medians 3.3 Nm (interquartile range 2.5 Nm) vs 4.1 Nm (2.0 Nm) in controls (P = 0.0003) for single pulse, 4.9 (4.7) vs 8.1 Nm (3.8) (P = 0.0001) for 2-pulse, 6.1 (6.3) vs 10.3 Nm (3.9) (P = 0.0009) for 3-pulse and 7.3 (6.4) vs 11.6 Nm (7.8), (P = 0.006) for 4-pulse stimulations, respectively. Contraction times were reduced and half-relaxation times increased compared with controls. CONCLUSIONS: Assessment of involuntary isometric skeletal muscle forces can be readily measured in critically ill patients. After one week of critical illness, these patients have decreased force compared with healthy controls. This assessment approach will be further evaluated in a long-term study with a larger patient population.

APACHE↗
PubMed1993

Manifesting carriers of Xp21 muscular dystrophy; lack of correlation between dystrophin expression and clinical weakness.

Ten females presenting with muscle weakness and a raised serum creatine kinase revealed abnormalities in the expression of dystrophin in their muscle biopsies and were diagnosed as manifesting carriers of Xp21 Duchenne/Becker muscular dystrophy. Seven cases, aged 3-22 yr at the time of biopsy, had a variable proportion of dystrophin-deficient fibres and an abnormal expression on immunoblot. These were confidently diagnosed as manifesting carriers. Results in the remaining three cases, aged 8-10 yr, were less clear-cut. Dystrophin expression on immunoblots was slightly reduced and some unevenness and reduction of immunolabelling was seen on sections, but dystrophin-deficient fibres were not a feature of these cases. The weakness in the ten carriers ranged from minimal to severe and there was no correlation between the degree of weakness and the number of dystrophin-deficient fibres. Two minimally weak girls had a high proportion of dystrophin-deficient fibres. Our results show that analysis of dystrophin expression is useful for the differential diagnosis of carriers of Xp21 dystrophy and autosomal muscular dystrophy, but that dystrophin expression does not correlate directly with the degree of clinical weakness.

Adult↗
PubMed1975

Nature of muscular change in osteomalacia: light- and electron-microscope observations.

Thirteen muscle biopsy specimens (mainly the gluteus maximus) from 12 patients with laboratory confirmation of osteomalacia and proximal muscle weakness in 10 were examined by light and electron microscopy. Light microscopy revealed mild diffuse non-specific atrophy of the muscle fibres in 10 cases, severe generalised atrophy in one and patchy group atrophy in one. There was no myopathic change in specimens from cases with either a nutritional aetiology, or a mixed aetiology. The former, mostly women gave a history of severe chronic malnutrition often accompanied by repeated pregnancies and prolonged lactation; those with a mixed aetiology gave, in addition, evidence of a metabolic or endocrine disorder such as hyperparathyroidism, hyperthyroidism, uraemia, or treatment with anti-epileptic drugs or were of uncertain origin. Electron-microscope examination of muscle from the nutritional group showed atrophic changes in the fibres, such as loss of myofibrils, prominence of mitochondria and glycogen, loosening and folding of the basement-membrane but good preservation of the remaining myofibrils. In contrast muscle from cases of mixed aetiology showed, in addition to the atrophic features, clear degenerative changes in the myofibrils and the mitochondria, accumulation of amorphous material at the site of myofibrillar loss and of lipofuscin in muscle fibres, vascular endothelium and satellite cells. The earliest degenerative change was in the "I" band, involving actin filaments and "Z" line. The triads were generally preserved but the sarcoplasmic reticulum appeared affected in a patient with tetany and severe mitochondrial degeneration. In a patient with thyrotoxicosis, proliferation of central nuclei, "Z" line streaming and formation of "T" tubular aggregates were seen. In one patient with hyperparathyroidism and hypercalcaemia, severe myofibrillar degeneration and mitochondria showing osmiophilic deposits, possibly of calcium phosphate, were encountered. It is concluded: (1) that all osteomalacic muscle weakness is not myopathic but a non-specific atrophy occurring probably on the basis of disuse and malnutrition, and (2) patients with an added metabolic or endocrinological disorder show in addition to the atrophy, degenerative changes in the muscle fibre and its sub-cellular components consistent with myopathy, and these patients should be clearly distinguished from those with a background of malnutrition only.

Adolescent↗
PubMed1986

Action of thyrotropin-releasing hormone (TRH) on the occurrence of fibrillation potentials and miniature end-plate potentials (MEPPs). An experimental study.

The effect of TRH on fibrillation potentials and MEPPs were studied to determine the sites of action of TRH on muscle weakness. Intravenous administration of 10(-4) U thyroid-stimulating hormone (TSH) did not change the fibrillation-frequency of the denervated muscles of rats, but subsequent intravenous administration of 1 mg TRH did. Drip application of 0.6 mg TRH directly onto the denuded denervated muscles of rats did not cause an increase in fibrillation. Application of 1 mg TRH to the rat diaphragm increased the frequency of MEPPs. Both the increase in frequency of fibrillation potentials and the increase in frequency of MEPPs by application of TRH suggest that TRH influences nerve terminals, and that TRH seems suitable for treatment of muscle weakness in patients with ALS.

Animals↗
PubMed2004

The effects of exercise on skeletal muscle in the aged.

Age-related sarcopenia leads to muscle weakness and a concomitant increase in gait problems and the risk of hip fracture due to falling in the elderly. Muscle weakness reduces general activity levels in elderly individuals which in turn elevates the risk of osteoporosis due to a decrease in overall mechanical loading of the skeleton. At the same time, age-related sarcopenia is also linked to an increase in the risk of metabolic disorders such as adult onset (Type II) diabetes. However, it is widely accepted that increased mechanical loading of the musculoskeletal system (e.g., resistive exercise) can have a beneficial effect on both skeletal muscle and the supporting skeleton resulting in a significant reduction in the risk of developing all of the above age-related problems. As such, unloading models that exhibit many if not all of the same responses observed in aged muscle, including the capacity of exercise to reverse these responses, may provide valuable insight into the skeletal muscle aging process.

Aged↗
PubMed1994

Exercise training and nutritional supplementation for physical frailty in very elderly people.

BACKGROUND: Although disuse of skeletal muscle and undernutrition are often cited as potentially reversible causes of frailty in elderly people, the efficacy of interventions targeted specifically at these deficits has not been carefully studied. METHODS: We conducted a randomized, placebo-controlled trial comparing progressive resistance exercise training, multinutrient supplementation, both interventions, and neither in 100 frail nursing home residents over a 10-week period. RESULTS: The mean (+/- SE) age of the 63 women and 37 men enrolled in the study was 87.1 +/- 0.6 years (range, 72 to 98); 94 percent of the subjects completed the study. Muscle strength increased by 113 +/- 8 percent in the subjects who underwent exercise training, as compared with 3 +/- 9 percent in the nonexercising subjects (P < 0.001). Gait velocity increased by 11.8 +/- 3.8 percent in the exercisers but declined by 1.0 +/- 3.8 percent in the nonexercisers (P = 0.02). Stair-climbing power also improved in the exercisers as compared with the nonexercisers (by 28.4 +/- 6.6 percent vs. 3.6 +/- 6.7 percent, P = 0.01), as did the level of spontaneous physical activity. Cross-sectional thigh-muscle area increased by 2.7 +/- 1.8 percent in the exercisers but declined by 1.8 +/- 2.0 percent in the nonexercisers (P = 0.11). The nutritional supplement had no effect on any primary outcome measure. Total energy intake was significantly increased only in the exercising subjects who also received nutritional supplementation. CONCLUSIONS: High-intensity resistance exercise training is a feasible and effective means of counteracting muscle weakness and physical frailty in very elderly people. In contrast, multi-nutrient supplementation without concomitant exercise does not reduce muscle weakness or physical frailty.

Aged↗
PubMed1989

[A case of Kennedy-Alter-Sung syndrome associated with external ophthalmoplegia--therapeutic efficacy of fluoxymesterone].

We reported a case with Kennedy-Alter-Sung syndrome (KAS) associated with bilateral external ophthalmoplegia. The patient had movement disturbance of bilateral infra-oblique muscles. The doll's eye phenomenon was not noted. It was suggested that the external ophthalmoplegia was due to the involvement of the oculomotor nucleus that innervated infra-oblique muscle. The serum levels of testosterone and gonadotropin were high, suggesting that the feminization of KAS patients was caused by androgen insensitivity. The feminization of KAS patients is similar to the incomplete form of testicular feminization syndrome except that they do not have feminization of genitals. Therefore, we proposed that abnormalities of androgen receptors might play a role in the pathogenesis of KAS. Fluoxymesterone therapy significantly improved the muscle weakness of the extremities of the patient, even though the therapeutic efficacy was shown temporarily. The therapeutic efficacy of fluoxymesterone for muscle weakness supports our hypothesis.

Androgen-Insensitivity Syndrome↗
PubMed2005

Changes in quadriceps twitch tension in response to resistance training in healthy sedentary subjects.

Magnetic stimulation of the femoral nerve has been shown to evoke maximal quadriceps twitch contraction (TwQ(max)). Its measurement as a nonvolitional index of muscle strength has been proposed as a means to follow the disability of patients with neuromuscular disorders or peripheral muscle weakness. The aim of the present study was to investigate TwQ(max) sensitivity to interventions known to develop peripheral muscle strength. We thus measured changes in TwQ(max) after a short-duration resistance training program, examining its reproducibility and comparing its changes with other indices of muscle strength, such as maximal voluntary contraction (MVC) and one-repetition maximum (1-RM). In 23 subjects, TwQ(max)was measured on two occasions. High within- and between-session intraclass coefficients of correlation were observed (r > 0.99). Within-session and between-session differences in TwQ(max)were low (2.2 +/- 1% and 5.4 +/- 2%, respectively). Eight subjects subsequently participated in a resistance training program of the knee extensors, 3 days per week for 8 weeks. TwQ(max) and 1-RM increased significantly after training (10.9 +/- 3.7 vs. 12.3 +/- 4.4 kg, P < 0.04; and 45 +/- 13 vs. 55 +/- 12 kg, P < 0.001, respectively), whereas the MVC increase did not reach significance (41.9 +/- 16 kg vs. 42.3 +/- 15 kg, P = 0.25). Responses to magnetic stimulation of the femoral nerve are highly reproducible and sensitive enough to detect improvement in muscle contractile mechanisms after resistance training in healthy subjects. Patient cooperation is not required, which may be an advantage in clinical situations.

Adolescent↗
PubMed1996

A distinctive type of infantile inflammatory myopathy with abnormal myonuclei.

Four infants developed progressive muscle weakness after a normal initial postnatal development. All patients had a moderate elevation of serum creatine kinase (CK) activity. Muscle biopsies revealed, in addition to myopathic features, endomysial and perivascular inflammation. Electron microscopy disclosed prominent myonuclear abnormalities. Corticosteroids in 3 patients were moderately beneficial. This appears to be a clinicopathologically distinct form of inflammatory myopathy of infants.

Adrenal Cortex Hormones↗
PubMed2006

Amyloid myopathy presenting with rhabdomyolysis: evidence of complement activation.

At age of 57 years, a man experienced an episode of rhabdomyolysis. On that occasion muscle biopsy was not performed, however monoclonal gammopathy of undetermined significance (MGUS) was diagnosed. Further he developed a moderate proximal muscle weakness with CK level persistently elevated (1000-1200U/l). When he came to our observation, at age 67, a muscle biopsy revealed an amyloid myopathy and multiple myeloma was at the same time disclosed. Terminal complement complex C5b9 (membrane attack complex) deposits were found in the vessel walls and muscle fibers surface depicted by amyloid. Our case suggests to keep in mind the possibility that amyloid myopathy may begin as an isolate episode of rhabdomyolysis. The detection of complement complex C5b9 suggests that complement cascade is implicated in the muscular damage of amyloid myopathy.

Aged↗