SEARCH · PubMed Health

Results for “Muscle Weakness”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources

PubMed2005

Streptomycin and EDTA decrease the number of desmin-negative fibers following stretch injury.

Streptomycin and ethylene diamine tetraacetic acid (EDTA) were used to examine the role of extracellular calcium in stretch-induced muscle injury. Streptomycin was injected in one group of rats, three times daily for 8 days (S, 300 mg.kg(-1).day(-1) intraperitoneally). In another group, EDTA was administered (150 mg.kg(-1) IP) 20 min before and 24 h after the injury protocol. Untreated rats (C) served as controls. Muscle injury was produced by 40 stretches of active dorsiflexor muscles by ankle rotation from 80 degrees to 130 degrees (velocity 1.75 rad.s(-1)). Ten minutes after the injury protocols, all animals lost the same amount of isometric force at both low and high stimulation frequencies (20 HZ; S, 56 +/- 6%; EDTA, 47 +/- 7%; C, 55 +/- 4%) and 120 HZ; S, 11 +/- 3%, EDTA, 13 +/- 3%; C, 11 +/- 3%). Tibialis anterior (TA) muscles were removed after 48 h for morphometric analysis. In both streptomycin-and EDTA-treated rats, the percent of injured (i.e., desmin-negative) myofibers in TA was reduced compared to untreated, injured muscles (S, 0.35 +/- 0.08%; EDTA, 0.64 +/- 0.19%; C, 1.81 +/- 0.43%). Thus, streptomycin and EDTA treatment did not alter the development of muscle weakness (i.e., isometric force deficit), but almost abolished the histopathologic changes. This study shows that the mechanisms for muscle weakness and histopathologic changes (inflammation) following repeated muscle strains can largely be dissociated from each other and helps explain why there is no correlation between isometric force deficits and the number of pathologic cells.

Animals↗

PubMed1997

[Effects of precurarization on oxygen arterial saturation measure with pulse oximetry and neuromuscular function].

OBJECTIVE: To study changes in arterial oxygen saturation (SpO2) measured by pulse oximetry, and the effect of neuromuscular function after precurarization with different nondepolarizing muscle relaxants. PATIENTS AND METHOD: One hundred twenty-four patients scheduled for elective surgery were randomly assigned to four groups according to the NDPMR received: d-tubocurarine 0.05 mg/kg, atracurium 0.05 mg/kg, vecuronium 0.01 mg/kg or pancuronium 0.015 mg/kg. We recorded SpO2 before precurarization and 4 minutes after administering the dose. We also recorded signs and symptoms of muscle weakness after the 4-minute period of precurarization. RESULTS: We observed a statistically significant decrease in SpO2 4 minutes after starting precurarization in the groups receiving pancuronium, vecuronium and atracurium. These three groups were also significantly different from the d-tubocurarine group with regard to signs and symptoms of muscle weakness; the incidences of such symptoms were similar among the three groups, the only exception being the greater difficulty patients in the pancuronium group had in maintaining the Valsalva maneuver for 10 seconds. The lowest incidence of clinical signs of muscle weakness were in the d-tubocurarine group. We found a significant relation between decreased SpO2 caused by precurarization and the variables of inability to maintain the Valsalva maneuver for 10 seconds and to raise the head for more than 4 seconds. CONCLUSIONS: SpO2 measured by pulse oximetry is an effective method for monitoring breathing function in the precurarized patient, as it detects early changes in arterial oxygen saturation related to respiratory muscle weakness. The agent d-tubocurarine is recommended for precurarization, because of its scarce effect on neuromuscular function at the dose used in this study.

Adolescent↗

PubMed2000

[A case of rhabdomyolysis with water intoxication confirmed by muscle biopsy].

A 32-year-old woman with chronic schizophrenia who took 8-10 liters of water for three years due to thirsty, admitted to our hospital because of convulsion and muscle weakness. Neurological finding on admission showed a mild disturbance of consciousness, moderate proximal muscle weakness, and muscle pain. Laboratory examination revealed marked serum hyponatremia(102 mEq/l) and high value of creatin kinase (1,259 IU/l). The level of creatin kinase reached a peak(39,700 IU/l) at the 5th hospital day. An analysis of the muscle biopsy specimen showed necrotic muscle fibers and opaque fibers, that was compatible with rhabdomyolysis. T 2 weighted magnetic resonance imaging of the brain showed a transient high signals in bilateral putamen but not in pons. She was diagnosed to have rhabdomyolysis due to water intoxication. The present case is the first rhabdomyolysis in Japan that was confirmed by muscle biopsy at an acute stage of water intoxication related with schizophrenia.

Adult↗

PubMed1996

[A family of hereditary motor and sensory neuropathy type I with a mutation (Arg98-->His) in myelin Po--report on a second Japanese family].

A 46-year-old housewife had complaints of insidiously progressive muscle weakness and paresthesia in the distal lower limbs. On neurological examination, a slight to moderate degree of muscle weakness with slight atrophy was observed in the bilateral intrinsic hand muscles. A severe degree of muscle weakness with moderate atrophy was observed in tibialis anterior, gastrocnemius and soleus muscles. Muscle stretch reflexes were decreased in the upper limbs and absent in the lower limbs, without pathologic reflexes. She had a steppage gait. Vibratory sensation was slightly decreased in the hands and moderately decreased in the feet. Touch, pain and temperature sensations were also moderately decreased only in the feet. On laboratory examination, glycosuria (5.6g/dl) was noted. Fasting blood sugar was 226mg/dl with an elevated hemoglobin A1C level (12.7%). The right median motor and sensory nerve conduction velocities were 14.8 and 20.3 m/sec, respectively, with a markedly prolonged distal latency. No muscle action potential was obtained from stimulation of the right tibial nerve. Also, no nerve action potential was elicited from stimulation of the right sural nerve. A fascicular biopsy of the right sural nerve revealed the presence of both demyelinated and remyelinated axons, and an onion-bulb formation with a marked decrease in the density of the myelinated fibers. Based on the neurological examination and nerve conduction studies of the family members, a younger sister, younger brother and an elder daughter of the proband were found to be affected by demyelinating polyneuropathy. Diabetes mellitus was not found among the family members with laboratory evidences of demyelinating polyneuropathy. Based on the family history, an uncle on the mother's side of the proband, the proband's grandmother and a younger daughter of a proband's brother were considered to be affected. The uncle and grandmother had diabetes mellitus. Therefore, we concluded that this family had HMSN type I with autosomal dominant inheritance. In the studies on fluorescence in situ hybridization, and restriction fragment length polymorphism of the genomic DNA of the proband, a DNA duplication in the 17p11.2-12 region was not observed. However, the direct sequencing analysis of DNA fragments from genomic DNA encoding the Po gene of the proband revealed a substitution of histidine for arginine at the codon 98 in the extramembranous domain of Po. She was heterozygous for the mutant allele and normal allele. Alterations in the tertiary structure of the extramembranous domain of Po may result in an impairment of the peripheral myelin compaction. This is the second Japanese family with the same mutation (Arg98-->His) of myelin Po as reported previously by us, and this type of case is rare in the literature. Therefore, the mutation at the codon 98 may play a critical role in the development of the myelin abnormality in HMSN type IB.

Arginine↗

PubMed1985

CT-scanning of skeletal muscle in arthrogryposis multiplex congenita.

CT-scanning of skeletal muscles was performed on 14 patients with arthrogryposis multiplex congenita (AMC), according to an eight-slice protocol. Adipose tissue replacement and atrophy of muscles was found in six patients with neurogenic or myopathic origin of AMC, associated with severe muscle weakness. In the remaining patients with other forms of AMC, in which muscle weakness was less marked or absent, muscular CT-scanning was normal. It is stated that muscular CT-scanning is not a routine investigation in a screening procedure of all cases of AMC. However, CT-scanning appears to be useful in cases of severe AMC with associated muscle weakness in detecting the neurogenic and myopathic forms. It also facilitates the selection of a suitable site for EMG and biopsy and may provide important information for orthopaedic management.

Adolescent↗

PubMed2005

Isolated mitochondrial myopathy associated with muscle coenzyme Q10 deficiency.

BACKGROUND: Primary coenzyme Q(10) (CoQ(10)) deficiency is rare. The encephalomyopathic form, described in few families, is characterized by exercise intolerance, recurrent myoglobinuria, developmental delay, ataxia, and seizures. OBJECTIVE: To report a rare manifestation of CoQ(10) deficiency with isolated mitochondrial myopathy without central nervous system involvement. METHODS: The patient was evaluated for progressive muscle weakness. Comprehensive clinical evaluation and muscle biopsy were performed for histopathologic analysis and mitochondrial DNA and respiratory chain enzyme studies. The patient began taking 150 mg/d of a CoQ(10) supplement. RESULTS: The elevated creatine kinase and lactate levels with abnormal urine organic acid and acylcarnitine profiles in this patient suggested a mitochondrial disorder. Skeletal muscle histochemical evaluation revealed ragged red fibers, and respiratory chain enzyme analyses showed partial reductions in complex I, I + III, and II + III activities with greater than 200% of normal citrate synthase activity. The CoQ(10) concentration in skeletal muscle was 46% of the normal reference mean. The in vitro addition of 50 micromol/L of coenzyme Q(1) to the succinate cytochrome-c reductase assay of the patient's skeletal muscle whole homogenate increased the succinate cytochrome-c reductase activity 8-fold compared with 2.8-fold in the normal control homogenates. Follow-up of the patient in 6 months demonstrated significant clinical improvement with normalization of creatine kinase and lactate levels. CONCLUSIONS: The absence of central nervous system involvement and recurrent myoglobinuria expands the clinical phenotype of this treatable mitochondrial disorder. The complete recovery of myopathy with exogenous CoQ(10) supplementation observed in this patient highlights the importance of early identification and treatment of this genetic disorder.

Biopsy↗

PubMed1998

Isokinetic strength testing does not predict hamstring injury in Australian Rules footballers.

OBJECTIVE: To determine the relation of hamstring and quadriceps muscle strength and imbalance to hamstring injury using a prospective observational cohort study METHOD: A total of 102 senior male Australian Rules footballers aged 22.2 (3.6) years were tested at the start of a football season. Maximum voluntary concentric and eccentric torque of the hamstring and quadriceps muscles of both legs was assessed using a Kin-Com isokinetic dynamometer at angular velocities of 60 and 180 degrees/second. Twelve (11.8%) players sustained clinically diagnosed hamstring strains which caused them to miss one or more matches over the ensuing season. RESULTS: There were no significant differences for any of the isokinetic variables comparing the injured and non-injured legs in players with unilateral hamstring strains (n=9). Neither the injured nor the non-injured leg of injured players differed from the mean of left and right legs in non-injured players for any isokinetic variable. The hamstring to opposite hamstring ratios also did not differ between injured and non-injured players. A hamstring to opposite hamstring ratio of less than 0.90 and a hamstring to quadriceps ratio of less than 0.60 were not associated with an increased risk of hamstring injury. A significantly greater percentage of players who sustained a hamstring strain reported a history of hamstring strain compared with non-injured players (p=0.02). However, this was not related to muscle weakness or imbalance. CONCLUSIONS: Isokinetic muscle strength testing was not able to directly discriminate Australian Rules football players at risk for a hamstring injury.

Adult↗

PubMedDate not supplied

[Myasthenia gravis: diagnosis and treatment].

INTRODUCTION: Myasthenia gravis is an autoimmune disorder characterized by fluctuating muscle weakness and fatigue of different muscle groups. Myasthenia gravis may affect persons of all ages, but especially women aged 20 to 40 years. DEVELOPMENT AND CONCLUSIONS: The ocular, facial and bulbar muscles are most often involved in this disease. The muscle weakness of patients with myasthenia gravis becomes worse with intercurrent episodes of infection, fever and physical or emotional exhaustion. Respiratory infection (bacterial or viral) is the most frequent trigger factor. The presence of antibodies to acetylcholine receptors in a patient with the clinical features of myasthenia gravis, confirms the diagnosis. Treatment is controversial. Each patient therefore has to be treated individually, as no single treatment is suitable for all patients. Treatment may include anticholinesterase drugs, corticosteroids, plasmapheresis, immunoglobulin, immunosuppressive drugs and thymectomy.

Adult↗

PubMedDate not supplied

Systemic lupus erythematosus presenting as amyotrophic lateral sclerosis.

We report a case of a 27-year-old Omani lady having a 3-year history of progressive skeletal muscle weakness with clinical and skeletal muscle changes of ALS, who during the course of investigations for ALS was found to have SLE. This association is not a simple coincidence but perhaps a causal relationship, opening vistas to explain the autoimmune pathogenesis and justification for immunosuppressive therapy in ALS. SLE presenting as ALS has not been reported earlier.

Adult↗

PubMed1999

New method of assessing outcome of treatment for cervical myelopathy (M/T method)--preliminary report.

In some patients with cervical radiculomyelopathy, neurological examination reveals extreme muscle weakness in an upper extremity with no, or a relatively insignificant, sensory deficit. In assessment of treatment outcome in these patients, the previous method used is thought to be unsuitable. We developed a new method of assessment (the M/T method) in which the recovery of upper extremity muscle weakness is assessed. The purpose of this study was to evaluate this new method. In the M/T method, change in the function of the spinal cord, including the anterior root, is expressed as an index number (recovery rate) in relation to the time-course. The function of the nerve tissue is expressed as the value for the manual muscle testing (MMT) of muscle power, and the muscle tested is represented by one that has the least MMT value before treatment. The unit of measurement of the time-course is 3 months. The index is the difference between the MMT value at the time of follow-up and that before treatment, divided by the number of time units after treatment. The index can be expressed in both fractional and decimal forms. Fractions are useful for examining an individual patient's progress and the decimal form is useful for comparing the data of multiple patients. The M/T method was employed in 16 patients (13 men, 3 women; age, 45-79 years; follow-up, 6 months - 8 years) whose chief complaints were muscle weakness in the upper extremities and who had undergone double-door laminoplasty. Seven patients had an M/T index of 1 or more; the score was 4 in one patient, 2 in four patients, and 1 in two patients. Two patients had an M/T index between 0 and 1; 0.17 and 0.25. Five patients had an index value of 0. The M/T index in two patients was less than 0; -0. 17 and -0.11. Using the M/T method, recovery can be presented as an index number, and as a result, it is easy to compare differences in the recovery rate among patients. The M/T method is useful for evaluation of the viability of the spinal cord, including the anterior root; in particular for those patients in whom neurological examination reveals extreme muscle weakness in an upper extremity with no, or a relatively insignificant, sensory deficit.

Aged↗

PubMed2026

Effects of exercise on muscle strength and characteristics in rheumatic diseases and sarcopenia: Protocol for the Care for Muscle (C4M) Study.

OBJECTIVE: Muscle weakness is prevalent in rheumatoid arthritis (RA), osteoarthritis (OA) and sarcopenia (SARC). Endurance exercises may improve mitochondrial function and oxidative capacity, while strength exercises are thought to stimulate myofibrillar protein synthesis. This study aims to compare the effects of strength and endurance exercise and explore the association between muscle characteristics and exercise outcomes in patients with RA, OA and SARC. We hypothesize that responses to endurance and strength exercises in patients with muscle weakness are influenced by intramuscular pathology including muscle morphology, mitochondrial function, and systemic inflammation, based on their disease pathology, potentially requiring personalized training schedules. METHODS: This two-arm, parallel-group exploratory trial will enroll 69 patients (23 RA, 23 OA, 23 SARC), randomized to endurance (n = 35) or muscle strength exercises (n = 34), using minimization to balance disease type and gender. The 8-week intervention includes two supervised sessions per week using a controlled cable pulley device (Reforter™) and fitness equipment, plus one weekly home-based session. The primary outcome is isokinetic muscle strength (peak torque), measured with the Biodex system®. Secondary outcomes include muscle morphology, mitochondrial function, systemic inflammation and muscle endurance (by Biodex and 6 Minute Walk test). Muscle morphology will be assessed via 3D ultrasound imaging of the vastus lateralis. Mitochondrial function will be analyzed using high-resolution respirometry on muscle biopsies. Systemic inflammation will be measured using multiplex assays or ELISA on serum samples. DISCUSSION: This study will explore differential responses to muscle endurance and muscle strength exercises in patients with RA, OA, and SARC, offering novel insights into the molecular mechanisms of muscle weakness. The findings may help identify potential mechanisms underlying variability in exercise response and provide effect size estimates to guide future confirmatory studies and more targeted exercise interventions. TRIAL REGISTRATION: ClinicalTrials.gov NCT06480643 (date of registration28-06-24).

Humans↗

PubMed1998

Apathy and hypersomnia are common features of myotonic dystrophy.

OBJECTIVES: Myotonic dystrophy is a disease characterised by myotonia and muscle weakness. Psychiatric disorder and sleep problems have also been considered important features of the illness. This study investigated the extent to which apathy, major depression, and hypersomnolence were present. The objective was to clarify if the apathy reported anecdotally was a feature of CNS involvement or if this was attributable to major depression, hypersomnolence, or a consequence of chronic muscle weakness. METHODS: These features were studied in 36 adults with non-congenital myotonic dystrophy and 13 patients with Charcot-Marie-Tooth disease. By using patients with Charcot-Marie-Tooth disease as a comparison group the aim was to control for the disabling effects of having an inherited chronic neurological disease causing muscle weakness. Standardised assessment instruments were used wherever possible to facilitate comparison with other groups reported in the medical literature. RESULTS: There was no excess of major depression on cross sectional analysis in these patients with mild myotonic dystrophy. However, apathy was a prominent feature of myotonic dystrophy in comparison with a similarly disabled group of patients with Charcot-Marie-Tooth disease (clinician rated score; Mann Whitney U test, p=0.0005). Rates of hypersomnolence were greater in the myotonic dystrophy group, occurring in 39% of myotonic dystrophy patients, but there was no correlation with apathy. CONCLUSION: These data suggest that apathy and hypersomnia are independent and common features of myotonic dystrophy. Apathy cannot be accounted for by clinical depression or peripheral muscle weakness and is therefore likely to reflect CNS involvement. These features of the disease impair quality of life and may be treatable.

Activities of Daily Living↗

PubMed1984

Submuscular transposition for the ulnar nerve at the elbow.

Forty patients who underwent submuscular transpositions of the ulnar nerve at the elbow (41 operations) were evaluated. A grading system was formulated to compare the preoperative and postoperative condition of each patient with respect to tenderness over the nerve, numbness, paresthesia, and muscle weakness. Thirty-seven of the 41 cases showed an improvement in grade. Of the 34 cases that demonstrated muscle weakness preoperatively, 25 improved following surgery, including five patients who had severe intrinsic muscle weakness with clawing of the ring and little finger. Muscle reattachment following nerve transposition was secure, even in a professional athlete.

Adolescent↗

PubMed2003

Gap junction protein beta 1 (GJB1) mutations and central nervous system symptoms in X-linked Charcot-Marie-Tooth disease.

OBJECTIVES: To clarify the clinical variability, including central nervous system (CNS) involvement, in X-linked Charcot-Marie-Tooth disease (CMTX) patients. MATERIAL AND METHODS: We clinically, pathologically and genetically studied six CMTX patients with distinct symptoms and four different GJB1 mutations. RESULTS: One patient with Val63Ile had deafness, low intelligence, saccadic eye movement, upper extremity distal dominant muscle weakness and normal sensation. Another patient with Glu186Lys had severe sensorineural deafness at the age of 6 years, but did not develop muscle weakness until the age of 20 years. Two patients with Arg22Gln had typical CMT1A-like clinical features, no CNS symptoms and obvious onion bulb formations. Two siblings with deletion of the entire GJB1 gene had mild to moderate lower extremity muscle weakness and sensory disturbance without CNS involvement. CONCLUSION: These findings suggest that some gain of function mutations of GJB1 may be related to CNS symptoms because the patients with GJB1 deletion only had peripheral neuropathy, although other unknown associated factors may contribute to their clinical phenotypes.

Adult↗

PubMed1984

Human mononuclear cell factors suppress contractility of isolated mouse soleus muscle.

Weakness in polymyositis-dermatomyositis is often greater than would be suggested by histologic evidence of fiber degeneration or necrosis. Mononuclear cell infiltration is the key pathologic feature of polymyositis-dermatomyositis, and previous studies suggest a role for cellular immunity. In this study, the effect of supernatants from mitogen-stimulated human blood mononuclear cells on contractility of isolated mouse normal soleus muscle was examined. Mononuclear cell factor-rich supernatants were generated in 5-day cultures by phytohemagglutinin P stimulation of mononuclear cells from normal volunteers. Mouse soleus muscle was mounted isometrically in a muscle bath filled with oxygenated Ringer's solution or RPMI-1640 and was stimulated electrically. In 10 individual experiments, all muscles exposed to mononuclear cell factor-rich supernatants showed a rapid and progressive decline in active force of isometric contraction; a 40% decrease in active force was observed 5 to 13 minutes (average, 8 minutes) after the addition of supernatant. The inhibitory effect was reversible on removal of mononuclear cell factor-rich supernatants. Control culture medium and supernatants from unstimulated cell cultures showed no appreciable effect on active force. The factor(s) producing suppression of muscle contractility was dialyzable and stable through several cycles of freezing and thawing. Gel chromatography (Sephadex G-25 fine) showed one active fraction corresponding to an apparent molecular weight of approximately 2000. These data indicate that factor(s) released by human mononuclear cells can directly suppress the contraction of normal skeletal muscle.

Animals↗

PubMed1997

[The diagnosis of amyotrophic lateral sclerosis supported by motor evoked potential and brain MRI studies].

A 57-year-old man developed severe muscle weakness and atrophy of the upper extremities within a five-month period. Neurological examination revealed severe weakness and atrophy in the scapular muscles and proximal and distal muscles of the upper extremities. Fasciculations were also observed in the various muscles of the upper extremities. There was neither muscle weakness, atrophy nor fasciculation in either his face, neck muscles or lower extremities. He had no pseudobulbar or bulbar signs. Tendon reflexes were mildly hyperactive in the jaw and lower extremities, and normal in the upper extremities. There were no pathological reflexes, spasticity or sensory disturbances. The needle EMG study revealed denervation potentials in all muscles of the upper extremities examined. The nerve conduction study revealed no findings of the conduction block. Cervical spine X-rays revealed the narrowing of the spinal foramens at the left C3/C4 and bilateral C4/C5, C5/C6, and C6/C7 intervertebral levels. In addition, magnetic resonance imaging (MRI) revealed compressions of the cervical cord at C4/C5 and C5/C6 intervertebral levels. These clinical and neuroradiological findings resembled those of the cervical spondylotic amyotrophy (CSA). However, the motor evoked potential (MEP) study revealed the pyramidal tract dysfunction above the levels of the pyramidal decussation. Furthermore, brain MRI revealed abnormal foci in both internal capsules which were characterized by hyperintense relative to cortical gray matter on T2-weighted images and still hyperintense to white matter on proton-density-weighted images. In addition, T2-weighted images demonstrated a low signal within the motor cortex and hyperintense lesions in the white matter of the precentral gyri. These MRI findings indicated the degeneration of the pyramidal tract and corresponded to those found in the patients with amyotrophic lateral sclerosis (ALS) which have been recently reported. It has been difficult to distinguish ALS from CSA. However, MEP and brain MRI studies were useful for distinguishing these two diseases in this patient. In addition, this patient showed typical MRI findings suggesting the degeneration of the pyramidal tract, although this patient had a relatively short course of illness and did not show obvious physical findings suggesting pyramidal tract dysfunction.

Amyotrophic Lateral Sclerosis↗

PubMed1998

Spontaneous thymoma rat as a model for myasthenic weakness caused by anti-ryanodine receptor antibodies.

The mechanism of muscle weakness in myasthenia gravis and its possible relation to antibodies that are directed against the ryanodine receptor (RyR) were studied by the use of the spontaneous thymoma rat (Buffalo/Mna strain). The present study focused on the motor dysfunction as complicated by impaired subcellular machineries and noted particularly in patients with thymus abnormalities. Rats began to develop skeletal muscle weakness soon after birth and worsened progressively. Rats aged 3 months showed a benign thymoma characterized by proliferative lymphocytes; epithelial cells were stained with anti-RyR peptide antibody. The rat serum contained anti-RyR antibodies, but no anti-acetylcholine receptor antibodies. The electrophysiological study in muscle showed a reduction of contractile force without abnormality in synaptic transmission and membrane properties, suggesting a defect in excitation-contraction coupling. Hypothetically, thymic epithelial cells and skeletal muscles share a common RyR antigen, so that anti-RyR antibodies that target the thymic tissue may react with a homologous target in the muscle.

Animals↗

PubMed2004

Colchicine myotoxicity: case reports and literature review.

Two of our patients experienced myotoxicity associated with colchicine administration. The first was a 54-year-old woman who was receiving dialysis and came to the emergency department with progressive generalized weakness and vomiting. She recently had taken colchicine for the treatment of gout. Physical examination revealed proximal muscle weakness and tenderness on palpation. Her creatine kinase (CK), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were elevated at 7185, 563, and 541 U/L, respectively. Drug-induced myopathy was suspected and colchicine was discontinued. The patient was discharged after symptom resolution 1 week later. The second patient was an 83-year-old woman with chronic renal insufficiency who came to the hospital with anorexia, diarrhea, and inability to get out of bed due to progressive weakness. Her colchicine dosage recently had been increased for gout management. Physical examination revealed generalized muscle weakness and tenderness on palpation. Her CK, ALT, and AST levels were elevated at 1797, 147, and 172 U/L, respectively. Electromyographic results were consistent with colchicine myopathy. The patient was discharged with minimal residual muscle weakness 1 week after discontinuation of colchicine. A literature search identified 82 documented cases of colchicine-induced myotoxicity. Most patients had a history of proximal weakness and pain with elevated CK, ALT, and AST levels. Onset of symptoms generally occurred days to weeks after initial administration of colchicine at the usual dosage in patients with renal impairment or a change in underlying disease state in those receiving long-term therapy. Muscle toxicity was not necessarily accompanied by gastrointestinal symptoms. Concomitantly administered drugs often were cyclosporine or corticosteroids. Diagnosis may be confirmed by electromyography or muscle biopsy. Colchicine-induced myotoxicity is a rare adverse effect but is well described in the literature. Clinicians should recognize that renal impairment is the primary risk factor for development of colchicine-induced myotoxicity, and that dosage adjustment or alternative therapy may be required.

Aged↗