Elevated Serum Creatine Kinase Research Articles

Exertional Rhabdomyolysis: A Case Report of an Exceptionally Elevated Serum Creatine Kinase (CK) Level

Exertional Rhabdomyolysis: A Case Report of an Exceptionally Elevated Serum Creatine Kinase (CK) Level

A recurrent rare intronic variant in CAPN3 alters mRNA splicing and causes autosomal recessive limb-girdle muscular dystrophy-1 in three Pakistani pedigrees.

Autosomal recessive limb-girdle muscular dystrophy-1 (LGMDR1) is an autosomal recessive disorder characterized by progressive weakness of the proximal limb and girdle muscles. Biallelic mutations in CAPN3 are reported frequently to cause LGMDR1. Here, we describe 11 individuals from three unrelated consanguineous families that present with typical features of LGMDR1 that include proximal muscle wasting, weakness of the upper and lower limbs, and elevated serum creatine kinase. Whole-exome sequencing identified a rare homozygous CAPN3 variant near the exon 2 splice donor site that segregates with disease in all three families. mRNA splicing studies showed partial retention of intronic sequence and subsequent introduction of a premature stop codon (NM_000070.3: c.379 + 3A>G; p.Asp128Glyfs*15). Furthermore, we observe reduced CAPN3 expression in primary dermal fibroblasts derived from an affected individual, suggesting instability and/or nonsense-mediated decay of mutation-bearing mRNA. Genome-wide homozygosity mapping and single-nucleotide polymorphism analysis identified a shared haplotype and supports a possible founder effect for the CAPN3 variant. Together, our data extend the mutational spectrum of LGMDR1 and have implications for improved diagnostics for individuals of Pakistani origin.

Elevated serum creatine kinase levels due to osimertinib: A case report and review of the literature

Osimertinib is a tyrosine kinase inhibitor that targets the epidermal growth factor receptor. Elevated serum creatine kinase level is an uncommon adverse event associated with osimertinib treatment for lung cancer. We report a previously healthy 56-year-old woman who developed elevated serum creatine kinase levels during osimertinib monotherapy for epidermal growth factor receptor mutation-positive lung adenocarcinoma. During treatment, she experienced leg cramps and her serum creatine kinase levels increased, peaking at 989 U/l. Further investigation revealed no evidence of cardiotoxicity or myositis; thus, osimertinib-induced myopathy was assumed to be the cause of her elevated serum creatine kinase levels. We successfully managed both lung cancer and osimertinib-induced myopathy using 1-week pauses of osimertinib therapy without dose reduction. Short-term suspension of osimertinib without dose reduction may be a reasonable option for osimertinib-induced myopathy.

Rhabdomyolysis After Implementing Whole-Body Electromyostimulation: A Case Study

Whole-body electromyostimulation is a new approach used to achieve weight loss and build muscles by activating different muscles groups through voluntary contractions generated by electrical impulses. This alternative approach is operated by a certified personal trainer, regulating the intensity of the electrical impulses to aid the muscular system to contract. Unaccustomed use of this technique leads to muscle destruction and a rise in creatine kinase level. A 25-year-old female began this therapy and experienced right flank tenderness associated with elevated serum creatine kinase (CK) levels. An impression of Rhabdomyolysis in the Emergency Department was given, followed by intravenous (IV) fluid administration. The patient consequently improved and was discharged with instructions. The study was projected to spread awareness regarding Whole-body electromyostimulation, which is tremendously promoted in Bahrain. This therapy may aid in client monitoring and improve the prognosis. Keywords: Adult; Electric stimulation therapy; Muscle; Musculoskeletal physiological phenomena; Rhabdomyolysis; Weight loss

MLIP causes recessive myopathy with rhabdomyolysis, myalgia and baseline elevated serum creatine kinase.

Striated muscle needs to maintain cellular homeostasis in adaptation to increases in physiological and metabolic demands. Failure to do so can result in rhabdomyolysis. The identification of novel genetic conditions associated with rhabdomyolysis helps to shed light on hitherto unrecognized homeostatic mechanisms. Here we report seven individuals in six families from different ethnic backgrounds with biallelic variants in MLIP, which encodes the muscular lamin A/C-interacting protein, MLIP. Patients presented with a consistent phenotype characterized by mild muscle weakness, exercise-induced muscle pain, variable susceptibility to episodes of rhabdomyolysis, and persistent basal elevated serum creatine kinase levels. The biallelic truncating variants were predicted to result in disruption of the nuclear localizing signal of MLIP. Additionally, reduced overall RNA expression levels of the predominant MLIP isoform were observed in patients' skeletal muscle. Collectively, our data increase the understanding of the genetic landscape of rhabdomyolysis to now include MLIP as a novel disease gene in humans and solidifies MLIP's role in normal and diseased skeletal muscle homeostasis.

The possible protective effect of Panax ginseng on experimentally induced colchicine myopathy in adult male albino rats: A histological study

Myopathy is one of the side effects of colchicine, manifested as pain, dysfunction, and weakness of muscles. Ginseng extract antioxidant and anti-inflammatory activities have been reported in muscular tissue. This study was conducted to investigate whether administration of ginseng ameliorates colchicine-induced skeletal muscles damage in adult male albino rats. Forty adult male albino rats were randomly divided into four groups (ten/group) – Group I (control group): rats received normal diet and orally given normal saline, Group II: ginseng extract was administered via oral gavage daily for one month at the doses of 300 mg/kg, Group III (Colchicine treated group): rats were given colchicine (50 μg/kg/day) via oral gavage for one month, and Group IV: concomitant administration of Ginseng and colchicine for one month. Serum creatine kinase (CK) levels were measured, and skeletal muscles specimens were processed for light and electron microscopic examination. Administration of colchicine (group III) showed elevated serum CK, and histologically myofibrillar disarray foci together with cellular infiltration and edema. Group IV showed reduction in most of those manifestations. Concomitant administration of ginseng with colchicine ameliorated most of the symptoms related to colchicine induced-myopathy.

Causes and outcome of rhabdomyolysis in patients admitted to medical wards in the Prince of Wales Hospital.

BackgroundRhabdomyolysis with a marked elevation of serum creatine kinase (CK) can be caused by various conditions. Acute kidney injury (AKI) is a potential complication of severe rhabdomyolysis and leads to a rapid increase in serum creatinine.MethodsThis study was performed to identify medical cases diagnosed with rhabdomyolysis and to examine the likely causes. Patients diagnosed with rhabdomyolysis during admission to the medical wards of Prince of Wales Hospital (PWH) in Hong Kong from January 1, 2004 to May 31, 2012 were identified by searching computer records. Details of hospital admissions were retrieved, and the underlying causes of the rhabdomyolysis and clinical outcomes were analyzed.ResultsThere were 95 Chinese patients with a median age of 72 years (range, 22–92 years) assigned a diagnosis of rhabdomyolysis. A mild degree of AKI was defined as an increase of serum creatinine more than 20% above the baseline value before onset of acute illness and with the highest creatinine greater than 120 µmol/L. Mild AKI was identified in 63 patients. Rhabdomyolysis appeared to contribute to a fatal outcome in eight patients who had multiple preexisting morbidities. The maximum CK had a median value of 9,829 U/L (range, 472–258,100 U/L). Twelve patients with peak CK levels <10× the upper limit of normal (ULN) may not have had rhabdomyolysis by this standard definition. Of the remaining 83 patients with maximum CK values >10× the ULN, the most common contributing factors were trauma (n=19) and infection (n=17). Other common underlying causes included drug abuse (heroin and alcohol) and ischemia/immobility.ConclusionsMost patients recovered with appropriate medical interventions and had a median hospital stay of 13 days. One patient was thought to have drug-related rhabdomyolysis due to taking bezafibrate during an episode of renal impairment.

Prevalence and clinical outcomes of dystrophin-associated dilated cardiomyopathy without severe skeletal myopathy.

Dilated cardiomyopathy (DCM) associated with dystrophin gene (DMD) mutations in individuals with mild or absent skeletal myopathy is often indistinguishable from other DCM forms. We sought to describe the phenotype and prognosis of DMD associated DCM in DMD mutation carriers without severe skeletal myopathy. At 26 European centres, we retrospectively collected clinical characteristics and outcomes of 223 DMD mutation carriers (83% male, 33 ± 15 years). A total of 112 individuals (52%) had DCM at first evaluation [n= 85; left ventricular ejection fraction (LVEF) 34 ± 11.2%] or developed DCM (n= 27; LVEF 41.3± 7.5%) after a median follow-up of 96 months (interquartile range 5-311 months). DCM penetrance was 45% in carriers older than 40 years. DCM appeared earlier in males and was independent of the type of mutation, presence of skeletal myopathy, or elevated serum creatine kinase levels. Major adverse cardiac events (MACE) occurred in 22% individuals with DCM, 18% developed end-stage heart failure and 9% sudden cardiac death or equivalent. Skeletal myopathy was not associated with survival free of MACE in patients with DCM. Decreased LVEF and increased left ventricular end-diastolic diameter at baseline were associated with MACE. Individuals without DCM had favourable prognosis without MACE or death during follow-up. DMD-associated DCM without severe skeletal myopathy is characterized by incomplete penetrance but high risk of MACE, including progression to end-stage heart failure and ventricular arrhythmias. DCM onset is the major determinant of prognosis with similar survival regardless of the presence of skeletal myopathy.

Carrier screening model for Duchenne muscular dystrophy for women of reproductive age based on a pre-pregnancy birth defect control platform

To establish a screening model for females of reproductive age carrying Duchenne muscular dystrophy (DMD) variants based on a current community health examination platform. A total of 61 870 participants were recruited between October 2017 and October 2019. Serum creatine kinase (CK) was measured with a Roche Cobasc 701/702 using an enzymatic rate method. Genetic testing was offered to those with a CK level of ≥ 200 U/L. For carriers of DMD variants, genetic counseling and follow up were provided. For the 61 870 females participating in the program, 1078 were found with raised serum CK (≥ 200 U/L), of which 618 (57.33%) accepted CK re-measurement after at least a two-week interval. One hundred and twenty cases were found with sustained serum CK elevation, of which 6 were confirmed to be definite DMD carriers regardless of family history. Genetic testing was provided to 33 females with a family history for DMD, and 13 were determined as definite carriers. An affected fetus was detected by prenatal diagnosis. After genetic counseling, the parents had opted induced abortion. Large-scale DMD carrier screening through a three-step approach based on the current community health examination platform is both feasible and cost effective.

Identification of a novel MICU1 nonsense variant causes myopathy with extrapyramidal signs in an Iranian consanguineous family

BackgroundCa2+ as a universal second messenger regulates basic biological functions including cell cycle, cell proliferation, cell differentiation, and cell death. Lack of the protein mitochondrial calcium uptake1 (MICU1), which has been regarded as a gatekeeper of Ca ions, leads to the abnormal mitochondrial Ca2+ handling, excessive production of reactive oxygen species (ROS), and increased cell death. Mutations in MICU1 gene causes a very rare neuromuscular disease, myopathy with extrapyramidal signs (MPXPS), due to primary alterations in mitochondrial calcium signaling which demonstrates the key role of mitochondrial Ca2+ uptake. To date, 13 variants have been reported in MICU1 gene in 44 patients presented with the vast spectrum of symptoms.Case presentationHere, we report a 44-year-old Iranian patient presented with learning disability, muscle weakness, easy fatigability, reduced tendon reflexes, ataxia, gait disturbance, elevated hepatic transaminases, elevated serum creatine kinase (CK), and elevated lactate dehydrogenase (LDH). We identified a novel nonsense variant c.385C>T; p.(R129*) in MICU1 gene by whole exome sequencing (WES) and segregation analysis.ConclusionsOur finding along with previous studies provides more evidence on the clinical presentation of the disease caused by pathogenic mutations in MICU1. Finding more variants and expanding the spectrum of the disease increases the diagnostic rate of molecular testing in screening of this kind of diseases and in turn improves the quality of counseling for at risk couples and helps them to minimize the risks of having affected children.

Decoding Neuromuscular Disorders Using Phenotypic Clusters Obtained From Co-Occurrence Networks.

Neuromuscular disorders (NMDs) represent an important subset of rare diseases associated with elevated morbidity and mortality whose diagnosis can take years. Here we present a novel approach using systems biology to produce functionally-coherent phenotype clusters that provide insight into the cellular functions and phenotypic patterns underlying NMDs, using the Human Phenotype Ontology as a common framework. Gene and phenotype information was obtained for 424 NMDs in OMIM and 126 NMDs in Orphanet, and 335 and 216 phenotypes were identified as typical for NMDs, respectively. ‘Elevated serum creatine kinase’ was the most specific to NMDs, in agreement with the clinical test of elevated serum creatinine kinase that is conducted on NMD patients. The approach to obtain co-occurring NMD phenotypes was validated based on co-mention in PubMed abstracts. A total of 231 (OMIM) and 150 (Orphanet) clusters of highly connected co-occurrent NMD phenotypes were obtained. In parallel, a tripartite network based on phenotypes, diseases and genes was used to associate NMD phenotypes with functions, an approach also validated by literature co-mention, with KEGG pathways showing proportionally higher overlap than Gene Ontology and Reactome. Phenotype-function pairs were crossed with the co-occurrent NMD phenotype clusters to obtain 40 (OMIM) and 72 (Orphanet) functionally coherent phenotype clusters. As expected, many of these overlapped with known diseases and confirmed existing knowledge. Other clusters revealed interesting new findings, indicating informative phenotypes for differential diagnosis, providing deeper knowledge of NMDs, and pointing towards specific cell dysfunction caused by pleiotropic genes. This work is an example of reproducible research that i) can help better understand NMDs and support their diagnosis by providing a new tool that exploits existing information to obtain novel clusters of functionally-related phenotypes, and ii) takes us another step towards personalised medicine for NMDs.

Clinical features and follow-up of pediatric patients hospitalized for COVID-19.

ObjectiveThis report summarizes the clinical features and 1‐month follow‐up observations for pediatric patients who were hospitalized with coronavirus disease 2019 (COVID‐19) in Wuhan Women and Children's Hospital.MethodsThe 1‐month follow‐up data included clinical manifestations and results from serum severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) IgG and IgM tests, reverse‐transcription polymerase chain reaction (RT‐PCR) for SARS‐CoV‐2, lung computed tomography (CT) scans, and laboratory tests.ResultsBetween January 20 and March 15, 2020, 127 patients aged 0–15 years were hospitalized for COVID‐19 treatment, including 3 severe cases and 124 mild or moderate cases. The main therapies included inhalation of aerosolized interferon‐α (122/127) and additional antiviral drugs (28/127). Among the 81 patients who had pneumonia at admission, 35 with right lobe pneumonia had the longest hospital stay (mean 14.5 ± 7 days); 17 with left lobe pneumonia had the highest creatine kinase (154 ± 106 U/L) and creatine kinase myocardial band (CK‐MB, 43 ± 48 U/L) levels; and 29 with bilateral pneumonia had the highest white blood cell counts (8.3 ± 4 × 109/L). Among the 46 patients who were successfully followed up 1 month after discharge, two notable findings were right lobe pneumonia in 22% (95% confidence interval [CI]: 11%–37%) of patients and persistently elevated serum creatine kinase and CK‐MB levels. The median duration of elevated CK‐MB was 45 days. The mean concentrations of serum SARS‐CoV‐2 IgG and IgM in 41 patients were 8.0 ± 7.5 and 98 ± 40 ng/ml, respectively. At follow‐up, four patients retested positive for SARS‐CoV‐2.ConclusionsThe involvement of different lung lobes in patients with COVID‐19 was associated with variations in the persistence of pneumonia and elevation of CK‐MB levels and body temperature.

Sarcoglycan A mutation in miniature dachshund dogs causes limb-girdle muscular dystrophy 2D

BackgroundA cohort of related miniature dachshund dogs with exercise intolerance, stiff gait, dysphagia, myoglobinuria, and markedly elevated serum creatine kinase activities were identified.MethodsMuscle biopsy histopathology, immunofluorescence microscopy, and western blotting were combined to identify the specific pathologic phenotype of the myopathy, and whole genome SNP array genotype data and whole genome sequencing were combined to determine its genetic basis.ResultsMuscle biopsies were dystrophic. Sarcoglycanopathy, a form of limb-girdle muscular dystrophy, was suspected based on immunostaining and western blotting, where α, β, and γ-sarcoglycan were all absent or reduced. Genetic mapping and whole genome sequencing identified a premature stop codon mutation in the sarcoglycan A subunit gene (SGCA). Affected dachshunds were confirmed on several continents.ConclusionsThis first SGCA mutation found in dogs adds to the literature of genetic bases of canine muscular dystrophies and their usefulness as comparative models of human disease.

Protective effects of ischemic postconditioning on skeletal muscle following crush syndrome in the rat.

ABSTRACTPurposeTo investigate the effect of ischemic postconditioning (IPostC) on skeletal muscle and its optimal protocol.MethodsThis article is about an animal study of rat model of crush syndrome. Sixty rats were randomized into nine different IPostC intervention groups and a control group. The anesthetized rats were subjected to unilateral hindlimb 3-kg compression with a compression device for 6 h, followed by nine different IPostC intervention protocols.ResultsSerum levels of creatine kinase (CK) at 3 h post-crush became 2.3-3.9 times among all 10 groups after crush. At 72 h post-crush, serum CK level was reduced to 0.28-0.53 time in all intervention groups. The creatinine (CREA) level in the control group was elevated to 3.11 times at 3 h post-crush and reduced to1.77 time at 72 h post-crush. The potassium (K+) level in the control group was elevated to 1.65 and 1.41 time at 3 and 72 h post-crush, respectively.ConclusionsOur IPostC intervention protocols can effectively protect rats from crush-induced elevation of serum CK, CREA, and K+ levels. The timing of IPostC intervention should be as early as possible, to ensure the protective effect.

Elevated serum creatine kinase levels in acne vulgaris patients treated with isotretinoin: A retrospective single-center study

Background: Oral isotretinoin is a highly effective and widely used therapeutic agent for acne; however, it requires close follow-up due to its potential to produce various side effects. Slightly increased levels of serum creatine kinase (CK) that are either associated or not associated with musculoskeletal symptoms have been commonly reported and are typically considered innocuous. Objectives: The aims of the study are to investigate the frequency of our acne vulgaris patients with elevated serum CK levels during isotretinoin treatment, to analyze their course, and to determine the potential risk factors. Materials and Methods: Data of the patients in an outpatient clinic who were treated with isotretinoin due to acne vulgaris were retrospectively analyzed. Results: A total of 154 patients with at least 3 months of follow-up were included in the study. Elevated serum CK levels were found in 31 patients, and two patients had elevated levels over 1000 IU/l. While male sex was found to be a significant risk factor of CK elevation (P

Clinical features, muscle biopsy scores, myositis specific antibody profiles and outcome in juvenile dermatomyositis

IntroductionJuvenile dermatomyositis (JDM) is the most common inflammatory myopathy of childhood. ObjectiveTo analyze clinical features, paraclinical examinations, MSAs, treatment response and long-term outcome in a JDM cohort Methods58 patients (35F, 23 M) from a tertiary referral center in the last two decades are included. ResultsMean age at onset was 8.1 ± 4.3, with a mean follow-up period of 5.66±3.59 years. Dermatological manifestations (91%) and muscle weakness (76%) were the key diagnostic elements. Elevated serum creatine kinase levels (86%), electromyography (23/25), muscle MRI (12/15), and muscle biopsy (n = 35) were compatible with the diagnosis. Out of 46 patients tested, 34 (76%) had autoantibodies, with NXP2 (21.7%), followed by TIF1g (17.4%), MDA5 (8.7%), and Mi-2 (8.7%). Presence of TIF1g and NXP2 indicated a severe course; and Ku a much severe course compared to previous studies. Corticosteroids (100%) combined with methotrexate (93%) was the initial treatment. Biological disease modifying anti-rheumatic drugs (DMARDs) were used in 22% of the cohort. Calcinosis (36%) was the most common long-term complication, associated with disease onset ≤6 years, higher muscle biopsy scores and MDA5 positivity.Complete remission was achieved in 65.5% of the patients in a median 24 (IQR 11.8–42.5) months with a relapse rate of 26.3%. 43.9% of NXP2 and 33.3% of TIF-1 g positive patients had a relapse. Course was monophasic (31%), polyphasic (17.2%), chronic (51.8%) without mortality. ConclusionIntegration of clinical features with laboratory and biopsy findings may help to predict prognosis and guide treatment in JDM. In our cohort calcinosis was associated with age, MDA5 autoantibodies, and muscle biopsy scores.

Three Individuals with PURA Syndrome in a Cohort of Patients with Neuromuscular Disease.

Pur-α protein (PURA) syndrome manifests in early childhood with core features such as neurodevelopmental and speech delay, feeding difficulties, epilepsy, and hypotonia at birth. We identified three cases with PURA syndrome in a cohort of patients with unexplained muscular weakness, presenting with a predominantly neuromuscular and ataxic phenotype. We further characterize the clinical presentation of PURA syndrome including myopathic facies and muscular weakness as the main clinical symptoms in combination with elevated serum creatine kinase levels. Furthermore, we report two novel variants located in the conservative domains PUR-I and PUR-II. For the first time, we present the muscle biopsies of PURA syndrome patients, showing myopathic changes, fiber size variability, and fast fiber atrophy as the key features. PURA syndrome should be taken into consideration as a differential diagnosis in pediatric patients with unexplained muscle weakness.

15397 Paraneoplastic dermatomyositis in a patient with an oligodendroglioma

A previously healthy 26-year-old white man presented with nausea, headache, and rash. Physical examination disclosed coalescing, erythematous to violaceous macules and patches on the eyelids, periorbital regions, cheeks, upper chest, shoulders, upper back, and posterior neck, and mild periorbital edema. Review of systems was positive for myalgias. Histopathologic examination of a shoulder lesion demonstrated vacuolar interface dermatitis and a sparse, superficial perivascular dermal lymphocytic infiltrate. Colloidal iron staining demonstrated dermal mucinosis. Based on these findings, the diagnosis of dermatomyositis was made. Labs demonstrated elevated serum creatine kinase (673 U/L); tests for rheumatoid factor, anti-nuclear antibodies, anti-SSA and anti-SSB antibodies, immunoglobulin subclasses, and a myomarker panel were within normal limits. A head MRI demonstrated a cystic mass in the right insula; stereotactic biopsy was consistent with an oligodendroglioma. He received a 60 mg oral dose of prednisone, and topical triamcinolone 0.1% and hydrocortisone 2.5% ointment. Within 10 days the rash completely resolved. He underwent a craniotomy for tumor resection several weeks after initial presentation. At follow-up four months later, he showed no recurrence of myalgias or rash. Ovarian, lung, and gastrointestinal cancers are most commonly associated with dermatomyositis in the Western world. To our knowledge, only 2 previous cases of dermatomyositis associated with an intracranial neoplasm have been reported: in a 39-year-old man following dendritic cell immunotherapy for an oligoastrocytoma and in a seven-year-old girl with a choroid plexus papilloma. Our case adds oligodendroglioma to the list of potential neoplasms to be considered when assessing a patient with dermatomyositis.

The lncRNA H19 alleviates muscular dystrophy by stabilizing dystrophin.

Dystrophin proteomic regulation in Muscular Dystrophies (MD) remains unclear. We report that a long noncoding RNA (lncRNA), H19, associates with dystrophin and inhibits E3 ligase-dependent poly-ubiquitination at Lys3584 (referred to as Ub-DMD) and its subsequent protein degradation. In-frame deletions in BMD and a DMD non-silent mutation (C3340Y) result in defects in the protein’s ability to interact with H19, causing elevated Ub-DMD levels and dystrophin degradation. Dmd C3333Y mice exhibited progressive muscular dystrophy, elevated serum CK, heart dilation, blood vessel irregularity, and respiratory failure with concurrently reduced dystrophin and increased Ub-DMD status. H19 RNA oligonucleotides conjugated with Agrin (AGR-H19) and Nifenazone competed-with/inhibited TRIM63. Dmd C3333Y animals, iPSC-derived skeletal muscle cells from BMD patients, or mdx mice subjected to exon-skipping exhibited inhibited dystrophin degradation, preserved skeletal/cardiac muscle histology, and improved strength/heart function following AGR-H19 or Nifenazone treatment. Our study paves the way to meaningful targeted therapeutics for BMD and certain DMD patients.

Cross-sectional investigation of serum creatine kinase concentration in Graves disease patients treated with oral antithyroid drugs.

Elevated serum creatine kinase (CK) concentration was reported in some Graves disease patients during the treatment with oral antithyroid drugs (ATD). The pathogenesis of this abnormal biochemical value was considered to be related to the therapeutic drug. However, the relevant epidemiological investigation was absent.Overall, 416 patients with Graves disease treated with oral ATDs were recruited from December 2017 to October 2019. Clinical characteristics such as the patient's medical history and therapeutic regimen were collected. Serum CK concentration and thyroid function were measured. Statistical analysis was adopted to clarify the relationship between serum CK level and these clinical parameters.Elevation of serum CK concentration was emerged in 13.5% patients who were treated with oral ATDs. The proportion was significantly higher among men than among women (19.5% vs 10.8%). There was no correlation between increased serum CK concentration and age. More than 60% of serum CK elevations occurred within 6 months after taking oral ATDs. Free triiodothyronine and free thyroxine are negatively correlated with serum CK concentration. The correlation coefficients are respectively –0.222 (P < .05) and –0.234 (P < .05). There is positive correlation between thyroid stimulating hormone and serum CK concentration. The correlation coefficient is 0.405 (P < .05). There was no statistical correlation between drug dosage and increased serum CK level.Increased serum CK level is a common adverse reaction of oral ATDs. It generally develops early after starting treatment. The cause of this adverse reaction is not clear. It is speculated that elevation of serum CK level is related to the fluctuation of thyroid function.