Serum Creatine Kinase Levels Research Articles

Reversible cardiac function and left ventricular hypertrophy in a Chinese man with mitochondrial myopathy: a case report

BackgroundMitochondrial myopathies (MMs) are a group of multi-system diseases caused by abnormalities in mitochondrial DNA (mtDNA) or mutations of nuclear DNA (nDNA). The diagnosis of mitochondrial myopathy (MM) is reliant on the combination of history and physical examination, muscle biopsy, histochemical studies, and next-generation sequencing. Patients with MMs have diverse clinical manifestations. In the contemporary literature, there is a paucity of reports on cardiac structure and function in this rare disease. We report a Chinese man with MM accompanied with both acute right heart failure and left ventricular hypertrophy.Case presentationA 49-year-old man presented with clinical features suggestive of MM, i.e., ophthalmoparesis, weakness of the pharyngeal and extremity muscles, and respiratory muscles which gradually progressed to respiratory insufficiency. He had a family history of mitochondrial myopathy. He had increased levels of serum creatine kinase and lactate. Muscle biopsy of left lateral thigh revealed 8% ragged red fibers (RRF) and 42% COX-negative fibers. Gene sequencing revealed a novel heterozygote TK2 variant (NM_001172644: c.584T>C, p.Leu195Pro) and another heterozygous variant (NM_004614.4:c.156+958G>A; rs1965661603) in the intron of TK2 gene. Based on these findings, we diagnosed the patient as a case of MM. Echocardiography revealed right heart enlargement, pulmonary hypertension, left ventricular hypertrophy, and thickening of the main pulmonary artery and its branches. The patient received non-invasive ventilation and coenzyme Q10 (CoQ10). The cardiac structure and function were restored at 1-month follow-up.ConclusionsThis is the first report of reversible cardiac function impairment and left ventricular hypertrophy in a case of adult-onset MM, nocturnal hypoxia is a potential mechanism for left ventricular hypertrophy in patients with MM.

Twenty-Four Percent of Wildland Firefighters Reach Critical Levels of Serum Creatine Kinase During 80-Hour Critical Training.

Wildland firefighters (WLFFs) must undergo a 2-wk critical training (CT) period prior to deployment to the field. This stress may result in clinical risks, including severe muscle damage and rhabdomyolysis. We aimed to document the effects of WLFFs' CT on physiologic markers of muscle damage and soreness. Two interagency hotshot crews (n=25) were followed during spring 2022 for 80 h of training. Activity counts as well as records of upper-body (US) and lower-body (LS) muscle soreness were collected daily. Body weight (BW) and skinfold measurements were recorded on Day 1 (D1) and D11 to estimate body fat (BF) and lean body weight (LBW). Blood was collected on D1 and D11 to measure muscle and liver damage markers. Critical training resulted in significant elevations in creatine kinase (CK) (216.9±57.4 U/L vs 5166.4±1927.8 U/L, P=0.017) and lactate dehydrogenase (LDH) (175.5±4.0 IU/L vs 340.0±42.6 IU/L, P=0.001) despite no significant changes in BW, BF, LBW, cortisol, or testosterone. Main effects of time were seen in US and LS, peaking on D11 (US: 5.2±0.4 cm, P<0.001; LS: 5.5±0.4 cm, P<0.001). Those who spent the most minutes with activity counts of >1500 counts/min showed the greatest increase in CK and LDH. These data suggest that WLFFs undergo significant physiologic stressors, resulting in muscle soreness and damage during CT, with 6 of the 25 subjects reaching critical levels of serum CK. It appears that much of the muscle damage and soreness occurred because of unaccustomed WLFF job-specific tasks.

Comparison of clinical outcomes between posterolateral approach and modified Hardinge approach in salvage total hip arthroplasty after medial buttress plate failure for femoral neck fractures.

The purpose of this study was to investigate the clinical outcomes of salvage total hip arthroplasty (THA) after medial buttress plate surgery for femoral neck fractures via the modified Hardinge approach (MHA) and posterolateral approach (PLA) through a retrospective analysis. From October 2016 to October 2020, a total of 41 patients with failed femoral neck fractures treated with cannulated screws and medial buttress plates underwent unilateral salvage THA, and a retrospective study was conducted. According to the surgical approach, patients were divided into PLA group and MHA group. Clinical and radiological data were evaluated. The primary outcome indicators were the Pain Visual Analog Scale (VAS) and Hip Harris Score (HHS). Secondary outcome indicators include hemoglobin (HGB), hematocrit (HCT), creatine kinase (CK), creatine kinase-MB (CK-MB), etc. The occurrence of postoperative complications was also recorded. There were no differences in demographic or clinical characteristics before surgery. There were no differences in postoperative HGB, HCT, CK-MB and radiological parameters. The surgical approach had no effect on the hospitalization period. The PLA group had earlier ambulation time, and the serum level of CK was also low. Analysis of the HHS and VAS showed that on postoperative day 3, the PLA group had superior scores. The incidence of complications did not significantly differ between groups. The posterolateral approach for salvage THA provides better functional recovery with less muscle damage in the early postoperative period.

Canonical transient receptor potential channel 1 aggravates myocardial ischemia-and-reperfusion injury by upregulating reactive oxygen species

The canonical transient receptor potential channel (TRPC) proteins form Ca2+-permeable cation channels that are involved in various heart diseases. However, the roles of specific TRPC proteins in myocardial ischemia/reperfusion (I/R) injury remain poorly understood. We observed that TRPC1 and TRPC6 were highly expressed in the area at risk (AAR) in a coronary artery ligation induced I/R model. Trpc1−/− mice exhibited improved cardiac function, lower serum Troponin T and serum creatine kinase level, smaller infarct volume, less fibrotic scars, and fewer apoptotic cells after myocardial-I/R than wild-type or Trpc6−/− mice. Cardiomyocyte-specific knockdown of Trpc1 using adeno-associated virus 9 mitigated myocardial I/R injury. Furthermore, Trpc1 deficiency protected adult mouse ventricular myocytes (AMVMs) and HL-1 cells from death during hypoxia/reoxygenation (H/R) injury. RNA-sequencing-based transcriptome analysis revealed differential expression of genes related to reactive oxygen species (ROS) generation in Trpc1−/− cardiomyocytes. Among these genes, oxoglutarate dehydrogenase-like (Ogdhl) was markedly downregulated. Moreover, Trpc1 deficiency impaired the calcineurin (CaN)/nuclear factor-kappa B (NF-κB) signaling pathway in AMVMs. Suppression of this pathway inhibited Ogdhl upregulation and ROS generation in HL-1 cells under H/R conditions. Chromatin immunoprecipitation assays confirmed NF-κB binding to the Ogdhl promoter. The cardioprotective effect of Trpc1 deficiency was canceled out by overexpression of NF-κB and Ogdhl in cardiomyocytes. In conclusion, our findings reveal that TRPC1 is upregulated in the AAR following myocardial I/R, leading to increased Ca2+ influx into associated cardiomyocytes. Subsequently, this upregulates Ogdhl expression through the CaN/NF-κB signaling pathway, ultimately exacerbating ROS production and aggravating myocardial I/R injury.

Clinical features of anti-melanoma differentiation-associated gene 5 antibody-positive dermatomyositis with macrophage activation syndrome.

This study aimed to describe the clinical features of patients with anti-melanoma differentiation-associated gene 5 (anti-MDA5) antibody-positive dermatomyositis (DM) who had macrophage activation syndrome (MAS). We retrospectively examined 44 patients with anti-MDA5-positive DM and compared the clinical features between patients with MAS (n = 11) and those without (n=33). Patients without MAS were selected randomly in the same year as those with MAS at a ratio of 3:1. Among patients with MAS, we compared the features between non-survivors and survivors. We used Fisher's exact test, Student's t test, the Mann-Whitney U test and the log-rank test for statistical analysis. Patients complicated with MAS had a significantly higher incidence of infection, heliotrope sign, Gottron's papule, V-neck sign, and higher serum levels of ferritin, aspartate aminotransferase (AST), lactic dehydrogenase (LDH), and creatine kinase (CK) than those without MAS (p<0.05). Among the 11 patients with MAS, 4 (36.4%) died after intensive treatment. Deceased patients were older, given more combination therapy with tofacitinib (TOF) and had a higher incidence of rapid progressive interstitial lung disease, infection, heart failure and renal impairment than those who survived (p<0.05). Among anti-MDA5-positive DM, Infection, DM typical rashes, and higher serum levels of ferritin, AST, LDH, and CK were more common in patients complicated with MAS. The mortality of patients with MAS was high, particularly among patients who were older, given more combination therapy with TOF, and had RP-ILD, infection, heart failure and renal impairment.

Clinical, pathological, and genetic characterization in a large Chinese cohort with female dystrophinopathy

We aimed to investigate the clinical, pathological, and genetic characteristics of Chinese female dystrophinopathy and to identify possible correlations among them. One hundred forty genetically and/or pathologically confirmed female DMD variant carriers were enrolled, including 104 asymptomatic carriers and 36 symptomatic carriers. Twenty of 36 symptomatic and 16 of 104 asymptomatic carriers were sporadic with no family history. Muscle pathological analysis was performed in 53 carriers and X chromosome inactivation (XCI) analysis in 19 carriers. In asymptomatic carriers, the median age was 35.0 (range 2.0–58.0) years, and the serum creatine kinase (CK) level was 131 (range 60–15,745) IU/L. The median age, age of onset, and CK level of symptomatic carriers were 15.5 (range 1.8–62.0) years, 6.3 (range 1.0–54.0) years, and 6,659 (range 337–58,340) IU/L, respectively. Four female carriers with X-autosome translocation presented with a Duchenne muscular dystrophy (DMD) phenotype. Skewed XCI was present in 70.0% of symptomatic carriers. Compared to Becker muscular dystrophy (BMD)-like carriers, DMD-like carriers were more likely to have an early onset age, rapidly progressive muscle weakness, delayed walking, elevated CK levels, severe reduction of dystrophin, and skewed XCI. Our study reports the largest series of symptomatic female DMD carriers and suggests that delayed walking, elevated CK levels, severe reduction of dystrophin, X-autosome translocation, and skewed XCI pattern are associated with a severe phenotype in female dystrophinopathy.

Fumigaclavine C ameliorates liver steatosis by attenuating hepatic de novo lipogenesis via modulation of the RhoA/ROCK signaling pathway

BackgroundNon-alcoholic fatty liver disease (NAFLD) has been well defined as a common chronic liver metabolism disorder. Statins as a first-line therapeutic treatment had some side effects. Here, we found that Fumigaclavine C (FC) was collected from endophytic Aspergillus terreus via the root of Rhizophora stylosa (Rhizophoraceae), had potential anti-adipogenic and hepatoprotective effects both in vitro and in vivo without obvious adverse side effects. However, the mechanisms of the prevention and management of FC for hepatic steatosis are incompletely delineated.MethodsThe pharmacodynamic effects of FC were measured in high-fat diet (HFD)-induced obese mice. Liver index and blood biochemical were examined. Histopathological examination in the liver was performed by hematoxylin & eosin or oil red O. The levels of serum TG, TC, LDL-c, HDL-c, FFA, T-bili, ALT, AST, creatinine, and creatine kinase were estimated via diagnostic assay kits. The levels of hepatic lipid metabolism-related genes were detected via qRT-PCR. The expression levels of hepatic de novo lipogenesis were quantitated with Western blot analysis. ResultsFC-treatment markedly reduced hepatic lipid accumulation in HFD-induced obese mice. FC significantly attenuated the hepatic lipid metabolism and ameliorated liver injury without obvious adverse side effects. Moreover, FC also could dose-dependently modulate the expressions of lipid metabolism-related transcription genes. Mechanically, FC notably suppressed sterol response element binding protein-1c mediated de novo lipogenesis via interfering with the RhoA/ROCK signaling pathway by decreasing the levels of geranylgeranyl diphosphate and farnesyl diphosphate.ConclusionsThese findings suggested that FC could improve hepatic steatosis through inhibiting de novo lipogenesis via modulating the RhoA/ROCK signaling pathway.

Unilateral Biportal Endoscopic Posterior Cervical Foraminotomy: An Outcome Comparison With the Full-endoscopic Posterior Cervical Foraminotomy.

Retrospective control study. To compare the curative effects of unilateral biportal endoscopic posterior cervical foraminotomy (UBE-PCF) with full-endoscopic posterior cervical foraminotomy (FPCF). There are few studies directly comparing outcomes between UBE-PCF and FPCF. The objective of this study was to compare outcomes between UBE-PCF and FPCF. A retrospective control study was conducted for 69 patients of cervical radiculopathy from July 2019 to December 2021. Clinical outcomes scores, including neck disability index, visual analog scale (VAS)-arm, and VAS-neck were evaluated. Serum creatine kinase levels and the size of the operating hole were measured. Postoperative neck disability index, VAS-neck, and VAS-arm scores showed statistically significant improvement over preoperative scores ( P <0.01). The operating time was significantly shorter in the UBE-PCF group ( P <0.001). No significant differences were found in serum creatine kinase levels between the 2 groups ( P >0.05). The mean area of the operating hole was 1.47+0.05cm 2 in the FPCF group and 1.79+0.11cm 2 in the UBE-PCF group. The difference was statistically significant ( P <0.001). Both UBE-PCF and FPCF are safe and effective procedures for cervical radiculopathy. Predictable and sufficient decompression could be achieved by UBE-PCF in a shorter operation time. Treatment Benefits Level III.

Clinical features and recovery pattern of secondary hypokalaemic paralysis.

Information regarding frequency, details of neurological signs and recovery patterns of patients with secondary hypokalaemic paralysis (HP) is limited. This study aimed to analyse the frequency, aetiology, clinical features and recovery patterns of patients with secondary HP. The clinical and laboratory records of 18 consecutive patients with secondary HP aged ≥ 18years admitted to our hospital between April 2011 and March 2022 were reviewed. Patients with inherited hypokalaemic periodic paralysis were excluded. Of the 18 patients, 16 had a common aetiology: chronic alcoholism, diarrhoea or an imbalanced diet. Initial symptoms, such as fatigue, were often atypical. Three patients had prominent asymmetric limb weakness and four had predominant upper limb weakness. On admission, the mean serum potassium and creatine kinase (CK) levels of the patients were 1.90mmol/L and 4488U/mL, respectively. Ten patients (56%) had decreased potassium levels after admission, despite potassium replacement treatment (rebound hypokalaemia). Twelve patients presented with increased CK levels even after 2-5days (delayed hyperCKaemia). Low serum magnesium levels significantly correlated with rebound hypokalaemia. Secondary HP can be caused by a variety of conditions, but mainly occurs due to lifestyle conditions/disorders. Secondary HP often presents with atypical symptoms, and the initial symptoms can be non-specific. Rebound hypokalaemia and delayed hyperCKaemia are common in secondary HP, despite potassium replacement. As such, careful serial monitoring is needed for patients with secondary HP.

HyperCKemia: An early sign of childhood-onset neutral lipid storage disease with myopathy

Neutral lipid-storage disease with myopathy (NLSDM) is an autosomal recessive neuromuscular disorder caused by mutations in PNPLA2, and the average age at onset is 30 years. To date, only eight patients with childhood-onset NLSDM have been reported in detail. We investigated 3 unreported patients with NLSDM detected in childhood and reviewed 8 childhood-onset and 82 adult-onset patients with NLSDM documented in the literature. In the childhood-onset cohort, NLSDM presented initially as asymptomatic or paucisymptomatic hyperCKemia in 6/11 patients, and follow-up data showed onset of muscle weakness in 6/11 childhood-onset patients. In the adult-onset cohort, 95.1% (78/82) of patients showed muscle weakness. Cardiac involvement developed in 6/11 childhood-onset patients. Hepatomegaly was observed in 3/11 childhood-onset patients. Serum creatine kinase levels were elevated greater than five-fold of the upper limit of normal (ULN) in most childhood-onset patients and were elevated to less than ten-fold of the ULN in most adult-onset patients. Peripheral blood smears and muscle biopsies showed cytoplasmic lipid droplets in leukocytes and myocytes. NLSDM can present in children with asymptomatic or paucisymptomatic hyperCKemia before the onset of muscle weakness. The presence of lipid droplets in leucocytes (Jordans' anomaly) aids in diagnosing and confirming the pathogenicity of PNPLA2 variants of uncertain significance. There were no clear genotype-phenotype correlations in patients with NLSDM.

Sildenafil increases AAV9 transduction after a systemic administration and enhances AAV9-dystrophin therapeutic effect in mdx mice.

Adeno-associated virus (AAV) vectors have been successfully used to deliver genes for treating rare diseases. However, the systemic administration of high AAV vector doses triggers several adverse effects, including immune response, the asymptomatic elevation of liver transaminase levels, and complement activation. Thus, improving AAV transduction and reducing AAV dosage for treatment is necessary. Recently, we found that a phosphodiesterase-5 inhibitor significantly promoted AAV9 transduction in vitro by regulating the caveolae and macropinocytosis pathways. When AAV9-Gaussian luciferase (AAV9-Gluc) and AAV9-green fluorescent protein (AAV9-GFP) were injected intravenously into mice pre-treated with sildenafil, the expressions of Gluc in the plasma and GFP in muscle tissues significantly increased (P < 0.05). Sildenafil also improved Evans blue permeation in tissues. Additionally, we found that sildenafil promoted Treg proliferation, inhibited B-cell activation, and decreased anti-AAV9 IgG levels (P < 0.05). Furthermore, sildenafil significantly promoted Duchenne muscular dystrophy gene therapy efficacy using AAV9 in mdx mice; it increased micro-dystrophin gene expression, forelimb grip strength, and time spent on the rotarod test, decreased serum creatine kinase levels, and ameliorated histopathology by improving muscle cell morphology and reducing fibrosis (P < 0.05). These results show that sildenafil significantly improved AAV transduction, suppressed the levels of anti-AAV9 IgG, and enhanced the efficacy of gene therapy.

Extremely elevated creatine kinase associated with rhabdomyolysis-induced acute kidney injury in a patient with Huntington’s disease: a case report

BackgroundRhabdomyolysis-induced acute kidney injury is a serious condition that can progress to acute renal failure if not promptly identified and treated. Rhabdomyolysis occurs when serum creatine kinase levels approach > 1000 U/L (five times the normal upper limit). The chance of acute kidney injury increases as the levels of creatine kinase increase. Although Huntington’s disease is associated with muscle atrophy, elevated baseline creatine kinase levels in these patients have not been routinely reported.Case presentationA 31-year-old African American patient presented to the emergency department after he was found unconscious from a fall attributed to the progression of his Huntington’s disease. On admission, he had an extremely high creatine kinase level of 114,400 U/L and was treated with fluids, electrolyte balance, and dialysis. However, his condition progressed to acute renal failure and he later developed posterior reversible encephalopathy syndrome, requiring transfer to the intensive care unit with placement on continuous renal replacement therapy. Eventually, his kidney function recovered and he was discharged home with 24/7 care by his family for persistent impairments related to his Huntington’s disease.ConclusionsThis case report underscores the importance of promptly recognizing elevated creatine kinase levels in patients with Huntington’s disease due to the risk of developing rhabdomyolysis-induced acute kidney injury. If not aggressively treated, the condition of these patients is likely to progress to renal failure. Anticipating the progression of rhabdomyolysis-induced acute kidney injury is paramount to improving clinical outcomes. Additionally, this case identifies a potential link between the patient’s Huntington’s disease and his abnormally elevated creatine kinase, a finding not described in the literature of rhabdomyolysis-induced kidney injuries to date and an important consideration for future patients with similar comorbidities.

Low-intensity pulsed ultrasound alleviates doxorubicin-induced cardiotoxicity via inhibition of S100a8/a9-mediated cardiac recruitment of neutrophils.

Doxorubicin (DOX)-induced cardiotoxicity limits its broad use as a chemotherapy agent. The development of effective and non-invasive strategies to prevent DOX-associated adverse cardiac events is urgently needed. We aimed to examine whether and how low-intensity pulsed ultrasound (LIPUS) plays a protective role in DOX-induced cardiotoxicity. Male C57BL/6J mice were used to establish models of both acute and chronic DOX-induced cardiomyopathy. Non-invasive LIPUS therapy was conducted for four consecutive days after DOX administration. Cardiac contractile function was evaluated by echocardiography. Myocardial apoptosis, oxidative stress, and fibrosis were analyzed using terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining, dihydroethidium (DHE) staining, and picrosirius red staining assays. RNA-seq analysis was performed to unbiasedly explore the possible downstream regulatory mechanisms. Neutrophil recruitment and infiltration in the heart were analyzed by flow cytometry. The S100a8/a9 inhibitor ABR-238901 was utilized to identify the effect of S100a8/a9 signaling. We found that LIPUS therapy elicited a great benefit on DOX-induced heart contractile dysfunction in both acute and chronic DOX models. Chronic DOX administration increased serum creatine kinase and lactate dehydrogenase levels, as well as myocardial apoptosis, all of which were significantly mitigated by LIPUS. In addition, LIPUS treatment prevented chronic DOX-induced cardiac oxidative stress and fibrosis. RNA-seq analysis revealed that LIPUS treatment partially reversed alterations of gene expression induced by DOX. Gene ontology (GO) analysis of the downregulated genes between DOX-LIPUS and DOX-Sham groups indicated that inhibition of neutrophil chemotaxis might be involved in the protective effects of LIPUS therapy. Flow cytometry analysis illustrated the inhibitory effects of LIPUS on DOX-induced neutrophil recruitment and infiltration in the heart. Moreover, S100 calcium binding protein A8/A9 (S100a8/a9) was identified as a potential key target of LIPUS therapy. S100a8/a9 inhibition by ABR-238901 showed a similar heart protective effect against DOX-induced cardiomyopathy to LIPUS treatment. LIPUS therapy prevents DOX-induced cardiotoxicity through inhibition of S100a8/a9-mediated neutrophil recruitment to the heart, suggesting its potential application in cancer patients undergoing chemotherapy with DOX.

Efficacy and muscle safety assessment of fukutin-related protein gene therapy

Limb-girdle muscular dystrophy type R9 (LGMDR9) is a muscle-wasting disease that begins in the hip and shoulder regions of the body. This disease is caused by mutations in fukutin-related protein (FKRP), a glycosyltransferase critical for maintaining muscle cell integrity. Here we investigated potential gene therapies for LGMDR9 containing an FKRP expression construct with untranslated region (UTR) modifications. Initial studies treated an aged dystrophic mouse model (FKRPP448L) with adeno-associated virus vector serotype 6 (AAV6). Grip strength improved in a dose- and time-dependent manner, injected mice exhibited fewer central nuclei and serum creatine kinase levels were 3- and 5-fold lower compared to those in non-injected FKRPP448L mice. Treatment also partially stabilized the respiratory pattern during exercise and improved treadmill running, partially protecting muscle from exercise-induced damage. Western blotting of C2C12 myotubes using a novel rabbit antibody confirmed heightened translation with the UTR modifications. We further explored the question of FKRP toxicity in wild-type mice using high doses of two additional muscle-tropic capsids: AAV9 and AAVMYO1. No toxic effects were detected with either therapeutic agent. These data further support the feasibility of gene therapy to treat LGMDR9.

Nursing outcomes of traditional Chinese medicine adjunctive therapy on osteofascial compartment syndrome: a review†

Abstract The rate of disability due to acute osteofascial compartment syndrome (OCS) is high, and the therapeutic effect of decompressive fasciotomy is not ideal. This paper retrospectively reviews the modern treatment of OCS, including Western medicine and Traditional Chinese medicine (TCM), mainly in the context of the advantages of TCM in the treatment process of decompressive fasciotomy or conservative treatment to the patients who are suffering from OCS. It was found that TCM treatment reduced the levels of serum creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST); it is beneficial to the elimination of swelling and pain. TCM adjunctive therapy promotes patients’ postoperative functional recovery and decreases the occurrence of fasciotomy in patients; TCM can relieve tissue hypoxia of compartments and prevent necrosis of muscle and nerve tissue. TCM treatment improves the quality of medical service and ensures the safety of OCS patients. This paper aims to summarize the function of TCM in the treatment of OCS, provide reference for the clinical treatment of OCS, and improve the nursing/medical outcomes of OCS.

Associations of Serum CXCL12α and CK Levels with Skeletal Muscle Mass in Older Adults.

Sarcopenia, a condition characterized by gradual loss of skeletal muscle mass and function, is a complex diagnosis; the decisive criterion in this diagnosis is the measurement of appendicular skeletal muscle index (ASMI). To identify potential serum markers predictive of sarcopenia in older adults, we evaluated correlations between ASMI, clinical data, and 34 serum inflammation markers in 80 older adults. Pearson's correlation analyses confirmed that ASMI was positively correlated with nutritional status (p = 0.001) and serum creatine kinase (CK) (p = 0.019) but negatively correlated with serum CXCL12α (p = 0.023), a chemoattractant for muscle stem cells. In the case group, ASMI was negatively correlated with serum interleukin (IL)-7 (p = 0.024), a myokine expressed and secreted from skeletal muscle cells in vitro. Multivariate binary logistic regression analyses identified four risk factors for sarcopenia in our study: advanced age (p = 0.012), malnutrition (p = 0.038), low serum CK levels (p = 0.044), and high serum CXCL12α levels (p = 0.029). Low CK and high CXCL12α levels serve as combinatorial serum markers of sarcopenia in older adults. The linear correlation between ASMI and CXCL12α levels may facilitate the development of new regression models for future studies on sarcopenia.

Severe muscle damage after a short period of ischemia and reperfusion in an animal model

BackgroundSkeletal muscle ischemia-reperfusion injuries result in a loss of contractile function, leading to limb disability or amputation. Ischemia causes hypoxia and cellular energy failure, which is aggravated by reperfusion due to the inflammatory response and oxidative stress. The consequences of the injury vary according to the duration of the period of ischemia and reperfusion. Therefore, the present work aims to evaluate ischemia-reperfusion injuries induced in the skeletal muscles of Wistar rats submitted to 3 different application periods based on morphological and biochemical parameters. MethodsFor this, a tourniquet was applied to the root of the animals’ hind limbs, occluding arterial and venous blood flow, and it was followed by reperfusion—the removal of the tourniquet. The groups were: control (without tourniquet); I30'/R60' (30 minutes of ischemia and 1 hour of reperfusion); I120'/R120' (2 hours and 2 hours); and I180'/R180' (3 hours and 3 hours). ResultsAll ischemia-reperfusion groups showed characteristics of muscle injury. Microscopic analyses of the extensor digitorum longus, soleus, tibialis anterior, and gastrocnemius muscles showed a significant increase in the number of injured muscle fibers in the ischemia-reperfusion groups compared to the control group. There were also significant differences between the ischemia-reperfusion groups in all muscles, showing a progressive increase in the degree of injury. The quantification of the number of injured muscle fibers between the muscles revealed that at I30'/R60', the soleus muscles had a higher number of injuries in relation to the other muscles, with statistical significance. In the I120'/R120' group, the gastrocnemius muscles presented a significantly greater number of injured fibers. There were no significant differences in the I180'/R180' group. The serum levels of creatine kinase in the I180'/R180' group were significantly higher than in the control and I30'/R60' groups. ConclusionsTherefore, it was evident that the 3 ischemia-reperfusion models used were capable of causing cell damage, with these findings being more pronounced in the I180'/R180' group.

Comparative Evaluation of Serum Urea, Uric Acid, and Creatine Kinase Levels in Oral Cancer and Potentially Malignant Disorders of the Oral Cavity: A Clinico-Biochemical Study.

Introduction Evidence suggests that oral potentially malignant disorders (OPMDs) are linked to increased possibilities of malignant transformation, creating a challenging situation.If oral cancer is detected early, the prognosis is better.The purpose of this study was to compare the serum levels of urea, uric acid (UA), and creatine kinase in patients with provisionally diagnosed and histopathologically confirmed cases of potentially malignant disorders and oral cancer to those of age- and sex-matched healthy controls. Materials and methods Eighty patients over the age of 18 with a clinical diagnosis of oral potentially malignant disorder (OPMD) or oral cancer and verified histopathology were included in the research. Using the kinetic methodology, the enzymatic colorimetric method, and the UV-kinetic approach, respectively, the serum concentrations of urea, uric acid, and creatine kinase were quantified in vitro following the venipuncture of 2 mL of venous blood. The Statistical Package for the Social Sciences (SPSS) version 20 (IBM SPSS Statistics, Armonk, NY, USA) was used for the statistical analysis. Results Comparing OPMD and oral cancer patients to healthy controls, serum urea levels were found to be greater, uric acid levels to be lower, and creatine kinase levels to be higher. Conclusion Prognostic markers for OPMDs and oral cancer may include urea, uric acid, and creatine kinase. However, this may be accomplished by large-scale prospective research.

The Effect of Short-term Administration of High-dose Vitamins E and C on Serum Creatine Kinase and Myoglobin in the Resting Phase of Elite Sanda Athletes: A Randomized Trial

Background: Muscle damage during continuous and intensive sports activities is common; therefore, experts in the field of sports medicine pay special attention to this issue. Objectives: We investigated the short-term effect of high-dose vitamin C and E supplements on serum levels of creatine kinase (CK) and myoglobin in elite athletes of the Sanda field. Methods: This research was a parallel single-blind randomized study design in which elite Sanda athletes were matched based on weight and randomly assigned to the vitamin C + E supplement (n = 10) and placebo groups (n = 10). Subjects took vitamin C (1400 U per day) and vitamin E (2000 U per day) supplements for 4 days (3 days before the competition and on the competition day). Blood sampling was done on the morning of the competition and 24 hours later (the following day) to measure serum levels of CK and myoglobin. Results: The serum CK level had a significant decrease in the supplement group (P = 0.001; mean ± SD: 237.2 ± 19.28), and myoglobin significantly increased (P = 0.001; mean ± SD, 41.1 ± 1.97) compared with the placebo group. Also, a paired sample t test showed that serum CK and myoglobin levels significantly decreased (P = 0.001; pretest, 307.7 ± 5.56; posttest, 237.2 ± 19.28) and increased (P = 0.005; pretest, 24.2 ± 2.7; posttest, 41.1 ± 1.97) in the supplement group, respectively, compared to the pretest values. However, no significant difference was observed in the placebo group. Conclusions: Short-term intake of high-dose vitamins C and E can facilitate recovery during competitive events such as Sanda. This claim can be defended based on the changes in CK and myoglobin in the blood serum of athletes.

Becker Muscular Dystrophy Accompanied by Anti-HMGCR Antibody-positive Immune-mediated Necrotizing Myopathy.

Becker muscular dystrophy (BMD) is an X-linked neuromuscular disease characterized by progressive muscle weakness that currently has no cure. Immune-mediated necrotizing myopathy (IMNM) is a type of autoimmune inflammatory myopathy characterized by proximal muscle weakness that is treated with immunosuppressive therapy. We herein report a patient diagnosed with BMD complicated with IMNM by a pathological analysis. Notably, the patient had an elevated serum anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase antibody level. Oral glucocorticoid and methotrexate treatment partially improved the muscle weakness with decreased levels of serum creatine kinase. An accurate diagnosis is important for therapeutic decisions in these complicated cases.