• Title/Summary/Keyword: Creatine kinase (CK)

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The characteristic laboratory findings of non-responsiveness to intravenous immunoglobulin in children with Kawasaki disease (가와사끼병 재 치료군의 특징적인 검사 지표)

  • Cho, Han Gil;Cho, Young Kuk;Ma, Jae Sook
    • Clinical and Experimental Pediatrics
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    • v.53 no.2
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    • pp.228-234
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    • 2010
  • Purpose : Although intravenous immunoglobulin (IVIG) treatment is an effective first-line treatment for Kawasaki disease, 10-20% of the patients develop persistent fever or coronary artery complications. Medical records of Kawasaki disease patients were reviewed to assess the characteristic laboratory findings of IVIG nonresponsiveness. Methods : We reviewed the clinical records of 118 children with Kawasaki disease who were treated at the Chonnam National University Hospital from March 2003 to February 2008. The laboratory findings of the IVIG-responder group (n=110) and the IVIG-nonresponder group (n=8) were compared at admission day and at 48 hours and 14 days after IVIG administration. Results : At admission, the level of creatine kinase (CK) was lower (P =0.03) and that of total protein was higher (P <0.01) in the nonresponders than in the responders. At 48 hours after IVIG administration, the white blood cell (WBC) count (P =0.04) and neutrophil% (P <0.01) was higher in the nonresponders than in the responders. The neutrophil% (P <0.01) and CK (P =0.01) level at admission was lower than that at 48 hours after IVIG administration in the responders; this decrease was not as apparent in the nonresponders. Conclusion : IVIG nonresponders have lower CK and higher total protein levels at admission and higher WBC count and neutrophil% at 48 hours after IVIG administration. The decrease in the neutrophil% and CK level between at admission and at 48 hours after IVIG administration is remarkably higher in responders than in nonresponders.

Comparison of the Muscle Damage and Liver Function in Ultra-Marathon Race (100 km) by Sections

  • Shin, Kyung-A;Kim, Young-Joo
    • Biomedical Science Letters
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    • v.18 no.3
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    • pp.276-282
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    • 2012
  • High-intensive endurance exercises induce cell changes in body, changes in structures and functions of the heart, the muscles, the cartilages, and the liver, as well as increase of inflammatory cytokine. The purpose of this study was to estimate the biochemical changes in the liver and muscles during ultra-marathon race (100 km) by sections. The blood of the subjects was collected before the marathon as a control in order to analyze serum creatine kinase (CK), lactic dehydrogenase (LDH), asprtate aminotransferase (AST), alanine aminotransferase (ALT), total(T)-bilirubin, direct(D)-bilirubin, total protein, albumin, uric acid, gamma-glutamyltranspeptidase (${\gamma}$-GTP), alkaline phosphatase (ALP), creatinine, blood urea nitrogen (BUN), and high sensitive C-reactive protein (hs-CRP) concentrations. The CK, LDH, D-bilirubin, AST and ALT concentrations at 50 km and 100 km were significantly increased compared to the control (P<0.05). The markers at 100 km were higher than those at 50 km (P<0.05). The T-bilirubin and hs-CRP concentrations showed no difference among the groups, whereas the markers at 100 km were higher than those of the control and at 50 km (P<0.05). In conclusion, this study shows that the ultra-marathon race (100 km) may induce the damage of the skeletal muscle, liver and kidney, intravascular hemolysis and inflammatory responses.

Immobilization-induced rhabdomyolysis patients with peripheral neuropathy: clinical, laboratory and imaging findings

  • Seok, Jung Im;Lee, In Hee;Ahn, Ki Sung;Kang, Gun Woo;Lee, Je Wan;Kwak, Sanggyu
    • Annals of Clinical Neurophysiology
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    • v.22 no.1
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    • pp.19-23
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    • 2020
  • Background: Peripheral nerve injury rarely occurs in patients with rhabdomyolysis. Based on our experience and previous reports, we consider prolonged immobilization a risk factor for the development of peripheral neuropathy in rhabdomyolysis patients. Methods: This study analyzed 28 patients with rhabdomyolysis due to prolonged immobilization. We analyzed their demographic and laboratory data, clinical and imaging findings, and outcomes, and compared these factors between patients with and without neuropathy. Results: Seven of the 28 patients had peripheral neuropathy, including sciatic neuropathy or lumbosacral plexopathy. Compared to those without neuropathy, the patients with neuropathy were younger (p = 0.02), had higher peak creatine kinase (CK) levels (p = 0.02), had higher muscle uptake in bone scans (p = 0.03), and more frequently exhibited abnormal muscle findings in computed tomography (CT) (p = 0.004). Conclusions: Patients with prolonged immobilization-induced rhabdomyolysis and neuropathy had higher CK levels, increased uptake on bone scans, and more-frequent abnormal muscles on CT than those without neuropathy. These findings indicate that peripheral neuropathy is more likely to develop in patients with severe muscle injury.

The Effect of Melatonin on Biochemical Changes after Ischemia-Reperfusion Injury of Rat Skeletal Muscle (흰쥐 골격근의 허혈-재관류 손상후 생화학적 변화에 미치는 Melatonin의 효과)

  • Park, Hye June;Burm, Jin Sik
    • Archives of Plastic Surgery
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    • v.32 no.6
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    • pp.683-688
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    • 2005
  • The ischemia-reperfusion injury of the skeletal muscles is caused by generation of reactive oxygen during ischemia and reperfusion. Melatonin or N-Acetyl-5-methoxy- tryptamine is suggested to have antioxidant effects in several tissues. In present study, we examined the protective effect of melatonin in a rat hind limb ischemia-reperfusion injury. Dimethyl-sulfoxide(DMSO) was also tested for comparison. Ischemia was induced for 4 hours by vascular clamping and followed by 1 hour or 24 hours of reperfusion. Muscle injury was evaluated in 4 groups such as single laparotomy group(control), ischemia-reperfusion group, DMSO group, melatonin group. Eedema ratio and malondialdehyde(MDA) of muscle tissue and serum level of creatine kinase(CK), were measeured at the end of reperfusion. DMSO and melatonin group showed significant amelioration of edema and serum CK compared with ischemia-reperfusion group. The decreasing effect was more prominent in melatonin group. The muscle tissue MDA concentration is significantly lower in melatonin group than in ischemia-reperfusion group. The results show that melatonin prevents and improves ischemia-reperfusion injury more effectively in a rat hind limb than DMSO dose. Thus, clinically the melatonin may be used for a beneficial treatment of such injuries

A Case Study of one Patient who has a ischemic heart disease(IHD) (허혈성 심질환(Ischemic heart disease) 환자(患者)의 사상(四象) 처방(處方) 투여 1례(例)에 대한 임상보고(臨床報告))

  • Kim, Hye-Won;Song, Jeong-Mo;Kim, Jeong-Ho
    • Journal of Sasang Constitutional Medicine
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    • v.14 no.2
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    • pp.125-131
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    • 2002
  • An ischemic heart disease(IHD) is a anemic state of heart caused by disproportion between heart's demand and supply of oxygen. A patient who has this IHD feels serious chest pain called angina pectoris. In a keen condition it leads to a necrosis of heart muscles, known as myocardial infarction. In an ischemic heart disease the ECG waves gives us useful information of patients' heart. And CK(creatine kinase) in serum and Troponin T are the principal factors in diagnosis of IHD. In this study, the IHD patient classified by Sasang Constitutional Medicine had a notable medical effects. The symptoms of patient are disappeared and waves of ECG is closed to normal. The result of CK in serum is also recovered. So we report the healing process and results of this patient in this study.

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Neogambogic acid relieves myocardial injury induced by sepsis via p38 MAPK/NF-κB pathway

  • Fu, Wei;Fang, Xiaowei;Wu, Lidong;Hu, Weijuan;Yang, Tao
    • The Korean Journal of Physiology and Pharmacology
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    • v.26 no.6
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    • pp.511-518
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    • 2022
  • Sepsis-associated myocardial injury, an invertible myocardial depression, is a common complication of sepsis. Neogambogic acid is an active compound in garcinia and exerts anthelmintic, anti-inflammatory, and detoxification properties. The role of neogambogic acid in sepsis-associated myocardial injury was assessed. Firstly, mice were pretreated with neogambogic acid and then subjected to lipopolysaccharide treatment to induce sepsis. Results showed that lipopolysaccharide treatment induced up-regulation of biomarkers involved in cardiac injury, including lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I (cTnI). However, pretreatment with neogambogic acid reduced levels of LDH, CK-MB, and cTnI, and ameliorated histopathological changes in the heart tissues of septic mice. Secondly, neogambogic acid also improved cardiac function in septic mice through reduction in left ventricular end-diastolic pressure, and enhancement of ejection fraction, fractional shortening, and left ventricular systolic mean pressure. Moreover, neogambogic acid suppressed cardiac apoptosis and inflammation in septic mice and reduced cardiac fibrosis. Lastly, protein expression of p-p38, p-JNK, and p-NF-κB in septic mice was decreased by neogambogic acid. In conclusion, neogambogic acid exerted anti-apoptotic, anti-fibrotic, and anti-inflammatory effects in septic mice through the inactivation of MAPK/NF-κB pathway.

Role of the Neutrophil-to-Lymphocyte Ratio at the Time of Arrival at the Emergency Room as a Predictor of Rhabdomyolysis in Severe Trauma Patients

  • Bae, Jin Chul;Sun, Kyung Hoon;Park, Yong Jin
    • Journal of Trauma and Injury
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    • v.33 no.2
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    • pp.96-103
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    • 2020
  • Purpose: In patients with trauma, rhabdomyolysis (RM) can lead to fatal complications resulting from muscle damage. Thus, RM must be immediately diagnosed and treated to prevent complications. Creatine kinase (CK) is the most sensitive marker for diagnosing RM. However, relying on CK tests may result in delayed treatment, as it takes approximately 1 hour to obtain CK blood test results. Hence, this study investigated whether the neutrophil-to-lymphocyte ratio (NLR) could predict RM at an earlier time point in patients with trauma, since NLR results can be obtained within 10 minutes. Methods: This retrospective study included 130 patients with severe trauma who were admitted to the emergency room of a tertiary institution between January 2017 and April 2020. RM was defined as a CK level ≥1,000 U/L at the time of arrival. Patients with severe trauma were categorized into non-RM and RM groups, and their characteristics and blood test results were analyzed. Statistical analysis was performed using SPSS version 26.0 for Windows. Results: Of the 130 patients with severe trauma, 50 presented with RM. In the multivariate analysis, the NLR (odds ratio [OR], 1.252; 95% confidence interval [CI], 1.130-1.386), pH level (OR, 0.006; 95% CI, 0.000-0.198), presence of acute kidney injury (OR, 3.009; 95% CI, 1.140-7.941), and extremity Abbreviated Injury Scale score (OR, 1.819; 95% CI, 1.111-2.980) significantly differed between the non-RM and RM groups. A receiver operating characteristic analysis revealed that a cut-off NLR value of 3.64 was the best for predicting RM. Conclusions: In patients with trauma, the NLR at the time of arrival at the hospital is a useful biochemical marker for predicting RM.

Curcumin Alleviates Dystrophic Muscle Pathology in mdx Mice

  • Pan, Ying;Chen, Chen;Shen, Yue;Zhu, Chun-Hua;Wang, Gang;Wang, Xiao-Chun;Chen, Hua-Qun;Zhu, Min-Sheng
    • Molecules and Cells
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    • v.25 no.4
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    • pp.531-537
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    • 2008
  • Abnormal activation of nuclear factor kappa B ($NF-{\kappa}B$) probably plays an important role in the pathogenesis of Duchenne's muscular dystrophy (DMD). In this report, we evaluated the efficacy of curcumin, a potent $NF-{\kappa}B$ inhibitor, in mdx mice, a mouse model of DMD. We found that it improved sarcolemmic integrity and enhanced muscle strength after intraperitoneal (i.p.) injection. Histological analysis revealed that the structural defects of myofibrils were reduced, and biochemical analysis showed that creatine kinase (CK) activity was decreased. We also found that levels of tumor necrosis factor alpha ($TNF-\alpha$), interleukin-1 beta ($IL-1\beta$) and inducible nitric oxide synthase (iNOS) in the mdx mice were decreased by curcumin administration. EMSA analysis showed that $NF-{\kappa}B$ activity was also inhibited. We thus conclude that curcumin is effective in the therapy of muscular dystrophy in mdx mice, and that the mechanism may involve inhibition of $NF-{\kappa}B$ activity. Since curcumin is a non-toxic compound derived from plants, we propose that it may be useful for DMD therapy.

The Effect of Ginseng on Muscle Injury and Inflammation

  • Alvarez, A.I.;De Oliveira, A.C. Cabral;Perez, A.C.;Vila, L.;Ferrando, A.;Prieto, J.G.
    • Journal of Ginseng Research
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    • v.28 no.1
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    • pp.18-26
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    • 2004
  • The effect of Panax ginseng administration in muscle inflammatory process induced after eccentric exercise, that causes myofibrillar disruption, was studied. Changes in lipid peroxidation, inflammation, glycogen levels in muscle and release of myocellular proteins to blood were measured. The analyses were performed immediately after eccentric exercise and over week since this period are necessary for the muscle damage-repair cycle. The ginseng extract (100 mg kg$^{-1}$ ) was orally administered to rats for three months, before the eccentric exercise performance. The results showed the protective role of ginseng against skeletal muscle damage. This effect could be associated with their membrane stabilising capacity since creatine kinase (CK) activity was significantly decreased 96 h post-exercise from 523$\pm$70 to 381$\pm$53 and 120 h post-exercise from 443$\pm$85 to 327$\pm$75 in treated animals. $\beta$-glucuronidase activity, as indicator of inflammation, showed a significant reduction of about 15-25% in soleus, vastus and triceps in these post-exercise times. The lipid peroxidation, measured by malondyaldehyde levels, was significantly decreased in the 24 h post-exercise period in soleus and vastus intermedius muscles and on the recovery period. Finally ginseng administration reduced significantly the decrease of the glycogen levels immediately after exercise and when the regenerative process took place (72-168 h post exercise). Collectively, the results have showed that ginseng did not inhibit the vital inflammatory response process associated with the muscle damage-repair cycle but presumably ameliorate the injury.

The Effect of Ginseng on Muscle Injury and Inflammation

  • Alvarez A.I.;Oliveira A. C. Cabral de;Perez A.C.;Vila L.;Ferrando A.;Prieto J.G.
    • Proceedings of the Ginseng society Conference
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    • 2002.10a
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    • pp.159-175
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    • 2002
  • The effect of Panax ginseng administration in muscle inflammatory process induced after eccentric exercise, that causes myofibrillar disruption, was studied. Changes in lipid peroxidation, inflammation, glycogen levels in muscle and release of myocellular proteins to blood were measured. The analyses were performed immediately after eccentric exercise and over week since this period are necessary for the muscle damage-repair cycle. The ginseng extract $(100\;mg\;kg^{-1})$ was orally administered to rats for three months, before the eccentric exercise performance. The results showed the protective role of ginseng against skeletal muscle damage. This effect could be associated with their membrane stabilising capacity since creatine kinase (CK) activity was significantly decreased 96 h post-exercise from $523{\pm}70\;to\;381{\pm}53$ and 120 h post-exercise from $443{\pm}85\;to\;327{\pm}75$ in treated animals. ${\beta}-glucuronidase$ activity, as indicator of inflammation, showed a significant reduction of about $15-25\%$ in soleus, vastus and triceps in these post-exercise times. The lipid peroxidation, measured by malondyaldehyde levels, was significantly decreased in the 24 h postexercise period in soleus and vastus intermedius muscles and on the recovery period. Finally ginseng administration reduced significantly the decrease of the glycogen levels immediately after exercise and when the regenerative process took place (72-168 h post exercise). Collectively, the results have showed that ginseng did not inhibit the vital inflammatory response process associated with the muscle damage-repair cycle but presumably ameliorate the injury.

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