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1.
Severe acute myopathy following SARS-CoV-2 infection: a case report and review of recent literature.
Islam, B, Ahmed, M, Islam, Z, Begum, SM
Skeletal muscle. 2021;(1):10
Abstract
BACKGROUND SARS-CoV2 virus could be potentially myopathic. Serum creatinine phosphokinase (CPK) is frequently found elevated in severe SARS-CoV2 infection, which indicates skeletal muscle damage precipitating limb weakness or even ventilatory failure. CASE PRESENTATION We addressed such a patient in his forties presented with features of severe SARS-CoV2 pneumonia and high serum CPK. He developed severe sepsis and acute respiratory distress syndrome (ARDS) and received intravenous high dose corticosteroid and tocilizumab to counter SARS-CoV2 associated cytokine surge. After 10 days of mechanical ventilation (MV), weaning was unsuccessful albeit apparently clear lung fields, having additionally severe and symmetric limb muscle weakness. Ancillary investigations in addition with serum CPK, including electromyogram, muscle biopsy, and muscle magnetic resonance imaging (MRI) suggested acute myopathy possibly due to skeletal myositis. CONCLUSION We wish to stress that myopathogenic medication in SARS-CoV2 pneumonia should be used with caution. Additionally, serum CPK could be a potential marker to predict respiratory failure in SARS-CoV2 pneumonia as skeletal myopathy affecting chest muscles may contribute ventilatory failure on top of oxygenation failure due to SARS-CoV2 pneumonia.
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Does Low-Level Laser Therapy Decrease Muscle-Damaging Mediators After Performance in Soccer Athletes Versus Sham Laser Treatment? A Critically Appraised Topic.
Bettleyon, J, Kaminski, TW
Journal of sport rehabilitation. 2020;(8):1210-1213
Abstract
Clinical Scenario: Low-level laser therapy (LLLT) is a controversial topic for its use in athletic recovery, mainly due to inconsistency in research regarding the application of LLLT. Articles on LLLT have assessed its effectiveness in untrained humans through pain scales, functional scales, and blood draws, and it has been found capable in nonathletic rehabilitative use. The controversy lies with LLLT in the recovering athlete. Not only do athletes need to perform at high levels, but each sport is unique in the metabolic demands placed on the athletes' bodies. This modality can alter chemical mediators of the inflammatory process, specifically blood lactate (BL) and creatine kinase (CK). During soccer contests, it is a common problem for athletes to have an average CK level of 800 U/L and BL of 8 mmol·L, increasing delayed-onset muscle soreness and fatigue. Micro-CK level elevation is associated with cellular membrane damage, localized hypoxia, and electrolyte imbalances, hindering the recovery process. Clinical Question: Does LLLT decrease muscle-damaging mediators effecting player fatigue and delayed-onset muscle soreness after performance in soccer athletes versus sham treatment? Summary of Key Findings: In 3 studies, preperformance, postperformance, or preperformance and postperformance LLLT was performed and evaluated BL (2 of 3) and CK (2 of 3). In each article, BL and CK showed a significant decrease (P < .05) when performed either preperformance or postperformance versus the control group. The greatest decrease in these mediators was noticed when postperformance laser therapy was performed. Clinical Bottom Line: LLLT at 10, 30, or 50 J performed at a minimum of 2 locations on the rectus femoris, vastus lateralis, and vastus medialis bilaterally for 10 seconds each is significant in decreasing blood serum levels of BL and CK when performed postexercise. Strength of Recommendations: All 3 articles obtained a Physiotherapy Evidence Database score of ≥8/10.
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Creatine kinase, neuromuscular fatigue, and the contact codes of football: A systematic review and meta-analysis of pre- and post-match differences.
Hagstrom, AD, Shorter, KA
European journal of sport science. 2018;(9):1234-1244
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Abstract
Physiological or performance tests are routinely utilised to assess athletes' recovery. At present, the ideal tool to assess recovery remains unknown. Therefore, the aim of this systematic review was to examine the change in creatine kinase (CK) and neuromuscular function as measured via a countermovement jump (CMJ) following a match in the contact codes of football. A comprehensive search of databases was undertaken with RevMan (V 5.3) used for statistical analysis. Our results demonstrated that CK pre- versus post-match (standardised mean difference (SMD) = 0.90, 95% CI = 0.50 to 1.31, p < .0001), CK pre- versus 24 h post-match (SMD = 1.50, 95% CI = 1.12 to 1.88, p < .00001), and CK pre- versus 48 h post-match all increased significantly (SMD = 0.90, 95% CI = 0.50 to 1.31, p < .0001), while CMJ peak power (PP) pre- versus post-match (SMD = -0.59, 95% CI = -1.12 to -0.06, p = .03), and pre- versus 24 h post-match (SMD = -0.80, 95% CI = -1.31 to -0.28, p = .002) decreased significantly. There was a significant relationship between the change in CK and the change in CMJ PP from immediately pre to immediately post (r = -0.924, p = .025), and between CMJ immediately following a match and 24 h CK change (r = -0.983, p = .017). In conclusion, CK levels increase and performance in the CMJ decreases following a match of a contact code of football. The identification of this relationship may allow coaching staff to implement a standalone measure of recovery.
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Approach to asymptomatic creatine kinase elevation.
Moghadam-Kia, S, Oddis, CV, Aggarwal, R
Cleveland Clinic journal of medicine. 2016;(1):37-42
Abstract
How to manage a patient who has an elevated serum creatine kinase (CK) level but no or insignificant muscle-related signs and symptoms is a clinical conundrum. The authors provide a systematic approach, including repeat testing after a period of rest, defining higher thresholds over which pursuing a diagnosis is worthwhile, and evaluating for a variety of nonneuromuscular causes. They also outline a workup for neuromuscular causes.
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[Myositides: What is the current situation?].
Rösler, KM, Scheidegger, O
Zeitschrift fur Rheumatologie. 2015;(6):496-506
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Abstract
This article gives a review of the classification, diagnostic procedures and treatment of idiopathic inflammatory myopathies from a neurological point of view. The myositis syndromes can be subdivided into four groups, polymyositis (PM), dermatomyositis (DM), inclusion body myositis (IBM) and necrotizing myopathy (NM), which substantially differ clinically and pathophysiologically. Myositis may also occur in association with cancer or autoimmune systemic diseases (overlap syndrome). Diagnosis of inflammatory myopathies is based on clinical symptoms, determination of creatine phosphokinase and acute phase parameters in blood (e.g. C-reactive protein and erythrocyte sedimentation rate), electromyography results and findings of magnetic resonance imaging (MRI) in muscle. A muscle biopsy is mandatory to confirm the diagnosis. High quality randomized controlled trials of treatment regimens for inflammatory myopathies are sparse; however, empirical experience indicates a clear effectiveness of immunosuppressive treatment of PM, DM and NM.
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The creatine kinase response to resistance exercise.
Koch, AJ, Pereira, R, Machado, M
Journal of musculoskeletal & neuronal interactions. 2014;(1):68-77
Abstract
Resistance exercise can result in localized damage to muscle tissue. This damage may be observed in sarcolemma, basal lamina, as well as, in the contractile elements and the cytoskeleton. Usually the damage is accompanied by release of enzymes such as creatine kinase (CK) and lactate dehydrogenase, myoglobin and other proteins into the blood. Serum CK has been proposed as one of the best indirect indicators of muscle damage due to its ease of identification and the relatively low cost of assays to quantify it. Thus, CK has been used as an indicator of the training intensity and a diagnostic marker of overtraining. However, some issues complicate CK's use in this manner. There is great interindividual variability in serum CK, which complicates the assignment of reliable reference values for athletes. Furthermore, factors such as training level, muscle groups involved, and gender can influence CK levels to a greater extent than differences in exercise volume completed. This review will detail the process by which resistance exercise induces a rise in circulating CK, illuminate the various factors that affect the CK response to resistance exercise, and discuss the relative usefulness of CK as a marker of training status, in light of these factors.
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Monitoring of lipids, enzymes, and creatine kinase in patients on lipid-lowering drug therapy.
Wiklund, O, Pirazzi, C, Romeo, S
Current cardiology reports. 2013;(9):397
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A number of plasma lipid parameters have been used to estimate cardiovascular risk and to be targets for treatment to reduce risk. Most risk algorithms are based on total cholesterol (T-C) or low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C), and most intervention trials have targeted the LDL-C levels. Emerging measures, which in some cases may be better for risk calculation and as alternative treatment targets, are apolipoprotein B and non-HDL-C. Other lipid measures that may contribute in risk analysis are triglycerides (TG), lipoprotein(a), and lipoprotein-associated phospholipase A2. The primary treatment target in cardiovascular prevention is LDL-C, and potential alternative targets are apoB and non-HDL-C. In selected individuals at high cardiovascular (CV) risk, TG should be targeted, but HDL-C, Lp(a), and ratios such as LDL-C/HDL-C or apoB/apoAI are not recommended as treatment targets. Lipids should be monitored during titration to targets. Thereafter, lipids should be checked at least once a year or more frequently to improve treatment adherence if indicated. Monitoring of muscle and liver enzymes should be done before the start of treatment. In stable conditions during treatment, the focus should be on clinical symptoms that may alert muscle or liver complications. Routine measurement of CK or ALT is not necessary during treatment with statins.
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Creatine and creatine analogues in hypertension and cardiovascular disease.
Horjus, DL, Oudman, I, van Montfrans, GA, Brewster, LM
The Cochrane database of systematic reviews. 2011;(11):CD005184
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BACKGROUND The creatine kinase system, the central regulatory system of cellular energy metabolism, provides ATP in situ at ATP-ases involved in ion transport and muscle contraction. Furthermore, the enzyme system provides relative protection from tissue ischaemia and acidosis. The system could therefore be a target for pharmacologic intervention. OBJECTIVES To systematically evaluate evidence regarding the effectiveness of interventions directly targeting the creatine kinase system as compared to placebo control in adult patients with essential hypertension or cardiovascular disease. SEARCH METHODS Electronic databases searched: Medline (1950 - Feb 2011), Embase (up to Feb 2011), the Cochrane Controlled Trials Register (issue 3, Aug 2009), Latin-American/Caribbean databank Lilacs; references from textbooks and reviews; contact with experts and pharmaceutical companies; and searching the Internet. There was no language restriction. SELECTION CRITERIA Randomized controlled trials comparing creatine, creatine phosphate, or cyclocreatine (any route, dose or duration of treatment) with placebo; in adult patients with essential hypertension, heart failure, or myocardial infarction. We did not include papers on the short-term use of creatine during cardiac surgery. DATA COLLECTION AND ANALYSIS The outcomes assessed were death, total myocardial infarction (fatal or non-fatal), hospitalizations for congestive heart failure, change in ejection fraction, and changes in diastolic and systolic blood pressure in mm Hg or as percent change. MAIN RESULTS Full reports or abstracts from 1164 papers were reviewed, yielding 11 trials considering treatment with creatine or creatine analogues in 1474 patients with heart failure, ischemic heart disease or myocardial infarction. No trial in patients with hypertension was identified. Eleven trials (1474 patients, 35 years or older) comparing add-on therapy of the creatine-based drug on standard treatment to placebo control in patients with heart failure (6 trials in 1226 / 1474 patients ), or acute myocardial infarction (4 trials in 220 / 1474 patients) or 1 in ischemic heart disease (28 / 1474 patients) were identified. The drugs used were either creatine, creatine phosphate (orally, intravenously, or intramuscular) or phosphocreatinine. In the trials considering heart failure all three different compounds were studied; creatine orally (Gordon 1995, Kuethe 2006), creatine phosphate via intravenous infusion (Ferraro 1996, Grazioli 1992), and phosphocreatinine orally (Carmenini 1994, Maggi 1990). In contrast, the acute myocardial infarction trials studied intravenous creatine phosphate only. In the ischemic heart disease trial (Pedone 1984) creatine phosphate was given twice daily through an intramuscular injection to outpatients and through an intravenous infusion to inpatients. The duration of the study intervention was shorter for the acute patients, from a two hour intravenous infusion of creatine phosphate in acute myocardial infarction (Ruda 1988, Samarenko 1987), to six months in patients with heart failure on oral phosphocreatinine therapy (Carmenini 1994). In the acute myocardial infarction patients the follow-up period varied from the acute treatment period (Ruda 1988) to 28 days after start of the symptoms (Samarenko 1987) or end of the hospitalization period (Zochowski 1994). In the other trials there was no follow-up after discontinuation of treatment, except for Gordon 1995 which followed the patients until four days after stopping the intervention.Only two out of four trials in patients with acute myocardial infarction reported mortality outcomes, with no significant effect of creatine or creatine analogues (RR 0.73, CI: 0.22 - 2.45). In addition, there was no significance on the progression of myocardial infarction or improvement on ejection fraction. The main effect of the interventions seems to be on improvement of dysrhythmia. AUTHORS' CONCLUSIONS This review found inconclusive evidence to decide on the use of creatine analogues in clinical practice. In particular, it is not clear whether there is an effect on mortality, progression of myocardial infarction and ejection fraction, while there is some evidence that dysrhythmia and dyspnoea might improve. However, it is not clear which analogue, dose, route of administration, and duration of therapy is most effective. Moreover, given the small sample size of the discussed trials and the heterogeneity of the population included in these reports, larger clinical studies are needed to confirm these observations.
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Serum markers in the diagnosis of tubal pregnancy.
Cabar, FR, Fettback, PB, Pereira, PP, Zugaib, M
Clinics (Sao Paulo, Brazil). 2008;(5):701-8
Abstract
The introduction of highly sensitive methods, such as transvaginal sonography and measurement of serum b-human chorionic gonadotropin, has dramatically improved ectopic pregnancy diagnosis in recent years. Early diagnosis is the key to successful and conservative management of women with ectopic pregnancy; however, approximately 50 percent of such women are initially misdiagnosed, resulting in significant morbidity and mortality. In order to improve diagnosis, several serum markers are being investigated including progesterone, CA 125, pregnancy-associated plasma protein-A, vascular endothelial growth factor, and maternal creatine kinase. Measurement of serum vascular endothelial growth factor, alone or together with other markers, could be a promising method for earlier and more accurate differential diagnosis. However, the clinical applicability of these findings remains to be evaluated in larger prospective studies.
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Should creatine kinase be checked in all boys presenting with speech delay?
Lundy, CT, Doherty, GM, Hicks, EM
Archives of disease in childhood. 2007;(7):647-9