Elevated Creatinine Kinase in Connection with Wilson Disease: Atypical Presentation with Musculoskeletal Symptoms or Associated Neuromuscular Disease

2016 ◽  
Vol 47 (S 01) ◽  
Author(s):  
N. Pfeifer ◽  
Marina Della ◽  
S. Kathemann ◽  
B. Hegen ◽  
S. Lutz ◽  
...  
Eye ◽  
2011 ◽  
Vol 26 (4) ◽  
pp. 613-614 ◽  
Author(s):  
W H Chan ◽  
S Biswas ◽  
J Ashworth ◽  
I Hughes ◽  
V Sharma ◽  
...  

2020 ◽  
Vol 38 (7) ◽  
pp. 1548.e1-1548.e3 ◽  
Author(s):  
Kok Hoe Chan ◽  
Iyad Farouji ◽  
Amany Abu Hanoud ◽  
Jihad Slim

2018 ◽  
Vol 63 (3) ◽  
pp. 82-86
Author(s):  
Deniz Can Guven ◽  
Abdulsamet Erden ◽  
Levent Kilic ◽  
Sevim Erdem Ozdamar ◽  
Omer Karadag

Background Immune-mediated necrotising myopathies are characterised clinically by the subacute onset of proximal limb weakness, accompanied by elevated creatinine kinase levels. They are distinguished from other myopathies by the absence of prominent infiltration of the muscle with inflammatory cells in the biopsies. Case presentation A 44-year-old man presented with upper extremity weakness and dysphagia. Laboratory tests included a creatinine kinase level of 4362 U/L (normal: 52–336 U/L). Rheumatological markers were all negative. A muscle biopsy showed multiple necrotic fibres with minimal inflammatory infiltration. One gram of methylprednisolone (IV) was given, followed by 1 mg/kg of methylprednisolone daily by the oral route. Intravenous immunoglobulin (0.4 mg/kg/day) was given for five days. Muscle weakness regressed and dysphagia disappeared with treatment. The patient remains well in the 23rd month of treatment, taking 5 mg/day prednisolone and monthly intravenous immunoglobulin. Conclusion Treatment of immune-mediated necrotising myopathy can be challenging as evidence-based therapeutic options are limited. It is generally accepted that early and extensive immunosuppression, including glucocorticoids as first-line agents, may be required.


2011 ◽  
Vol 31 (03) ◽  
pp. 319-326 ◽  
Author(s):  
Sheetal Wadera ◽  
Margret Magid ◽  
Mark McOmber ◽  
David Carpentieri ◽  
Tamir Miloh

2021 ◽  
Vol 12 ◽  
Author(s):  
Allison Jordan ◽  
Arun Nagaraj ◽  
J. Chad Hoyle ◽  
Amro Maher Stino ◽  
W. David Arnold ◽  
...  

Introduction: Serum Creatinine Kinase (CK) is a non-specific marker of muscle damage. There has been limited investigation of the association between peripheral neuropathy and CK elevation (hyperCKemia).Methods: We performed a chart review to investigate the CK level in peripheral neuropathies. Demographics, clinical history, physical exam, electrodiagnostic data, CK level, statin use, etiology of neuropathy, and concomitant neuromuscular disorders were recorded. HyperCKemia was defined using our laboratory cutoff values of >180 U/L (women) and >220 U/L (men).Results: We identified 450 patients with peripheral neuropathy who had CK testing, 92 (20.4%) of whom had hyperCKemia. Sixty-one of those patients (13.5% of the total figure) had a concomitant etiology that could explain the CK elevation. Thirty-one patients (6.9%) had no other identifiable etiology for their hyperCKemia beyond the neuropathy. The average CK level in the latter cohort with hyperCKemia was 376 U/L (women: 312 U/L; men: 444 U/L). The frequency of cramping was greater in patients with elevated vs. normal CK (p < 0.0001).Discussion: HyperCKemia can occur in patients with peripheral neuropathy and appears to associate with cramping.


Rheumatology ◽  
2006 ◽  
Vol 45 (5) ◽  
pp. 594-594
Author(s):  
A. Al-Ansari ◽  
C. Clarke ◽  
G. Kallarackal

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