This will create a ratio that is used as a diagnostic method. If there is no evidence of heart problems or skeletal muscle breakdown, then the kidneys may be the cause of the increased levels of CKMB.
Chronic muscle diseases, alcohol abuse, or low levels of thyroid hormones have also been known to cause positive test results. Exercise and contact sports are known to create moderately high levels of CKMB.
A negative CKMB test results means that no damage has occurred and the cause of the bothersome symptoms is related to a different health condition. It may also indicate that a cardiac event could have occurred, but do so several days before the test.
There are numerous reasons why an individual may experience chest pain that do not include a heart attack or a symptom of coronary heart disease. There are numerous muscles in the chest that can be pulled or strained to create chest pain.
Lung problems are also known to cause chest pain, as can something as simple as indigestion. Stress is also known to cause chest pain, as can regular exercise.
It is important to seek medical assistance when the chest pain lasts longer than a few minutes. What do the results mean? If your results show you have a higher than normal level of CK, it may mean you have an injury or disease of the muscles, heart, or brain. A small amount of CK in the blood is normal. Higher amounts can mean a health problem. Depending on the type and level of CK found, it can mean you have damage or disease of the skeletal muscles, heart, or brain.
High CK-MB levels also show up in a blood test if there are other reasons for damage to the heart. This is a brain-specific enzyme that produces elevated CK levels if the brain has suffered any injury.
This was done because not all CK elevations in patients with IIM are due to the underlying disease and clinicians must be diligent to rule out other causes of myositis when this scenario is encountered. However, in 34 of 35 of these cases, the CK elevation was indeed attributed to IIM activity and it could be argued that this created a higher than expected percentage of patients in the IIM category.
Three of the 29 patients first presented with respiratory symptoms and interstitial lung disease, three patients were already known to have IIM and developed an elevated CK without concurrent symmetric, proximal muscle weakness, and one patient was diagnosed with IBM, which is known to present with both proximal and distal asymmetric weakness.
Three of these patients were diagnosed with statin-induced myositis. One of these patients had a muscle biopsy without mention of widespread necrosis to suggest autoimmune necrotizing myopathy. The other two patients were followed for 1 and 4 years without recurrence.
Of the remaining non-IIM patients with symmetric proximal weakness, two were diagnosed with muscular dystrophy, two were attributed to trauma complicated by an underlying neurologic disease multiple sclerosis and polyneuropathy that explained the proximal weakness, one patient had severe hypothyroidism with a TSH with a thyroid stimulating hormone level of 76, one patient had a self-limiting episode of myositis that was felt to be viral in etiology, and one patient had an isolated elevation in CK with a suspected metabolic myopathy but a normal muscle biopsy.
Taken together, these findings emphasize the importance of clinical features such as proximal muscle weakness, interstitial lung disease, or features of an overlap syndrome or antisynthetase syndrome when considering an IIM as the cause of a markedly elevated CK concentration.
Fig 2 Other distinguishing features found to be significantly different between IIM and non-IIM patients like age, gender, location of consultation, duration of symptoms, medical comorbidities, antinuclear antibodies, and anti-Jo-1 antibodies can then be used to raise or lower clinical suspicion. However, true statin-associated myopathy with a significant elevation in creatine kinase is rare [ 20 ].
The diagnosis of statin-associated myopathy was primarily based on the temporal relation of the onset and resolution of myositis with statin exposure and withdrawal, respectively. Thus, while statin-associated myopathy is rare, it is a relatively common diagnosis in the scenario examined in this study.
It should also be noted that 13 of the IIM patients had a history of prior exposure to statins. Each of these patients had persistent CK elevation and weakness despite discontinuing the statin and none were restarted on a statin after the diagnosis of IIM was made.
Only one patient had a biopsy with features suggestive of a statin-induced autoimmune necrotizing myopathy. This study has some limitations. First, all patients were treated at a single medical center and therefore the findings could have been influenced by local referral practices. For example, there were very few neuromuscular disorders and metabolic myopathies found in this cohort, likely because these patients were sent to neurology without obtaining a rheumatology referral.
This practice could be different in other medical centers. In addition, the study was a chart review so data were recorded for clinical purposes. As mentioned above, some patients had missing data on liver function tests, creatinine levels, and duration of treatment. Furthermore, only anti-Jo-1 antibodies were available in this cohort but other myositis specific antibodies and anti-HMGcoA antibodies are relatively new and currently are send-out tests in our institution; therefore, they were not recorded in the Synthetic Derivative database.
Furthermore, when evaluating patients with severely elevated CK concentrations, clinicians should be aware that in the absence of symmetric proximal muscle weakness, interstitial lung disease, or features of an overlap or antisynthetase syndrome, an IIM is less likely to be the cause of the elevated CK. National Center for Biotechnology Information , U.
Clin Rheumatol. Author manuscript; available in PMC Jun 1. David Leverenz , M. Crofford , M. Chung , M. Leslie J. Cecilia P. Author information Copyright and License information Disclaimer. Corresponding author: Cecilia P. Chung, M. Copyright notice. The publisher's final edited version of this article is available at Clin Rheumatol. See other articles in PMC that cite the published article.
Abstract Introduction Patients with severely elevated creatine kinase CK concentrations are commonly referred to rheumatologists to evaluate for the presence of an idiopathic inflammatory myopathy IIM. Results A total of patients were included for analysis. Keywords: idiopathic inflammatory myopathies, creatine kinase, polymyositis, dermatomyositis, myositis.
Introduction Creatine kinase is an enzyme primarily found in muscle tissue that catalyzes the conversion of creatine and adenosine triphosphate ATP into phosphocreatine and adenosine diphosphate ADP. Materials and Methods Data collection was performed using the Vanderbilt Synthetic Derivative, a de-identified copy of over 2 million patient records.
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