Positive troponin T without cardiac involvement in inclusion body myositis

Schwarzmeier, Josef D.; Hamwi, Ahmad; Preisel, Martin; Resl, Christoph; Preusser, Matthias; Sluga, E; Horcher, Ernst; Shehata, Medhat

doi:10.1016/j.humpath.2005.06.009

Cited by 13 publications

(10 citation statements)

References 22 publications

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“…As a simple illustration using example (a), we shall choose the initial CK-value as 983.33 Ul/L, P as 250.0 Ul/L, the steroid (S) as 62.5 mg every second day with the natural product (Ambrotose) being taken daily. The calculated CK-value decreases with time to reach a constant value of CK = 226.63 (P = 26.56); example (b), we choose the initial CK-value as 226.63, P as Our findings support other studies indicating that up-regulation of CK-MB and cTnT is common in inflammatory muscle diseases [7][8][9][10]19] . The source of the elevated cTnT has not been established, however there are a number of possibilities.…”

Section: Discussionsupporting

confidence: 81%

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An Analysis of the Creatine Kinase Isoenzyme and Cardiac Troponin T Levels in a Polymyositis Patient

Rm¹,

Giles²,

Sokoya³

2008

American J. of Immunology

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From an extensive model developed to interpret physiological processes we are able to show that the observed elevated creatine kinase-myoglobin (CK-MB) and serum concentration of cardiac troponin T (cTnT) values for a particular patient are associated with the inflammatory disease, polymyositis, and not myocardial injury. This highlights that caution must be exercised in using elevated CK-MB and cTnT levels as evidence for myocardial damage in patients with chronic muscle degeneration such as polymyositis.

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Section: Discussionsupporting

confidence: 81%

“…Some studies have reported that cTnT can be used to discriminate between myocardial disease and skeletal muscle disease [6] . However, other conditions such as polymyositis/dermatomyositis [7,8] , inclusion body myositis [9,10] , trauma [11] and rhabdomyolysis [12] have been reported to also result in increased levels of cTnT.…”

Section: Introductionmentioning

confidence: 99%

An Analysis of the Creatine Kinase Isoenzyme and Cardiac Troponin T Levels in a Polymyositis Patient

Rm¹,

Giles²,

Sokoya³

2008

American J. of Immunology

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“…6,8 Increased plasma concentrations of cTnT have been described in individual cases and small sample size reports of patients with various myopathies. 9,[11][12][13]34 In some skeletal muscle myopathies such as Duchenne muscular dystrophy, the heart is known to be affected, which might explain increased cTnT levels. 35 Hypertrophic cardiomyopathy is a characteristic feature in patients with classic infantile Pompe disease (but not in the childhood and adult forms of Pompe disease) and in most cases it is known to respond well to ERT.…”

Section: Discussionmentioning

confidence: 99%

Elevated Plasma Cardiac Troponin T Levels Caused by Skeletal Muscle Damage in Pompe Disease

Wens

Schaaf

Michels

et al. 2016

Circ Cardiovasc Genet

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Background— Elevated plasma cardiac troponin T (cTnT) levels in patients with neuromuscular disorders may erroneously lead to the diagnosis of acute myocardial infarction or myocardial injury. Methods and Results— In 122 patients with Pompe disease, the relationship between cTnT, cardiac troponin I, creatine kinase (CK), CK-myocardial band levels, and skeletal muscle damage was assessed. ECG and echocardiography were used to evaluate possible cardiac disease. Patients were divided into classic infantile, childhood-onset, and adult-onset patients. cTnT levels were elevated in 82% of patients (median 27 ng/L, normal values <14 ng/L). Cardiac troponin I levels were normal in all patients, whereas CK-myocardial band levels were increased in 59% of patients. cTnT levels correlated with CK levels in all 3 subgroups ( P <0.001). None of the abnormal ECGs recorded in 21 patients were indicative of acute myocardial infarction, and there were no differences in cTnT levels between patients with and without (n=90) abnormalities on ECG (median 28 ng/L in both groups). The median left ventricular mass index measured with echocardiography was normal in all the 3 subgroups. cTnT mRNA expression in skeletal muscle was not detectable in controls but was strongly induced in patients with Pompe disease. cTnT protein was identified by mass spectrometry in patient-derived skeletal muscle tissue. Conclusions— Elevated plasma cTnT levels in patients with Pompe disease are associated with skeletal muscle damage, rather than acute myocardial injury. Increased cTnT levels in Pompe disease and likely other neuromuscular disorders should be interpreted with caution to avoid unnecessary cardiac interventions.

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“…Arguments against hereditary IBM, however, are the late onset, muscle cramps, the lack of weakness, and the family history suggesting dominant inheritance although GNE mutations are usually recessive. Cardiac abnormalities have been only rarely reported in patients with IBM [8]. Affection of the myocardium in IBM may be primarily classified as symptomatic or asymptomatic.…”

Section: Discussionmentioning

confidence: 99%

Left ventricular hypertrabeculation/noncompaction in hereditary inclusion body myopathy

Finsterer

Stöllberger

Höftberger³

2011

International Journal of Cardiology

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Positive troponin T without cardiac involvement in inclusion body myositis

Cited by 13 publications

References 22 publications

An Analysis of the Creatine Kinase Isoenzyme and Cardiac Troponin T Levels in a Polymyositis Patient

An Analysis of the Creatine Kinase Isoenzyme and Cardiac Troponin T Levels in a Polymyositis Patient

Elevated Plasma Cardiac Troponin T Levels Caused by Skeletal Muscle Damage in Pompe Disease

Left ventricular hypertrabeculation/noncompaction in hereditary inclusion body myopathy

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