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Letters |
Departments of
1
Medical Biochemistry, and
2
Cardiac Services, Flinders Medical Centre, Flinders Drive, Bedford Park, South Australia 5042, Australia
aAuthor for correspondence. Fax 61-8-8204-4466; e-mail Graham.White{at}fmc.sa.gov.au.
To the Editor:
Increased troponins have been reported in dermatomyositis (1). We report in more detail a case of increased cardiac troponin T (cTnT) in a patient presenting with chest pain and undiagnosed dermatomyositis (2).
A 72-year-old man, previously well apart from treated gout, presented
to the Emergency Department after 3 days of pleuritic-type chest pain,
breathlessness, and sweating and 5 weeks of a flu-like illness and
productive cough. He complained of recent proximal muscle aches and
weakness in his arms and legs. He had no history of cardiac or
respiratory problems and no known cardiac risk factors except for a
family history of ischemic heart disease. To exclude acute coronary
syndrome as a cause of the chest pain, creatine kinase (CK) activity
(at 37 °C, using CK NAC reagent sets on a Hitachi 917; Roche
Diagnostics) and CK-MB mass (AxSYM analyzer using CK-MB reagent packs;
Abbott Laboratories) were measured, and an electrocardiogram (ECG) was
recorded. The ECG showed no ischemic changes, and serial ECGs and an
echocardiogram were normal. The temporal pattern of increased serial
cardiac markers was not consistent with a clinical diagnosis of acute
myocardial infarction (Table 1
). The patient was diagnosed and treated for bronchopneumonia.
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cTnT was measured (third-generation Troponin T STAT; cat. no. 2017423;
Elecsys 1010 immunoassay analyzer; Roche Diagnostics) retrospectively
on the admission and day 3 specimens, and was increased in both (Table 1
). Renal and thyroid function were normal. All assays were performed
according to the manufacturers’ instructions on plasma collected into
lithium-heparin gel tubes (Vacuette; Greiner Pty. Ltd).
Further clinical findings included an erythematous facial rash,
periorbital edema, Gottron papules, thickened fingertip skin, and
abnormal capillary dilatation of nail folds. The patient could not rise
from the crouch position, and had reduced power in the shoulder and
neck muscles and normal strength distally in the upper and lower limbs.
The results of immunological tests were as follows: rheumatoid factor
<1/20 IU/mL (upper reference limit <1/40); antinuclear
antibody titer positive at 1:2560 (upper reference limit <1/80) with a
speckled pattern; antibodies to extractable nuclear antigens positive
with an unidentified precipitin line. Dermatomyositis was diagnosed on
the basis of the clinical and laboratory findings; muscle biopsy was
considered unnecessary. After 3 months of standard prednisolone
treatment, the symptoms resolved; the total CK activity and cTnT
normalized within 10 months (Table 1
).
Chronic inflammatory muscle diseases can increase CK-MB to 50% of total CK (3). In our patient we assume that the initial CK changes reflected fluctuations of the untreated inflammatory muscle process. During steroid treatment, CK decreased disproportionately more rapidly than CK-MB, thereby increasing the CK-MB index. We suggest that this discordance could reflect a differential steroid effect on the release of total CK as a result of the inflammatory process and on the abnormal production of B subunits in the regenerating muscle.
After 3 weeks of steroid treatment, cTnT increased (0.87 µg/L compared with 0.50 µg/L) as total CK decreased. This may possibly be attributable to a nonsystematic heparin effect (4), but we suggest that it could reflect either an exacerbation of subclinical myocardial damage or a differential response to prednisolone by the myocardial and skeletal muscle. Our patient was negative for rheumatoid factor, and the cTnT normalized following treatment. We conclude that the increased TnT in our patient reflected subclinical myocardial damage that occurred during the active phase of dermatomyositis.
If the admission cTnT had been used as the sole cardiac marker for the initial clinical assessment, the result would have been misleading. Where Emergency Departments use admission cTnT results to assist initial clinical assessments of chest pain, we suggest that CK markers remain a useful adjunct and that cTnT results require careful interpretation in patients with dermatomyositis.
References
The following articles in journals at HighWire Press have cited this article:
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  J S Hamilton and P C Sharpe Two cases of inflammatory muscle disease presenting with raised serum concentrations of troponin T J. Clin. Pathol., December 1, 2005; 58(12): 1323 - 1324. [Abstract] [Full Text] [PDF]
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