Rheumatology Advance Access originally published online on March 16, 2006
Rheumatology 2006 45(5):643-644; doi:10.1093/rheumatology/kel093
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LETTER TO THE EDITOR |
An unusual cause of acute rhabdomyolysis
1 Department of Rheumatology and Clinical Immunology, 2 Department of Neuropathology, 3 Department of Cardiology, 4 Department of Radiology, 5 Department of Nuclear Medicine and 6 Department of Virology, Albert-Ludwigs University Medical School, Freiburg, Germany
Correspondence to: Ulrich A. Walker, MD, Albert-Ludwigs University Medical School, Dept of Rheumatology and Clinical Immunology, Hugstetterstr. 55, D-79106 Freiburg, Germany. E-mail: ulrich.walker{at}klinikum.uni-freiburg.de
SIR, Last February, a previously healthy 27-year-old male was admitted to our hospital with a 2-day history of afebrile abrupt onset malaise and myalgias involving arms, legs and trunk. Because of simultaneous cephalgias and rhinorrhoea, the primary care physician had suspected influenza and immediately prescribed oseltamivir, a neuraminidase inhibitor. The patient had massive tissue oedema and a rapidly progressive paresis of the proximal and distal muscles of all extremities. His heart rate was 132/minute, his blood pressure 130/90. The ESR was 12 in the first hour. His serum creatine kinase (CK) levels were 125 860 U/l (CK-MB1080 U/l), troponin T was negative, the pro-brain derived natriuretic peptide (proBNP) was 1492 µg/l (normal <125). His leucocyte count was 17 800 µl (79% neutrophils), serum CRP was 105 mg/l, creatinine 13 mg/l, ALT 764 U/l and urate 105 mg/l. There was hypocalcaemia (1.6 mmol/l) and hyperphosphataemia (79 mg/l). The patient voided dark brown urine (200 ml within the first 12 h). The urine peroxidase reaction was positive and in the absence of erythrocytes indicative of myoglobin.
The patient denied recent trauma, drug use and a family history of muscle disease. Chest X-ray, ECG and echocardiogram were normal. MRI and 99mTc pyrophosphate scintigraphy revealed a disseminated muscle oedema (Fig. 1A). A muscle biopsy performed at day 2 of admission from an involved region (M. vastus lateralis) showed a regular checkerboard distribution of type I and type II fibres, intact enzyme activities and normal PAS and oil red stains. Single fibre necrosis was observed very rarely, myophagocytosis and inflammatory infiltrations were completely absent. Electron microscopy showed activated satellite cells, an intact myofibrillar lattice and disrupted sarcoplasmic membranes (Fig. 1B).
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Serum carnitine and acetyl carnitine, carnitine palmitoyl transferase and ANA were within normal limits [1]. Legionella pneumophila antigen was negative in the urine, as were serum antibodies for HIV, parainfluenza, adeno-, influenza A, cytomegalo-, Epstein–Barr and herpes simplex viruses.
Blood drawn at admission yielded a positive ELISA result for influenza B virus IgG (22.9 U; cutoff at 9.0 U), a repeat serum after 15 days showed an almost 8-fold rise (174.0 U). RT-PCR for influenza B virus RNA from the muscle biopsy specimen was negative.
Twelve hours after admission, the patient was unable to lift arms and legs from the bed. The CK had doubled (265300 U/l). Despite instantaneous urine alkalinization, volume substitution (9 l within the first 24 h) and treatment with recombinant urate oxidase, there was renal failure requiring haemodialysis. Plasmapheresis was performed on three consecutive days. After 12 days, the myalgias diminished, muscle strength began to improve and the CK had declined (5700 U/l). At the same time troponin T (which was measured daily) became positive and proBNP had increased (11304 µg/l). Chest X-ray and repeat echocardiograms were normal, as were ECG curves with the exception of sinus tachycardia (110/min). After 4 weeks, the patient had no muscle tenderness, was able to walk, CK had normalized and haemodialysis was discontinued.
Although myalgias are common in influenza, myositis has only been described in a few adults. Almost all adult cases were caused by influenza A. Our case is unusual in its association with influenza B and its magnitude of CK elevation.
The lack of prevention by oseltamivir of this influenza B-associated complication and the late-onset myocardial involvement deserve consideration. Rhabdomyolysis was previously observed in a 51-year-old man who had received oseltamivir for influenza A infection and in whom muscle breakdown developed shortly after the flu symptoms had resolved [2]. This temporal course has raised the possibility of a drug-related aetiology [2].
Our case is the first to visualize widespread muscle involvement, the mechanism of which is unknown. Cytokines may contribute to skeletal muscle breakdown [3]. Viral antigen and myxovirus-like particles were detected in the muscle only rarely [4], although direct infection, replication and cytopathic effects have been demonstrated in mononucleate myoblasts and multinucleate myotubes [5]. The muscle of adult animals appears to be resistant to infection [4, 6], but denervation and muscle regeneration may promote susceptibility. In this context, it is interesting that our patient was a karate fighter in whom micro-injuries during training sessions may have initiated muscle regeneration.
Influenza myositis should be included in the differential diagnosis even in afebrile patients. Nasal swabs and repeat serology are the most reliable way of diagnosis.
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References
- Kelly KJ, Garland JS, Tang TT, Shug AL, Chusid MJ. Fatal rhabdomyolysis following influenza infection in a girl with familial carnitine palmitoyl transferase deficiency. Pediatrics 1989;84:312–6.
[Abstract/Free Full Text] - Zulfiqar M, Doshi P, Brainard A, Piko C. Oseltamivir inducing rhabdomyolysis in influenza A. J Invest Med 2000;48:272.
- Konrad RJ, Goodman DB, Davis WL. Tumor necrosis factor and coxsackie B4 rhabdomyolysis. Ann Intern Med 1993;119:861–2.
[Free Full Text] - Gamboa ET, Eastwood AB, Hays AP, Maxwell J, Penn AS. Isolation of influenza virus from muscle in myoglobinuric polymyositis. Neurology 1979;29:1323–35.[Web of Science][Medline]
- Servidei S, Miranda AF, Gamboa ET. Infectivity of influenza B virus in cultured human muscle. Acta Neuropathol 1987;73:67–76.[CrossRef][Medline]
- Wagner RR. A pantropic strain of influenza virus: generalized infection and viremia in the infant mouse. Virology 1955;1:497–515.[Medline]
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