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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 40  |  Issue : 3  |  Page : 141-144

Varicella-zoster virus-induced rhabdomyolysis: A case report and literature review


1 Department of Internal Medicine, Division of Infectious Diseases and Tropical Medicine, National Defense Medical Center, Tri-Service General Hospital, Taipei, Taiwan
2 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, National Defense Medical Center, Tri-Service General Hospital, Taipei, Taiwan
3 Department of Internal Medicine, Division of Nephrology, National Defense Medical Center, Tri-Service General Hospital, Taipei, Taiwan
4 Department of Family Medicine, National Defense Medical Center, Song-Shan Branch, Tri-Service General Hospital, Taipei, Taiwan

Date of Submission09-Jun-2019
Date of Decision30-Jun-2019
Date of Acceptance15-Aug-2019
Date of Web Publication04-Oct-2019

Correspondence Address:
Dr. Yao-Hsien Huang
Department of Family Medicine, National Defense Medical Center, Song.Shan Branch, Tri-Service General Hospital, National Defense Medical Center, No. 131, Jiankang Road, Songshan District, Taipei
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmedsci.jmedsci_114_19

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  Abstract 


Infection is a possible cause of rhabdomyolysis. We describe the case of a 63-year-old male with malaise and erythematous papules on the right C5–C7 dermatomes, consistent with herpes zoster. Serum antibody and Tzanck tests of the skin lesion were positive. Increased serum creatine kinase (CK) and myoglobin levels and cola-colored urine indicated the development of rhabdomyolysis. Acute kidney injury was also observed. After excluding other possible predisposing factors, the patient was diagnosed with varicella-zoster virus (VZV)-induced rhabdomyolysis. Extracellular volume with alkalized fluids and topical acyclovir was administered. While CK levels declined to normal by day 13, the renal function was not restored. The skin lesion crusted by day 8 and scaled off gradually by day 13. Our case and literature review highlighted the necessity for systemic antiviral treatment and that poor VZV infection control could lead to irreversible kidney injury. In addition, systemic acyclovir should be administered carefully due to its complication of nephrotoxicity.

Keywords: Rhabdomyolysis, varicella-zoster virus, acyclovir, kidney injury


How to cite this article:
Chen KY, Shen CH, Wang SH, Wei KY, Huang YH. Varicella-zoster virus-induced rhabdomyolysis: A case report and literature review. J Med Sci 2020;40:141-4

How to cite this URL:
Chen KY, Shen CH, Wang SH, Wei KY, Huang YH. Varicella-zoster virus-induced rhabdomyolysis: A case report and literature review. J Med Sci [serial online] 2020 [cited 2020 Jul 12];40:141-4. Available from: http://www.jmedscindmc.com/text.asp?2020/40/3/141/268569




  Introduction Top


Rhabdomyolysis is not an uncommon syndrome encountered in clinical practice. It can be caused by trauma, excessive exercise, immobilization, drugs, toxins, thermal extremes, grand mal seizures, metabolic and electrolyte disorders, genetic disorders, and infections. The viral infections reported to have caused rhabdomyolysis worldwide include influenza virus, human immunodeficiency virus, cytomegalovirus, herpes simplex virus, Epstein–Barr virus, Coxsackievirus, West Nile virus, and dengue virus.[1],[2] A few cases of varicella-zoster virus (VZV)-induced rhabdomyolysis have been reported. Herein, we present the first case of VZV-induced rhabdomyolysis in Taiwan and reviewed VZV-induced rhabdomyolysis. We also discussed subsequent acute kidney injury (AKI) and provided possibly appropriate treatment.


  Case Report Top


A 63-year-old male presented to our hospital with a 1-week history of malaise, decreased appetite, and multiple painful erythematous skin rashes on his left anterior chest and shoulder. Cola-colored urine occurred 2 days after admission. The patient had no underlying disease, current medication treatment, or weight loss in the past year. His vital signs were normal without any signs of fever, tachycardia, or hypotension. Physical examination revealed moist oral mucosa and pustular papules and fluid-full vesicles at different stages of the development on a red base were noted at the right C5, C6, and C7 dermatomes. Serum antibody including IgG and IgM of VZV and Tzanck tests of the skin lesion performed by dermatologists revealed positive results. Blood analysis showed elevated creatine kinase (CK) (20,000 U/L), myoglobin (1389 ng/mL), aspartate aminotransferase (474 U/L), alanine transaminase (103 U/L), and lactate dehydrogenase (718 U/L) levels. Urinalysis revealed a positive occult blood reaction in the absence of red blood cells in a high-power field. The patient was diagnosed with rhabdomyolysis. Other blood tests showed the following: white blood cell count, 8570/μL; hemoglobin, 11.9 g/dL; platelet count, 176 × 10[3]/μL; C-reactive protein, 13.32 mg/dL; creatinine, 3.0 mg/dL; urea, 35 mg/dL; sodium, 134 mmol/L; potassium, 3.2 mmol/L; pH of the vein, 7.35; and bicarbonate, 24.8 mEq/L. His renal function was in the normal range 3 weeks prior to admission. His glomerular filtration rate on admission was 22 mL/min. The tests for influenza, HIV, cytomegalovirus, and Epstein–Barr virus were negative.

On admission, twice daily topical acyclovir was prescribed for the skin lesion. Extracellular volume with vigorous alkalized fluids was administered to maintain a urine output of up to 2 mL/kg/h. His CK levels slowly declined and returned to normal through day 13, but his renal function was not restored [Figure 1]. The skin lesion crusted by day 8 and scaled off gradually by day 13 [Figure 2]. An episode of hospital-acquired pneumonia with a deterioration of renal function developed after completing the treatment for rhabdomyolysis (day 19). However, the patient refused resuscitation and died several days later.
Figure 1: While the plasma creatine kinase (U/L) concentration slowly declined and was within the normal range until day 13, there was no reduction in plasma creatinine levels (Cr, mg/dL)

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Figure 2: The crusted skin lesion scaled off gradually by day 13

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  Discussion Top


The possible causes of rhabdomyolysis in this patient, including trauma, exhausting exercise, seizure, shock, or electrolyte imbalance, were excluded from the study. VZV infection was the most predisposing factor for rhabdomyolysis. The normalization of CK level was consistent with the convalescent phase of herpes zoster, strengthening the diagnosis of VZV-induced rhabdomyolysis.

Rhabdomyolysis caused by VZV is not common, especially when presented with herpes zoster. A review of reported cases of VZV-induced rhabdomyolysis in the English-language literature indicated that most presented with varicella and only one case presented with herpes zoster [Table 1].[3],[4],[5],[6],[7],[8],[9],[10],[11] The proposed mechanisms for infection-induced rhabdomyolysis include direct pathogen invasion of muscle, tissue hypoxia, low oxidative and glycolytic enzyme activity, activation of lysosomal enzymes, and mechanisms implicating endotoxins.[1] Seven of ten (70%) cases experienced AKI, which is higher than previous reports.[12] However, all of the reported cases had restored renal function except for our case.
Table 1: Characteristics of reported patients with varicella-zoster virus-induced rhabdomyolysis

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The indications for antiviral treatment in patients with herpes zoster include age ≥50 years, moderate or severe pain, severe rash, involvement of the face or eye, other complications of herpes zoster, and immunocompromised state. Oral or intravenous antiviral treatments are recommended.[13] In other reported cases, systemic acyclovir was administered. However, in our case, only topical acyclovir was applied to the visible skin lesion. Despite vigorous volume supplement with alkalized fluids, irreversible AKI still occurred. This may be attributed to the nature of rhabdomyolysis or inadequate infection control under topical antiviral treatment. Therefore, thorough and timely suppression or eradication of the pathogen may be the crucial strategy for the treatment of VZV-induced rhabdomyolysis. Further, research and evidence are needed to confirm this supposition.

Systemic acyclovir is a well-documented nephrotoxic agent. Aldehyde metabolites and crystal precipitation of acyclovir in renal tubules due to low solubility are factors that can result in acute tubular necrosis.[14] The nephrotoxicity of systemic acyclovir may have contributed to the higher prevalence of AKI in patients with VZV-induced rhabdomyolysis. In the case reported by Lee et al.,[4] renal function recovered after replacing acyclovir with antibodies against VZV. Another case with AKI had restored renal function after discontinuation of acyclovir.[6] Famciclovir and brivudine are reported to be safe substitutes for patients with acyclovir-induced nephrotoxicity.[15],[16]


  Conclusion Top


Rhabdomyolysis is considered a possible complication in patients with VZV infection that might be underdiagnosed, because CK levels are not routinely checked in clinical practice. To the best of our knowledge, this is the first case of VZV-induced rhabdomyolysis in Taiwan. The associated literature review highlighted that systemic antiviral treatment was suggested and that poor infection control could lead to irreversible kidney injury. The use of systemic acyclovir should be cautioned due to the complication of nephrotoxicity.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

The study was approved by Tri-Service General Hospital, National Defense Medical Center. Approval number: 2-107-05-099 & Approval Date: 2018/7/23.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Khan FY. Rhabdomyolysis: A review of the literature. Neth J Med 2009;67:272-83.  Back to cited text no. 1
    
2.
Huang SY, Lee IK, Liu JW, Kung CT, Wang L. Clinical features of and risk factors for rhabdomyolysis among adult patients with dengue virus infection. Am J Trop Med Hyg 2015;92:75-81.  Back to cited text no. 2
    
3.
Roberts DE. Varicella zoster infection, massive rhabdomyolysis, myoglobinuria, and renal failure. J Am Board Fam Pract 1995;8:52-4.  Back to cited text no. 3
    
4.
Lee S, Ito N, Inagaki T, Okajima T, Muramatsu A, Ito Y, et al. Fulminant varicella infection complicated with acute respiratory distress syndrome, and disseminated intravascular coagulation in an immunocompetent young adult. Intern Med 2004;43:1205-9.  Back to cited text no. 4
    
5.
Will MJ, Hecker RB, Wathen PI. Primary varicella-zoster-induced rhabdomyolysis. South Med J 1996;89:915-20.  Back to cited text no. 5
    
6.
Pirounaki M, Liatsos G, Elefsiniotis I, Skounakis M, Moulakakis A. Unusual onset of varicella zoster reactivation with meningoencephalitis, followed by rhabdomyolysis and renal failure in a young, immunocompetent patient. Scand J Infect Dis 2007;39:90-3.  Back to cited text no. 6
    
7.
Beby-Defaux A, Brabant S, Chatellier D, Bourgoin A, Robert R, Ruckes T, et al. Disseminated varicella with multiorgan failure in an immunocompetent adult. J Med Virol 2009;81:747-9.  Back to cited text no. 7
    
8.
Martínez-Martínez ML, Córdoba-Soriano JG, Calbo-Mayo J, Melero Bascones M. Varicella complicated by rhabdomyolysis. Actas Dermosifiliogr 2013;104:448-9.  Back to cited text no. 8
    
9.
Hollenstein U, Thalhammer F, Burgmann H. Disseminated intravascular coagulation (DIC) and rhabdomyolysis in fulminant varicella infection – Case report and review of the literature. Infection 1998;26:306-8.  Back to cited text no. 9
    
10.
Kim GU, Ku BD. Varicella zoster virus meningoencephalitis accompanied by rhabdomyolysis without skin eruption. Neurol Sci 2012;33:623-5.  Back to cited text no. 10
    
11.
Bhargava P, Bhutani C, Feng Q, Alavi A, Zhuang H. Varicella zoster infection associated rhabdomyolysis demonstrated by Tc-99m MDP imaging. Clin Nucl Med 2003;28:594-5.  Back to cited text no. 11
    
12.
Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine (Baltimore) 1982;61:141-52.  Back to cited text no. 12
    
13.
Cohen JI. Clinical practice: Herpes zoster. N Engl J Med 2013;369:255-63.  Back to cited text no. 13
    
14.
Gunness P, Aleksa K, Bend J, Koren G. Acyclovir-induced nephrotoxicity: The role of the acyclovir aldehyde metabolite. Transl Res 2011;158:290-301.  Back to cited text no. 14
    
15.
Htwe TH, Bergman S, Koirala J. Famciclovir substitution for patients with acyclovir-associated renal toxicity. J Infect 2008;57:266-8.  Back to cited text no. 15
    
16.
Aksoy B, Altaykan-Hapa A, Cengiz A, Mete Aksoy H, Atakan N. Disseminated cutaneous herpes zoster complicated by acyclovir nephrotoxicity and successfully treated with Brivudin. Eur J Dermatol 2010;20:247-8.  Back to cited text no. 16
    


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