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CASE REPORT Table of Contents  
Ahead of print publication
Rhabdomyolysis in hepatitis A: Uncommon complication of a common infection


 Department of General Medicine, JSS Medical College and Hospital, JSSAHER, Mysore, Karnataka, India

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Date of Submission06-Dec-2020
Date of Acceptance07-Jan-2021
Date of Web Publication12-Jan-2022
 

  Abstract 


Hepatitis A is usually a mild self-limiting infection of liver. Rhabdomyolysis complicating acute nonfulminant hepatitis A is exceedingly rare. We present here a case report of 19-year-old young male with hepatitis A, who developed rhabdomyolysis with acute renal failure. He underwent dialysis and made a complete recovery with normalization of laboratory tests.

Keywords: Acute renal failure, hepatitis A virus, hepatitis A, rhabdomyolysis


How to cite this URL:
Babu M S, Ashoka H G, Adusumilli A. Rhabdomyolysis in hepatitis A: Uncommon complication of a common infection. APIK J Int Med [Epub ahead of print] [cited 2022 Sep 25]. Available from: https://www.ajim.in/preprintarticle.asp?id=335654





  Introduction Top


Hepatitis A is an inflammatory liver disease caused by infection with the hepatitis A virus (HAV). HAV infection occurs worldwide, either sporadically or in epidemic outbreaks. In general, the prognosis is excellent. Rare complications in hepatitis A include acute renal failure, interstitial nephritis, pancreatitis, red blood cell aplasia, agranulocytosis, bone marrow aplasia, transient heart block, Guillain-Barré syndrome, acute arthritis, Still disease, lupus-like syndrome and Sjogren syndrome. The exact mechanism for acute renal failure in hepatitis A is uncertain but glomerulonephritis, acute tubular necrosis and hepatorenal syndrome have been postulated. We report here a rare case of hepatitis A with acute renal failure resulting from rhabdomyolysis.


  Case Report Top


A 19-year-old male presented with a history of fever, vomiting, and loose stools for 1 day followed few days later by yellowish discoloration of eyes and urine with increasing pain in the thighs and weakness of both lower limbs to an extent of being restricted to bed. The patient was anuric for 16 h before admission. On examination, the patient was conscious, coherent, afebrile, with deep icterus, mild pallor, and no pedal edema. Abdomen examination showed mild hepatomegaly. Cardiac and respiratory system examination was unremarkable. Central nervous system examination showed bilateral lower limb weakness Grade 1/5 with diminished reflexes and bilateral flexor plantar response. At admission, investigations revealed hemoglobin percent – 8 g%, total leukocyte count – 12,840/cc, platelets – 0.46l/cc, peripheral blood smear showed normocytic normochromic anemia with neutrophilicleucocytosis, and thrombocytopenia. Blood urea – 227 mg%, serum creatinine – 5.7 mg%, serum potassium – 6.6 mEq/l, total bilirubin – 33 mg%, direct bilirubin – 29.8 mg%, total protein – 4.6 g%, serum albumin – 2.8 g%, aspartate aminotransferase – 1561u/l, alanine aminotransferase – 435u/l, and creatinine kinase (CK)-NAC-20,000 U/LLDH – 1607/U/L. Ultrasonography abdomen showed raised cortical echoes of bilateral kidneys and mild hepatomegaly. Test for hepatitis B surface antigen, hepatitis C virus, hepatitis E virus, HIV, dengue, leptospira, rickettsia, malaria, IgM antibodies for herpes simplex, toxoplasma, rubella, and cytomegalovirus was negative; ANA – negative. Blood culture showed no significant bacterial growth. IgM Elisa for antihepatitis A virus (HAV) was positive; Kit name – DIA. PRO; OD of the test sample 2.6; cutoff value 0.324; S/Co of the sample 8.0; Interpretation: S/Co the sample <0.8 negative, 0.8–1.2 equivocal, >1.2 positive. The patient received PRBCs transfusion and underwent dialysis. There was clinical improvement over days with decreasing pain, improvement of power in the lower limbs, and normalization of renal function test, liver function test, CKNAC, and complete blood count parameters.


  Discussion Top


Rhabdomyolysis complicating acute nonfulminant hepatitis A is exceedingly rare. Very few case reports of rhabdomyolysis associated with HAV infection have been reported in the literature.[1] The proposed mechanisms for infection-induced rhabdomyolysis include tissue hypoxia, direct bacterial invasion of muscle, low oxidative and glycolytic enzyme activity, activation of lysosomal enzymes, and mechanisms implicating endotoxins.[2] Investigations in rhabdomyolysis commonly show an elevation in the acute phase reactants, white blood cell count, CK, and other muscle enzymes with a decline in these values in 3–5 days of muscle injury. Serum CK levels are usually elevated to at least five times the upper limit of normal but range from approximately 1500 to over 100,000 IU/L. Acute renal failure (ARF) complicating acute nonfulminantviral hepatitis A is rare although it is not an uncommon association in cases of fulminant hepatitis with massive hepatic necrosis due to hepatitis A.[3] The mechanism of HAV-associated ARF is uncertain. Several possible mechanisms have been considered which include prerenal failure secondary to dehydration caused by nausea, vomiting and diarrhea, immune complex-mediated nephritis, endotoxemia with systemic hypotension, renal vasoconstriction, release of cytokines and activation of neutrophils, and a direct cytopathic effect of HAV have been postulated. Factors favoring development of ARF following rhabdomyolysis include hypovolemia, acidosis or aciduria, tubular obstruction, and the nephrotoxic effects of myoglobin. Treatment includes prompt and aggressive fluid resuscitation, correction of electrolyte and metabolic abnormalities, and dialysis. Dialysis is considered for patients with rising or elevated potassium level, persistent acidosis, or oliguric renal failure with fluid overload. Our patient recovered with normalization of blood investigations in 1 month after initial hospitalization. To conclude, rhabdomyolysis with ARF is an uncommon complication of hepatitis A. When treated early and aggressively, rhabdomyolysis with ARF in hepatitis A has a good prognosis with complete recovery of renal function.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their 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.

Acknowledgment

Dr. Deepak Suvarna, Associate Professor of Gastroenterology, JSS Medical College and Hospital, JSSAHER, Mysuru, Karnataka, India.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ann SH, An GH, Lee SY, Oak JH, Moon HI, Moon SK, et al. A case of rhabdomyolysis during hospitalization for acute hepatitis A. Korean J Hepatol 2009;15:85-9.  Back to cited text no. 1
    
2.
Nachbaur K, König P, Rumpelt HJ, Schobel B, Lhotta K, Vogel W. Acute renal failure complicating non-fulminant hepatitis A. Clin Nephrol 1996;45:398-400.  Back to cited text no. 2
    
3.
Blanco JR, Zabalza M, Salcedo J, Echeverria L, García A, Vallejo M. Rhabdomyolysis of infectious and non-infectious causes. South Med J 2002;95:542-4.  Back to cited text no. 3
    

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Correspondence Address:
M Suresh Babu,
E and F Block, Kuvempunagar, Mysore - 570 023, Karnataka
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_98_20





 

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Abstract
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