To the Editors:
We read with interest the report by Ebbeson et al, of a pediatric case with rhabdomyolysis, acute renal failure, and compartment syndrome caused by parainfluenza type 1 infection. To date, only 5 cases of parainfluenza virus-induced rhabdomyolysis infection in children have been described in the literature, 2 attributed to parainfluenza type 1, 2 to parainfluenza type 2, and 1 to type 3.1–5 The latter had a fatal outcome. Of the 2 cases with rhabdomyolysis due to type 1, both were complicated with acute renal failure syndrome. On the contrary, our case is the first one with rhabdomyolysis due to parainfluenza type 1 virus, without renal dysfunction and having a favorable outcome.
A 10-year-old boy presented with complaints of severe muscle weakness and refusal to walk. His visited after 5 days of a sore throat, myalgias, and 2 days of profound muscle weakness. In the morning of admission, his urine was brown.
On physical examination, he had no edema, rashes, or lymphadenopathy. His joints were of normal appearance and mobility. Laboratory investigation revealed erythrocyte sedimentation rate, 37 mm/h; C-reactive protein, 3.2 mg/dL; hemoglobin, 129 g/L; red blood cells, 4.5 × 1012/L; white blood cells, 4.7 × 109/L (lymphocytes, 69%; neutrophils, 31%); and PLT, 358 × 109/L. Urinalysis revealed protein, 2+; blood, 1+; glucose negative; nitrite negative; leukocyte esterase negative; pH 5; ketone, 1+; urobilinogen negative, and bilirubin negative. Microscopic examination of the sediment revealed 1 to 2 white blood cells per high-power field but no red blood cells. Serum biochemical analysis revealed urea, 32 mg/dL; creatinine, 0.8 mg/dL; alkaline phosphatase, 161 U/L; alanine aminotransferase, 69 U/L; and aspartate aminotransferase, 71 U/L. The diagnosis of rhabdomyolysis was made by measuring the serum enzymes: CK, 7.563 U/L (normal, 10–70 U/L); CK-MB, 1 U/L (normal <10 U/L); and lactate LDH, 617 U/L (normal, 100–350 U/L). Additional laboratory work obtained indicated that initial blood and urine culture was negative and that he was seronegative for Epstein-Barr virus, herpes virus, cytomegalovirus, human immunodeficiency virus, respiratory syncytial virus, enterovirus, adenovirus, influenza A and B, Legionella, and Mycoplasma pneumoniae. Parainfluenza type 1 virus was identified by direct immunofluorescence antibody assay in the nasopharyngeal aspirate.
He was given initially symptomatic treatment with a large oral fluid intake to induce diuresis. There was no need for urine alkalization or diuretic use, as he had almost normal kidney function. CK values gradually decreased and reached its reference values 9 days later. His symptoms improved in 4 days and the urine was macroscopically clear and negative for protein and blood by dipstick. During the 1-year follow-up, he had febrile infections but no evidence for myositis.
To our knowledge, this is the first pediatric case reported with a parainfluenza type 1 induced rhabdomyolysis, which had favorable progression and outcome.
Zoe Dorothea Pana, MD, MSc
Athanasios Tragiannidis, MD, PhD
2nd University Pediatric Department AHEPA Hospital Thessaloniki, Greece
Stergianna Douma, MD, PhD
Karteridou Chrisa, MD, PhD
Pediatric Department General Hospital of Kilkis Kilkis, Greece
1. Zvolanek J. Benign acute childhood myositis associated with parainfluenza type 2 infection. Pediatr Infect Dis J
2. O'Connor JV, Iyer SK. Myoglobinuria associated with parainfluenza type 2 infection. N Y State J Med
3. Ueda K, Robbins DA, Iitaka K, et al. Fatal rhabdomyolysis associated with parainfluenza type 3 infection. Hiroshima J Med Sci
4. Ebbeson RL, De Kock MJ, Penny N, et al. Rhabdomyolysis, acute renal failure, and compartment syndrome in a child with parainfluenza type 1 infection. Pediatr Infect Dis J
5. Vrsalovic R, Tesovic G, Mise B. Rhabdomyolysis and acute renal failure in a child with para-influenza type 1 infection. Pediatr Nephrol