Journal of Infection (I99O) 21, 3o3-3o4
CASE REPORT Influenza A and rhabdomyolysis W i l l i a m Foulkes,* Jeremy Rees and Caroline S e w r y t
Department of Medicine and t Jerry Lewis Muscle Research Centre, Royal Postgraduate Medical School, Hammersmith Hospital, Du Cane Rd, London WI2 oNN, U.K. Accepted for publication IO May 199o Summary A case of influenza A H3N ~ resulting in unusually severe rhabdomyolysis and myoglobinuria is described. Although a rare complication of viral infection, prompt treatment with intravenous fluids can prevent the serious complications which may follow.
Introduction Influenza A caused m u c h ill health between November 1989 and early January 199o. Influenza A/England/427/88 H~ N 2 was responsible for the majority of cases reported during the outbreak. We report here a case of influenza A H 3N 2 occurring during the recent outbreak which resulted in unusually severe rhabdomyolysis and myoglobinuria.
Case report A 31-year-old West Indian woman presented to the Casualty Department with a I days' history of passing ' black urine '. This had never occurred before. She had been feeling unwell for the previous 5 days with fever, chills and myalgia. She had noticed generalised muscle weakness, most marked in the limb girdle regions, for 3 days before admission but it improved during the following 2 days. She had been under investigation for iron deficiency until January I989 but otherwise had an unremarkable past medical history. On examination she had a temperature of 37"5°C, mild pharyngeal inflammation and moderate proximal muscle weakness, especially of the pelvic girdle. T h e rest of the examination was normal. Urinalysis with clinistix revealed protein + + + + and blood + + + . Microscopy showed proteinaceous debris but no red blood cells. Myoglobinuria was determined by spectrophotometry and later confirmed by the Regional Protein Reference Unit, Queen Mary's University Hospital, Roehampton. Other investigations showed haemoglobin lO-6 g/dl, mean cell volume 77fl, no evidence of haemolysis on the blood film and normal haptoglobin and glucose-6-phosphate dehydrogenase values. She did not have sickle cell trait. Aspartate transaminase (AST) was 2772 IU/1 and creatine kinase (CK) > 1o0000 IU/1 * Address correspondence to: Dr William Foulkes, H u m a n Immunogenetics Laboratory, Imperial Cancer Research Fund, Lincoln's Inn Fields, London WC2A 3PX, U.K.
oi63-4453/9o/o6o3o3+o2 $oz.oo/o 12
© I99o T h e British Society for the Study of Infection JIN21
304
W. FOULKES E T A L .
(normal < 200 IU/1). A u t o - a n t i b o d y screen, including antiskeletal muscle antibody, was negative. C-reactive protein was 3o mg/1 (normal < 5 mg/1). A biopsy from the left quadriceps muscle I day after admission s h o w e d disruption of myofibrils and an increase in acid phosphatase activity, consistent with, b u t not diagnostic of, myositis. In order to exclude other causes of rhabdomyolysis, a repeat biopsy was taken 3 weeks later w h e n the patient's m u s c u l a r strength had returned to normal. T h i s showed positive fetal m y o s i n staining and a high level of R N A expression, confirming considerable regeneration. E l e c t r o m y o g r a p h y p e r f o r m e d within 5 days o f admission d e m o n s t r a t e d classical features of polymyositis. Paired sera taken 8 days apart revealed recent seroconversion to influenza A. F u r t h e r studies at the Virus Reference L a b o r a t o r y , Central Public H e a l t h L a b o r a t o r y Service ( P H L S ) Colindale, confirmed a rising haemagglutination inhibition titre with 8 A D antigen f r o m < IO to 320 for influenza A H 3 N 2. T h e patient m a d e an uneventful recovery after treatment with plentiful intravenous fluids and mild analgesics. She was discharged from hospital after 5 days. T h r e e weeks later the C K had fallen to 81o I U / 1 and the A S T had r e t u r n e d to the normal range.
Discussion
Influenza A is a rare cause o f myositis, b u t a n u m b e r of well d o c u m e n t e d , b i o p s y - p r o v e n cases have been reported. T M W h a t is especially unusual a b o u t o u r patient is the m a n n e r in which she presented. Nearly all the cases previously described complained mainly ofmyalgia, the m y o g l o b i n u r i a usually being r e p o r t e d only after the patient had sought medical attention. In this case the history of myalgia was elicited only after direct questioning. As far as it is possible to k n o w from voluntary reporting, it seems that this was the only case o f influenzal polymyositis resulting in m y o g l o b i n u r i a n o t e d during the recent outbreak [S. Young, ( P H L S ) personal communication]. It is a rare complication o f viral infection b u t early identification and p r o m p t treatment with intravenous fluids can prevent serious complications following severe r h a b d o m y o l y s i s and myoglobinuria. (We would like to thank Dr H. J. F. Hodgson for allowing us to report this case and Dr R. P. F. Watkins for helpful discussions. The muscle biopsies were performed by Dr N. H. Thomas. Dr Sewry is supported by the Muscular Dystrophy Group of Great Britain.) References I. Minow RA, Gorbach S, Johnson BL et al. Myoglobinuria associated with influenza A infection. Ann lntern Med I974; 8o: 359-361. 2. Di Bona FJ, Morens DM. Rhabdomyolysis associated with influenza A. J Paediatr I977; 9 r : 943-945. 3. Cunningham E, Kohli R, Rocco CV. Influenza-associated myoglobinuric renal failure. f f A M A r979; 242: 2428-2429. 4- Gamboa ET, Eastwood AB, Hays AP et aL Isolation of influenza virus from muscle in myoglobinuric polymyositis. Neurology 1979; 29: I323-I335.
CASE REPORT Influenza A and rhabdomyolysis W i l l i a m Foulkes,* Jeremy Rees and Caroline S e w r y t
Department of Medicine and t Jerry Lewis Muscle Research Centre, Royal Postgraduate Medical School, Hammersmith Hospital, Du Cane Rd, London WI2 oNN, U.K. Accepted for publication IO May 199o Summary A case of influenza A H3N ~ resulting in unusually severe rhabdomyolysis and myoglobinuria is described. Although a rare complication of viral infection, prompt treatment with intravenous fluids can prevent the serious complications which may follow.
Introduction Influenza A caused m u c h ill health between November 1989 and early January 199o. Influenza A/England/427/88 H~ N 2 was responsible for the majority of cases reported during the outbreak. We report here a case of influenza A H 3N 2 occurring during the recent outbreak which resulted in unusually severe rhabdomyolysis and myoglobinuria.
Case report A 31-year-old West Indian woman presented to the Casualty Department with a I days' history of passing ' black urine '. This had never occurred before. She had been feeling unwell for the previous 5 days with fever, chills and myalgia. She had noticed generalised muscle weakness, most marked in the limb girdle regions, for 3 days before admission but it improved during the following 2 days. She had been under investigation for iron deficiency until January I989 but otherwise had an unremarkable past medical history. On examination she had a temperature of 37"5°C, mild pharyngeal inflammation and moderate proximal muscle weakness, especially of the pelvic girdle. T h e rest of the examination was normal. Urinalysis with clinistix revealed protein + + + + and blood + + + . Microscopy showed proteinaceous debris but no red blood cells. Myoglobinuria was determined by spectrophotometry and later confirmed by the Regional Protein Reference Unit, Queen Mary's University Hospital, Roehampton. Other investigations showed haemoglobin lO-6 g/dl, mean cell volume 77fl, no evidence of haemolysis on the blood film and normal haptoglobin and glucose-6-phosphate dehydrogenase values. She did not have sickle cell trait. Aspartate transaminase (AST) was 2772 IU/1 and creatine kinase (CK) > 1o0000 IU/1 * Address correspondence to: Dr William Foulkes, H u m a n Immunogenetics Laboratory, Imperial Cancer Research Fund, Lincoln's Inn Fields, London WC2A 3PX, U.K.
oi63-4453/9o/o6o3o3+o2 $oz.oo/o 12
© I99o T h e British Society for the Study of Infection JIN21
304
W. FOULKES E T A L .
(normal < 200 IU/1). A u t o - a n t i b o d y screen, including antiskeletal muscle antibody, was negative. C-reactive protein was 3o mg/1 (normal < 5 mg/1). A biopsy from the left quadriceps muscle I day after admission s h o w e d disruption of myofibrils and an increase in acid phosphatase activity, consistent with, b u t not diagnostic of, myositis. In order to exclude other causes of rhabdomyolysis, a repeat biopsy was taken 3 weeks later w h e n the patient's m u s c u l a r strength had returned to normal. T h i s showed positive fetal m y o s i n staining and a high level of R N A expression, confirming considerable regeneration. E l e c t r o m y o g r a p h y p e r f o r m e d within 5 days o f admission d e m o n s t r a t e d classical features of polymyositis. Paired sera taken 8 days apart revealed recent seroconversion to influenza A. F u r t h e r studies at the Virus Reference L a b o r a t o r y , Central Public H e a l t h L a b o r a t o r y Service ( P H L S ) Colindale, confirmed a rising haemagglutination inhibition titre with 8 A D antigen f r o m < IO to 320 for influenza A H 3 N 2. T h e patient m a d e an uneventful recovery after treatment with plentiful intravenous fluids and mild analgesics. She was discharged from hospital after 5 days. T h r e e weeks later the C K had fallen to 81o I U / 1 and the A S T had r e t u r n e d to the normal range.
Discussion
Influenza A is a rare cause o f myositis, b u t a n u m b e r of well d o c u m e n t e d , b i o p s y - p r o v e n cases have been reported. T M W h a t is especially unusual a b o u t o u r patient is the m a n n e r in which she presented. Nearly all the cases previously described complained mainly ofmyalgia, the m y o g l o b i n u r i a usually being r e p o r t e d only after the patient had sought medical attention. In this case the history of myalgia was elicited only after direct questioning. As far as it is possible to k n o w from voluntary reporting, it seems that this was the only case o f influenzal polymyositis resulting in m y o g l o b i n u r i a n o t e d during the recent outbreak [S. Young, ( P H L S ) personal communication]. It is a rare complication o f viral infection b u t early identification and p r o m p t treatment with intravenous fluids can prevent serious complications following severe r h a b d o m y o l y s i s and myoglobinuria. (We would like to thank Dr H. J. F. Hodgson for allowing us to report this case and Dr R. P. F. Watkins for helpful discussions. The muscle biopsies were performed by Dr N. H. Thomas. Dr Sewry is supported by the Muscular Dystrophy Group of Great Britain.) References I. Minow RA, Gorbach S, Johnson BL et al. Myoglobinuria associated with influenza A infection. Ann lntern Med I974; 8o: 359-361. 2. Di Bona FJ, Morens DM. Rhabdomyolysis associated with influenza A. J Paediatr I977; 9 r : 943-945. 3. Cunningham E, Kohli R, Rocco CV. Influenza-associated myoglobinuric renal failure. f f A M A r979; 242: 2428-2429. 4- Gamboa ET, Eastwood AB, Hays AP et aL Isolation of influenza virus from muscle in myoglobinuric polymyositis. Neurology 1979; 29: I323-I335.
