Severe rhabdomyolysis caused by Plasmodium vivax malaria in the Brazilian Amazon

Severe rhabdomyolysis (creatine phosphokinase = 29,400 U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for infection with Plasmodium vivax. Treatment led to myoglobinuria and acute renal failure. After hemodialysis, the patient improved and a musc...

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Published inThe American journal of tropical medicine and hygiene Vol. 83; no. 2; pp. 271 - 273
Main Authors Siqueira, André M, Alexandre, Márcia A A, Mourão, Maria P G, Santos, Valquir S, Nagahashi-Marie, Suely K, Alecrim, Maria G C, Lacerda, Marcus V G
Format Journal Article
LanguageEnglish
Published United States The American Society of Tropical Medicine and Hygiene 05.08.2010
SeriesCase Report
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Abstract Severe rhabdomyolysis (creatine phosphokinase = 29,400 U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for infection with Plasmodium vivax. Treatment led to myoglobinuria and acute renal failure. After hemodialysis, the patient improved and a muscle biopsy specimen showed no myophosphorylase or deaminase deficiency. This case of rhabdomyolysis associated with P. vivax infection showed no comorbidities. The pathogenesis is still unclear. Although rhabdomyolysis is generally reported as a complication of Plasmodium falciparum malaria, leading to metabolic and renal complications,1 it has been reported in a patient with P. vivax infection with myoadenylate deaminase deficiency.2 We report a case in a patient without typical muscle enzyme deficiencies in which severe rhabdomyolysis developed while the patients was being treated with chloroquine for a confirmed P. vivax infection.
AbstractList Severe rhabdomyolysis (creatine phosphokinase = 29,400U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for infection with Plasmodium vivax . Treatment led to myoglobinuria and acute renal failure. After hemodialysis, the patient improved and a muscle biopsy specimen showed no myophosphorylase or deaminase deficiency. This case of rhabdomyolysis associated with P. vivax infection showed no comorbidities. The pathogenesis is still unclear. Although rhabdomyolysis is generally reported as a complication of Plasmodium falciparum malaria, leading to metabolic and renal complications,1 it has been reported in a patient with P. vivax infection with myoadenylate deaminase deficiency.2 We report a case in a patient without typical muscle enzyme deficiencies in which severe rhabdomyolysis developed while the patients was being treated with chloroquine for a confirmed P. vivax infection.
Severe rhabdomyolysis (creatine phosphokinase = 29,400 U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for infection with Plasmodium vivax. Treatment led to myoglobinuria and acute renal failure. After hemodialysis, the patient improved and a muscle biopsy specimen showed no myophosphorylase or deaminase deficiency. This case of rhabdomyolysis associated with P. vivax infection showed no comorbidities. The pathogenesis is still unclear. Although rhabdomyolysis is generally reported as a complication of Plasmodium falciparum malaria, leading to metabolic and renal complications,1 it has been reported in a patient with P. vivax infection with myoadenylate deaminase deficiency.2 We report a case in a patient without typical muscle enzyme deficiencies in which severe rhabdomyolysis developed while the patients was being treated with chloroquine for a confirmed P. vivax infection.
Severe rhabdomyolysis (creatine phosphokinase = 29,400U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for infection with Plasmodium vivax . Treatment led to myoglobinuria and acute renal failure. After hemodialysis, the patient improved and a muscle biopsy specimen showed no myophosphorylase or deaminase deficiency. This case of rhabdomyolysis associated with P. vivax infection showed no comorbidities. The pathogenesis is still unclear. Although rhabdomyolysis is generally reported as a complication of Plasmodium falciparum malaria, leading to metabolic and renal complications, 1 it has been reported in a patient with P. vivax infection with myoadenylate deaminase deficiency. 2 We report a case in a patient without typical muscle enzyme deficiencies in which severe rhabdomyolysis developed while the patients was being treated with chloroquine for a confirmed P. vivax infection.
Author Alecrim, Maria G C
Alexandre, Márcia A A
Nagahashi-Marie, Suely K
Lacerda, Marcus V G
Siqueira, André M
Santos, Valquir S
Mourão, Maria P G
AuthorAffiliation Tropical Medicine Foundation of Amazonas, Manaus, Amazonas, Brazil; University of the Amazonas State, Manaus, Amazonas, Brazil; Nilton Lins University Center, Manaus, Amazonas, Brazil; Faculdade de Medicina, Departamento de Neurologia, University of São Paulo, São Paulo, São Paulo, Brazil
AuthorAffiliation_xml – name: Tropical Medicine Foundation of Amazonas, Manaus, Amazonas, Brazil; University of the Amazonas State, Manaus, Amazonas, Brazil; Nilton Lins University Center, Manaus, Amazonas, Brazil; Faculdade de Medicina, Departamento de Neurologia, University of São Paulo, São Paulo, São Paulo, Brazil
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Snippet Severe rhabdomyolysis (creatine phosphokinase = 29,400 U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for...
Severe rhabdomyolysis (creatine phosphokinase = 29,400U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for...
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StartPage 271
SubjectTerms Adolescent
Animals
Brazil
Humans
Malaria, Vivax - complications
Malaria, Vivax - drug therapy
Male
Plasmodium vivax
Rhabdomyolysis - complications
Rhabdomyolysis - parasitology
Title Severe rhabdomyolysis caused by Plasmodium vivax malaria in the Brazilian Amazon
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