Severe epidemic myalgia with an elevated level of serum interleukin-6 caused by human parechovirus type 3: a case report and brief review of the literature.

BACKGROUND: Human parechovirus type 3 (HPeV-3) is known to cause cold-like symptoms, diarrhea, or severe infections such as sepsis in infants and children. In adults, HPeV-3 infection is rarely diagnosed because the symptoms are generally mild and self-limiting; however, this infection has been linked to epidemic myalgia, regardless of the presence of underlying diseases, immunosuppression, or sex. CASE PRESENTATION: We describe an adult case of severe systemic myalgia and orchiodynia after infection with HPeV-3, which was transmitted from the child of the patient. Interleukin-6 (IL-6) level was found to be elevated in the patient's serum. CONCLUSION: Severe myalgia associated with HPeV-3 infection is potentially caused by an elevated serum level of IL-6.

Absent neutrophil alkaline phosphatase in the eosinophilia myalgia syndrome associated with L-tryptophan use.

The clinical constellation of leukocytosis, thrombocytosis, and low or absent stainable neutrophil alkaline phosphatase (NAP) is considered characteristic of chronic myelogenous leukemia (CML). CML with eosinophilic differentiation (eosinophilic leukemia) is well described, and leukemia and other clonal hematologic malignancies are associated with the syndrome of eosinophilic fasciitis. We describe leukocytosis, thrombocytosis, eosinophilia, mild basophilia, and absent stainable NAP, initially suggesting the diagnosis of CML in a patient with the eosinophilia myalgia syndrome associated with L-tryptophan use, a condition resembling eosinophilic fasciitis. Cytogenetic and molecular genetic studies failed to demonstrate a clonal proliferation of eosinophils.

Does fever or myalgia indicate reduced physical performance capacity in viral infections?

To study prospectively the effects of a brief febrile viral infection on parameters of muscle and circulatory function, seven volunteers were inoculated with sandfly fever virus and two control subjects with sterile saline. During but not after fever, decreased isometric and dynamic strength and endurance were recorded in various muscles. Impairment could not be explained by altered activities of relevant muscle enzymes in serum or muscle tissue or by altered muscle ultrastructure, but correlated with the severity of perceived symptoms, including myalgia, as rated by each subject. Compared to baseline, cardiac stroke volume was lower during and after fever. During fever, an increased heart rate maintained cardiac output at pre-inoculation values, whereas cardiac output fell in early convalescence. This decrease in cardiac output correlated significantly with the severity of fever. Thus, in brief viral infections a transient impairment of muscle performance capacity is correlated to subjective symptoms such as myalgia, rather than to fever, whereas a decreased cardiac output following such infections seems to be associated with the fever reaction.