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Título

Mitochondrial Myopathy Manifested After Zika Virus Viral Infection: Case Report

RESUMO

Case Report Female patient, 49 years old, report that for 5 years she has been progressing with urinary incontinence, sleep apnea using Continuous Positive Airway Pressure (CPAP), dysphagia, generalized fatigue, severe pain intensity in lower and upper limbs, mild hearing loss, decreased vocal tone and constipation. Activities likebrush the hair, going up and down stairs and walking short distances have become obstacles due to fatigue and pain. She said it all started after Zika virus infection in 2016 (confirmed by IgG antibody). She denied any similar family history. After analyzing the case, two possible differential diagnoses for the case were presented: mitochondrial myopathy and myasthenia gravis and, complementary exams were requested. The electroneuromyography performed in association with the repetitive stimulation test revealed the presence of some action potentials of the motor unit, from the examined proximal muscles, with myopathic characteristics. The lactic acid at rest was 5.8 mg / dl and lactic acid after 15 minutes of walking was 22.2 mg / dl showing an increase of 3.83 times. The acetylcholine anti-receptor antibody was not found. With the history and clinical examination associated with the complementary exams, it was possible to infer as a probable diagnosis of mitochondrial myopathy. Treatment with coenzyme Q10 at a daily dose of 800 mg was instituted and the patient presented a complete remission of the vast majority of symptoms using the coenzyme for 5 months. Discussion Just as infection by the Zika virus has been linked to the occurrence of neurological manifestations, other viruses have also been shown to have similar actions. Reports in the literature prove the relationship between arbovirus infection and the involvement of the nervous system. In the case report presented, the Zika virus was associated with a neurological manifestation different from those reported so far in the available literature, mitochondrial myopathy. The relationship can be established since even before the arbovirus infection, the patient denies any symptoms of mitochondrial dysfunction. However, it is not possible to say whether viral infection was the triggering factor of the dysfunction or the environmental activator of the mutation, with the appearance of clinical manifestations. Final comments Knowledge of the pathogenic mechanisms involved in Zika virus infection and its consequences for adults is still very limited.

Palavras Chave

Zika virus, neurological manifestations, mitochondrial myopathy.