Human parechovirus type 3 (HPeV3) can cause serious conditions in neonates, such as sepsis and encephalitis, but data for adults are lacking. The case of a pregnant woman with HPeV3 infection is reported herein. A 28-year-old woman at 36 weeks of pregnancy was admitted because of myalgia and muscle weakness. Her grip strength was 6.0kg for her right hand and 2.5kg for her left hand. The patient's symptoms, probably due to fasciitis and not myositis, improved gradually with conservative treatment, however labor pains with genital bleeding developed unexpectedly 3 days after admission. An obstetric consultation was obtained and a cesarean section was performed, with no complications. A real-time PCR assay for the detection of viral genomic ribonucleic acid against HPeV showed positive results for pharyngeal swabs, feces, and blood, and negative results for the placenta, umbilical cord, umbilical cord blood, amniotic fluid, and breast milk. The HPeV3 was genotyped by sequencing of the VP1 region. The woman made a full recovery and was discharged with her infant in a stable condition.
Valacyclovir, a prodrug of acyclovir, is the first-line treatment for herpes zoster, but the renal function must be monitored, because acyclovir is metabolized by the kidneys. We herein report a case of valacyclovir-induced neurotoxicity with no preceding renal impairment. An 88-year-old man was admitted because of an impaired consciousness after the administration of valacyclovir at 3,000 mg daily for herpes zoster on the chest. His consciousness level gradually improved with hydration and valacyclovir withdrawal. It was later confirmed that the level of acyclovir on admission had been 35.45 μg/mL in the blood and 36.45 μg/mL in the cerebrospinal fluid.
A 49-year-old woman with hepatic failure owing to alcoholic liver cirrhosis went into a deep coma. Her serum ammonia concentration was elevated at 436 μg/dl, and she had a generalized convulsion. Electroencephalogram and cerebrospinal fluid examination did not suggest encephalitis and epilepsy. Hyperammonemia may be occur because of generalized convulsions; however, it can spontaneously resolve if the convulsions are stopped. If hyperammonemia is the primary cause of generalized convulsion, the serum ammonia concentration will remain high until the cause is eliminated. However, despite stopping the convulsions, her ammonia concentration remained high. Diffusion-weighted brain MRI revealed symmetric high-intensity lesions in the frontal, temporal, and parietal cortices, especially the cingulate and insular cortices of the bilateral hemispheres. These findings were in line with those of previous reports that revealed symmetric cortical lesions, including cingulate and insula cortices that are distinctive in acute hyperammonemic encephalopathy. Therefore, we diagnosed that the coma, generalized convulsions, and abnormal brain MRI findings were caused by acute hyperammonemic encephalopathy.
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