Objective/Background : This study was performed to clarify whether sleep disordered breathing (SDB) contributes to increases in sympathetic nerve (SN) activity during sleep and the development of hypertension.
Patients/Methods : Polysomnography and pulse rate variability (PRV) analysis using a photoplethysmograph were performed simultaneously in 153 male subjects and evaluated by instantaneous time-frequency analysis using the complex demodulation method. Parasympathetic nerve (PN) activity and SN activity were assessed by the amplitude of high-frequency (HF) and the ratio of low-frequency (LF) to HF amplitude (LF/HF ratio), respectively. Blood pressure (BP) before going to bed and early in the morning were measured in all subjects.
Results : The subjects were classified according to the severity of SDB as normal (apnea hypopnea index (AHI) <5 events/h, n＝99), mild SDB (5≤AHI<15 events/h, n＝28), and moderate-to-severe SDB groups (AHI≥15 events/h, n＝26). The mean LF/HF ratio was higher according to sleep stage in the order REM sleep>light sleep>slow wave sleep in all groups. The mean LF/HF ratio in each sleep stage and BP both before going to bed and early in the morning were significantly higher in the moderate-to-severe SDB group compared with normal subjects and the mild SDB group and showed a significant correlation with arousal index. The multiple regression model showed that independent associations for the systolic BP early in the morning were age, BMI, cumulative ％ time with SpO₂<90％ (CT90) as an index of hypoxemia during sleep, and decreased sleep efficiency.
Conclusion : The findings of this study suggested that the frequent arousal due to SDB may contribute to the increased SN activity, and that hypoxemia during sleep and sleep disturbance in addition to age and obesity may be associated with increased SBP early in the morning in moderate-to-severe SDB.

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Hemophagocytic lymphohistiocytosis (HLH) is a rare, life-threatening hyperinflammatory syndrome that is characterized by uncontrolled activation and proliferation of proinflammatory cytokines. We describe the case of a 7-day-old female neonate with an HLH-like illness associated with coxsackie virus B2 (CVB2) infection. Her perinatal history was normal. She presented with fever and was unwell on the 7th post-natal day. Laboratory examinations revealed typical abnormalities of disseminated intravascular coagulation (DIC) ; thrombocytopenia ; and increased levels of serum ferritin, aspartate aminotransferase, and lactate dehydrogenase. Her symptoms and laboratory data partially fulfilled the proposed HLH diagnosis criteria (2004), and we initiated treatment for DIC and intravenous immunoglobulin for the HLH-like illness. Her symptoms and laboratory parameters gradually improved, and she was discharged at the age of 30 days without any sequelae. Her development and growth were normal at the age of 1 year. Subsequently, virological analyses of the patient's serum and throat swab detected the presence of CVB2 using the PCR method. Thus, we arrived at a diagnosis of an HLH-like illness caused by CVB2 infection, which is only the 2nd case report to the best of our knowledge. CVB2 is an important virus that can cause hypercytokinemia that sometimes leads to HLH, requiring specific therapy. HLH is a potentially lethal childhood illness ; therefore, early diagnosis and timely treatment by pediatricians are crucial.

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