[HLA-DRB and -DQB allele contribution to narcolepsy susceptibility in Chinese patients with narcolepsy].

OBJECTIVES: To study the association of narcolepsy with HLA class II alleles in Chinese narcoleptic patients. METHODS: 31 patients with narcolepsy underwent brain computed tomography (CT) scan and magnetic resonance imaging (MRI) testing. All patients received a MSLT test following a routine night's sleep, and serological HLA typing for HLA DR(2). 21 patients received PCR-SSP HLA DR and DQ typing. RESULTS: All patients had sleepiness and cataplexy. There was no evidence for other functional or structural diseases. Sleep paralysis was elicited in 45%; hypnagogic hallucinations, in 61%. Mean sleep latency on MSLT was 2.1 min +/- 1.3 min; sleep-onset rapid eye movement (SOREM) occurred during 2/5 naps in 30 of 31 patients. The average number and latency of SOREM episodes were 4.2 +/- 1.0 episodes and 4.0 min +/- 1.8 min, respectively. All patients but one were HLA DR(2) positive and 86% were HLADRB(1) * 1501-HLADQB(1)*0602 positive. CONCLUSIONS: HLA DR(2) and HLADQw6 are markers for narcolepsy-cataplexy in Chinese.

[Influence of different sleep stages on respiratory regulation in normal humans].

OBJECTIVE: To understand the influence of different sleep stages on respiratory regulation in normal people. METHODS: We measured ventilation (VE) and occlusion pressure (P0.1) responses to hyperoxia hypercapnia (deltaVE/deltaPaCO2, deltaP0.1/deltaPaCO2) and isocapnic hypoxia (deltaVE/deltaSaO2 and deltaP0.1/deltaSaO2) in eleven non-snoring healthy people during wakefulness and during non-rapid eye movement (NREM) I + II, NREM III+IV, and rapid eye movement (REM) sleep stages. RESULTS: During NREM I + II and NREM III+IV, the normal subjects showed no significant decrease in P0.1, deltaP0.1/deltaSaO2 and deltaP0.1/deltaPaCO2 (P > 0.05), but deltaVE/ deltaSaO2 and deltaVE/ deltaPaCO2 decreased significantly (P < 0.05). During REM sleep, P0.1 maintained the level during wakefulness, but both hypoxic and hypercapnic responses decreased significantly (P < 0.05). CONCLUSIONS: Sleep has significant influence on respiratory regulation in normal people. The respiratory drive (P0.1) in both NREM and REM sleep stages could maintain the awake level due to an effective compensation to the increase of upper airway resistance. The P0.1 responses to both hypoxia and hypercapnia decrease only in REM sleep stage, which is in consistent with the clinical phenomenon that sleep disordered breathing occurs in REM in normal people.

[Acute respiratory failure and noninvasive positive pressure ventilation treatment in patients with severe acute respiratory syndrome].

OBJECTIVE: To describe the blood gas features and short-term outcomes of noninvasive positive pressure ventilation (NPPV) treatment for acute respiratory failure (ARF) in patients with severe acute respiratory syndrome (SARS) in this retrospective case series study sought. METHODS: Between April 22 and May 1, 2003, 120 clinically compatible SARS patients were admitted to a special hospital for infectious diseases in Beijing. All patients' records were reviewed. The outcome variables of NPPV therapy were analyzed. RESULTS: At 6 weeks of SARS onset, 25% (30/120) patients had respiratory failure with ALI/ARDS. 16 (53%) had hypercapnia (PaCO(2) > 45 mm Hg) during the course of SARS. 28 of them received NPPV therapy. One was intolerable to NPPV treatment. In the remaining 27 patients, NPPV was initiated 1.2 +/- 1.6 (0 - 10) days after onset of respiratory failure. One hour of NPPV therapy led to significant increases in PaO(2), SpO(2) and PaO(2)/FiO(2), and decrease in respiratory rate (all P < 0.01). 18 of the 27 patients were weaned successfully from NPPV. The mean duration of NPPV use was 10 +/- 6 (5 - 30) days. In addition to one patient who was intolerable to NPPV treatment, intubation was required in other 9 patients who initially had a favorable response to NPPV. Remarkable pulmonary barotrauma was noted in 7 of the 120 (5.8%) patients with SARS, among which 1 developed 2 days after intubation, and 6 occurred while the patients were on NPPV, the incidence being 22% (6/27) in patients using NPPV. The fatality rate at 13 weeks of SARS onset was 6.7% (8/120) in the patient cohort, and 26.7% (8/30) in the ALI/ARDS patients. No SARS occurred in medical staff taking care of NPPV patients. CONCLUSIONS: Some of the SARS patients with ALI/ARDS could experience CO(2) retention, which might be related to the impairment of respiratory muscles. It is proved to be feasible and appropriate for NPPV treatment of respiratory failure in SARS patients who were at high risk of intubation related complications. As there was a high incidence of remarkable barotrauma, a careful lung protective strategy is necessary during the administration of NPPV as well as invasive mechanical ventilation.

[Respiratory control during sleep and the development of nocturnal hypoxia in patients with obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: It is assumed that the reduced ventilatory control during sleep may be related to the nocturnal hypoxia in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) and daytime CO(2) retention. METHODS: Oxygen desaturation index (ODI(4)), sleep time spent when SaO(2) was below 90% (SIT(90)), the lowest SaO(2) (LSaO(2)) and the mean SaO(2) (MSaO(2)) during sleep were measured in 24 OSAHS patients with daytime PaCO(2) > or = 45 mm Hg and 39 with PaCO(2) < 45 mm Hg. Hypoxic (DeltaP(0.1)/DeltaSaO(2)) and hypercapnic (DeltaP(0.1)/DeltaPaCO(2)) responsiveness were measured in 11 eucapnic and 4 hypercapnic patients during wakefulness, NREM and REM sleep stages. RESULTS: Compared with the eucapnic patients, all the hypercapnic patients had more severe hypoxia during sleep (P < 0.05). Although both groups had similar chemical responsiveness during wakefulness, the hypercapnic patients had lower DeltaP(0.1)/DeltaSaO(2) and DeltaP(0.1)/DeltaPaCO(2) during both REM and NREM sleep (P < 0.05). CONCLUSION: The depressed chemical responsiveness during sleep plays an important role in the development of nocturnal hypoxia in OSAHS patients with daytime CO(2) retention.