Corticosteroid might reduce serum levels of pro-inflammatory cytokines in fulminant hepatitis: A case series.

AIM: There are no beneficial therapies except for emergency liver transplantation for acute liver failure (ALF). However, in Japan, which has a serious problem in the shortage of donor livers, therapies other than transplantation must be further investigated for patients with ALF. Pro-inflammatory cytokines promoting tissue destruction are predominant at an early phase of ALF. Corticosteroid (CS) influences monocyte/macrophage differentiation, by suppressing pro-inflammatory genes, indicating CS treatment might be beneficial during the early phase of ALF. Our aim was to elucidate the efficacy of CS pulse therapy in decreasing pro-inflammatory cytokine levels in the early stage of ALF. METHODS: Ten consecutive adult Japanese patients with fulminant hepatitis in the early stage, three treated with artificial liver support (ALS) and CS pulse therapy (ALS + CS group) and seven treated with ALS (ALS group), were enrolled. Clinical and biochemical data on admission were matched between the groups and retrospectively analyzed for serum concentrations of interleukin-6, tumor necrosis factor-α, and interleukin-1ß over a 2-week period. RESULTS: Mean cytokine levels on admission were not different between the two groups. Tumor necrosis factor-α was significantly reduced on day 7 in patients with CS. Serum levels of pro-inflammatory cytokines tended to be reduced in patients with CS compared to those without during the observation period, although the differences were not significant. CONCLUSIONS: It might be possible that introduction of CS pulse therapy in the early stage of ALF could reduce levels of pro-inflammatory cytokines, which might inhibit the cascade of progression of ALF.

Prompt prediction of successful defibrillation from 1-s ventricular fibrillation waveform in patients with out-of-hospital sudden cardiac arrest.

PURPOSE: Ventricular fibrillation (VF) is a common cardiac arrest rhythm that can be terminated by electrical defibrillation. During cardiopulmonary resuscitation, there is a strong need for a prompt and reliable predictor of successful defibrillation because myocardial damage can result from repeated futile defibrillation attempts. Continuous wavelet transform (CWT) provides excellent time and frequency resolution of signals. The purpose of this study was to evaluate whether features based on CWT could predict successful defibrillation. METHODS: VF electrocardiogram (ECG) waveforms stored in ambulance-located defibrillators were collected. Predefibrillation waveforms were divided into 1.0- or 5.12-s VF waveforms. Indices in frequency domain or nonlinear analysis were calculated on the 5.12-s waveform. Simultaneously, CWT was performed on the 1.0-s waveform, and total low-band (1-3 Hz), mid-band (3-10 Hz), and high-band (10-32 Hz) energy were calculated. RESULTS: In 152 patients with out-of-hospital cardiac arrest, a total of 233 ECG predefibrillation recordings, consisting of 164 unsuccessful and 69 successful episodes, were analyzed. Indices of frequency domain analysis (peak frequency, centroid frequency, and amplitude spectral area), nonlinear analysis (approximate entropy and Hurst exponent, detrended fluctuation analysis), and CWT analysis (mid-band and high-band energy) were significantly different between unsuccessful and successful episodes (P < 0.01 for all). However, logistic regression analysis showed that centroid frequency and total mid-band energy were effective predictors (P < 0.01 for both). CONCLUSIONS: Energy spectrum analysis based on CWT as short as a 1.0-s VF ECG waveform enables prompt and reliable prediction of successful defibrillation.

The influence of nicardipine-, nitroglycerin-, and prostaglandin E(1)-induced hypotension on cerebral pressure autoregulation in adult patients during propofol-fentanyl anesthesia.

UNLABELLED: We investigated the influence of drug-induced hypotension at a mean arterial pressure (MAP) of 60-70 mm Hg on cerebral pressure autoregulation in 45 adult patients during propofol-fentanyl anesthesia. Time-averaged mean blood flow velocity in the right middle cerebral artery (Vmca) was continuously measured at a PaCO(2) of 39-40 mm Hg by using transcranial Doppler ultrasonography. Hypotension was induced and maintained with a continuous infusion of nicardipine, nitroglycerin, or prostaglandin E(1). Cerebral autoregulation was tested by a slow continuous infusion of phenylephrine to induce an increase in MAP of 20-30 mm Hg. From the simultaneously recorded data of Vmca and MAP, cerebral vascular resistance (CVR) was calculated as MAP/Vmca. Furthermore, the index of autoregulation (IOR) was calculated as DeltaCVR/DeltaMAP, where DeltaCVR = change in CVR and DeltaMAP = change in MAP. The test was performed twice for each condition on each patient: baseline and hypotension. The IOR during baseline was similar among the groups. During nitroglycerin- and prostaglandin E(1)-induced hypotension, IOR was not different from baseline. In contrast, during nicardipine-induced hypotension, IOR significantly decreased compared with baseline (0.37 +/- 0.08 versus 0.83 +/- 0.07, P < 0.01). In conclusion, nicardipine, but not nitroglycerin or prostaglandin E(1), significantly attenuates cerebral pressure autoregulation during propofol-fentanyl anesthesia. IMPLICATIONS: Vasodilators may influence cerebral autoregulation by changing cerebral vascular tone. Nicardipine, but not nitroglycerin or prostaglandin E(1), attenuated cerebral pressure autoregulation in normal adult patients during propofol-fentanyl anesthesia.