Use of a modified early warning score system to reduce the rate of in-hospital cardiac arrest.

BACKGROUND: Physiological abnormalities are often observed in patients prior to cardiac arrest. A modified early warning score (MEWS) system was introduced, which aims to detect early abnormalities by grading vital signs, and the present study investigated its usefulness. METHODS: Based on previous reports, the Chubu Tokushukai Hospital-customized MEWS was developed in Okinawa, Japan. The MEWS was calculated among all inpatients, and the rates of in-hospital cardiac arrests (IHCAs) were compared according to the score. The warning zone (WZ) was set as 7 or more because of the high possibility of acute deterioration. The MEWS system was introduced to provide immediate interventions for patients who reached the WZ in accordance with the callout algorithm. The numbers of IHCAs were compared between the 18 months before and after introduction of the MEWS system. RESULTS: The numbers of patients who experienced IHCA with each score were as follows: score of 6, 1 of 556 patients (0.18 %); score of 7, 4 of 289 (1.40 %); score of 8, 2 of 114 (1.75 %); and score of 9 or more, 2 of 56 (3.57 %). There was no significant difference in the mean age or sex between before and after the introduction of the MEWS system. The rate of IHCAs per 1000 admissions decreased significantly from 5.21 (79/15,170) to 2.05 (43/17,961) (p < 0.01). CONCLUSIONS: The Chubu Tokushukai Hospital-customized MEWS was applied to all inpatients, and the rate of IHCA decreased owing to the introduction of the system, as the system enables early interventions for patients who have the possibility of acute deterioration.

Acquired immune-deficiency syndrome with focal onset of Mycobacterium avium infection displaying a histological/genetic pattern of disseminated mycobacteria.

A 66-year-old man with human immunodeficiency virus (HIV) infection was admitted for treatment of Pneumocystis pneumonia. Upon admission, a tumor mass adjacent to the thoracic descending aorta was revealed on computed tomography. Histology revealed an exudative granuloma with histiocytes packed with numerous acid-fast bacilli. Mycobacterium avium was isolated from the tissue. A genetic examination of the isolates demonstrated this strain to be located in the cluster consisting of strains that cause systemic infection. The patient's baseline CD4+ cell count was 9/µL and the HIV-RNA viral load was 43,800 copies/mL. This case suggests the possibility of a localized onset of disseminated M. avium infection.

Antiallergic drugs, azelastine hydrochloride and epinastine hydrochloride, inhibit ongoing IgE secretion of rat IgE-producing hybridoma FE-3 cells.

We asked whether or not antiallergic drugs, azelastine hydrochloride and epinastine hydrochloride, inhibit IgE secretion from IgE-producing hybridoma FE-3 cells. FE-3 cells were cultured in the presence of azelastine or epinastine for 24 h, washed in phosphate-buffered saline , and then recultured in the medium in the absence of the antiallergic drugs. IgE levels in the cultured medium as well as those in the cytoplasm of FE-3 cells were measured by enzyme-linked immunosorbent assay. mRNA levels of Cepsilon, activation-induced cytidine deaminase (AID), XBP-1, and Bip were estimated by northern blot or reverse transcriptase polymerase chain reaction analysis. The activities of nuclear factor-kappa B (NF-kappaB) were analyzed by electrophoretic mobility shift assay (EMSA). Phosphorylation of I kappa B alpha (IkappaBalpha) was analyzed by immunoprecipitation followed by western blot analysis. IgE levels in the cultured medium and in the microsome fraction were lower on the treatment with 10(-5) M azelastine or epinastine than those on the treatment with vehicle. Cepsilon and AID mRNA levels were lower on the treatment with 10(-5) M azelastine than those on the treatment with vehicle, but were not decreased on the treatment with 10(-5) M epinastine. XBP-1 and Bip mRNA levels were not altered following treatment of the antiallergic drugs. Azelastine at 10(-5) M, but not epinastine, reduced DNA binding activity of NF-kappaB and also diminished IkappaBalpha phosphorylation, leading to sustaining IkappaBalpha protein levels. These findings suggest that azelastine exerts its inhibitory effect on the IgE secretion from FE-3 cells through the inhibition of Cepsilon mRNA expression, and that the inhibitory effect of epinastine is, at least in part, due to suppression of IgE synthesis at the post-transcriptional level.

Azelastine and suplatast shorten the distribution half-life of IgE in rats.

We aim to clarify whether suplatast and azelastine (anti-allergic drugs) can shorten the half-life of imnunoglobulin E (IgE) in the circulating blood. Thirty Wistar rats were divided into six groups. Distilled water or anti-allergic drugs were given orally for 6 days after the first sensitization. Two milligrams of monoclonal dinitrophenyl (DNP)-specific rat IgE was administered to the rats, which had been given suplatast or azelastine orally. The level of DNP-specific rat IgE in the serum was estimated by IgE-capture enzyme-linked immunosorbent assay, and the turnover of IgE was analyzed from its pharmacokinetic parameters. The elimination half-life of rat IgE was about 12 h irrespective of the sensitized state. The intercompartmental rate constants (Kct and Ktc) in the suplatast-administered or azelastine-administered group were larger than those of the distilled water-administered group under non-sensitized conditions. These findings suggested that the anti-allergic drugs used in the present study facilitated the excretion of IgE from the circulation in rats.