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Yasuyuki Goto

Publications and source records attributed to Yasuyuki Goto.

At least 19 recordsLinked to original sources
PubMed2006

Bioinformatic identification of tandem repeat antigens of the Leishmania donovani complex.

With large amounts of parasite gene sequence available, additional bioinformatic tools to screen these sequences for identifying genes encoding antigens are needed. Proteins containing tandem repeat (TR) domains are often B-cell antigens, and antibody responses toward TR domains of the proteins are dominant in human infected with certain parasites. We hypothesized that antigens of serological significance could be identified with a search for TR domains. Here we show the result of bioinformatic screening of the gene sequence database of the parasitic protozoan Leishmania infantum. Of 8,191 genes scanned, 64 genes contained TR domains. Of the 64 genes, 22 encoded previously characterized antigens; the remaining 42 genes were previously uncharacterized. By using sera from Sudanese visceral leishmaniasis patients, we confirmed that the TR domains of LinJ11.0070, LinJ25.1100, LinJ27.0400, and LinJ29.0110, which were from the 42 uncharacterized proteins, are also antigenic. The results suggest the validity of this approach for identifying leishmanial antigens of serological significance.

Animals↗
PubMed2006

Grb2-associated binder 1 polymorphism was associated with the risk of Helicobactor pylori infection and gastric atrophy.

BACKGROUND: Various single nucleotide polymorphisms (SNPs) have explained the association between Helicobacter pylori (H. pylori) and gastric atrophy and cancer. This study investigated the associations of Grb2 associated binder 1 (Gab1) polymorphism and the combination of PTPN11 gene encoding src homology 2 domain-containing protein tyrosine phosphatase-2 (SHP2) and Gab1 gene with gastric cancer and gastric atrophy among H. pylori seropositive subjects. METHODS: A single nucleotide polymorphism at intron 2 of Gab1 (JST164345) was examined for 454 Japanese health checkup examinees (126 males and 328 females) aged 35 to 85 without a history of gastric cancer and 202 gastric cancer patients (134 males and 68 females) aged 33 to 94 with pathologically confirmed diagnosis of gastric adenocarcinoma. RESULTS: The decreased OR of the Gab1 A/A for H. pylori seropositivity was 0.25 (95% confidence interval (CI): 0.08-0.71). Among seropositive healthy controls, the OR of the Gab1 G/A+A/A for gastric atrophy was significant (OR=1.95, 95% CI: 1.12 -3.40). Seropositive individuals with PTPN11 G/G and Gab1 G/A+A/A demonstrated the highest risk of gastric atrophy with significance (OR=3.49, 95% CI: 1.54-7.90) relative to PTPN11 G/A+A/A and Gab1 G/G, the lowest risk combination, as a reference. However, the gene-gene interaction between PTPN11 and Gab1 was not observed (OR=1.39, 95% CI: 0.41-4.66). Compared to gastric cancer case, the Gab1 did not influence the step of atrophy/metaplasia-gastric cancer sequence. CONCLUSIONS: This study represents that the Gab1 polymorphism was associated with the low risk of H. pylori infection and the high risk of gastric atrophy among seropositive healthy controls, and that seropositive individuals with PTPN11 G/G and Gab1 G/A+G/G were associated with the greatest risk of gastric atrophy. These findings require confirmation in much larger studies.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Inducible nitric oxide synthase polymorphism is associated with the increased risk of differentiated gastric cancer in a Japanese population.

AIM: To examine the association of inducible nitric oxide synthase (iNOS) C150T polymorphism with gastric cancer, as well as with gastric atrophy and H pylori seropositivity. METHODS: A single nucleotide polymorphism of iNOS C150T was examined for 454 Japanese health checkup examinees (126 males and 328 females) aged 35 to 85 years without a history of cancer and 202 gastric cancer patients (134 males and 68 females) aged 33 to 94 years with pathologically confirmed diagnosis of gastric adenocarcinoma. RESULTS: The iNOS C150T polymorphism was not associated with gastric atrophy or with H pylori seropositivity. The odds ratio (OR) of the C/T + T/T for gastric cancer was increased without statistical significance (OR = 1.19, 95% confidence interval (CI): 0.68-2.08). In the differentiated subgroup (n = 113), however, the OR of the C/T genotype for gastric cancer was significant (OR = 2.02, 95% CI: 1.04-3.92) relative to the C/C genotype. In addition, considering the location of gastric cancer (n = 105), there were significant differences between the controls and non-cardia group with the OR of 2.13 (95% CI: 1.08-4.18) for C/T and 1.94 (95% CI: 1.00-3.78) for C/T + T/T. CONCLUSION: The iNOS C150T polymorphism is associated with the risk of H pylori-related gastric cancer in a Japanese population. This polymorphism may play an important role in increasing the risk of gastric cancer in Asian countires with the highest rates of gastric cancer.

Adult↗
PubMed2006

Eradication rate of Helicobacter pylori according to genotypes of CYP2C19, IL-1B, and TNF-A.

BACKGROUND: Lansoprazole, amoxicillin, and clarithromycin are commonly used drugs for eradication of Helicobacter pylori (H. pylori). A few studies reported that the eradication rate was influenced by the functional polymorphism of CYP2C19, whose product metabolizes proton pomp inhibitors including lansoprazole. METHODS: This study examined the eradication rate among 67 participants in the polymorphism study who visited Daiko Medical Center, Nagoya University from July 2004 to October 2005. The participants aged 20 to 69 years were classified into three group according to CYP2C19 genotype; rapid metabolizers (RM) with *1*1 genotype, intermediate metabolizers (IM) with *1*2 or *1*3 genotype, and poor metabolizers (PM) with *2*2, *2*3, or *3*3 genotype. For the genotype classification, G681A (681G for *1 and 681A for *2) and G636A (636G for *1 and 636A for *3) were genotyped by PCR with confronting two-pair primers (PCR-CTPP). They were also genotyped for IL-1B T-31C and TNF-A T-1031C by a duplex PCR-CTPP. RESULTS: The eradication rate was 70.0% for RM, 93.9% for IM, and 85.7% for PM. The difference in the rate between RM and IM+PM was statistically significant (p=0.025). The eradication rate was highest for those with IL-1B -31CC; the p value was marginal among the whole subjects (chi2=3.78, p=0.05) and not significant among the RM group (chi2=1.60, p=0.21). The genotypes of TNF-A T-1031C had no associations with the eradication rate. But among the RM group, the odd ratio (OR) of the TNF-A CT for the eradication rate relative to TT was marginally reduced (OR=0.05, 95% confidence interval, 0.002-1.19). CONCLUSIONS: The present study confirmed the low eradication rate for RM. The reproduced finding provides evidence that the CYP2C19 genotype is useful to predict the success of the treatment. For the RM group, alternative regimens expected to be with a higher eradication rate will be recommended, especially to those with the TNF-A -1031C allele.

Journal Article↗
PubMed2006

Genetic factors involved in the development of Helicobacter pylori-related gastric cancer.

Developmental process to gastric cancer by Helicobacter pylori infection consists of three steps: (1) H. pylori infection; (2) gastric atrophy development; and (3) carcinogenesis. In each step, genetic traits may influence the process, interacting with lifestyle. In the step of H. pylori infection, two lines of genetic polymorphisms were assumed: one influencing gastric acid inhibition interacting with smoking, and the other concerning innate immune response attenuation. The former includes functional polymorphisms of IL-1B (C-31T or tightly linked T-511C), and TNF-A (T-1031C and C-857T), and the latter possibly includes NQO1 C609T. In the step to gastric atrophy, polymorphisms pertaining to the signal transduction from cytotoxin-associated gene A (PTPN11 A/G at intron 3) and to T-cell responses (IL-2 T-330G and IL-13 C-1111T) were hypothesized. There are a limited number of epidemiological genotype studies on the final step of literal carcinogenesis, potentially interacting with smoking, a low vegetable and fruit intake, and salty foods, the well-documented risk factors. In past case-control studies on the associations between genotype and gastric cancer risk, the cases consisted of H. pylori-related and unrelated gastric cancer patients and the controls consisted of individuals including the uninfected (H. pylori unexposed and exposed) and the infected with and without gastric atrophy. Accordingly, it was not clear whether the observed risk was for H. pylori-related or -unrelated gastric cancer, nor which step was involved in the observed associations even when nearly all cases were H. pylori-related. In order to elucidate the genetic traits of H. pylori-related gastric cancer, stepwise evaluation will be required.

Genetic Predisposition to Disease↗
PubMed2006

Causal role of Helicobacter pylori infection in gastric cancer.

Gastric cancer is the second most frequent cancer in the world, accounting for a large proportion of all cancer cases in Asia, Latin America, and some countries in Europe. Helicobacter pylori (H pylori) is regarded as playing a specific role in the development of atrophic gastritis, which represents the most recognized pathway in multistep intestinal-type gastric carcinogenesis. Recent studies suggest that a combination of host genetic factors, bacterial virulence factors, and environmental and lifestyle factors determine the severity of gastric damage and the eventual clinical outcome of H pylori infection. The seminal discovery of H pylori as the leading cause of gastric cancer should lead to effective eradication strategies. Prevention of gastric cancer requires better screening strategies to identify candidates for eradication.

Antigens, Bacterial↗
PubMed2006

Association between serum pepsinogens and polymorphismof PTPN11 encoding SHP-2 among Helicobacter pylori seropositive Japanese.

Helicobacter pylori (H. pylori) plays a crucial role in the development of gastric atrophy and cancer, and cagA-positive strains, which are universal in Japan, increase the risk of these outcomes substantially. The CagA protein is injected from attached H. pylori into gastric epithelial cells and undergoes Src-dependent tyrosine phosphorylation and activation of the eukaryotic phosphatase SHP-2. The CagA/SHP-2 interactions elicit cellular changes that increase the risk of carcinogenesis. We investigated the association of a frequent single nucleotide polymorphism (SNP; JST057927; G-to-A) in the PTPN11 gene that encodes SHP-2 with gastric atrophy and gastric cancer in Japan. Gastric atrophy was assessed by measuring serum pepsinogen I and II levels. The subjects comprised 454 healthy controls (126 males; mean age, 58.4) and 202 gastric cancer cases (134 males and 68 females; mean age, 66.7). All gastric cancer cases and 250 (55%) controls were H. pylori seropositive; 179 (89%) of the gastric cancer cases had gastric atrophy compared to 137 (55%) of the H. pylori seropositive controls (p < 0.001). Among HP seropositive controls compared to the common PTPN11 G/G genotype, the odds ratio of atrophy was nonsignificantly reduced with the G/A genotype (0.70; 95% CI = 0.39-1.25) and significantly reduced with the A/A genotype (0.09; 95% CI = 0.01-0.72). Lower risk for gastric atrophy had a gene-dose association with the A allele (p = 0.01, trend test). There was a clear deficiency of the A/A genotype in those with atrophy compared to those without (1 subject in the gastric atrophy group vs. 8 in the group without). Cancer cases differed from controls in frequencies of PTPN11 G/A genotype only because of a higher prevalence of atrophy among the cancer cases. The G/A SNP in the PTPN11 gene appears to be a risk factor for gastric atrophy in subjects infected with cagA-positive H. pylori. This may explain why only a proportion of CagA-positive individuals develop gastric atrophy and gastric cancer, even though infection with cagA strains is universal in Asian countries such as Japan. The functional consequences of the G/A polymorphism remain to be elucidated.

Atrophy↗
PubMed2006

Associations of TNF-A-1031TT and -857TT genotypes with Helicobacter pylori seropositivity and gastric atrophy among Japanese Brazilians.

BACKGROUND: Our previous study in a Japanese population showed elevated Helicobacter pylori seropositivity in those with tumor necrosis factor (TNF) A -1031TT and -857TT genotypes. This study examined the associations of this seropositivity and serum pepsinogen (PG) levels with these genotypes in Japanese Brazilians. METHODS: The subjects were 963 individuals (399 males and 564 females), aged 33 to 69 years, from four regions (Sao Paulo, Curitiba, Mogi das Cruzes, and Mirandopolis) in Brazil. Gastric atrophy was evaluated with serum pepsinogens (PGI < 70 ng/dl and PGI/II < 3), and TNF T-1031C and C-857T were genotyped by polymerase chain reaction with confronting two-pair primers (PCR-CTPP). RESULTS: The frequency of TNF-A T-1031C was 68.4% TT, 28.4% TC, and 3.3% CC, and that of C-857T was 64.5% CC, 31.7% CT, and 3.8% TT, whose distributions were in Hardy-Weinberg equilibrium. No significant associations of the genotypes with H. pylori seropositivity or gastric atrophy were found. However, male participants with TNF-A -1031CC and -857CC showed the lowest seropositivity (43.8% out of 16), and males with TNF-A -1031TT and -857TT showed the highest (61.5% out of 13). CONCLUSION: This study demonstrated that the associations between H. pylori seropositivity and TNF-A genotypes were not marked for Japanese Brazilians. The genotypes were not associated with gastric atrophy among the seropositive individuals.

Adult↗
PubMed2006

Cloning, characterization, and serodiagnostic evaluation of Leishmania infantum tandem repeat proteins.

Visceral leishmaniasis (VL) is a form of leishmaniasis, which is caused by infection with the protozoan parasite Leishmania, and is often fatal unless it is treated. Rapid and accurate diagnosis of VL is important for effective treatment. Here we report the cloning of previously undescribed tandem repeat (TR) proteins of Leishmania infantum and an evaluation of VL patient antibody responses to the corresponding proteins. By screening an L. infantum expression library with sera from human VL patients or infected hamsters, we identified 43 genes encoding B-cell antigens. Surprisingly, 19 of the 43 genes (44%) were TR proteins, and that percentage was significantly higher than that for genes picked randomly from the database. We then expressed the TR regions of LinJ16.1750, LinJ22.1590, and LinJ33.2870 and the entire LinJ28.2310 protein. These recombinant proteins were all recognized by Sudanese VL patient sera in an enzyme-linked immunosorbent assay. Recombinant LinJ16.1750 (rLinJ16.1750) showed the best performance among these antigens in terms of both sensitivity and specificity. Serological evaluation revealed that 97% (34 of 35) of Sudanese VL patients had significantly elevated antibody levels to rLinJ16.1750. Furthermore, when eight of the patient sera which had low reactivities to rK39 were tested with the novel recombinant antigens, some of the sera showed stronger antibody responses to these antigens than to rK39. Our results suggest that TR regions from the novel L. infantum proteins identified in this study are immunodominant B-cell epitopes and may represent good candidates for serodiagnosis of VL.

Animals↗
PubMed2006

Alternative genotyping method of GSTT1 null/present polymorphism.

Glutathione S-transferase (GST) theta is an enzyme to detoxify xenobiotic compounds. The gene GSTT1 has a null/present polymorphism in one of the targets for cancer susceptibility research. The polymorphism is classified into two types: present type with at least one present allele (heterozygote and homozygote) and null type without a present allele. Although one report showed a method to distinguish the heterozygote from the present homozygote, its use has been limited possibly owing to the difficulty of successful genotyping of long DNA sequences (1460 base pairs). This article reports an alternative method utilizing typical PCR primers specific to the null allele (566 base pairs) and the present allele (458 base pairs). All samples of the GSTT1 null genotype processed by the present PCR method (n = 331), were correctly classified as the null genotype by a conventional method, and the samples of heterozygous (n = 364) or present homozygous (n = 108) genotype as the present genotype; this indicates that it is appropriate for future research to utilize three genotypes of the GSTT1 null/present polymorphism.

Disease↗
PubMed2005

Association between Helicobacter pylori seropositivity and NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism observed in outpatients and health checkup examinees.

BACKGROUND: Significant associations of Helicobacter pylori (H. pylori) seropositivity have been found with several host polymorphisms. This study investigated the associations of functional polymorphisms of the NQO1, GSTM1, and GSTT1 genes of detoxification enzymes, with the seropositivity, as well as with pepsinogen levels, as markers of gastric atrophy. METHODS: The subjects were 241 noncancer outpatients who had participated in an H. pylori eradication program (HPE) at Aichi Cancer Center Hospital, and 465 health checkup examinees in Nagoya (HCE). The NQO1 C609T, GSTM1, and GSTT1 polymorphisms were determined by triplex polymerase chain reaction with confronting two-pair primers (PCR-CTPP). RESULTS: The sex- and age-group-adjusted odds ratio (OR) of NQO1 C/C for H. pylori seropositivity relative to T/T was highly significant; OR, 1.92; 95% confidence interval (95% CI), 1.22-3.03. The ORs of the GSTM1 present type and GSTT1 present type for H. pylori seropositivity were not significant; OR, 0.87; 95% CI, 0.64-1.20 and OR, 1.14; 95% CI, 0.83-1.57, respectively. The association of the NQO1 C/C genotype with H. pylori seropositivity was observed only for never-smokers; OR, 2.25; 95% CI, 1.33-3.79. The genotypes of the NQO1, GSTM1, and GSTT1 genes were not associated with the development of atrophic gastritis among the H. pylori-seropositive subjects. CONCLUSION: This is the first study to report a significant association of the NQO1 C609T polymorphism with H. pylori seropositivity. The biological mechanism explaining the significant association with the seropositivity remains to be elucidated.

Adult↗
PubMed2005

No association between EGF gene polymorphism and gastric cancer.

The etiology of gastric cancer is not well-understood. Epidermal growth factor (EGF) transduces growth signals to mitogen-activated protein kinase via RAS and BRAF, and EGF/EGF receptor interaction is important for tumor growth and progression. Previous studies have reported that the EGF +61 (A/G) single nucleotide polymorphism in the 5'-untranslated region of the EGF gene is functional, and is associated with gastric cancer and various malignancy. Individuals with the EGF A/A genotype produce less EGF than individuals with G/G or G/A. We investigated a single nucleotide polymorphism at exon 1 of EGF, named rs4444903 in NCI dbSNP, in 454 Japanese subjects undergoing a health checkup and 202 patients with gastric cancer. Genotype was determined by PCR with confronting two-pair primers. Results showed that EGF polymorphism was not associated with gastric cancer but that the EGF A/A genotype showed a protective effect (odds ratios, 0.58; 95% confidence interval, 0.29-1.17 relative to G/G). Furthermore, when we divided cases into two groups, a differentiated type and an undifferentiated type, the A/A and G/A combined was found to be lower frequency in the latter type than in the former type without significance (OR, 0.81; 95% confidence interval, 0.44-1.49 relative to G/G). As is the case with any malignancy, other factors are involved, including environmental and host factors. The present results show that although EGF is necessary for cancer, it is not sufficient. We also found ethnic heterogeneity in the functional EGF polymorphism. Because the relationship between EGF polymorphism and malignancy remains inconsistent, confirmation of the role of EGF polymorphism in gastric cancer requires a much larger study.

Adult↗
PubMed2003

Applications of recombinant Leishmania amazonensis expressing egfp or the beta-galactosidase gene for drug screening and histopathological analysis.

Leishmania amazonensis recombinants expressing the enhanced green fluorescent protein (egfp) gene or beta-galactosidase gene (lacZ) were constructed for drug screening and histopathological analysis. The egfp or lacZ in a leishmanial transfection vector, p6.5, was introduced into L. amazonensis promastigotes, and egfp or lacZ-carrying recombinant L. amazonensis, La/egfp and La/lacZ, respectively, were obtained. Expression of egfp or lacZ in both promastigotes and amastigotes could be clearly visualized by fluorescence microscopy or by light microscopy with 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X-Gal), respectively. Fluorescence signal and beta-galactosidase activity measured by a colorimetric reaction with chlorophenol red beta-D-galactopyranoside (CPRG) were well correlated to the numbers of these parasites. The inhibitory concentration (IC50) of a leishmanicidal drug, amphotericin B, in L. amazonensis promastigotes measured using La/egfp and La/lacZ was similar to that measured by conventional methods such as cell counting, thymidine incorporation and colorimetric assay. Furthermore, the fluorescence signal and absorbance of CPRG correlated well with the numbers of La/egfp and La/lacZ amastigotes in macrophages, respectively, suggesting La/egfp and La/lacZ can be a convenient and useful tool for drug screening not only in promastigotes, but also in amastigotes of L. amazonensis. La/lacZ collected from mouse tissues four weeks after the parasite infection were stained well with X-Gal. La/lacZ allowed parasite detection at high sensitivity in the tissues of infected mice and will be useful for following infections in macrophages in vivo. Thus, the marker-transfected Leishmania parasites constructed in this study will be useful for analyses of Leishmania parasites, especially at the intracellular stage.

Animals↗
PubMed2002

[Perioperative mortality and morbidity in the year 2000 in 502 Japanese certified anesthesia-training hospitals: with a special reference to ASA-physical status--report of the Japan Society of Anesthesiologists Committee on Operating Room Safety].

Perioperative mortality and morbidity in Japan from Jan. 1 to Dec. 31, 2000 were studied retrospectively. Committee on Operating Room Safety in Japanese Society of Anesthesiologists (JSA) sent confidential questionnaires to 794 certified training hospitals of JSA and received answers from 67.6% of the hospitals. We analyzed their answers with a special reference to ASA physical status (ASA-PS). The total number of anesthesia available for this analysis was 897,733. The percentages of patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E are 38.0, 40.3, 8.5, 0.4, 4.3, 5.3, 2.5, and 0.7%, respectively. Mortality and morbidity from all kinds of causes including anesthetic management, intraoperative events, co-existing diseases, and surgical problems were as follows. The incidences of cardiac arrest (per 10,000 cases of anesthesia) were 1.11, 3.26, 12.25, 54.60, 0.77, 4.46, 21.08 and 217.75 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The incidences of critical events including cardiac arrest, severe hypotension, and severe hypoxemia were 6.89, 20.22, 62.18, 148.21, 6.71, 20.38, 106.72 and 592.21 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The mortality rates (death during anesthesia and within 7 postoperative days) after cardiac arrest were 0.26, 0.77, 3.69, 41.60, 0.00, 1.06, 9.42 and 163.31 per 10,000 cases of anesthesia in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The overall mortality rates were 0.32, 1.38, 9.75, 70.20, 0.26, 2.12, 29.15 and 353.02 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. Overall mortality and morbidity were higher in emergency anesthesia than in elective anesthesia. ASA-PS correlated well with overall mortality and morbidity, regardless of etiology. The incidences of cardiac arrest totally attributable to anesthesia were 0.23, 0.50, 1.32, 0.00, 0.00, 0.85, 2.69 and 4.95 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The incidences of all critical events totally attributable to anesthesia were 3.13, 5.56, 11.46, 5.20, 3.87, 5.94, 13.90 and 14.85 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The mortality rates after cardiac arrest totally attributable to anesthesia were 0.03, 0.03, 0.00, 0.00, 0.00, 0.21, 0.45 and 3.30 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The overall mortality rates totally attributable to anesthesia were 0.03, 0.06, 0.00, 0.00, 0.00, 0.21, 0.45 and 6.60 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The overall mortality rate totally attributable to anesthesia among patients with good physical status (ASA-PS of I, II, I E, II E) was 0.05. Anesthetic management was mainly responsible for critical events in patients with good physical status, while coexisting diseases were in those with poor physical status. Surgical problems including procedures and massive hemorrhage were the leading causes of mortality in patients with good physical status. We reconfirmed that ASA-PS is useful to predict perioperative mortality and morbidity. It also seems likely that we should make much more efforts to reduce anesthetic morbidity in patients with good physical status, and to improve preanesthetic assessment and preparation in those with poor physical status. Reducing mortality and morbidity from surgical problems is also required for improving perioperative mortality.

Anesthesia↗
PubMed2002

[Annual report of perioperative mortality and morbidity for the year 2000 at certified training hospitals of Japanese Society of Anesthesiologists: with a special reference to anesthetic methods--report of the Japanese Society of Anesthesiologists Committee on Operating Room Safety].

The Committee on Operating Room Safety of Japan Society of Anesthesiologists (JSA) sends annually confidential questionnaires of perioperative mortality and morbidity (cardiac arrest, severe hypotension, severe hypoxia) to Certified Training Hospitals of JSA. This report is a special reference to anesthetic methods in perioperative mortality and morbidity in 2000. Five hundreds and twenty hospitals reported perioperative mortality and morbidity referred to anesthetic methods and total numbers of reported cases were 910,007. The percentage of cases reported by each anesthetic method was as follows; inhalation anesthesia 45.47%, total intravenous anesthesia (TIVA) 6.15%, inhalation anesthesia + epidural or spinal or conduction block 24.48%, TIVA + epidural or spinal or conduction block 6.33%, spinal with continuous epidural block (CSEA) 3.67%, epidural anesthesia 1.92%, spinal anesthesia 10%, conduction block 0.47% and others 1.49%. The incidence of cardiac arrest per 10,000 cases due to all etiology (anesthetic management, preoperative complications, intraoperative complications, surgery, others) is estimated to be 6.55 cases in average; 5.36 cases in inhalation anesthesia, 30.72 cases in total intravenous anesthesia (TIVA), 4.62 cases in inhalation anesthesia + epidural or spinal or conduction block, 2.6 cases in TIVA + epidural or spinal or conduction block, 1.2 cases in spinal with continuous epidural block (CSEA), 0.57 cases in epidural anesthesia, 1.65 cases in spinal anesthesia, 2.36 cases in conduction block and 46.38 cases in other methods. However, the incidence of cardiac arrest per 10,000 cases totally attributable to anesthetic management is estimated to be 0.54 cases in average; 0.34 cases in inhalation anesthesia, 1.07 cases in TIVA, 0.58 cases in inhalation anesthesia + epidural or spinal or conduction block, 0.17 cases in TIVA + epidural or spinal or conduction block, 0.9 cases in CSEA, 0.57 cases in epidural anesthesia, 0.99 cases in spinal anesthesia, zero case in conduction block and 1.47 cases in other methods. The incidence of severe hypotension per 10,000 cases due to all etiology is estimated to be 11.14 cases in average; 11.31 cases in inhalation anesthesia, 36.61 cases in TIVA, 9.29 cases in inhalation anesthesia + epidural or spinal or conduction block, 6.59 cases in TIVA + epidural or spinal or conduction block, 3.59 cases in CSEA, 6.3 cases in epidural anesthesia, 4.39 cases in spinal anesthesia, 2.36 cases in conduction block and 23.56 cases in other methods. On the other hand, the incidence of severe hypotension per 10,000 cases totally attributable to anesthetic management is estimated to be 1.25 cases in average; 0.97 cases in inhalation anesthesia, 0.89 cases in TIVA, 1.39 cases in inhalation anesthesia + epidural or spinal or conduction block, 1.39 cases in TIVA + epidural or spinal or conduction block, 2.09 cases in CSEA, 3.44 cases in epidural anesthesia, 1.87 cases in spinal anesthesia, zero case in conduction block and zero case in other methods. The incidence of severe hypoxia per 10,000 cases due to all etiology is estimated to be 4.8 cases in average; 6.35 cases in inhalation anesthesia, 9.64 cases in TIVA, 3.82 cases in inhalation anesthesia + epidural or spinal or conduction block, 2.26 cases in TIVA + epidural or spinal or conduction block, 0.3 cases in CSEA, 1.15 case in epidural anesthesia, 1.21 cases in spinal anesthesia, zero case in conduction block and 5.89 cases in other methods. On the other hands, the incidence of severe hypoxia per 10,000 cases totally attributable to anesthetic management is estimated to be 1.98 cases in average; 3.09 cases in inhalation anesthesia, 2.32 cases in TIVA, 1.3 cases in inhalation anesthesia + epidural or spinal or conduction block, 0.87 cases in TIVA + epidural or spinal or conduction block, zero case in CSEA, zero case in epidural anesthesia, 0.55 cases in spinal anesthesia, zero case in conduction block and zero case in other methods. The mortality rate of cardiac arrest within 7 postoperative days per 10,000 cases due to all etiology is estimated to be 3.55 (54.2%) cases in average; 3.12 (58.1%) cases in inhalation anesthesia, 19.29 (62.8%) cases in TIVA, 1.17 (25.2%) cases in inhalation anesthesia + epidural or spinal or conduction block, 0.52 (20%) cases in TIVA + epidural or spinal or conduction block, zero cases in CSEA, zero case in epidural anesthesia, 0.33 (20%) cases in spinal anesthesia, zero case in conduction block and 39.76 (85.7%) cases in other methods. On the other hands, the mortality rate of cardiac arrest per 10,000 cases totally attributable to anesthesia is estimated to be 0.07 (12.2%) case in average, 0.07 (21.4%) case in inhalation anesthesia, 0.18 (16.8%) case in TIVA, zero case in inhalation anesthesia + epidural or spinal or conduction block, zero case in TIVA + epidural or spinal or conduction block, zero case in CSEA, zero case in epidural anesthesia, 0.11 (11.1%) case in spinal anesthesia, zero case in conduction block and 0.74 (50%) case in other methods. Five major combinations of listed critical incidents, causes and anesthetic methods were as follows: 18.93 cases in TIVA, preoperative complications and severe hypotension; 18.75 cases in TIVA, preoperative complications and cardiac arrest; 11.07 cases in TIVA, surgery and severe hypotension; 6.79 cases in TIVA, surgery and cardiac arrest; 5.24 cases in inhalation anesthesia, preoperative complications and severe hypotension. In summary: 1. There was no significant difference with regard to perioperative mortality and morbidity due to anesthetic management among anesthetic methods. 2. The percentage of each anesthetic method in 2000 was not different significantly from that in 1999 in spite of increased cases reported. 3. Incidence of severe hypotension due to all etiology of TIVA in 2000 decreased significantly compared with that in 1999 (P < 0.05). This may be attributed to the decreased incidence in preoperative complication (shock) and massive bleeding due to surgery.

Anesthesia↗
PubMed2002

[Perioperative mortality and morbidity for the year 2000 in 532 Japanese Society of Anesthesiologists certified training hospitals: with a special reference to surgical sites--report of the Japan Society of Anesthesiologists Committee on Operating Room Safety].

Perioperative mortality and morbidity in Japan for the year 2000 were analyzed with special reference to operative regions. The total number of analyzed cases was 903,086. The percentages for each operative region were as follows, CRANIOTOMY 4.5%, THORACOTOMY 3.5%, HEART and GREAT-VESSELS 3.7%, THORACOTOMY with LAPAROTOMY 0.7%, LAPAROTOMY 30.4%, CESARIAN SECTION 3.3%, HEAD-NECK-ENT 14.7%, CHEST-ABDOMEN-PERINEUM 14.0%, SUPINE 3.6%, EXTREMITY including PERIPHERAL-VESSEL 17.2%, OTHERS 4.4%. The incidence of serious events, including cardiac arrest and severe hypotension and hypoxemia developing to cardiac arrest, was 26.74 per 10,000 anesthetics in all operative regions. The events were observed more frequently in HEART and GREAT-VESSELS 170.39, THORACOTOMY with LAPAROTOMY 85.84 and THORACOTOMY 63.63, and less frequently in CHEST-ABDOMEN-PERINEUM 10.49, CESARIAN SECTION 10.95 and EXTREMITY including PERIPHERAL-VESSEL 13.42. Regarding the prognosis of events, the cases with no sequelae were 63.4% in all operative regions. While there were fewer cases with no sequelae in CRANIOTOMY 49.0%, THORACOTOMY with LAPAROTOMY 43.4% and HEART and GREAT-VESSELS 44.4%, there were more cases in HEAD-NECK-ENT 86.9% and CHEST-ABDOMEN-PERINEUM 89.5%. The incidence of serious events totally attributable to anesthetic management was 5.24 per 10,000 anesthetics in all operative regions. The events were observed more frequently in THORACOTOMY 12.91 and SPINE 8.02, and less frequently in LAPAROTOMY except CESARIAN SECTION 4.11 and EXTREMITY including PERIPHERAL-VESSEL 4.65. The main cause of events in THORACOTOMY was inadequate airway management and in SPINE was inadequate airway management and the overdose or miss selection for drugs. Regarding the prognosis of events totally attributable to anesthetic management, the cases with no sequelae were 91.8% in all operative regions. There were fewer cases with no sequelae in HEART and GREAT-VESSELS 82.6%. The incidence of serious events totally attributable to anesthetic management was one fifth of all serious events in all operative regions. While the total deaths from 903,086 cases, including deaths in the operating room or within 7 postoperative days, were 641 cases (7.10 per 10,000 cases), the deaths totally attributable to anesthesia were 9 cases (0.10 per 10,000 cases).

Anesthesia↗
PubMed2002

[Annual study of anesthesia-related mortality and morbidity in the year 2000 in Japan: the outlines--report of Japanese Society of Anesthesiologists Committee on Operating Room Safety].

This report contains anesthesia-related mortality and morbidity in Japanese Society of Anesthesiologists Certified Training Hospitals (JSACTH) in the year 2000, as a part of the second series of annual studies started in 1999. JSA Committee on Operating Room Safety (CORS) sent confidential questionnaires to 794 JSACTH and received effective answers from 65.5% of hospitals. A total number of 941,217 anesthetics were documented. The respondents were asked to report all cases of cardiac arrests and other critical incidents (serious hypotension, serious hypoxemia and others), and their outcomes (death in operating room, death within 7 days, transfer to vegetative state and rescue without sequelae) as well as one principal cause for each incident from the list of 52 items. They were also requested to submit the tabulation of patients by ASA physical status, age distribution, surgery sites and anesthetic methods. Analysis was made by total incidents under anesthesia/surgery, and also by incidents totally attributable to anesthetic management (AM), due to preoperative complications (PC), due to intraoperative pathological events (IP) and due to surgery (SG). This paper focused analysis on entire patients, since analyses with special reference to ASA physical status, age distribution, surgery sites and anesthetic methods were reported previously. Total incidence of cardiac arrest under anesthesia/surgery was 6.52 per 10,000 anesthetics. PC, IP and SG occupied 46.4%, 19.1% and 23.0% of principal causes of total cardiac arrest, respectively. AM occupied only 8.1% of the principal causes and the incidence was 0.53 per 10,000. The most frequent cause of cardiac arrest in 52 more detailed classification of principal causes was preoperative hemorrhagic shock that occupied 23.3% of all cardiac arrests. The second was massive hemorrhage and/or hypovolemia due to surgical procedures (10.6%), and the third was surgery itself (9.5%). Prognosis of the cardiac arrest was worst in that due to PC, 73.7% of cardiac arrests died in the operating room or within 7 days after surgery and only 20.4% survived without sequelae. The best prognosis was found in cardiac arrest due to AM, 76.0% survived without sequelae and 12.0% died. The mortality rate after cardiac arrest was 3.52 per 10,000 anesthetics, of them 0.06 was due to AM, 0.39 due to IP, 2.23 due to PC and 0.76 due to SG. The mortality rate after critical incidents other than cardiac arrest such as severe hypotension and severe hypoxemia was 3.48, and of them 0.03 was due to AM, 0.18 due to IP, 2.45 due to PC and 0.81 due to SG. The final mortality rate attributable to anesthesia/surgery including deaths after cardiac arrest and after other critical incidents was 7.00 per 10,000 anesthetics and very close to 7.18 [6.22, 8.13], that of mean [95%C.I.] in 1994-1998, and 7.19 in 1999. The final mortality rate totally attributable to AM was 0.10 per 10,000 anesthetics, which was significantly improved from 0.21 [0.15, 0.27], that of mean [95%C.I.] in 1994-1998, but not different from 0.13 in 1999. IP, PC and SG showed the final mortality rate of 0.56, 4.69 and 1.57, respectively. Five major causes of all critical incidents were massive hemorrhage due to surgical procedures (13.8%), preoperative hemorrhagic shock (13.1%), surgical technique (8.6%), inappropriate airway management (6.2%) and preoperative respiratory complication (5.7%). Drug overdose or wrong choice (2.7%) as a human error occupied the 10th. In conclusion, the obtained incidences as to death, other critical incidents and their outcomes as well as the occurrence of principal causes in 2000 study were remarkably close to those in 1999 study. We expect that this second series of annual studies for five-years should reveal precise and definite direction for us to reduce anesthesia-related mortality and morbidity.

Anesthesia↗