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Biomedical subjects

S Saitoh

Publications and source records attributed to S Saitoh.

At least 55 records · Page 3Linked to original sources
PubMed2001

[Night-eating syndrome].

Morning anorexia, evening hyperphagia and insomnia characterized night-eating syndrome. This syndrome is described in 1955 by Stunkard, et al. It occurred during periods of stress and was associated with a poor outcome of efforts at weight reduction. The prevalence of this syndrome was about 26% of severely obese population in US. In Japan, there is few clinical study of this syndrome. It is thought that this syndrome increases in prevalence with increasing adiposity. The behavior study showed that a coherent pattern of behavior was found in subjects with night-eating syndrome. And neuroendocrine study indicated that the leptin, which was produced from the adipocyts, related this syndrome and night eating behavior.

Feeding and Eating Disorders↗
PubMed2001

[Evaluation of cerebrovascular events in patients with rheumatoid arthritis].

OBJECTIVE: We evaluated cerebrovascular events (cerebral infarction or cerebral bleeding) in patients with rheumatoid arthritis (RA). METHODS: Prognosis and the causes of death among 1100 RA patients from 1995 to 1999, were analyzed. 34 RA patients were complicated by cerebrovascular events. About them, hemoglobin, platelet, C-reactive protein, rheumatoid factor, total cholesterol, triglyceride, duration of disease, functional class, and dose of steroids per day were measured. RESULT: Among 1100 patients with RA, 90 died at the age of 70.2. Of these patients, 24 (26.7%) died of cerebrovascular events, 19 (21.1%) of heart failure, 16 (17.8%) of infectious diseases, 10 (11.1%) of malignant tumors, and 9 (10%) of renal failure. When RA patients who died of cerebrovascular events were compared with those who died of other causes, the dose of steroid was significantly lower and the age was higher in RA patients who died of cerebrovascular events. However, there were no significant differences in total cholesterol and triglyceride levels between the two groups. Although the major cause of death in RA patients was reported to be complication by cardiovascular diseases, infectious diseases, or renal failure, the frequency of deaths was higher in elderly RA patients complicated by cerebrovascular events. When the frequency of complication by cerebrovascular events was investigated in all RA patients including those who survived, 24 died and 10 survived. The frequency of complication by cerebral infarction was higher than that of complication by cerebral bleeding in RA patients who died of cerebral events. CONCLUSION: RA patients can live longer with improvements in care and treatment, the number of elderly RA patients who may died of complication by cerebrovascular events may gradually increase.

Aged↗
PubMed2001

[Standard therapy of CPT-11 for colorectal cancer].

Irinotecan (CPT-11) is a potent inhibitor of topoisomerase I, and has demonstrated antitumor activity against metastatic colorectal cancer. In phase II studies, CPT-11 showed promising activity. Combining irinotecan with 5-fluorouracil (5-FU) and Leucovorin (LV) has shown benefits for patients with metastatic colorectal cancer CPT-11/5-FU/LV therapy is considered as a standard therapy. Weekly or biweekly administration of CPT-11 is most recommended.

Antineoplastic Agents, Phytogenic↗
PubMed2000

Polymorphisms of UDP-glucuronosyltransferase gene and irinotecan toxicity: a pharmacogenetic analysis.

Irinotecan unexpectedly causes severe toxicity of leukopenia or diarrhea. Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) 1A1 enzyme. Genetic polymorphisms of the UGT1A1 would affect an interindividual variation of the toxicity by irinotecan via the alternation of bioavailability of SN-38. In this case-control study, retrospective review of clinical records and determination of UGT1A1 polymorphisms were performed to investigate whether a patient with the variant UGT1A1 genotypes would be at higher risk for severe toxicity by irinotecan. All patients previously received irinotecan against cancer in university hospitals, cancer centers, or large urban hospitals in Japan. We identified 26 patients who experienced severe toxicity and 92 patients who did not. The relationship was studied between the multiple variant genotypes (UGT1A1*28 in the promoter and UGT1A1*6, UGT1A1*27, UGT1A1*29, and UGT1A1*7 in the coding region) and the severe toxicity of grade 4 leukopenia (< or =0.9 x 10(9)/liter) and/or grade 3 (watery for 5 days or more) or grade 4 (hemorrhagic or dehydration) diarrhea. Of the 26 patients with the severe toxicity, the genotypes of UGT1A1*28 were homozygous in 4 (15%) and heterozygous in 8 (31%), whereas 3 (3%) homozygous and 10 (11%) heterozygous were found among the 92 patients without the severe toxicity. Multivariate analysis suggested that the genotype either heterozygous or homozygous for UGT1A1*28 would be a significant risk factor for severe toxicity by irinotecan (P < 0.001; odds ratio, 7.23; 95% confidence interval, 2.52-22.3). All 3 patients heterozygous for UGT1A1*27 encountered severe toxicity. No statistical association of UGT1A1*6 with the occurrence of severe toxicity was observed. None had UGT1A1*29 or UGT1A1*7. We suggest that determination of the UGT1A1 genotypes might be clinically useful for predicting severe toxicity by irinotecan in cancer patients. This research warrants a prospective trial to corroborate the usefulness of gene diagnosis of UGT1A1 polymorphisms prior tb irinotecan chemotherapy.

Adult↗