[Perspectives in treatment of peptic ulcer disease].
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Anti-Inflammatory Agents, Non-Steroidal↗
Biomedical subjects
Yasuhiro Fujiwara
Publications and source records attributed to Yasuhiro Fujiwara.
[Prostaglandin derivatives--indication and critical points].
After discovery of H. pylori, management of peptic ulcer disease (PUD) is getting much easier. However, four thousands a year still died caused by this disease in Japan. Ten to twenty percent of the non-NSAIDs ulcer could be expected to remain after complete eradication of H. pylori; The number could be still 100,000-200,000 a year in Japan. Furthermore, NSAIDs ulcer would not decrease in number in the post-H. pylori era. Recurrence of ulcer is related to the quality of ulcer healing. Deficiency of prostaglandins(PG) in the mucosa is another main reason than H. pylori infection of poor quality of ulcer healing. Therefore, a PG analogue may be a most reasonable tool for treatment of H. pylori-negative PUD including NSAIDs ulcer, but is often poorly tolerated because of diarrhea and abdominal pain. The mucosal damage caused by NSAIDs is also gastric acid-dependent and so, an H2-receptor antagonist is to some extent effective although the efficacy is far behind of that with a PG-analogue. Recently, a proton-pump inhibitor has been reported to exert the same effect as a PG-analogue in healing of gastroduodenal mucosal damage caused by NSAIDs and the superior effect in preventing recurrence of the damage with better tolerance. This results suggest that strong acid inhibition is highly effective for such damage. Whether such strong acid inhibition causes disturbance of absorption of NSAIDs is not clear, which might result in poor antiinflammatory effect. Elderly patients often have tendency of constipation and less possibility of pregnancy. Therefore, a PG-analogue may be not only safe but also more favorable for such patients.
Aged↗
Diagnosis of complete response to neoadjuvant chemotherapy using diagnostic imaging in primary breast cancer patients.
Advances in the therapeutic agents used for neoadjuvant chemotherapy (NAC) have recently achieved higher response rates and induced a greater number of pathologic complete responses (pCR) than ever before. The aim of this study is the diagnosis of pCR after NAC by diagnostic imaging of clinical complete response (cCR) patients. This study included 35 breast cancer patients who demonstrated cCR after receiving NAC with a combination of anthracycline and taxane from May 1998 to August 2003. Surgical treatment included breast-conserving therapy followed by radiotherapy or mastectomy. The identity of post-NAC lesions as either a complete response (CR) or partial response (PR) were made by mammography, ultrasonography, and contrast-enhanced computed tomography (CT). Among the 35 patients, 11 achieved pCR, including the disappearance of both invasive and intraductal components. Of the patients achieving pCR, eight were defined as CR and three were determined to be PR by CT. There was a significant relationship between the pCR and the determination of CR by CT. The determination of CR by ultrasonography was indicative of the disappearance of pathologic invasive components. While mammography appeared to reflect the observed histologic results, we did not observe any statistical differences. A subset of cases exhibited discrepancies between the imaging and pathologic results, likely due to the replacement of destroyed tumor cells by fibrosis and granulomatous tissue. The evaluation of CR by CT was significantly indicative of pCR. The positive predictive value, however, was not large enough to avoid surgical treatment. Further studies will be needed to establish a diagnosis of pCR.
Adult↗
Long-term effect of Helicobacter pylori eradication on quality of life, body mass index, and newly developed diseases in Japanese patients with peptic ulcer disease.
BACKGROUND/AIMS: Eradication of Helicobacter pylori is known to reduce ulcer recurrence in patients with peptic ulcer disease, however, other long-term effects after eradication therapy are not well known. The aim of this study is to examine the long-term effect of H. pylori eradication on clinical symptoms, quality of life, body mass index, newly emerging symptoms, and newly developed diseases. METHODOLOGY: One hundred and ninety-two Japanese patients with peptic ulcer disease who received H. pylori eradication therapy at Department of Gastroenterology, Osaka City University Hospital between 1993 and 1995 were asked to fill in specially a prepared questionnaire. RESULTS: One hundred and fourteen patients returned the questionnaires; out of them 98 could be analyzed in this study. Successful eradication (n = 88) resulted in alleviation of symptoms, improvement of quality of life and increase of body mass index while failure of eradication (n = 10) had much less or no effects. A relatively high incidence of hyperlipidemia (25.0%) was observed in patients with successful H. pylori eradication. Development of hyperlipidemia was associated with significant improvement of quality of life especially the item concerning eating and drinking habits but not with increased body mass index. In the elderly, no significant change in body mass index was observed, however, post-eradication body mass index was significantly higher in patients with hyperlipidemia than those without. CONCLUSIONS: Cure of H. pylori infection alleviates symptoms and improves quality of life of treated patients, but might be associated with an increased incidence of hyperlipidemia.
Body Mass Index↗
Validation of the limited-sampling models for carboplatin AUC in combination chemotherapy with taxanes.
We previously developed limited-sampling models (LSM) for estimation of the area under the concentration curve (AUC) of free carboplatin (Anticancer Res 17: 4571-4576, 1997). The one-point model was: AUC (mg/ml x min) = 0.93 x C3h + 0.47 and the two-point model was: AUC (mg/ml x min) = 0.16 x C1h + 2.26 x C8h + 0.75, in which C3h, C1h and C8h represented the plasma concentration, sampled at 3 h, 1 h and 8 h after the start of a 1-h carboplatin infusion, respectively. In this study, we tried to confirm the utility of our LSMs in combination chemotherapy with taxanes. We obtained 29 data series from 29 patients who received carboplatin in combination with docetaxel (n = 16) or paclitaxel (n = 13). The actual AUC was strongly correlated with the AUC calculated from both one- and two-point models (one-point model; the mean prediction error (MPE) = -4.44 +/- 2.15%, the root mean squared error (RMSE) = 12.22 +/- 0.84%, two-point model; MPE = -1.89 +/- 1.66%, RMSE = 8.99 +/- 0.81%). Our LSMs proved to be unbiased and precise and are also useful for calculating carboplatin AUC in combination with taxanes.
Aged↗
UGT1A10 is responsible for SN-38 glucuronidation and its expression in human lung cancers.
BACKGROUND: We previously reported that upregulation of glucuronidation activity catalyzed by uridine 5'diphosphoglucuronosyltransferase (UGT) is one of the mechanisms associated with irinotecan hydrochloride/7-ethyl-10-hydroaxycamptothecin (CPT-11/SN-38) resistance. In order to extend this result to the clinical setting, it is important to elucidate the role of SN-38 glucuronidation by UGT1A isoforms in CPT-11/SN-38 resistance in vivo. MATERIALS AND METHODS: We examined SN-38 glucuronidation activity in COS-7 cells transfected with full-length cDNAs for human UGT isoforms (UGT1A1, UGT1A3, UGT1A6 and UGT1A10). The gene expression levels of UGT isoforms were examined in lung cancer cell lines and 14 lung cancer samples by semi, quantitative RT-PCR. RESULTS: Our HPLC assay results showed that both UGT1A1 and UGT1A10 are responsible for SN-38 glucuronidation. The levels of UGT1A1 and UGT1A10 expression in a CPT-11/SN-38-resistant cell line were increased compared to levels in the parent cell line. Furthermore, there was considerable intersubject variability in 14 lung cancer samples, but UGT1A1 and UGT1A10 expression levels were significantly correlated (r=0. 70, p=0.004). Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.
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