Abstract. A pregnant 26-year-old woman was referred for evaluation and management of progressive hypertension and hypokalemia at 14 weeks of gestation. Her plasma aldosterone level was markedly elevated and magnetic resonance imaging showed a right adrenal tumor. Primary aldosteronism due to an aldosterone producing-adenoma was diagnosed. Because of progressive severe hypertension, a laparoscopic adrenalectomy was performed at 17 weeks of gestation. The procedure was completed without complication, and plasma aldosterone and potassium levels rapidly improved postoperatively. However, her hypertension persisted and the growth retardation of the fetus was found. Regrettably, intrauterine fetal death was confirmed at 26 weeks of gestation. Histological examination of the placenta revealed that the placental artery had very thick walls which had apparently caused a critical failure in fetal blood flow. The optimal timing of laparoscopic surgery during pregnancy and perioperative management were subsequently discussed. PRIMARY aldosteronism is not a rare cause of hypertension [1], and its association with pregnancy has been reported. However, we found that only 23 cases have been described in the literature published in English since the first report of primary aldosteronism in pregnancy described by Crane et al. in 1964 [2]. A recent evolution in adrenal surgery, including minimally invasive laparoscopic surgery, has largely improved modality and QOL of patients with primary aldosteronism. As of yet, however, there has been little discussion of performing laparoscopic adrenalectomy on a pregnant woman. We report a case of primary aldosteronism during pregnancy that was treated by a laparoscopic adrenalectomy and discuss the feasibility of this procedure on pregnant women. Case ReportA 26-year-old Japanese woman was hypertensive when she registered for prenatal care at 14 weeks and 4 days of gestation. She had been healthy before becoming pregnant; however, the initial laboratory assessment revealed low potassium and high plasma aldosterone levels. She was told three years ago that she had mild hypertension that could be controlled
The importance of cancer-mesenchymal interactions in the aggressive behavior of scirrhous gastric cancer is supported by experimental and clinical evidences. We have previously reported that gastric fibroblasts secretion of keratinocyte growth factor (KGF) underline the remarkable proliferation of scirrhous gastric cancer cells. Cyclooxygenase-2 (COX-2) is not only expressed in cancer cells, but also in interstitial fibroblasts in gastric carcinoma. To clarify the mechanisms responsible for the antiproliferation effect of COX-2 inhibitors, effect of COX-2 inhibitor on the paracrine epithelial-mesenchymal interactions of growth was examined. Scirrhous gastric cancer cell line, OCUM-2M, gastric fibroblasts, NF-21, and COX-2 inhibitor, JTE-522, were used. Growth-interaction was examined by calculating the number of cancer cells or by measuring [ Key words: COX-2; K-samII; keratinocyte growth factor; epithelialmesenchymal interaction; JTE-522; fibroblasts; scirrhous gastric cancer Recent epidemiologic studies have shown that nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of developing and/or dying from colon cancer and gastric cancer.
XELOX plus bevacizumab is an effective treatment strategy and has a manageable tolerability profile when administered to Japanese patients with metastatic colorectal cancer (mCRC). In this study, we retrospectively reviewed cases in which XELOX plus bevacizumab were administered in order to evaluate its efficacy and safety in clinical practice. In total, 40 patients with mCRC who presented at Fuchu Hospital received XELOX plus bevacizumab as a first-line treatment between September, 2009 and April, 2012. Eligible patients had histologically confirmed mCRC. XELOX consisted of a 2-h intravenous infusion of oxaliplatin 130 mg/m on day 1 plus oral capecitabine 1,000 mg/m twice daily for 2 weeks of a 3-week cycle. Overall survival (OS) and survival benefit were analyzed when patients continued with XELOX plus bevacizumab beyond disease progression. The median progression-free survival (PFS) was 290 days [95% confidence interval (CI): 222-409 days] and the median OS was 816 days (95% CI: 490 days-not calculated). The response rate (RR; complete plus partial response) was 67.5%, and the disease control rate (RR plus stable disease) was 90%. The most common adverse events observed following administration of XELOX plus bevacizumab were neurosensory toxicity (82.5%), anorexia (50%), hypertension (45%) and a decrease in the platelet count (40%). The most common grade 3/4 adverse events were neurosensory toxicity (15%) and fatigue (15%). In conclusion, XELOX plus bevacizumab may be considered a routine first-line treatment option for patients with mCRC. Notably, the combination of capecitabine and bevacizumab was safe with an acceptable toxicity profile and induced a significant rate of disease control.
We report an unusual case of a prepancreatic postduodenal portal vein (PPPV), incidentally discovered during total gastrectomy. If it had not been noticed, this portal vein might have been ligated and divided with disastrous consequences. This anomaly was not diagnosed preoperatively, but it could have been. Although embryological anomalies of the portal venous system, such as PPPV and preduodenal portal vein, are rarely encountered in abdominal surgery, surgeons must be aware of their possibility and be able to recognize them to avoid major intraoperative injury.
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