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老年胃癌患者围手术期并发症及其处理 总被引:2,自引:0,他引:2
目的 研究老年胃癌患者的临床特点,总结老年胃癌患者的年龄、术前各种合并症等对术后并发症发生的影响.方法 总结自2005年1月至2007年1月接受手术的181例胃癌患者的临床资料,其中老年患者(年龄大于65岁者)65例,回顾性分析老年胃癌患者的年龄、术前各种合并症与术后并发症发生的关系.结果 老年胃癌组术前合并症总发生率为83%,非老年胃癌组为59%;老年胃癌组中有52%存在2种或2种以上合并症,发生率最高的合并症为高血压,达40%;老年胃癌患者的根治率为86%,非老年胃癌组的根治率为93%;老年胃癌组术后并发症的发生率为37%,术前合并高血压、糖尿病、肺部疾病、低蛋白血症、贫血者术后并发症发生率较高.结论 老年胃癌患者手术治疗后的总并发症发生率和病死率与非老年胃癌患者相比无差异. 相似文献
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Breast cancer is the most frequently encountered carcinoma in women worldwide. Pain is the most distressing symptom in patients with breast carcinoma and can occur at all stages of the disease due to the cancer per se as well as due to various diagnostic and treatment modalities. A proper pain assessment helps in identification of pain syndromes and guides in formulating analgesic strategies. Primary therapies of breast carcinoma like surgery, chemotherapy, and radiotherapy for bony metastases can cause substantial pain relief. However, multimodal analgesic approaches incorporating pharmacological, interventional as well as non-conventional techniques should be employed prior to, in conjunction with, and after primary therapies of breast cancer. The prevalence of chronic neuropathic pain following breast cancer surgery may exceed 50% by current estimates, and with the increase in life expectancy of these patients, providing adequate pain relief is of paramount importance to improve their quality of life. In this review, we discuss prevailing methods of evaluation and management of pain in patients of breast carcinoma and the new techniques that may become the mainstay of pain management protocols in future. 相似文献
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SUMMARY Analysis of the age of onset of diabetes amongst insulin-treatedpatients in a large African diabetic clinic revealed a bimodaltype of distribution, 23 per cent having an age of onset before30 years and 77 per cent with onset at 30 years of age. All66 of the young insulin-treated group (21.7±4.8 years(mean±1 SD)), and a random selection of 50 older insulin-treatedpatients (49.7±10 years), were studied. The older groupwere better controlled (HbA1 8.4±1.7 per cent vs. 10.8±2.6per cent, p<0.001), on lower doses of insulin (49±23vs. 71±23 u/day, p<0.001) and had higher body massindex (26.0±5.6 vs. 21.8±3.5, p<0.001). SerumC-peptide (0.24±0.15 vs. 0.07±0.10 nmol/l, p<0.0001),and C-peptide/glucose ratio (2.57±2.65 vs. 0.56+0.98nmol/mmolx 102, p<0.001) were very significantly higher inolder patients. Patients with later onset disease thus had betterpreservation of pancreatic function, higher body mass indexand better glycaemic control on lower doses of insulin. Thesefeatures suggest that older insulin-treated patients could infact be Type 2 or non-insulin dependent patients,and the condition may be controllable with diet and/or oralhypoglycaemic agents, at least in some. 相似文献
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Wu H Chen G Wyburn KR Yin J Bertolino P Eris JM Alexander SI Sharland AF Chadban SJ 《The Journal of clinical investigation》2007,117(10):2847-2859
Ischemia/reperfusion injury (IRI) may activate innate immunity through the engagement of TLRs by endogenous ligands. TLR4 expressed within the kidney is a potential mediator of innate activation and inflammation. Using a mouse model of kidney IRI, we demonstrated a significant increase in TLR4 expression by tubular epithelial cells (TECs) and infiltrating leukocytes within the kidney following ischemia. TLR4 signaling through the MyD88-dependent pathway was required for the full development of kidney IRI, as both TLR4(-/-) and MyD88(-/-) mice were protected against kidney dysfunction, tubular damage, neutrophil and macrophage accumulation, and expression of proinflammatory cytokines and chemokines. In vitro, WT kidney TECs produced proinflammatory cytokines and chemokines and underwent apoptosis after ischemia. These effects were attenuated in TLR4(-/-) and MyD88(-/-) TECs. In addition, we demonstrated upregulation of the endogenous ligands high-mobility group box 1 (HMGB1), hyaluronan, and biglycan, providing circumstantial evidence that one or more of these ligands may be the source of TLR4 activation. To determine the relative contribution of TLR4 expression by parenchymal cells or leukocytes to kidney damage during IRI, we generated chimeric mice. TLR4(-/-) mice engrafted with WT hematopoietic cells had significantly lower serum creatinine and less tubular damage than WT mice reconstituted with TLR4(-/-) BM, suggesting that TLR4 signaling in intrinsic kidney cells plays the dominant role in mediating kidney damage. 相似文献
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SR Kulkarni MS Gohel RA Bulbulia MR Whyman KR Poskitt 《Annals of the Royal College of Surgeons of England》2009,91(3):210-213