氧化亚氮联合利多卡因行无痛人工流产术280例临床分析

目的: 探讨吸入 50%氧化亚氮 (N2O) 与 50%氧气 (O2 ) 的混合气体联合宫颈注射 2%利多卡因进行无痛人工流产术 (人流术) 的有效性和安全性。方法: 将人流术 580例分为A、B两组。其中A组 280例吸入 50%氧化亚氮 (N2O)与 50%氧气的混合气体联合宫颈注射 2%利多卡因进行无痛人流术, 称为联合组; B组 300例, 不用任何药物, 为对照组, 分析比较两组手术中镇痛效果, 宫口松弛情况, 手术出血量, 人流综合反应。结果: 联合组镇痛完全, 有效率达 97 5%。宫口完全松弛率 97 9%。两组比较有显著性差异 (P<0 05)。结论: 吸入氧化亚氮联合宫颈注射利多卡因进行无痛人流术, 镇痛效果确定, 人流时受术者意识处于朦胧状态, 安静, 无痛苦, 不良反应少, 苏醒快等。     

Mechanism of adrenocortical toxicity induced by quinocetone and its bidesoxy-quinocetone metabolite in porcine adrenocortical cells in vitro

Quinocetone (QCT) is a new feeding antibacterial agent in the QdNOs family. The mechanism of its adrenal toxicity is far from clear. This study was conducted to estimate the adrenal cell damage induced by QCT and its bidesoxy-quinocetone (B-QCT) metabolite and to further investigate their mechanisms. Following doses of QCT increasing from 5 to 50 μM, cell apoptosis and necrosis, mitochondrial dysfunction and redox imbalance were observed in porcine adrenocortical cells. The mRNA levels of the six components of intermediary enzymes and the adrenal renin-angiotensin-aldosterone system (RAAS) displayed a dysregulation induced by QCT, indicating that QCT might influence aldosterone secretion not only through the upstream of the production but also through the downstream of the adrenal RAAS pathway. In contrast, B-QCT had few toxic effects on the cell apoptosis, mitochondrial dysfunction and redox imbalance. Moreover, LCMS-IT-TOF analysis showed that no desoxy metabolites of QCT were found in either cell lysate or supernatant samples. In conclusion, we reported on the cytotoxicity in porcine adrenocortical cells exposed to QCT via oxidative stress, which raised awareness that its toxic effects resulted from N→O groups, and its toxic mechanism might involve the interference of the steroid hormone biosynthesis pathway.     

ACS合并AHF患者治疗中RAAS抑制剂对CI-AKI发病的影响

目的 探讨肾素血管紧张素醛固酮系统（RAAS）抑制剂在急性冠状动脉综合征（ACS）合并急性心力衰竭（AHF）患者经皮冠状动脉介入术（PCI）中对比剂致急性肾损伤（CI-AKI）中的作用。方法 回顾性分析成功行PCI手术ACS合并AHF患者504例,并于术后24～48 h内复查肾功能。分别按照有无CI-AKI及有无应用RAAS抑制剂进行分组,对比相关观察指标,并将差异有统计学意义的观察指标进行Logistics回归分析。结果 504例患者中144例（28.6%）患者发生CI-AKI。CI-AKI组RAAS抑制剂使用比例、高血压、糖尿病患病率与非CI-AKI组比较,差异有统计学意义（P?<0.05）。CI-AKI组反映心脏功能超声指标LVEF、LVEDD、PAP、NT-proBNP、hs-CRP及Hcy水平与非CI-AKI组比较,差异有统计学意义（P?<0.05）。将上述指标引入Logistic回归分析发现,应用RAAS抑制剂对CI-AKI影响消失。而高血压、NT-proBNP、Hcy、hs-CRP、LVEF、PAP仍为心力衰竭患者CI-AKI发生高危因素。结论 对ACS合并AHF患者需行PCI治疗患者,常规应用RAAS抑制剂并不增加CI-AKI发生风险。     

Dietary Interventions for Heart Failure in Older Adults: Re-Emergence of the Hedonic Shift

Dietary non-adherence to sodium restriction is an important contribution to heart failure (HF) symptom burden, particularly in older adults. While knowledge, skills, and attitudes toward sodium restriction are important, sodium intake is closely linked to the ability to taste salt. The ‘hedonic shift’ occurs when sodium restriction induces changes in an individual’s salt taste that lower subsequent salt affinity. Older adults often have compromised salt taste and higher dietary salt affinity due to age-related changes. Older HF patients may have additional loss of salt taste and elevated salt appetite due to comorbid conditions, medication use, and micronutrient or electrolyte abnormalities, creating a significant barrier to dietary adherence. Induction of the hedonic shift has the potential to improve long-term dietary sodium restriction and significantly impact HF outcomes in older adults.     

Pathophysiologic mechanisms in diabetic kidney disease: A focus on current and future therapeutic targets

Diabetic kidney disease (DKD) is the primary cause of chronic kidney disease around the globe and is one of the main complications in patients with type 1 and 2 diabetes. The standard treatment for DKD is drugs controlling hyperglycemia and high blood pressure. Renin angiotensin aldosterone system blockade and sodium glucose cotransporter 2 (SGLT2) inhibition have yielded promising results in DKD, but many diabetic patients on such treatments nevertheless continue to develop DKD, leading to kidney failure and cardiovascular comorbidities. New therapeutic options are urgently required. We review here the promising therapeutic avenues based on insights into the mechanisms of DKD that have recently emerged, including mineralocorticoid receptor antagonists, SGLT2 inhibitors, glucagon-like peptide-1 receptor agonist, endothelin receptor A inhibition, anti-inflammatory agents, autophagy activators and epigenetic remodelling. The involvement of several molecular mechanisms in DKD pathogenesis, together with the genetic and epigenetic variability of this condition, makes it difficult to target this heterogeneous patient population with a single drug. Personalized medicine, taking into account the genetic and mechanistic variability, may therefore improve renal and cardiovascular protection in diabetic patients with DKD.     

重症急性胰腺炎持续血液净化治疗观察

目的探讨持续性血液净化技术在重症急性胰腺炎治疗中的效果。方法23例患者接受传统临床药物治疗,23患者在此基础上加上持续性血液净化技术,对比两组患者炎性因子等指标改善的情况。结果治疗24h后,观察组IL-1、IL-6、IL-8、TNF-α分别为（246．52±31．84）pg／ml、（15．12±1．07）pg／ml、（16．05±1．08）pg／ml、（1．42±0．31）ng／L,治疗48h后,观察组IL-1、IL-6、IL-8、TNF-α分别为（190．46±27．65）pg／ml、（11．07±1．87）pg／ml、（11．04±1．57）pg／ml、（0．68±0．34）ng／L,均显著低于治疗前,差异有统计学意义（P〈0．05）,且观察组指标明显低于对照组。治疗24h后,观察组Ang-Ⅰ、Ang-Ⅱ、E、ALD分别为（1．34±1．17）ng／L、（0．72±5．37）ng／L、（1．05±0．21）ng／ml、（145．27±15．34）pg／ml,治疗48h后,观察组Ang-Ⅰ、Ang-Ⅱ、E、ALD分别为（9．28±1．16）ng／L、（48．42±4．10）ng／L、（0．63±0．11）ng／ml、（99．31±11．16）pg／ml,均显著低于治疗前,差异有统计学意义（P〈0．05）,且观察组指标明显低于对照组。结论CBP可以明显缓解SAP病情,促进炎性因子和RAAS系统的改善。     

Proteinuric renal disease in type 2 diabetes—Is remission of proteinuria associated with improved mortality and morbidity?

Aims

Patients with type 2 diabetes and macroalbuminuria are at high risk for end stage renal disease (ESRD), cardiovascular disease and death, but remission of proteinuria may improve prognosis. We examine the effectiveness of currently recommended treatments on inducing remission of proteinuria, and on morbidity and mortality.

Methods

Observational study of 78 patients with type 2 diabetes (46 male) with mean age (SD) of 61.5 (11) years, with a urinary albumin/creatinine ratio (ACR) ≥ 50 mg/mmol. All were treated with agents blocking the renin–angiotensin system. Follow-up was from recognition of ACR ≥ 50 mg/mmol until death or March 2011 (median 6 years). Remission of proteinuria was defined as ≥70% reduction from peak ACR, sustained for ≥1 year.

Results

Only 22 of 78 patients (28%) achieved remission of proteinuria. Thirty-six (46%) had at least one major event (death, dialysis or cardiovascular). Remission of proteinuria was associated with lower incidence of ESRD/death (9% vs 36%; p = 0.02) but cardiovascular events were not reduced (32% vs 30%). A third of patients had no retinopathy when albuminuria was first recognised, suggesting that non-diabetic renal pathologies were prominent. There was a significant interaction between the severity of diabetic retinopathy and remission of proteinuria on the risk of ESRD/death (p = 0.0003).

Conclusions

Remission of proteinuria was achieved in only a third of patients despite efforts to achieve blood pressure targets <130/80 mmHg. Failure to attain remission of proteinuria was associated with increased risk of ESRD or death, a risk compounded by the presence of severe diabetic retinopathy.