类固醇糖尿病——糖皮质激素治疗中必须警惕的不良反应

糖皮质激素(glucocorticoid,GC)是所有药物中对糖代谢影响最大的药物.自20世纪40年代考的松成功治疗类风湿关节炎(RA)后,人工合成的GC制剂如泼尼松、泼尼松龙、甲泼尼龙及地塞米松等陆续上市,它们以超生理剂量的形式在减轻感染性或非感染性炎性反应、减少渗出、抗过敏和免疫抑制、抗休克、抗毒素等方面发挥了重要的药理作用.但是,GC的药理特性恰是一把"双刃剑",在发挥治疗作用的同时,也可能产生一系列不良反应如并发糖尿病、各种感染、骨质疏松、消化性溃疡等,这是我们在临床工作中必须要高度重视的问题.     

糖尿病一级预防任重道远

糖尿病肆虐全球!其“高死亡、高致残”使各大洲不同肤色、不同民族的人民深受其害。目前世界范围内的糖尿病总人数为1．71亿,到2030年将达到3．66亿,发展中国家的糖尿病发病率高于发达国家,糖尿病人数前4位的国家依次是：印度、中国、美国和印度尼西亚。2000年全球死于糖尿病的人数290万,占总死亡率的5．2％,排列为主要死亡原因的第8位。糖尿病心脑血管、肾脏及眼并发症的高额医疗花费已经成为世界各国政府和人民的沉重负担。鉴于现行的治疗方法已被证明很难有效地阻止糖尿病并发症的发生和发展,     

Implantable cardioverter-defibrillator therapy in clinical practice

Pharmacologic treatment of heart failure has led to dramatic improvements in survival and quality of life. Nonetheless, heart failure often progresses despite treatment with diuretics, angiotensin-converting enzyme inhibitors, beta-adrenergic blockers, aldosterone antagonists, and digoxin. Further, despite a steady decline in the risk of death from pump failure, many patients remain at high risk for sudden cardiac death. The annual incidence of sudden cardiac death in the U.S. alone has been estimated at 184,000 to over 400,000 cases. During the past decade, substantial advances have been made in the use of device-based therapy for this population. The role of the implantable cardioverter-defibrillator (ICD) continues to evolve in routine heart failure management. The current status of ICD therapy in the treatment of heart failure patients based on randomized clinical trial results and published practice guidelines is summarized in this review.     

Percutaneous coronary intervention following intravenous fibrinolytic therapy: should it be a must?

Of the two methods of reperfusion therapy for acute myocardialinfarction, primary percutaneous coronary intervention (PCI)is more difficult to implement but offers the best results whenperformed in an optimal setting.¹ Although intravenous fibrinolytictherapy is easier to use, it has a lesser capacity to open theculprit artery and therefore is less likely to ensure adequatereperfusion of the jeopardized myocardium; in addition, evenin the case where the artery can be reopened, the result achievedwith fibrinolysis appears less ‘stable’ than thatachieved with primary PCI and exposes the patient to a riskof re-infarction.¹ Combining fibrinolysis with early PCI mightoffer a unique opportunity to associate the practicability ofan easily available intravenous treatment with the capacityof PCI to either reopen persistently occluded arteries or maintainan optimal patency of arteries already reopened by the     

Central pressure should be used in clinical practice

The original purpose for recording brachial blood pressure (BP) more than 100 years ago was to estimate central (aortic) BP. While high brachial BP is an important cardiovascular risk factor, it is clear that major differences in central systolic BP (SBP; e.g. >30 mmHg) can occur among people with similar brachial SBP. It is also proven that central SBP responses to antihypertensive therapy can differ substantially from brachial SBP responses, such that true treatment effects cannot be gauged from conventional brachial BP. Importantly, assessment of central BP results in: 1) improved predictive accuracy of future cardiovascular events beyond brachial BP and other cardiovascular risk factors; 2) superior diagnostic accuracy over brachial BP and; 3) different patient management than usual care guided by brachial BP. Collectively, the above illustrates that central BP is a better cardiovascular risk biomarker than brachial BP. As with all medical advances there are areas of research need and international consensus is required on issues such as standardization of techniques. However, central BP can now be accurately estimated (with appropriate waveform calibration) using brachial cuff methods in an approach that is familiar to clinicians, acceptable to patients and amenable to widespread use. In other words, this modern BP technique can finally satisfy the original purpose for measuring central aortic BP as intended more than 100 years ago. Although the tipping point towards routine use is yet to be reached, the body of evidence continues to favour the view that central BP should be used in clinical practice.     

Central pressure should not be used in clinical practice

The heart, brain and kidneys are key targets of pulsatile damage in older people and in patients with longstanding hypertension. These central organs are exposed to central systolic and pulse pressures, which may differ from the corresponding peripheral pressures measured in the brachial artery. Studies employing the generalized transfer function as a means to estimate central pressure have demonstrated a large difference between central and peripheral systolic and pulse pressure that diminishes with age but remains substantial even in octogenarians. As a result of this persistent difference, some have advocated that central pressure may represent a more robust indicator of risk for target organ damage and major cardiovascular disease events. From the perspective of risk prediction, it is important to acknowledge that a new technique must add incremental predictive value to what is already commonly measured. Thus, in order to justify the added complexity and expense implicit in the measurement, central pressure must be shown to add significantly to a risk factor model that includes standard cardiovascular disease risk factors. A limited number of studies have shown marginally better correlations between central pressure pulsatility and continuous measures of target organ damage in the heart. A similarly limited number of prospective studies in unique cohorts have suggested that central pressure may provide marginally better risk stratification, although no reclassification analysis has been published. Thus, currently available evidence does not provide sufficient justification for widespread adoption and routine use of central pressure measurements in clinical practice.     

Implantable cardioverter-defibrillator therapy in clinical practice.

Pharmacologic treatment of heart failure has led to dramatic improvements in survival and quality of life. Nonetheless, heart failure often progresses despite treatment with diuretics, angiotensin-converting enzyme inhibitors, beta-adrenergic blockers, aldosterone antagonists, and digoxin. Further, despite a steady decline in the risk of death from pump failure, many patients remain at high risk for sudden cardiac death. The annual incidence of sudden cardiac death in the U.S. alone has been estimated at 184,000 to over 400,000 cases. During the past decade, substantial advances have been made in the use of device-based therapy for this population. The role of the implantable cardioverter-defibrillator (ICD) continues to evolve in routine heart failure management. The current status of ICD therapy in the treatment of heart failure patients based on randomized clinical trial results and published practice guidelines is summarized in this review.     

Dose escalation of infliximab in clinical practice: improvements seen may be explained by a regression-like effect

OBJECTIVE: To determine whether increased infliximab doses result in better clinical outcome in rheumatic diseases. METHODS: Subjects were 124 patients with rheumatoid arthritis treated with biological agents at a single institute. Index cases were 44 patients whose infliximab doses had been increased. Controls were patients treated with infliximab without dose increase (n = 44), and patients treated with etanercept (n = 36). Disease activity score (DAS28), ACR28 swollen joint counts, and numerical ACR responses were compared before and after dose increases. For the controls, the point at which the DAS28 value showed any increase (despite infliximab/etanercept treatment) was used as the reference time point. Comparisons were made between three sets of outcomes: best outcome achieved before the dose increase (cases) or before the reference time point (controls); outcomes at this point; and best outcomes after this point. RESULTS: Following dose increase, disease activity showed modest but statistically significant improvements. The improvement achieved after dosage escalation was equal to, but not better than, the best values before dose escalation. While this finding could be interpreted as "recapturing" the previous response, similar improvements were seen in both control groups. Thus the same pattern of worsening and subsequent improvement was seen with or without the infliximab dose increase. CONCLUSIONS: Clinical improvement with increased infliximab dose, and the impression that a previous response can be "recaptured" with higher doses, cannot be taken at face value, as similar improvements occurred in two control groups. The use of infliximab at doses higher than 3 mg/kg needs to be evaluated further.