The Role of Allergic Contact Dermatitis in Diaper Dermatitis

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A Randomized Trial of Intravenous Streptokinase Versus Tissue Plasminogen Activator for the Treatment of Acute Myocardial Infarction: Results Using an Aggressive Approach

Seventy-six patients presenting within 6 hours of the onset of an acute myocardial infarction were randomized to either treatment with 1.5 million units of Streptokinase or 100 mg of recombinant tissue plasminogen activator intravenously. Patients not demonstrating clinical reperfusion within 1 hour were taken emergently for “salvage” angioplasty or coronary bypass surgery. Those patients demonstrating clinical reperfusion underwent early (12 to 72 hours) elective angiography and either elective angioplasty or bypass surgery. The mean time from pain onset to treatment was 149 minutes in the Streptokinase group and 134 minutes in the recombinant tissue plasminogen activator group (P = NS). There were no statistical differences between groups with regard to prior myocardial infarction, infarct location, prior coronary bypass surgery and Killip classification. Clinical reperfusion was demonstrated in 56% of the Streptokinase group and 53% of the recombinant tissue plasminogen activator group (P - NS). Angiographic patency was demonstrated in 70% of the Streptokinase group and 66% of the recombinant tissue plasminogen activator group (P = NS). Left ventricular ejection fraction at discharge was no different: 47% in the Streptokinase group and 43% in the recombinant tissue plasminogen activator group (P = NS). Recurrent ischemic events were found more often in the recombinant tissue plasminogen activator group, 18%, versus the Streptokinase group 3% (P = 0.05). Treatment outcomes did not differ between groups. There was one (3%) death in the Streptokinase group versus two (6%) deaths in the recombinant tissue plasminogen activator group (P = NS). There was a trend toward a greater need for emergent coronary bypass surgery after attempted angioplasty in the recombinant tissue plasminogen activator group, four of 18 patients (22%) versus one of 23 patients (4%) in the Streptokinase group (P = 0.14). In summary, in the setting of acute myocardial infarction treated by thrombolysis, those patients treated with recombinant tissue plasminogen activator experienced significantly more recurrent ischemic events and required emergent coronary bypass surgery more frequently for failed angioplasty compared to those treated with Streptokinase. The results suggest there may be agent specific increases in complications dependent upon the thrombolytic agent of choice when salvage or early coronary angioplasty is used.     

Intravenous Drug Therapy in Premature Infants: Practical Aspects

Most decisions regarding the methods used for intravenous drug delivery are made by nurses. For this reason, neonatal nurses must recognize the unique problems associated with drug delivery to the low birth weight infant. A review of the associated problems is presented along with suggested solutions to aid the nurse in choosing a therapeutic method for intravenous drug administration.     

Thermal Facilitation of Lymphocyte Trafficking Involves Temporal Induction of Intravascular ICAM‐1

Objective: Fever is associated with improved survival, although its beneficial mechanisms are poorly understood. Previous studies indicate that the thermal element of fever augments lymphocyte migration across high endothelial venules (HEVs) of lymphoid organs by increasing the intravascular display of a gatekeeper trafficking molecule, intercellular adhesion molecule‐1 (ICAM‐1). Here, we evaluated the spatio‐temporal relationship between the thermal induction of intravascular ICAM‐1 and lymphocyte trafficking. Methods: Intravascular ICAM‐1 density was quantified by immunofluorescence staining in mice exposed to fever‐range whole‐body hyperthermia (39.5±0.5°C). ICAM‐1–dependent lymphocyte trafficking was measured in short‐term homing assays. Results: A linear relationship was observed between the duration of heat treatment and intravascular ICAM‐1 density in HEVs with maximal responses requiring sustained (i.e., five hours) thermal stress. Circulating lymphocytes were found to sense incremental changes in ICAM‐1 on HEVs, such that trafficking is proportional to the intravascular density of ICAM‐1. We further identified a hydroxamate‐sensitive shedding mechanism that restores ICAM‐1 expression to homeostatic levels following the cessation of thermal stress. Conclusions: The time‐dependent response to thermal stress indicates that ICAM‐1 density governs the efficiency of lymphocyte interactions with HEVs in vivo. These studies highlight the dynamic role of the microcirculation in promoting immune surveillance during febrile inflammatory responses.     

The Effect of Acute Versus Delayed Remote Ischemic Preconditioning on Reperfusion Induced Ventricular Arrhythmias

Remote Ischemic Preconditioning and Cardiac Arrhythmias. Introduction: The effect of remote ischemic preconditioning (RIPC) on arrhythmias in in vivo models is unknown. Our purpose was to determine effects of both acute and delayed RIPC on arrhythmias. Methods and Results: In the acute protocol anesthetized open chest rats were exposed to 5 minutes of proximal left coronary artery occlusion (CAO) and 10 minutes of reperfusion. Rats were either untreated (ischemia/reperfusion, IR group, n = 17) or received RIPC (n = 14) with 5 minutes bilateral femoral occlusions followed by 5 minutes of reperfusion times 3, started 30 minutes before CAO. At reperfusion, onset of ventricular tachycardia (VT) was delayed in RIPC group (25.7 seconds) versus IR (8.8 seconds; P = 0.04). Number of episodes of VT was 17.0 in IR versus 3.0 in the RIPC group (P = 0.01) and duration of VT was 54.1 seconds in IR versus 4.9 seconds in RIPC (P = 0.019). Number of ventricular premature complexes (VPC) was 26.0 in IR and 10.0 in RIPC rats (P = 0.04). Levels of reperfusion injury salvage kinases (RISK), that is, phospho‐Akt and phospho‐p70S6 in the risk area of IR and RIPC hearts were similarly higher compared to the nonischemic areas both at 1 and 10 minutes into reperfusion. Delayed RIPC was induced on day 1 and on day 2, myocardial IR was induced. Delayed RIPC did not affect VT or VPC. Conclusion: Acute RIPC of the lower limbs induced a powerful delay in/and reduction in IR induced ventricular arrhythmias, but without evoking the RISK pathway; a late protective phase of RIPC on arrhythmias did not occur. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1374‐1383, December 2012)