Iron complex, dabigatran and toxic epidermal necrolysis syndrome: a case-report.

WHAT IS KNOWN AND OBJECTIVE: Toxic Epidermal Necrolysis Syndrome falls in the spectrum of acute idiosyncratic bullous disorders with medications being the major aetiological factor. The authors review the relevant literature and report a case of Toxic Epidermal Necrolysis Syndrome where two medications, iron protein succinylate and dabigatran, not previously associated with the disorder might have acted as precipitants to it. CASE SUMMARY: An 86-year-old female recently introduced to iron protein succinylate and dabigatran, presented with a widespread rash consisting of erythematous macules symmetrically distributed on her torso and both upper and lower limbs, down to her extremities. She was diagnosed with Toxic Epidermal Necrolysis Syndrome. None of the drugs previously implicated with the disorder were listed in her recent prescriptions. It was therefore concluded that the two most recently initiated medications, iron protein succinylate and dabigatran, might have been the cause. They were both discontinued to good effect for our patient. WHAT IS NEW AND CONCLUSION: Although neither iron protein succinylate nor dabigatran has been incriminated as causative of Toxic Epidermal Necrolysis Syndrome, we believe that either one of these or their interaction might have acted as the precipitant to this condition. We suggest that the possibilities of the above associations should be further explored.

Metabolic management of coronary heart disease: adjunctive treatment with trimetazidine decreases QT dispersion in patients with a first acute myocardial infarction.

PURPOSE: The metabolic management of ischemic heart disease represents a promising new therapeutic approach for acute coronary syndromes. Trimetazidine has been suggested to exert anti-ischemic properties on myocardium without affecting myocardial oxygen consumption or supply. The aim of this study was to investigate whether the administration of trimetazidine, as an adjunct to conventional treatment, decreases QT dispersion in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: The study was prospective, randomized, double-blind and included 55 out of 86 consecutive patients aged < or = 80 years, admitted with a first AMI. Excluded from the study subjects with atrial fibrillation or pacing-rhythm, bundle branch block, pericardial or valvular heart disease or cardiogenic shock. Also were excluded patients treated with inotropic and antiarrhythmic agents, except for beta blockers. Enrolled patients were randomized into 2 groups: Trimetazidine group (n=29) and control group (n = 26). All patients were treated conventionally and, in addition, trimetazidine group patients were received trimetazidine 20 mg orally every 8 hours started after randomization and continued throughout hospitalization. The QT and QTc (corrected QT) dispersion were measured manually on 3 and 7 post-AMI days. The mean values of QT and QTc dispersion were significantly lower in trimetazidine group on both days, compared to control group: Day 3, QTD = 52+/-24 ms vs 68+/-30 ms (p = 0.034), QTcD = 52+/-21 ms vs 75+/-34 ms (p = 0.004). Day 7, QTD = 39+/-17 ms vs 60+/-20 ms (p < 0.0001), QTcD 40+/-17 ms vs 62+/-20 ms (p < 0.0001). Between days 3 and 7 the mean values of QT (p = 0.003) and QTc dispersion (p = 0.002) were decreased significantly only in trimetazidine group. An analysis with respect to the use of thrombolysis revealed that trimetazidine sub-groups had lower QT and QTc dispersion mean values on day 7, both in patients treated (p < 0.05) and non-treated (p = 0.001) with thrombolysis. CONCLUSIONS: It is concluded that trimetazidine decreases QT and QTc dispersion after acute myocardial infarction. Further investigation is needed to evaluate the mechanism and the clinical implications of this effect.