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BACKGROUND: In 2011 a list of 20 drugs linked to drug-induced Tako-Tsubo cardiomyopathy (TCM) was published. Thus, the objectives were both to identify cases of drug-induced TCM, and update the 2011 list of drugs as possible triggers of this cardiomyopathy. METHOD: As the 2011 report of drug-induced TCM, case reports of drug-induced TCM were identified by a comprehensive search in Medline/PubMed database. From December 2010 to March 2015 search terms were Takotsubo cardiomyopathy, Takotsubo cardiomyopathy, stress cardiomyopathy, transient-left-ventricular ballooning syndrome, ampulla cardiomyopathy, apical ballooning syndrome, OR broken heart syndrome; together with "iatrogenic", "drug-induced", OR "induced by". Publications limited to English, Spanish, and French, in humans, and with full texts were retrieved. Articles that recognized any drug as a possible trigger of TCM were selected. RESULTS: Overall, 405 different references were retrieved and 67 were selected (62 case reports and 5 case series) involving 78 patient cases with TCM possibly associated to drugs were reviewed. At total of 44 drugs were recognized as possible drug-induced TCM, mainly with sympathetic effect, and 37 (84.1%) were different to those 20 identified in the 2011 review; therefore, a list of 57 drugs associated to TCM was obtained. CONCLUSION: There are new case reports that linked drug-use with the development of TCM. The list of 57 drugs obtained is principally integrated by drugs that generate sympathetic overstimulation. Consequently, the recommendation "drug-induced TCM would be considered in patients with TCM, particularly those in which no clear emotional or stress trigger could be identified" is endorsed.

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Adriamycin is a potent and broad-spectrum antineoplastic agent that plays a major role in cancer chemotherapy. Unfortunately, its use has been hampered by conventional toxicities and cardiotoxicity manifested by congestive cardiomyopathy. Adriamycin is particularly toxic to heart tissue and constitutes a major cause of morbidity and mortality due to its complex pathogenesis. In this review, the different forms of cardiotoxicity produced by adriamycin as well as the biochemical changes induced by this drug are summarized. Secondly, the current hypotheses proposed to explain adriamycin-induced myocardial damage (the iron and free-radical hypothesis, the metabolic hypothesis, the "unifying hypothesis" and apoptosis) and the attempts to reduce adriamycin-induced myocardial toxicity are discussed (e.g. dose limitation, close cardiac monitoring, alteration of dosage schedules, development of new anthracycline analogs, and the administration of protective agents and liposomal encapsulation). Finally, we summarized our own experimental and clinical experience in ameliorating and or preventing adriamycin-induced cardiotoxicity and the latest attempts to prevent and/or monitor cardiac function. According to this, a combination of usual doses of calcium antagonist drugs plus vitamins A and E seems advisable.

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La porfiria cutánea tarda esclerodermiforme (PCTE) es una forma poco frecuente de la presentación de la porfiria cutánea tarda (PCT), representando el 18-33 por ciento de los casos. Se caracteriza por manifestarse con placas esclerodermiformes de aparición insidiosa y tardía en el curso de la enfermedad. El déficit de la actividad de la enzima uroporfirinógeno decarboxilasa (UPDC), lleva a la acumulación de metabolitos intermedios responsables de las manifestaciones clínicas y bioquímicas. Se presentan cuatro pacientes con PCTE estudiados en nuestro Servicio, en un período de cuatro años (1992-1996)

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