[Toxic epidermal necrolysis: idiosyncratic reaction to drugs]. / Necrólisis epidérmica tóxica: reacción idiosincrática a neurofármacos.

Toxic epidermal necrolysis (NET) and Steven Johnson syndrome (SJS) are infrequent mucocutaneous hypersensitivity reactions with systemic involvement. They are predominantly caused by drugs. We report the case of a patient over 60 years of age who presented with extensive mucocutaneous and ophthalmic injury with hemodynamic failure, associated with the rapid onset of lamotrigine in a short period of time. Although the incidence is low, the mortality rate is high. It requires early suspicious and diagnosis in addition to an interdisciplinary therapeutic approach.

[Hypoxic hepatitis in a patient with endomyocardial fibrosis]. / Hepatitis hipóxica en paciente con endomiocardiofibrosis.

Endomyocardial fibrosis is a restrictive cardiomyopathy with high morbidity and mortality rates, prevalent in the sub-Saharan Africa region but infrequent in our population. It has a close relation with blood hypereosinophilia. Hypoxic hepatitis is frequently observed in intensive care units and its diagnosis is clinical. It shows a typical enzyme pattern with high mortality too. There are multiple mechanisms responsible for this condition, such as ischemia, passive congestion and dysoxia. We described the case of a 35 year-old cocaine addict woman diagnosed with endomyocardial fibrosis and hypereosinophilic syndrome who developed cardiogenic shock with hypoxic hepatitis. The patient evolved favorably with the appropriate treatment.

La endomiocardiofibrosis es una causa de miocardiopatía restrictiva frecuente en la región de áfrica subsahariana, aunque poco frecuente en nuestra población. Posee estrecha relación con la presencia de hipereosinofilia en sangre y tiene alta morbimortalidad. La hepatitis hipóxica es una afección clínica con un patrón enzimático característico, muy prevalente en unidades de cuidados intensivos y elevada mortalidad. Se reconocen múltiples mecanismos fisiopatológicos, como la isquemia, la congestión venosa y la alteración en la utilización de oxígeno del hepatocito. Describimos el caso de u na paciente de 35 años, consumidora de cocaína, con diagnóstico de endomiocardiofibrosis secundario a síndrome hipereosinofílico idiopático que presentó shock cardiogénico y hepatitis hipóxica asociada. Evolucionó favorablemente con el tratamiento de sostén adecuado.

Hepatitis hipóxica en paciente con endomiocardiofibrosis / Hypoxic hepatitis in a patient with endomyocardial fibrosis

La endomiocardiofibrosis es una causa de miocardiopatía restrictiva frecuente en la región de África subsahariana, aunque poco frecuente en nuestra población. Posee estrecha relación con la presencia de hipereosinofilia en sangre y tiene alta morbimortalidad. La hepatitis hipóxica es una afección clínica con un patrón enzimático característico, muy prevalente en unidades de cuidados intensivos y elevada mortalidad. Se reconocen múltiples mecanismos fisiopatológicos, como la isquemia, la congestión venosa y la alteración en la utilización de oxígeno del hepatocito. Describimos el caso de u na paciente de 35 años, consumidora de cocaína, con diagnóstico de endomiocardiofibrosis secundario a síndrome hipereosinofílico idiopático que presentó shock cardiogénico y hepatitis hipóxica asociada. Evolucionó favorablemente con el tratamiento de sostén adecuado.

Endomyocardial fibrosis is a restrictive cardiomyopathy with high morbidity and mortality rates, prevalent in the sub-Saharan Africa region but infrequent in our population. It has a close relation with blood hypereosinophilia. Hypoxic hepatitis is frequently observed in intensive care units and its diagnosis is clinical. It shows a typical enzyme pattern with high mortality too. There are multiple mechanisms responsible for this condition, such as ischemia, passive congestion and dysoxia. We described the case of a 35 year-old cocaine addict woman diagnosed with endomyocardial fibrosis and hypereosinophilic syndrome who developed cardiogenic shock with hypoxic hepatitis. The patient evolved favorably with the appropriate treatment.

[Hypokalemic rhabdomyolisis and schizophrenia]. / Rabdomiólisis hipokalémica y esquizofrenia.

The purpose of this report is to emphasize the necessity to periodically explore internal environment variables, as certain metabolic alterations often go unnoticed during antipsychotic treatment. Early detection of such alterations may prevent catastrophic syndromes. We will also stress the clinical relevance of cognitive perseverations in schizophrenic patients, as these often condition habits of consumption which can alter the internal environment. In this clinical case of a schizophrenic patient, a chain of events led to a catastrophic syndrome: a trivial home accident (fall from own height) developed into a condition characterized by oligoanuria, hypokalemia, creatine phosphokinase (CPK) elevation (125,000 IU / L) and acute renal failure with dialysis requirement. This episode was non lethal due to the early implementation of support measures. We performed a revision of the available literature in order to discern the cause of the elevation of CPK. Here we aim to highlight the importance of 1) careful clinical and laboratory monitoring of psychopharmacological treatment, 2) interactions resulting from consumption habits capable of generating unforeseen consequences, 3) the role of the psychiatrist in the context of multidisciplinary work.

[Takotsubo cardiomyopathy: The mind-body continuum]. / Enfermedad de Takotsubo: el binomio mente-cuerpo.

Takotsubo disease, also called "apical ballooning syndrome", "stress cardiomyopathy" or "broken-heart syndrome" is a potentially lethal entity. It is usually triggered by psychological or physical stress, either individual or collective, as a traumatic experience which is sudden and acute. Clinical presentation is usually accompanied by severe myocardial failure, which generally requires hemodynamic support in Cardiovascular Care Unit.

[Mixed Munchausen Syndrome with organic comorbidity]. / Síndrome de Munchausen mixto con comorbilidad orgánica.

We present a detailed case report that shows a woman patient who has Factitious Disorder manifested by the coexistence both of: A) typical/direct Munchausen and B) Munchausen by proxy or indirect: being the frst one (A) about the own person and the second one (B) about other people (most cases about their own young children). Furthermore, in the reported case we observed that the patient shown the particularity of having positive biological markers for Myasthenia Gravis (serology markers), and having inconsistent clinical manifestations that are typically observed in the exacerbation phase when she still continued in remission phase. In our own bibliographic research we couldn`t fnd anything about this case of "Mixed Munchausen Syndrome with organic comorbidity". In the same way as we tried to get information about the diagnostic algorithms and the possible therapeutic treatment strategies we found nothing like this reported before. Finally, this clinical presentation constitutes a blind spot for the scientifc community generating a lack of recognition for this diagnostic category and above all of the confusion that this mental disorder can generate in: a) the inadequate use of therapeutic resources, b) the irrational use of drugs, c) the distortion of institutional instances, and d) the medical behaviors that occurred in this case.

[The century of the receptor, history of ideas that launched psychopharmacology]. / El siglo del receptor, historia de ideas que iniciaron la psicofarmacología.

Nowadays, the term receptor is obvious in psychopharmacology. However, this was not so obvious a century ago. To try to explain how drugs act, European scientists began to develop theories that turned into deeds with the scientific progress. Thus, the receptor concept and their applications in medicine and psychiatry began to gain substance. In this paper we relate the facts that have led to the current knowledge of receptor, the cornerstone of pharmacology.

[Thalidomide and its legacy, the rational inside the irrational]. / La talidomida y su legado, lo racional dentro de lo irracional.

Thalidomide was synthesized by Chemie Grünenthal from Germany and launched at October 1957, as a sedative and antiemetic drug. In only four years after being widely and freely prescribed to pregnant women, unleashed an epidemic of teratogenicity that revolutionized health and public opinion. From that moment, world regulation on drugs and its development was radically changed, the clinical trial as a tool was completely revised, while pharmacovigilance as a discipline was established. In a second chance, its irrational use as psychotropic drug was changed to use as immunomodulator, context in which it is prescribed today. This paper aims to highlight some historical aspects of thalidomide to draw conclusions for rational use of psychotropic drugs.

[Cocaine-induced agitated delirium, a different consequence of cocaine addiction]. / Delirium agitado fatal, una consecuencia diferente de la adicción a la cocaína.

In the past 10 years, chronic drug abuse health problems have become complex medical-legal problems. These include Cocaine-Induced Agitated Delirium, an idiosyncratic illness appears 1-2 hours after regular drug intake and can cause death without overdose is detected at autopsy. This review studies the molecular changes caused by cocaine abuse that derived into Cocaine-Induced Agitated Delirium. The molecular-clinical correlation links the phenomena induced by the abuse expressed at different levels of complexity, from the biochemical to the social. The purpose here is to induce a greater awareness of this illness to improve its prevention, to obtain its early diagnosis and to achieve its appropriate therapeutic-legal approach. Cocaine-Induced Agitated Delirium should be considered as the result of several unseen changes, that if they reach a critical threshold trigger the fatal outcome. This makes the abuse of cocaine and the individual predisposition solely responsible for its appearance.

Delirium agitado fatal, una consecuencia diferente de la adicción a la cacaína / Cocaine-induced agitated delirium, a different consequence of cocaine addiction

Los problemas sanitarios por el consumo crónico de sustancias de abuso, se han transformado en problemas médico-legales en los últimos 10 años. Entre estos se destaca el Delirium Agitado Fatal por Cocaína, cuadro idiosincrático que deviene luego de 1 a 2 horas de una ingesta habitual y que puede causar la muerte sin que se detecte sobredosis en la autopsia. Esta revisión tiene como objetivo estudiar los cambios moleculares que provoca el consumo crónico de cocaína vinculados con el Delirium Agitado Fatal por Cocaína. La correlación molecular-clínica permite vincular los fenómenos inducidos por el consumo abusivo que se expresan en los distintos niveles de complejidad, desde lo bioquímico a lo social. De esta forma se pretende inducir un mayor conocimiento de este cuadro a fin mejorar su prevención, su diagnóstico temprano y su abordaje terapéutico-legal. En suma, el Delirium Agitado Fatal por Cocaína debe ser considerado como la consecuencia de varias modificaciones inadvertidas que, alcanzado un umbral crítico desencadena el cuadro fatal. Esto hace al consumo abusivo de cocaína y a la predisposición individual los únicos responsables de su aparición.(AU)

In the past 10 years, chronic drug abuse health problems have become complex medical-legal problems. These include Cocaine-Induced Agitated Delirium, an idiosyncratic illness appears 1-2 hours after regular drug intake and can cause death without overdose is detected at autopsy. This review studies the molecular changes caused by cocaine abuse that derived into Cocaine-Induced Agitated Delirium. The molecular-clinical correlation links the phenomena induced by the abuse expressed at different levels of complexity, from the biochemical to the social. The purpose here is to induce a greater awareness of this illness to improve its prevention, to obtain its early diagnosis and to achieve its appropriate therapeutic-legal approach. Cocaine-Induced Agitated Delirium should be considered as the result of several unseen changes, that if they reach a critical threshold trigger the fatal outcome. This makes the abuse of cocaine and the individual predisposition solely responsible for its appearance.(AU)

Delirium agitado fatal, una consecuencia diferente de la adicción a la cacaína / Cocaine-induced agitated delirium, a different consequence of cocaine addiction

Los problemas sanitarios por el consumo crónico de sustancias de abuso, se han transformado en problemas médico-legales en los últimos 10 años. Entre estos se destaca el Delirium Agitado Fatal por Cocaína, cuadro idiosincrático que deviene luego de 1 a 2 horas de una ingesta habitual y que puede causar la muerte sin que se detecte sobredosis en la autopsia. Esta revisión tiene como objetivo estudiar los cambios moleculares que provoca el consumo crónico de cocaína vinculados con el Delirium Agitado Fatal por Cocaína. La correlación molecular-clínica permite vincular los fenómenos inducidos por el consumo abusivo que se expresan en los distintos niveles de complejidad, desde lo bioquímico a lo social. De esta forma se pretende inducir un mayor conocimiento de este cuadro a fin mejorar su prevención, su diagnóstico temprano y su abordaje terapéutico-legal. En suma, el Delirium Agitado Fatal por Cocaína debe ser considerado como la consecuencia de varias modificaciones inadvertidas que, alcanzado un umbral crítico desencadena el cuadro fatal. Esto hace al consumo abusivo de cocaína y a la predisposición individual los únicos responsables de su aparición.

In the past 10 years, chronic drug abuse health problems have become complex medical-legal problems. These include Cocaine-Induced Agitated Delirium, an idiosyncratic illness appears 1-2 hours after regular drug intake and can cause death without overdose is detected at autopsy. This review studies the molecular changes caused by cocaine abuse that derived into Cocaine-Induced Agitated Delirium. The molecular-clinical correlation links the phenomena induced by the abuse expressed at different levels of complexity, from the biochemical to the social. The purpose here is to induce a greater awareness of this illness to improve its prevention, to obtain its early diagnosis and to achieve its appropriate therapeutic-legal approach. Cocaine-Induced Agitated Delirium should be considered as the result of several unseen changes, that if they reach a critical threshold trigger the fatal outcome. This makes the abuse of cocaine and the individual predisposition solely responsible for its appearance.