[Adenosine triphosphate in the treatment of supraventricular paroxysmal tachycardia: a comparison with verapamil]. / Trifosfato de adenosina en el tratamiento de la taquicardia paroxística supraventricular: comparación con verapamilo.

AIMS: There are multiple drugs options in the treatment of Paroxysmal Supraventricular Tachycardia (PST) after inefficacious vagal stimulus. In this study we compare two of these treatments: verapamil versus adenosin triphosphate (ATP). METHODS: Fifty patients with PST were randomly treated with either Verapamil (5 to 10 mg) or ATP (5 to 20 mg). The basal features of each group, and the efficacy and safety of the two drugs were compared. Verapamil failures were treated with ATP and vice versa. RESULTS: The characteristics of both groups of treatment were similar. 86% of PST episodes were resolved with Verapamil use, versus 83% after ATP administration. Finally all patients were successfully treated with these drugs. No adverse effects were observed with Verapamil, whereas these effects were frequent with ATP use, but in any case requiring specific intervention. CONCLUSIONS: Both Verapamil and aTP are an equally safe and effective treatment of PST, but transient and minor side effects are frequent after ATP administration.

[The coronary sulcus and ischemic cardiopathy: an independent association of risk factors]. / Surco coronario y cardiopatía isquémica: una asociación independiente de los factores de riesgo.

BACKGROUND: Coronary sulcus of the auricular lobe has been related to the presence of ischemic cardiopathy although the nature of this relation has not been well defined. The aim of the present study was to determine whether there is a relation between the sulcus and the classical coronary risk factors, or whether the association between coronariopathy and sulcus is independent of such factors. METHODS: Patients admitted into an intensive care unit (n = 222) were divided into two groups according to whether coronary sulcus was present and the following analysis were performed: 1) comparative study between the groups for the variables: age, sex, coronariopathy, hyperglycemia, hyperlipidemia, hypertension, index of body mass, and tobacco habit. 2) logistic regression analysis used as a variable to study the existence of coronary sulcus and as independent factors the different coronary risk factors. 3) calculation of sensitivity and specificity of the coronary sulcus as a marker of ischemic cardiopathy. RESULTS: In the comparison between groups the individuals with coronary sulcus had greater age, cholesterolemia, index of body mass, with greater frequency found in females with ischemic cardiopathy. In the logistic regression analysis the presence of coronary sulcus was only associated by order of statistical significance to the variables of age and the female sex. In this study, coronary sulcus was a sensitive (87.6%) although unspecific (41.2%) marker of coronariopathy. CONCLUSIONS: The prevalence of coronary sulcus increases with age, and is greater in patients with ischemic cardiopathy. This relation is independent of the classical coronary risk factors.

[Acute polyneuropathy and encephalopathy caused by arsenic poisoning]. / Encefalopatía y polineuropatía agudas causadas por arsénico.

INTRODUCTION: Acute arsenic toxicity is a multisystemic disease with pleural and pericardial effusions, gastrointestinal symptoms and pancytopenia. The most frequent neurological complication of inorganic arsenic intoxication is a distal symmetrical polyneuropathy. CASE REPORT: We report here a patient who developed a systemic illness followed with severe acute polyneuropathy. Electrophysiological findings suggested a Guillain-Barré syndrome (GBS). Finally an acute encephalopathy appeared which led to reconsideration of the diagnosis. A 24-hour heavy metal urine, nail and hair analysis was performed. A diagnosis of arsenic toxicity was made. Instead of chelating therapy patient died due to respiratory failure. CONCLUSIONS: A misdiagnosis of GBS in inorganic arsenic polyneuropathy is not infrequent. Atypical progression compels to rule out arsenic or heavy metal intoxication. In our case the appearance of the encephalopathy was the key to the diagnosis. It has been suggested that axonal degeneration and segmental demyelination might be equally prominent pathological features of the neuropathy, depending on the dosage and the length of time of exposure to arsenic. The exact pathophysiology of arsenic polyneuropathy remains unclear and a interference with pyruvate oxidation has been postulated.

[Acute thoracic syndrome]. / Síndrome torácico agudo.

The acute chest syndrome is a clinical entity appearing in patients suffering from sickle cell anaemia. It presents with pleuritic pain, fever, leucocytosis and pulmonary infiltrates in the thoracic radiology. The etiological diagnosis is difficult, and it is necessary to distinguish between pneumonia and pulmonary infarction. This syndrome is quite frequent among the patients at risk, and can be lethal according to the severity and the etiology of the event. A case of acute chest syndrome due to a S. pneumoniae sepsis is presented. The interest of the case lies in the rareness of this disease in our population and the peculiar evolutive clinical features of this case, with the development of intracranial hypertension and death.

[Osteochondroplastic tracheopathy. Diagnostic confirmation. Experience with 8 cases]. / Traqueopatía osteocondroplásica. Confirmación diagnóstica. Experiencia en 8 casos.

We report our experience in 8 patients with osteochondroplastic tracheopathy and consider the importance of its diagnosis y biopsy in order to confirm histology and if possible etiology, because specific treatment could change the course of the disease. Methods such as radiology, CT-scan, respiratory function tests only give diagnostic suspicion, which is a previous step before confirmation by bronchoscopy with biopsy. To date, with the exception of a few cases, the diagnosis is made by necropsy. Thus, this justifies our emphasis in the diagnosis of this rare disease when it is suspected in living patients.

¿Qué temas eligen los internistas jóvenes en las oposiciones? / No disponible

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Encefalopatía y polineuropatía agudas causadas por arsénico / Acute polyneuropathy and encephalopathy caused by arsenic poisoning

Introducción. La intoxicación por arsénico inorgánico es una enfermedad multisistémica con derrames pericárdico y pleural, síntomas gastrointestinales y pancitopenia. La complicación neurológica más frecuente es la aparición de una polineuropatía distal simétrica. Caso clínico. Se describe la evolución de un paciente con un cuadro sistémico de tres meses de evolución, consistente fundamentalmente en sintomatología abdominal, que desarrolló una tetraparesia rápidamente progresiva asociada a una polineuropatía aguda desmielinizante, atribuida en un primer momento a un síndrome de Guillain-Barré (SGB) postinfeccioso. La aparición de un cuadro encefalopático asociado hizo descartar otras posibilidades diagnósticas; entre ellas, la intoxicación por metales pesados, y se detectaron unos niveles elevados de arsénico en el pelo, las uñas y la orina. A pesar del tratamiento quelante, el paciente falleció por complicaciones respiratorias. Conclusiones. La confusión diagnóstica con un SGB en la polineuropatía por arsénico no es infrecuente. La progresión atípica obliga a descartar intoxicación por metales pesados, entre otras patologías. En nuestro caso, la aparición de un cuadro encefalopático fue clave para el diagnóstico. Las neuropatías por arsénico, tanto desde el punto de vista electrodiagnóstico como anatomopatológico, pueden ser de tipo axonal o desmielinizante, según la dosis y el tiempo de exposición al mismo. Se postula la interferencia con el ciclo de Krebs como mecanismo fisiopatológico (AU)

Introduction. Acute arsenic toxicity is a multisystemic disease with pleural and pericardial effusions, gastrointestinal symptoms and pancytopenia. The most frequent neurological complication of inorganic arsenic intoxication is a distal symmetrical polyneuropathy. Case report. We report here a patient who developed a systemic illness followed with severe acute polyneuropathy. Electrophysiological findings suggested a Guillain-Barré syndrome (GBS). Finally an acute encephalopathy appeared which led to reconsideration of the diagnosis. A 24-hour heavy metal urine, nail and hair analysis was performed. A diagnosis of arsenic toxicity was made. Instead of chelating therapy patient died due to respiratory failure. Conclusions. A misdiagnosis of GBS in inorganic arsenic polyneuropathy is not infrequent. Atypical progression compels to rule out arsenic or heavy metal intoxication. In our case the appearance of the encephalopathy was the key to the diagnosis. It has been suggested that axonal degeneration and segmental demyelination might be equally prominent pathological features of the neuropathy, depending on the dosage and the length of time of exposure to arsenic. The exact pathophysiology of arsenic polyneuropathy remains unclear and a interference with pyruvate oxidation has been postulated (AU)