Colestasis canalicular inducida por anabolizantes esteroideos / Canalicular cholestasis induced by anabolic steroids

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Clinical pattern and acute and long-term management of hereditary angioedema due to C1-esterase inhibitor deficiency

Background: Hereditary angioedema due to C1-esterase inhibitor deficiency (HAE-C1-INH) is a life-threatening disease. Objectives: To describe the clinical characteristics and management of patients with HAE-C1-INH during routine clinical practice. Methods: An observational, retrospective study was performed in patients with HAE-C1-INH. Demographic, clinical, and analytical data were collected from 2 periods: period A (October 2009-September 2010) and period B (October 2007-September 2009). Results: We studied 112 patients with HAE-C1-INH (57.1% females). Age at onset of symptoms was 14.4 years (lower in patients who had experienced attacks in the previous year). In period B (n=87), 62.1% of patients presented at least 1 edema attack (median, 3.5 attacks/patient/2 years), and 19.1% of attacks were treated. In period A (n=77), 58.4% of patients were on maintenance therapy. Stanozolol was the most widely used drug (48.9%), with a mean weekly dose of 6.7 mg. At least 1 attack was recorded in 72.7% of patients (median, 3.0 attacks/patient/year), and 31.5% of the attacks were treated. Treatment of acute attacks increased by 12.4%. Conclusion: Age at onset of symptoms is associated with clinical expression of disease. The higher age at onset of symptoms, the fewer number of attacks per patient and year, and the lower dose of attenuated androgens necessary to control the disease than in other series lead us to hypothesize that HAE-C1-INH could have a less severe expression in Spain. Acute attacks seem to be treated increasingly often (AU)

Antecedentes: El angioedema hereditario por déficit del inhibidor de la C1 esterasa (AEH-C1-INH) es potencialmente mortal. Objetivos: Describir las características clínicas y el manejo de pacientes con AEH-C1-INH durante la práctica clínica habitual. Métodos: Estudio retrospectivo observacional de pacientes con AEH-C1-INH. Se recogieron datos demográficos, clínicos y analíticos en los periodos A (Octubre 2009-Septiembre 2010) y B (Octubre 2007-Septiembre 2009). Resultados: Se estudiaron 112 pacientes con AEH-C1-INH (57,1% mujeres) con edad de inicio de los síntomas de 14,4 años (inferior en aquellos pacientes con ataques en el último año). En el periodo B (n=87) 62,1% tuvo al menos un ataque (mediana: 3,5 ataques/paciente /2 años) y el 19,9% de los ataques se trataron. En el periodo A (n=77) 58,4% recibieron tratamiento de mantenimiento, siendo el estanozolol el fármaco más utilizado (48,9%) (dosis media semanal 6,7mg). El 72,7% de los pacientes tuvo al menos un ataque (mediana: 3,0 ataques / paciente / año), el 31,5% se trataron. Hubo un incremento del 12,4% de tratamientos de ataques agudos. Conclusiones: La edad de inicio de los síntomas está relacionada con la expresión clínica de la enfermedad. La edad superior del inicio de los síntomas, el menor número de ataques por paciente/año, y una dosis inferior de andrógenos atenuados para controlar la enfermedad, comparado con otros países, permite hipotetizar que el AEH-C1-INH en España tendría una expresión clínica menos grave. Existe una tendencia al alza en la frecuencia de tratamiento de ataques agudos (AU)

Stanozolol-induced bland cholestasis

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Prolonged treatment with the anabolic–androgenic steroid stanozolol increases antioxidant defences in rat skeletal muscle

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Testosterone and its synthetic derivatives anabolic–androgenic steroids have been shown to increase skeletal muscle work capacity and fatigue resistance, but the molecular basis for these effects remains uncertain. Since muscle performance has been related to redox status of exercising muscles, this investigation was aimed at testing whether a treatment with suprapharmacological doses of the anabolic–androgenic steroid stanozolol, (2 mg/kg body weight, 5 days/week, for 8 weeks), either alone or in conjunction with treadmill training (12 weeks), enhanced antioxidant defences in rat muscles. Stanozolol treatment did not modify thiobarbituric acid reactive substances and glutathione content in soleus and extensor digitorum longus (EDL) homogenates. In soleus from sedentary rats, superoxide dismutase and glutathione reductase activities were increased by 25% (P < 0.05) and by 40% (P < 0.01) after stanozolol administration, whereas catalase and glutathione peroxidase activities were not modified. This response was similar to that induced by training alone. In EDL from sedentary rats, stanozolol increased only superoxide dismutase activity (20%, P < 0.05). In no case, the effects of steroid administration and training were additive. HSP72 levels were up-regulated in soleus (1.5-fold, P < 0.01) and EDL (threefold, P < 0.001) following training but remained unchanged after stanozolol treatment. Endurance capacity, assessed in a treadmillendurance test, was similar for treated and control rats. We conclude that stanozolol treatment increases antioxidant capacity in selected skeletal muscles from sedentary rats. However, the steroid was not effective in improving endurance capacity or enhancing the training effects on muscle antioxidant defence systems (AU)

Colestasis inducida por consumo de estanozolol / Cholestatic injury by stanozolol intake

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Atrofia blanca con buena respuesta a estanozolol y ácido acetilsalicílico / Atrophic blanche with good response to stanozol. Case report and literature review

La atrofia blanca es un proceso ulcerativo de los miembros inferiores que, en su evolución, da lugar a lesiones atróficas, rodeadas de pigmentación hemosiderótica y telangiectasias, La mayoría de los casos se asocian a insuficiencia venosa crónica, aunque en otras ocasiones se han relacionado con enfermedades sistémícas. Considerada anteriormente como un cuadro de origen vasculltico, actualmente se describe como una vasculopatía trombogénica, en la que se han descrito numerosos tratamientos para corregir las alteraciones de la microcirculación existentes en estos pacientes (AU)

Atrophie blanche is a lower leg ulcerative condition, which develops atrophic lesions, with hemosiderotic changes and telangiectasia. Most cases are associated with chronic venous insufficiency, although underlying systemic diseases have also been described. Although the process was previously considered to be of vasculitic origin, currently it is described as a thrombogenic vasculopathy, with a wide range of therapies aimed at correcting impaired microcirculation in these patients (AU)