RESUMO
Transcriptomics, proteomics and pathogen-host interactomics data are being explored for the in silico-informed selection of drugs, prior to their functional evaluation. The effectiveness of this kind of strategy has been put to the test in the current COVID-19 pandemic, and it has been paying off, leading to a few drugs being rapidly repurposed as treatment against SARS-CoV-2 infection. Several neglected tropical diseases, for which treatment remains unavailable, would benefit from informed in silico investigations of drugs, as performed in this work for Dengue fever disease. We analyzed transcriptomic data in the key tissues of liver, spleen and blood profiles and verified that despite transcriptomic differences due to tissue specialization, the common mechanisms of action, "Adrenergic receptor antagonist", "ATPase inhibitor", "NF-kB pathway inhibitor" and "Serotonin receptor antagonist", were identified as druggable (e.g., oxprenolol, digoxin, auranofin and palonosetron, respectively) to oppose the effects of severe Dengue infection in these tissues. These are good candidates for future functional evaluation and clinical trials.
Assuntos
Antivirais/uso terapêutico , Dengue/tratamento farmacológico , Transcriptoma , Adenosina Trifosfatases/antagonistas & inibidores , Antagonistas Adrenérgicos/farmacologia , Antagonistas Adrenérgicos/uso terapêutico , Antivirais/farmacologia , Encéfalo/metabolismo , Simulação por Computador , Dengue/sangue , Dengue/genética , Dengue/metabolismo , Descoberta de Drogas , Avaliação Pré-Clínica de Medicamentos , Reposicionamento de Medicamentos , Humanos , Fígado/metabolismo , Redes e Vias Metabólicas/efeitos dos fármacos , NF-kappa B/metabolismo , Antagonistas da Serotonina/farmacologia , Antagonistas da Serotonina/uso terapêutico , Dengue Grave/sangue , Dengue Grave/tratamento farmacológico , Dengue Grave/genética , Dengue Grave/metabolismo , Baço/metabolismoRESUMO
BACKGROUND AND PURPOSE: ß-Adrenoceptors are expressed in human and experimental animal breast cancer cells. However, the effect of the agonists and antagonists reported on cell proliferation and tumour growth was paradoxical, precluding their utilization as possible adjuvant therapy, mainly in the cases of refractory tumours. EXPERIMENTAL APPROACH: ß-Adrenoceptor expression was analysed by immunofluorescence and RT-PCR. Cell proliferation was assessed by [(3) H]-thymidine incorporation, tumour growth by measuring with a calliper and ERK 1/2 phosphorylation by Western blotting. KEY RESULTS: ß(2) -Adrenoceptor expression was confirmed in the mouse and human cells tested. Cell proliferation was increased by adrenaline (by α(2) -adrenoceptor action) and decreased in every tested cell line by the ß-adrenoceptor agonist isoprenaline and the ß(2) -adrenoceptor agonist salbutamol. Isoprenaline and salbutamol reduced tumour growth in every tumour tested (mouse C4-HD and CC4-3-HI and human IBH-4, IBH-6 and MDA-MB-231 cell lines growing as xenografts in nude mice). These effects were reversed by the ß-adrenoceptor antagonist propranolol. The α(2) -adrenoceptor antagonist rauwolscine and the ß(2) -adrenoceptor agonist salbutamol were equally effective in diminishing tumour growth. ERK 1/2 activation analysed in IBH-4 tumours correlated with tumour growth, with the ß-adrenoceptor agonists decreasing its activation. Inhibition of ERK 1/2 phosphorylation in vitro was mainly mediated by the PKA pathway. CONCLUSIONS AND IMPLICATIONS: In our experimental models, the ß-adrenoceptor agonists inhibited breast cancer cell proliferation and tumour growth, probably mediated by inhibition of ERK 1/2 phosphorylation. The ß-adrenoceptor agonists were as effective as the α(2) -adrenoceptor antagonist rauwolscine, providing possible novel adjuvant treatments for breast cancer.
Assuntos
Agonistas Adrenérgicos/uso terapêutico , Antineoplásicos/uso terapêutico , Neoplasias da Mama/tratamento farmacológico , Receptores Adrenérgicos alfa 2/metabolismo , Receptores Adrenérgicos beta 2/metabolismo , Agonistas Adrenérgicos/farmacologia , Antagonistas Adrenérgicos/farmacologia , Antagonistas Adrenérgicos/uso terapêutico , Albuterol/farmacologia , Animais , Antineoplásicos/farmacologia , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Feminino , Humanos , Isoproterenol/farmacologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Propranolol/farmacologia , Ensaios Antitumorais Modelo de Xenoenxerto , Ioimbina/farmacologiaRESUMO
BACKGROUND: Children with scorpion envenomation have massive sympathetic activation and variable degrees of left ventricular systolic dysfunction. OBJECTIVE: To evaluate a rescue protocol for children with severe left ventricular dysfunction secondary to scorpion envenomation. METHODS: Four children, after scorpion envenomation, were subjected to a rescue protocol for acute left ventricular dysfunction: Endotracheal intubation and respiratory assistance, electrocardiograms, chest x-Ray, echocardiograms and blood samples for norepinephrine and troponin I serum levels. Samples and echocardiograms were repeated at 12, 24 and 48 hours. Intravenous medications: Dobutamine: 4-6 microg/kg/min. Amiodarone: 3 mg/kg during a 2 hour period. Maintenance: 5 mg/kg/day. Furosemide: 0.5 mg/kg/dose. Diuretics were given when the systemic blood pressure was above percentile fifty. Amiodarone, Dobutamine and Furosemide were administered during the first 48 hours. Beta-adrenergic blockers and angiotensin converting enzyme were given, at 48 hours after admission, once the left ventricular Ejection fraction > 0.35 and the clinical status had improved. RESULTS: On admission, norepinephrine was 1,727.50 +/-794.96 pg/ml, troponin I 24.53 +/- 14.09 ng/ml and left ventricular ejection fraction 0.20 +/- 0.056. At twelve hours, norepinephrine and troponin I serum levels were down to half of the initial values and the ejection fraction increased to 0.32 +/- 0.059. During the next 24 and 48 hours, the ejection fraction rose to 0.46 +/- 0.045, (p<0.01) and norepinephrine and troponin diminished to 526.75 +/- 273.73 (p < 0.02) and 2.20 +/- 2.36 (p<0.02) respectively. CONCLUSION: Amiodarone, by acting as a neuromodulator, is very likely responsible for the early and progressive decrease of serum norepinephrine.
Assuntos
Antagonistas Adrenérgicos/uso terapêutico , Amiodarona/uso terapêutico , Venenos de Escorpião/intoxicação , Disfunção Ventricular Esquerda/tratamento farmacológico , Adolescente , Criança , Pré-Escolar , Protocolos Clínicos/normas , Feminino , Humanos , Masculino , Disfunção Ventricular Esquerda/induzido quimicamenteRESUMO
Fundamentos: As crianças picadas por escorpião, pressintam ativação maciça do sistema nervoso simpática com vários graus de disfunção sistólica ventricular esquerda. Oobjetivo: Testar um protocolo de resgate em crianças com grave disfunção ventricular esquerda causada por picada de escorpião. Métodos: Quatro crianças após serem picadas por escorpião foram submetidas a: Encubação endotraqueal e suporte respiratório, eletrocardiograma, radiografia de tórax, ecocardiograma e determinação sérica da norepinefrina e troponina I. As análises foram repetidas após 12, 24 e 48 horas. As seguintes medicações intravenosas foram administradas: dobutamina 4-6 μg/kg/min; amiodarona 3 mg/kg durante duas horas, com dose de manutenção de 5 mg/kg/dia; e furosemida 0,5 mg/kg. Amiodarona, dobutamina e furosemida foram administradas durante as primeiras 48 horas. Bloqueadores beta-adrenérgicos e inibidores da enzima conversora da angiotensina foram administrados até 48 após a internação, uma vez que o estado clínico havia melhorado e a fração de ejeção ventricular esquerda encontrava-se acima de 0,35 por cento. Resultados: Na admissão, a dosagem da norepinefrina foi 1.727,50± 794,96 pg/ml, a de troponina I 24,53 ± 14,09 ng/ml e a fração de ejeção do ventrículo esquerdo foi 0,20 ± 0,056. Após 12 horas, os níveis séricos de norepinefrina e de troponina I diminuíram para a metade dos valores iniciais e a fração de ejeção aumentou para 0,32 ± 0,059. Durante as 24 e 48 horas subseqüentes, a fração de ejeção elevou-se para 0,46 ± 0,045 (p<0,01) e a norepinefrina e de troponina I diminuíram para 526,75 ± 273,73 (p< 0,02) e 2,20 ± 2,36 (p<0,02) respectivamente. Conclusão: É bem provável que a amiodarona, ao agir como neuromodulador, seja responsável pela redução rápida e progressiva dos níveis séricos de norepinefrina.
Background: Children with scorpion envenomation have massive sympathetic activation and variable degrees of left ventricular systolic dysfunction. Objective: To evaluate a rescue protocol for children with severe left ventricular dysfunction secondary to scorpion envenomation. Methods: Four children, after scorpion envenomation, were subjected to a rescue protocol for acute left ventricular dysfunction: Endotracheal intubation and respiratory assistance, electrocardiograms, chest x-Ray, echocardiograms and blood samples for norepinephrine and troponin I serum levels. Samples and echocardiograms were repeated at 12, 24 and 48 hours. Intravenous medications: Dobutamine: 4-6 μg/kg/min. Amiodarone: 3 mg/kg during a 2 hour period. Maintenance: 5 mg/kg/day. Furosemide: 0.5 mg/kg/dose. Diuretics were given when the systemic blood pressure was above percentile fifty. Amiodarone, Dobutamine and Furosemide were administered during the first 48 hours. Beta-adrenergic blockers and angiotensin converting enzyme were given, at 48 hours after admission, once the left ventricular Ejection fraction > 0.35 and the clinical status had improved. Results: On admission, norepinephrine was 1,727.50 ±794.96 pg/ml, troponin I 24.53 ± 14.09 ng/ml and left ventricular ejection fraction 0.20 ± 0.056. At twelve hours, norepinephrine and troponin I serum levels were down to half of the initial values and the ejection fraction increased to 0.32 ± 0.059. During the next 24 and 48 hours, the ejection fraction rose to 0.46 ± 0.045, (p<0.01) and norepinephrine and troponin diminished to 526.75 ± 273.73 (p < 0.02) and 2.20 ± 2.36 (p<0.02) respectively. Conclusion: Amiodarone, by acting as a neuromodulator, is very likely responsible for the early and progressive decrease of serum norepinephrine.
Fundamento: Los niños con picaduras de escorpión sufren activación masiva del sistema nervioso simpático con varios grados de disfunción sistólica ventricular izquierda. Objetivo: Probar un protocolo de rescate en niños con disfunción ventricular severa izquierda ocasionada por picadura de escorpión. Métodos: Cuatro niños tras un escorpión picarlas se sometieron a: incubación endotraqueal y soporte respiratorio, electrocardiograma, radiografía de tórax, ecocardiograma y determinación sérica de la norepinefrina y troponina I. Los análisis se repitieron tras 12, 24 y 48 horas. Las siguientes medicaciones intravenosas se administraron: dobutamina 4-6 mcg/kg/min; amiodarona 3 mg/kg durante dos horas, con dosis de mantenimiento de 5 mg/kg/día; y furosemida 0.5 mg/kg. Amiodarona, dobutamina y furosemida se administraron durante las primeras 48 horas. Bloqueante betaadrenergicos e inhibidores de la enzima convertidora de la angiotensina se administraron hasta 48 tras la internación, una vez que el estado clínico había mejorado y la fracción de eyección ventricular izquierda se hallaba superior a un 0,35 por ciento. Resultados: Al ingreso, la dosificación de la norepinefrina fue 1727,50± 794,96 pg/ml, la de troponina I 24,53 ± 14,09 ng/ml y la fracción de eyección del ventrículo izquierdo fue 0,20 ± 0,056. Tras 12 horas, los niveles séricos de norepinefrina y de troponina I disminuyeron para la mitad de los valores iniciales y la fracción de eyección aumentó para 0,32 ± 0,059. Durante las 24 y 48 horas subsiguientes, la fracción de eyección se elevó para 0,46 ± 0,045 (p<0,01) y la norepinefrina y de troponina I se redujeron para 526,75 ± 273,73 (p< 0,02) y 2,20 ± 2,36 (p<0,02) respectivamente. Conclusión: Es bien probable que la amiodarona, al actuar como neuromodulador, sea responsable de la reducción rápida y progresiva de los niveles séricos de norepinefrina.
Assuntos
Adolescente , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Antagonistas Adrenérgicos/uso terapêutico , Amiodarona/uso terapêutico , Venenos de Escorpião/intoxicação , Disfunção Ventricular Esquerda/tratamento farmacológico , Protocolos Clínicos/normas , Disfunção Ventricular Esquerda/induzido quimicamenteRESUMO
The selective serotonin reuptake inhibitors (SSRIs) are considered the first-line pharmacological treatment for PTSD. However, even when treated with this class of drugs, response rates rarely exceed 60% and less than 20-30% of the patients achieve full remission. The aim of this study was to address this limitation by systematically reviewing the options left for the treatment of PTSD when patients do not respond satisfactorily to or tolerate SSRIs. A systematic review covering all original articles, letters and brief reports published in any language until October 2008 was conducted through searches in the ISI/Web of Science, PubMed and PILOTS databases. The search terms included the pharmacological class of each agent or its generic name plus "PTSD" or "stress disorder" in the title, in the abstract or as a keyword. Sixty-three articles were selected, covering the following categories: antipsychotics, anticonvulsants, adrenergic-inhibiting agents, opioid antagonists, benzodiazepines and other agents. None of the identified agents reached the level A of scientific evidence, 5 reached level B, 7 level C and 13 level D. The non-antidepressant agent with the strongest scientific evidence supporting its use in PTSD is risperidone, which can be envisaged as an effective add-on therapy when patients did not fully benefit from previous treatment with SSRIs. Prazosin, an adrenergic-inhibiting agent, is a promising alternative for cases of PTSD where nightmares and insomnia are prominent symptoms. So far, there is no consistent empirical support for using benzodiazepines in the prevention or in the treatment of PTSD, although these drugs could alleviate some associated non-specific symptoms, such as insomnia or anxiety. Further controlled clinical trials and meta-analysis are needed to guide clinicians in their search of effective pharmacological alternatives to antidepressants in PTSD.
Assuntos
Antidepressivos/uso terapêutico , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Transtornos de Estresse Pós-Traumáticos/psicologia , Antagonistas Adrenérgicos/uso terapêutico , Animais , Anticonvulsivantes/uso terapêutico , Antipsicóticos/uso terapêutico , Benzodiazepinas/uso terapêutico , Humanos , Antagonistas de Entorpecentes/uso terapêuticoRESUMO
OBJECTIVES: In this narrative review, we aimed to describe different pharmacological strategies for the treatment of patients with post-traumatic stress disorder who display different levels of intolerance, resistance, refractoriness, or who are unable to take to antidepressants, especially serotonin reuptake inhibitors. METHOD: We searched the ISI web of science and the PubMed for original studies focusing in the treatment of PTSD in different clinical scenarios. RESULTS: Preliminary evidence pointed towards the efficacy of drugs such as risperidone, olanzapine, lamotrigine and prazosin as strategies to be employed in the above mentioned clinical scenarios. The choice of a specific "second line" drug should take into account not only symptoms, but also pattern of comorbidities, previous response to other treatments, pharmacological interactions, side-effects, and patient's physical conditions. CONCLUSIONS: Future randomized controlled trials should be performed in order to unveil which drugs should be prescribed in the absence of adequate treatment and response to serotonin reuptake inhibitors.
Assuntos
Antagonistas Adrenérgicos/uso terapêutico , Anticonvulsivantes/uso terapêutico , Antipsicóticos/uso terapêutico , Inibidores Seletivos de Recaptação de Serotonina/uso terapêutico , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Benzodiazepinas/uso terapêutico , Humanos , Lamotrigina , Olanzapina , Prazosina/uso terapêutico , Ensaios Clínicos Controlados Aleatórios como Assunto , Risperidona/uso terapêutico , Falha de Tratamento , Triazinas/uso terapêuticoRESUMO
OBJETIVOS: Nesta revisão narrativa, o objetivo foi descrever as opções farmacológicas para o tratamento do transtorno de estresse pós-traumático nos casos de intolerância, resistência, refratariedade ou impossibilidade de utilizar antidepressivos, especialmente inibidores seletivos da recaptação da serotonina. MÉTODO: Consulta às bases de dados ISI Web of Science e PubMed em busca de estudos originais sobre o tratamento farmacológico do transtorno de estresse pós-traumático em diferentes cenários clínicos. RESULTADOS: Evidências preliminares apontam para a utilidade de drogas como a risperidona, a olanzapina, a lamotrigina e o prazosin como estratégias para o cenário clínico em tela. A escolha do medicamento de segunda linha deve levar em conta não só os sintomas, como também as comorbidades, os tratamentos prévios, as interações farmacológicas, os efeitos colaterais e as condições físicas do paciente. CONCLUSÕES: Futuros ensaios clínicos randomizados ainda são necessários para estabelecer com clareza alternativas farmacológicas aos antidepressivos para o tratamento do transtorno de estresse pós-traumático.
OBJECTIVES: In this narrative review, we aimed to describe different pharmacological strategies for the treatment of patients with post-traumatic stress disorder who display different levels of intolerance, resistance, refractoriness, or who are unable to take to antidepressants, especially serotonin reuptake inhibitors. METHOD: We searched the ISI web of science and the PubMed for original studies focusing in the treatment of PTSD in different clinical scenarios. RESULTS: Preliminary evidence pointed towards the efficacy of drugs such as risperidone, olanzapine, lamotrigine and prazosin as strategies to be employed in the above mentioned clinical scenarios. The choice of a specific "second line" drug should take into account not only symptoms, but also pattern of comorbidities, previous response to other treatments, pharmacological interactions, side-effects, and patient's physical conditions. CONCLUSIONS: Future randomized controlled trials should be performed in order to unveil which drugs should be prescribed in the absence of adequate treatment and response to serotonin reuptake inhibitors.
Assuntos
Humanos , Antagonistas Adrenérgicos/uso terapêutico , Anticonvulsivantes/uso terapêutico , Antipsicóticos/uso terapêutico , Inibidores Seletivos de Recaptação de Serotonina/uso terapêutico , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Benzodiazepinas/uso terapêutico , Prazosina/uso terapêutico , Ensaios Clínicos Controlados Aleatórios como Assunto , Risperidona/uso terapêutico , Falha de Tratamento , Triazinas/uso terapêuticoRESUMO
AIMS: To describe the pathophysiology, diagnosis and clinical manifestations of the neurological complications that critically ill patients often develop in intensive care units, and to discuss their treatment and prognosis, in the light of the most significant contemporary literature. DEVELOPMENT: The most frequent complication suffered by critically ill patients is sepsis, with encephalopathy as the main manifestation, and this has a direct effect on their prognosis. Polyneuropathy of the critically ill patient is linked to sepsis, as the main precipitating factor, as well as to the presence of high levels of glucose, which plays an important role in deciding whether mechanical ventilation can be withdrawn or not. Myopathy of the critically ill patient is related to the use of fluorinated steroids and neuromuscular blockers, which are frequently administered to these patients. All these entities represent a significant diagnostic challenge for the physician and are accompanied by important sequelae that continue after the patient's discharge from hospital, as well as myopathies and neuropathies associated to the use of drugs that are commonly administered to critically ill patients. It is therefore necessary to be familiar with the pathophysiology of the damage and with the associated factors, if a suitable diagnostic approach is to be employed. CONCLUSIONS: The incidence of these pathologies and their complications makes them important conditions that require a swift, accurate diagnosis so that treatment can be established early on and a prognosis can also be determined.
Assuntos
Estado Terminal , Doenças Neuromusculares , Antagonistas Adrenérgicos/efeitos adversos , Antagonistas Adrenérgicos/uso terapêutico , Aminoglicosídeos/efeitos adversos , Aminoglicosídeos/uso terapêutico , Amiodarona/efeitos adversos , Amiodarona/uso terapêutico , Anestésicos Intravenosos/efeitos adversos , Anestésicos Intravenosos/uso terapêutico , Antiarrítmicos/efeitos adversos , Antiarrítmicos/uso terapêutico , Anti-Infecciosos/efeitos adversos , Anti-Infecciosos/uso terapêutico , Antiulcerosos/efeitos adversos , Antiulcerosos/uso terapêutico , Anticonvulsivantes/efeitos adversos , Anticonvulsivantes/uso terapêutico , Ciclosporina/efeitos adversos , Ciclosporina/uso terapêutico , Diagnóstico Diferencial , Humanos , Imunossupressores/efeitos adversos , Imunossupressores/uso terapêutico , Unidades de Terapia Intensiva , Labetalol/efeitos adversos , Labetalol/uso terapêutico , Metronidazol/efeitos adversos , Metronidazol/uso terapêutico , Doenças Neuromusculares/tratamento farmacológico , Doenças Neuromusculares/etiologia , Doenças Neuromusculares/patologia , Doenças Neuromusculares/fisiopatologia , Omeprazol/efeitos adversos , Omeprazol/uso terapêutico , Fenitoína/efeitos adversos , Fenitoína/uso terapêutico , Polineuropatias/etiologia , Polineuropatias/metabolismo , Prognóstico , Propofol/efeitos adversos , Propofol/uso terapêutico , Sepse/complicações , Sepse/metabolismo , Tacrolimo/efeitos adversos , Tacrolimo/uso terapêuticoRESUMO
OBJECTIVE: The objective was to compare the safety and efficacy of intravenous labetalol and intravenous hydralazine for acutely lowering blood pressure in pregnancy. STUDY DESIGN: Two hundred women with severe hypertension in pregnancy were randomized to receive hydralazine (5 mg as a slow bolus dose given intravenously, and repeated every 20 min up to a maximum of five doses) or labetalol (20-mg intravenous bolus dose followed by 40 mg if not effective within 20 min, followed by 80 mg every 20 min up to a maximum dose of 300 mg). The primary end point was successful lowering of blood pressure and maternal hypotension. RESULTS: Women were similar with respect to characteristics at randomization. No significant differences were observed for maternal hypotension or persistent severe hypertension; only two patients in the hydralazine group presented with hypotension. Palpitations (p=0.01) and maternal tachycardia (p=0.05) occurred significantly more often in patients treated with hydralazine. The main neonatal outcomes were very similar per group; however, hypotension and bradycardia were significantly more frequent in the labetalol group. There were two neonatal deaths per antihypertensive drug group. CONCLUSIONS: This randomized clinical trial shows that labetalol and hydralazine fulfill the criteria required for an antihypertensive drug to treat severe hypertension in pregnancy.
Assuntos
Antagonistas Adrenérgicos/uso terapêutico , Anti-Hipertensivos/uso terapêutico , Hidralazina/uso terapêutico , Hipertensão/tratamento farmacológico , Labetalol/uso terapêutico , Vasodilatadores/uso terapêutico , Antagonistas Adrenérgicos/administração & dosagem , Anti-Hipertensivos/administração & dosagem , Feminino , Humanos , Hidralazina/administração & dosagem , Hipotensão/induzido quimicamente , Labetalol/administração & dosagem , Pré-Eclâmpsia/prevenção & controle , Gravidez , Resultado da Gravidez , Taquicardia/induzido quimicamente , Vasodilatadores/administração & dosagemRESUMO
En el campo de la Urología, una de las causas més frecuentes de consulta la constituye la patología prostática y dentro de ésta, la hiperplasia benigna de la próstata. Esta consiste en un incremento de células en el área periuretral prostática, lo que puede ser debido a una proliferación celular aumentada, a una alteración de la apoptosis, o a una combinación de ambos mecanismos. Entre las principales opciones terapÚuticas actuales para la hiperplasia prostática benigna están: - Tratamiento quirúrgico, que continua siendo la principal alternativa de terapia, representado principalmente por la resección transuretral. Tratamiento farmacológico, utilizado como alternativa y/o complemento a la cirugía y representado por dos grandes grupos de fármacos: los antagonistas adrenÚrgicos y la terapia endocronológica (finasteride). El presente trabajo es una revisión bibliográfica actualizada sobre las distintas opciones de tratamiento disponibles para la hiperplasia prostática benigna y sus respectivas indicaciones.