Descrição das notificações de queixas técnicas de medicamentos recebidas pelafarmacovigilância do Hospital de Clínicasde Porto Alegre / Description of technical drugs complaintsat the pharmacovigilance of Hospital deClínicas de Porto Alegre

Introdução: Farmacovigilância é definida como o conjunto de atividades relativas à detecção, avaliação, compreensão e prevenção de efeitos adversos ou queixas técnicas dos medicamentos. Objetivo: Descrever as notificações espontâneas de produtos com suspeita de desvios de qualidade, recebidas pela farmacovigilância do Hospital de Clínicas de Porto Alegre no período de 2008 a 2012. Método: Realizado estudo descritivo com dados recebidos pela farmacovigilância e Serviço de Parecer Técnico da instituição, tendo como variáveis: notificadores, produtos, desvios de qualidade, presença de erros de medicação e medidas adotadas após avaliação do produto. Resultados: No período, foram recebidas 191 notificações espontâneas de produtos com suspeita de desvio de qualidade, sendo os funcionários da farmácia (48,7%) e a enfermagem (35,1%) os responsáveis pelo maior número de notificações.Das notificações, em 12,6% foram identificados erros de medicação, 60,2% foram encaminhas para avaliação da indústria e 13% receberam parecer desfavorável para uso na instituição. Conclusão: É fundamental que os profissionais de saúde façam a notificação dos problemas detectados para que se mantenha ou melhore a qualidade e segurança dos produtos.

Background: Pharmacovigilance is defined as a set of activities related to detection, assessment, understanding, and prevention of adverse effects and drug-related technical complaints. Aims: To describe spontaneous reports about products with suspected quality defects filed at the Pharmacovigilance Department of Hospital de Clínicas de Porto Alegre between 2008 and 2012.Method: Descriptive study with data from the Pharmacovigilance Department and Technical Expert Service of the hospital including the following variables: author of the report, products, quality defects, medication errors, measures adopted after product assessment. Results: In the period assessed, there were 191 spontaneous reports of products with suspected quality defects. Pharmacists and nurses accounted for most reports (48.7 and 35.1%, respectively). Of all reports, 12.6% described medication errors, 60.2% were forwarded to the pharmaceutical industry for assessment, and 13% resulted in drugs not being recommended for use at the hospital. Conclusion: Consistent reporting of drug-related problems by health professionals is extremely important to maintain and improve product quality and safety.

Urinary TGF-beta1 reduction related to a decrease of systolic blood pressure in patients with type 2 diabetes and clinical diabetic nephropathy.

With the aim to determine the influence of reducing systolic blood pressure in urinary TGF-beta1 of type 2 diabetes (DM2) with diabetic nephropathy (DN), 21 subjects with type 2 diabetes and proteinuria >500 mg/24 h were studied. Amlodipine and ramipril were added to their previous antihypertensive treatment for 12 weeks. Urinary TGF-beta1 (UTGF-beta1) was determined at 0, 4, 8 and 12 weeks. Plasma TGF-beta1 was determined at 0 and 12 weeks. Subjects whose mean systolic blood pressure (SBP) during treatment were under 140 mmHg were grouped as the better SBP controlled group (n = 11) and those with SBP equal to or greater than 140 mHg were grouped in a moderate SBP controlled group (n = 10). Compared to baseline, mean log UTGF-beta1 at 4, 8 and 12 weeks decreased (-0.22 +/- 0.15 pg/mg; p = 0.04) in better SBP controlled group but not in the moderate SBP controlled group (-0.12 +/- 0.08 pg/mg, p = 0.82). Mean SBP correlated with UTGF-beta1 (r = 0.458, p = 0.0357), and this effect was independent of HbA1c (p = 0.042). By controlling SBP in DM2 subjects with DN we might decrease UTGF-beta1. We propose that reduction of UTGF-beta1 is due to a decrease in renal TGF-beta1 production.

Increased urinary TGF-beta1 and cortical renal GLUT1 and GLUT2 levels: additive effects of hypertension and diabetes.

BACKGROUND/AIM: Diabetes and mesangial stretch caused by hypertension increase mesangial matrix deposition which is induced by local production of transforming growth factor beta 1 (TGF-beta1). Both conditions are associated with cortical GLUT1 overexpression. We evaluated the effect of genetically determined hypertension and its association with diabetes on urinary TGF-beta1 and cortical GLUT1 and GLUT2 expression. METHODS: We studied Wistar-Kyoto rats (controls, C) and spontaneously hypertensive rats (SHR), weighing approximately 210 g, 30 days after the injection of streptozotocin (diabetic, D) or citrate buffer (10 C, 9 SHR, 12 C-D and 15 SHR-D). Twenty-four-hour urine was collected for glucose, albumin, and TGF-beta1 determinations. Catheters were implanted into the femoral artery to measure the arterial blood pressure in conscious animals 1 day later. Then GLUT1 and GLUT2 protein levels (Western blotting) in renal cortex and medulla were evaluated. RESULTS: The cortical GLUT1 levels were 5, 2, and 7 times higher in SHR, C-D, and SHR-D groups versus C group (p < 0.05); the GLUT2 contents were 1.5, 1.8, and 2.3 times higher in SHR, C-D and SHR-D groups versus C group (p < 0.05). The urinary TGF-beta1 level was elevated by diabetes and diabetes and hypertension, but not by hypertension alone: 1.39 +/- 0.2, 2.34 +/- 0.6, 18.2 +/- 3.2, and 28.8 +/- 7.6 ng/24 h, respectively, in C, SHR, C-D, and SHR-D groups (p < 0.05). CONCLUSIONS: Diabetes, hypertension, and especially their association increase the renal cortical GLUT1 and GLUT2 levels. The magnitude of GLUT1 overexpression caused by hypertension is higher than that induced by diabetes alone. The impact on urinary TGF-beta1 occurs when diabetes and hypertension are associated, suggesting an effect that is triggered in the presence of GLUT1 overexpression and hyperglycemia.