Feeds:
Posts
Comentários

Archive for the ‘Material de apoio’ Category

 

Roteiro básico

Veja uma série de recomendações, baseadas no chamado Protocolo Spikes (modelo construído por estudiosos americanos visando transmitir o diagnóstico aos pacientes de câncer):

Objetivos

:: Escutar o paciente com a finalidade de conhecer o seu grau de informação sobre a doença, suas expectativas e seu preparo para receber a má notícia.

:: Transmitir informação médica de maneira inteligível, de acordo com as possibilidades, as necessidades e os desejos do paciente.

:: Dar suporte ao paciente, utilizando habilidades profissionais para reduzir o impacto emocional e a sensação de isolamento experimentados por quem recebe a má notícia.

:: Desenvolver uma estratégia, sob a forma de um plano de tratamento, com a contribuição e a colaboração do paciente.

Etapas e recomendações

ETAPA 1 – Como planejar a entrevista

:: Rever os dados que fundamentam a má notícia: resultados de exames, tratamentos anteriores, literatura médica e informações gerais sobre o paciente.

:: Avaliar seus próprios sentimentos – positivos e negativos – sobre a transmissão da má notícia para esse paciente.

:: Buscar ambiente com privacidade; informar sobre restrições de tempo ou interrupções que possam ser inevitáveis; desligar o celular ou pedir a um colega para atender.

:: Envolver pessoas importantes, se esse for o desejo do paciente.

:: Sentar-se e colocar-se disponível para o paciente.

ETAPA 2 – Como avaliar a percepção do paciente: “Antes de contar, pergunte”

:: Procurar saber como o paciente percebe sua situação médica (o que tem, se é sério ou não), o que já lhe foi dito sobre o seu quadro clínico e o que procurou saber por fontes leigas ou profissionais, internet etc., qual é a sua compreensão sobre as razões pelas quais foram feitos os exames.

:: Perceber se o paciente está comprometido com alguma variante de negação da doença: pensamento mágico, omissão de detalhes médicos essenciais, mas desfavoráveis sobre a doença ou expectativas não realistas do tratamento.

:: Corrigir desinformações e moldar a má notícia para a compreensão e a capacidade de absorção do paciente.

ETAPA 3 – Como avaliar o desejo de saber do paciente e obter o seu pedido por informações

:: Procurar saber, desde o início do tratamento, se o paciente deseja informações detalhadas sobre o diagnóstico, o prognóstico e os pormenores dos tratamentos ou se quer ir pedindo informações gradativamente.

:: Oferecer-se para responder a qualquer pergunta ou para falar com familiares ou amigos.

:: Negociar a transmissão de informação no momento em que se pedem exames: se o paciente vai querer detalhes sobre os resultados ou apenas um esboço que possibilite a discussão do plano de tratamento.

ETAPA 4 – Como transmitir a notícia e as informações ao paciente

:: Anunciar com delicadeza que más notícias estão por vir, dar tempo ao paciente para se dispor a escutá-las.

:: Evitar termos técnicos, adaptando-se ao vocabulário e ao nível de compreensão do paciente.

:: Evitar a dureza excessiva, amenizando a transmissão de detalhes desnecessários.

:: Informar aos poucos, buscando conferir o progresso de sua compreensão.

:: Quando o prognóstico é ruim, evitar transmitir desesperança e desistência, valorizando, ao contrário, os cuidados paliativos, o alívio dos sintomas e o acompanhamento solidário.

ETAPA 5 – Como validar a expressão de sentimentos e oferecer respostas afetivas às emoções dos pacientes (e de familiares)

:: Favorecer a expressão de pacientes e familiares sobre o impacto da má notícia, dando voz a seus sentimentos e emoções para ajudá-los a superar estados de choque e evitar o descontrole.

:: Acolher a legítima expressão de sentimentos de ansiedade, raiva, tristeza ou inconformismo de pacientes e familiares, dando-lhes algum tempo para se acalmarem e abrindo-lhes as possibilidades de continuidade do acompanhamento.

:: Buscar respostas de reconhecimento e sintonia afetiva, ensaiar perguntas exploratórias que favoreçam a expressão dos sentimentos e das preocupações em jogo, assim como afirmativas reasseguradoras da legitimidade dessas expressões para reduzir os sentimentos de isolamento do paciente e de familiares, expressar solidariedade e validar seus sentimentos e pensamentos.

ETAPA 6 – Como resumir e traçar estratégias

:: Resumir as principais questões abordadas e traçar uma estratégia ou um plano de tratamento para ajudar os pacientes a sentirem-se menos ansiosos e inseguros.

:: Antes de discutir um plano de tratamento, perguntar aos pacientes se eles estão prontos para essa discussão e se aquele é o momento.

:: Compartilhar responsabilidades na tomada de decisão com o paciente (o que pode também reduzir qualquer sensação de fracasso da parte do médico quando o tratamento não é bem-sucedido).

:: Avaliar o não entendimento de pacientes sobre a discussão, prevenindo sua tendência a superestimarem a eficácia ou não compreenderem o propósito do tratamento.

:: Ser honesto sem destruir a esperança ou a vontade de viver dos pacientes.

Fonte: Clic RBS

 

Anúncios

Read Full Post »

Metformin is one of the oldest oral treatments to reduce hyperglycaemia in people with diabetes. Gastrointestinal side effects are common, and metformin should be used with caution in patients with renal impairment because of the slight risk of lactic acidosis. In the United Kingdom Prospective Diabetes Study (UKPDS) patients treated with metformin had a significant reduction in myocardial infarction and mortality that was not demonstrated in patients treated with sulphonylureas or insulin. The fact that metformin significantly reduces cardiovascular events plus reduces weight has meant that metformin is the drug of first choice in guidelines for the treatment of type 2 diabetes. There are no longer concerns about using metformin in patients with chronic heart failure, other than in patients with associated renal failure, or during episodes of acute left ventricular failure when metformin should be temporarily stopped.

Introduction

The prevalence of type 2 diabetes mellitus (T2DM) is reaching epidemic proportions. Metformin therapy has been used in the treatment of T2DM for many years. Despite an increased armoury of agents for treating hyperglycaemia, only metformin has been shown to improve prognosis as a primary end point in a randomised-controlled trial.[1] Clinical studies have shown that the effects of metformin go beyond improving glycosylated haemoglobin (HbA1c) and include reductions in cardiovascular end points. Despite the evidence base for the benefits of metformin, concerns remain about its side effects, including the perceived risk of lactic acidosis, particularly in the presence of cardiac and renal failure. Evidence confirming its safety, even in the setting of cardiac and renal failure, has resulted in metformin being accepted globally as the first-line treatment for overweight patients (body mass index [BMI] >25 kg/m2) with T2DM.

The proposed mechanisms of action of metformin, which are not fully understood, are illustrated in figure 1. It can lower blood glucose in several ways. It acts by countering insulin resistance, particularly in liver and skeletal muscle. It suppresses hepatic gluconeogenesis, increases peripheral insulin sensitivity in insulin sensitive tissues such as muscle and adipose tissue, and enhances peripheral glucose utilisation. The protective effect on the cardiovascular system cannot be fully explained by its blood glucose-lowering properties. These effects may be partly mediated via beneficial effects on circulating markers of endothelial function (vascular cell adhesion molecule-1 [VCAM-1], E-selectin), fibrinolysis (plasminogen activator inhibitor-1 [PAI-1]) and chronic inflammation (C-reactive protein [CRP]). There are several other potential mechanisms postulated to explain the cardiovascular benefits beyond blood glucose lowering, including disruption of respiratory chain oxidation in mitochondria and activation of the enzyme adenosine monophosphate (AMP)-activated protein kinase (AMPK).[2,3] AMPK is a protein kinase ubiquitously expressed in mammalian tissues and involved in regulating energy balance. Activation of AMPK stimulates adenosine triphosphate (ATP)-producing catabolic pathways, while inhibiting ATP-consuming anabolic pathways, thereby, maintaining cellular energy stores. In skeletal muscle, activation of AMPK increases glucose uptake and lipid oxidation. In liver, activation of AMPK inhibits gluconeogenesis and lipid synthesis but increases lipid oxidation. Finally, in adipose tissue, activation of AMPK reduces both lipolysis and lipogenesis. Therefore, activation of AMPK in skeletal muscle, liver and adipose tissue results in decreased circulating glucose, lipids and ectopic fat accumulation, as well as enhanced insulin sensitivity.

Metformin has a short half-life of around six hours and undergoes renal excretion with 90% being eliminated within 24 hours. It can be prescribed as 500 mg or 850 mg tablets. It should be started at the 500 mg dose and increased in weekly increments until the maximum tolerated dose is achieved, normally 2 g/day. It should be taken with food to reduce the potential for gastrointestinal side effects. Occasionally higher doses are given depending on clinical response and tolerability. Hypoglycaemia is not usually a side effect of metformin therapy and it tends not to result in significant weight gain. The main side effect of concern is its association with lactic acidosis particularly in the setting of renal and cardiac failure.

Metformin is licensed to be given on its own in patients who have failed to improve with dietary modifications or it can be given in combination with sulphonylureas, thiazolidinediones, repaglinide/nateglinide, dipeptidyl peptidase-4 (DPP4) inhibitors (sitipliptin, vildagliptin, saxagliptin), glucagon-like peptide-1 (GLP-1) agonists (exenatide or liraglutide), acarbose or insulin. Indeed, given that the benefits of metformin are considered to go beyond glycaemic control, all overweight patients with T2DM should be on metformin, if tolerated. There is limited evidence to support the use of a slow-release preparation of metformin (Glucophage SR®) on the basis of fewer gastrointestinal side effects.

Evidence for Improved Glycaemic Control

The United Kingdom Prospective Diabetes Study (UKPDS) study, initiated in 1977 and reported in 1998, demonstrated that improved glycaemic control was associated with a reduced incidence of microvascular complications (such as nephropathy and retinopathy).[1] While no significant effect of lowering blood glucose was observed on cardiovascular complications, epidemiological analysis of the UKPDS data has demonstrated a continuous association between the risk of cardiovascular complications and glycaemic control. Metformin has been shown to improve glycaemic control compared with placebo or diet. When compared with placebo, metformin shows improvement in HbA1c and fasting plasma glucose, but there are no significant differences for BMI or weight, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, triglycerides, or blood pressure.[4] When compared with diet, metformin shows improvement in HbA1c and total cholesterol, but no difference for fasting plasma glucose, BMI or weight, HDL-cholesterol, LDL-cholesterol, triglycerides, or blood pressure. Metformin and sulphonylureas have similar effects on HbA1c, and there is no significant difference in HbA1c between those using metformin and those using insulin. UKPDS was the first randomised trial to demonstrate improved outcome with metformin treatment. The UKPDS trial allocated patients to either conventional (initial dietary modification with addition of a sulphonylurea for fasting plasma glucose >15 mmol/L) or a more intensive glycaemic control strategy (which could include metformin, sulphonylurea or insulin therapy).

Evidence for Cardiovascular Benefit

Within the UKPDS cohort there was a substudy looking at overweight patients (54% with obesity). Those allocated to metformin (n=342) had improved outcomes compared with those on conventional treatment (n=411). Randomisation to metformin was associated with dramatic relative risk reductions in diabetes-related death (–42%), myocardial infarction (–39%), stroke (–42%) any diabetes-related end point (–32%) and all-cause mortality (–36%) when compared with diet. This is in contrast to the relative risk reductions with sulphonylurea or insulin in diabetes-related death (–20%), myocardial infarction (–21%), stroke (‘14%) any diabetes-related end point (–7%) and all-cause mortality (–8%) when compared with diet. There were no significant differences between metformin and other comparison arms for other outcomes such as stroke, peripheral arterial disease and microvascular disease. Mean HbA1c after follow-up in the diet group and metformin group were 8% and 7.4%, respectively, and there was no clear difference in the glucose-lowering effect between metformin, sulphonylurea and insulin.

Given that the glucose-lowering effects of metformin, sulphonylurea and insulin were similar, it has been proposed that metformin must confer additional vascular benefits beyond those of glycaemia alone. The UKPDS Post-Trial monitoring results suggest a legacy effect with continuing benefit of metformin therapy. There is maintenance of the relative risk reductions for any diabetes-related end point (–21%), myocardial infarction (–33%) and all-cause mortality (–27%), despite loss of within-trial blood glucose and therapy differences.[5]

Discussion

Clinical studies in T2DM have shown that the effects of metformin go beyond improving HbA1c and include reductions in cardiovascular end points. Metformin is considered to be the first drug of choice for the treatment of T2DM in overweight patients. There is increasing evidence to show that in the absence of tissue hypoxia and/or moderate-to-severe renal impairment, metformin will not result in lactic acidosis. Importantly, metformin should no longer be contraindicated in patients with chronic stable heart failure and may even have morbidity and mortality benefits. There is a clear need for prospective randomised-controlled studies of metformin therapy in patients with T2DM and the traditional contraindications of heart and renal failure. In the meantime, a pragmatic approach is recommended including temporarily stopping metformin during an acute illness where tissue hypoxia is suspected, which will include patients with an acute myocardial infarction, acute left ventricular failure or septicaemia, or when an individual is due to get radiological investigations using iodine-based contrast medium. Particular care should be taken in patients with chronic renal failure with a lower clinical threshold to temporarily discontinue in the aforementioned circumstances. However, chronic renal failure in itself is not an absolute contraindication to metformin use when the decision to prescribe or not is based on the potential prognostic benefits weighed against the likelihood of harm.

references

  1. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998;352:854–65.
  2. Owen MR, Doran E, Halestrap AP. Evidence that metformin exerts its anti-diabetic effects through inhibition of complex 1 of the mitochondrial respiratory chain. Biochem J 2000;348:607–14.
  3. Zhou G, Myers R, Li Y et al. Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest 2001;108:1167–74.
  4. Saenz A, Fernandez-Esteban I, Mataix A, Ausejo M, Roque M, Moher D. Metformin monotherapy for type 2 diabetes mellitus. Cochrane Database Syst Rev 2005;(3):CD002966.
  5. Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year follow-up of intensive glucose control in type 2 diabetes (UKPDS 80). N Engl J Med 2008;359:1577–89.
  6. Salpeter S, Greyber E, Pasternak G, Salpeter E. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev 2006;(1):CD002967.
  7. Emslie-Smith AM, Boyle DI, Evans JM, Sullivan F, Morris AD. Contraindications to metformin therapy in patients with type 2 diabetes—a population-based study of adherence to prescribing guidelines. Diabet Med 2001;18:483–8.
  8. Cusi K, Consoli A, DeFronzo RA. Metabolic effects of metformin on glucose and lactate metabolism in non insulin-dependent diabetes mellitus. J Clin Endocrinol Metabol 1996;81:4059–67.
  9. Eurich DT, McAlister FA, Blackburn DFet al. Benefits and harms of antidiabetic agents in patients with diabetes and heart failure: systematic review. BMJ 2007;335:497–501.
  10. National Institute for Health and Clinical Excellence. Type 2 diabetes: the management of type 2 diabetes (update). NICE Guideline CG66. London: NICE, 2008. Available from: http://www.nice.org.uk

Read Full Post »

New reports of ADEs appear in the medical literature each month. These publications can provide pediatric health care providers with valuable information to guide drug selection, dosing, and monitoring to avoid or reduce the potential for adverse events in their patients.

Adverse Events in Pediatric Intensive Care

A collaborative group of 15 PICUs published a retrospective evaluation of adverse events documented during the last four months of 2005. A total of 734 patient records were evaluated; 1,488 adverse events were identified, including 256 adverse drug events (ADEs). This resulted in a rate of 4.9 ADEs per 100 patient-days, or an adjusted cumulative risk for an ADE of 1.6% per PICU day. Surgical patients had a higher incidence of both adverse events and ADEs. There was also a relationship between the risk for ADEs and age, with a 4% increase in the adjusted ADE rate for every year increase in age. The authors suggest that these data may be useful in developing areas of focus for prevention strategies. Agarwal S, Classen D, Larsen G, et al. Prevalence of adverse events in pediatric ICUs in the United States. Pediatr Crit Care Med 2010; (epub ahead of print).

Analgesics and Anti-inflammatories in Sports

The June 2010 issue of Pediatric Clinics of North America includes an extensive review of the benefits and risks of analgesics and anti-inflammatory medications in young athletes. The authors describe the mechanism of action, pharmacokinetic and pharmacodynamic properties, and dosing recommendations for these drugs, as well as their adverse effect profiles. They include both oral agents and topical products. This article, with its extensive tables and bibliography, will be a useful reference for health care providers who provide care for adolescents with sports-related injuries. Feucht CL, Patel DR. Analgesics and anti-inflammatory medications in sports: use and abuse. Pediatr Clin N Am 2010;57:751–74.

Antiepileptic Safety Monitoring

Anderson and Choonara have studied the methods for ADE reporting during randomized controlled trials (RCTs) of antiepileptic drugs in children over the 10-year period from 1998 to 2007. Of the 29 RCTs identified, only three analyzed data from pediatric patients separately. Six of the trials (20%) described a standardized method for obtaining and documenting ADE information. Only three studies utilized an independent safety monitoring committee to ensure thorough, unbiased assessment of adverse event reports. Based on their assessment, the authors recommend significant changes in antiepileptic study design to improve safety monitoring and ADE reporting. Anderson M, Choonara I. A systematic review of safety monitoring and drug toxicity in published randomized controlled trials of antiepileptic drugs in children over a 10-year period. Arch Dis Child 2010; (epub ahead of print).

Guillain-barré Syndrome After H1cn1 Vaccine

Tremblay and colleagues describe a case of Guillain-Barré Syndrome (GBS) in an 11-year-old boy after administration of the H1N1 vaccine during the fall of 2009. The patient presented to the hospital with facial diplegia, abdominal, forehead, neck, and thigh pain 13 days after receiving a subcutaneous injection of the Arepanrix® H1N1 vaccine. Neurologic examination demonstrated symmetric paralysis of the eighth cranial nerve, along with proximal weakness of the shoulder and pelvis. After exclusion of alternative diagnoses and further investigation, the authors concluded that there was a probable relationship between the patient’s condition and the vaccine. While the CDC reports only 12 probable cases of GBS from approximately 46 million doses of vaccine administered during 2009 (MMWR 2009;58:1–6), this case serves as a reminder of the potential for this condition in children. Tremblay M, Closon A, D’Anjou G, et al. Guillain-Barré syndrome following H1N1 immunization in a pediatric patient. Ann Pharmacother 2010;44:1330–3.

 

Valproate-induced Metabolic Effects

Long-term use of valproate has long been associated with the potential for weight gain and insulin resistance in children with epilepsy. A two part study was recently conducted to address the mechanism for these adverse effects. The first part, a cross-sectional study of children previously diagnosed with epilepsy was designed to evaluate insulin sensitivity and weight gain. Patients were divided into 3 groups: those who had not yet received valproate, patients currently receiving treatment, and those who had discontinued valproate at least 1 year previously. The second part of the study was a prospective longitudinal follow-up of the children in the first group after they began treatment with valproate. Sixty children were enrolled, with 20 continuing on to the longitudinal portion of the study.

When the children were divided into the 3 groups, there were no differences in age, or baseline glucose and insulin levels. There were, however, significant differences in body mass index (BMI) and measurements of insulin resistance. The group currently receiving valproate had a significantly higher BMI than the group who had not been treated (20.22±4.11 compared to 15.97±1.70, p = 0.0002). There was also higher insulin resistance in this group (1.67±1.08 versus 1.04±0.38, p = 0.003). No differences were found between the treatment group and those who had discontinued valproate. Significant correlations were found in the treatment group between the daily valproate dose and both insulin resistance (r = 0.663) and fasting insulin levels (r = 0.765). The longitudinal study revealed significant increases in fasting and post-glucose challenge insulin values at the one year follow-up, however the degree of insulin resistance eventually leveled off over time. The information gained from this study suggests a need for routine monitoring of weight and blood glucose values in children receiving long-term treatment.Masuccio F, Verrotti A, Chiavaroli V, et al. Weight gain and insulin resistance in children treated with valproate: the influence of time. J Child Neurol 2010; 25:941–7.

 

Fonte: Medscape Pharmacist

Read Full Post »

Clinical Context

 

A recent study, published in the current issue of the American Journal of Respiratory and Critical Care Medicine, conducted by Amberbir and colleagues reported that acetaminophen use was associated with increased risk of wheeze, but not eczema, in a small cohort of patients in Ethiopia.

Previously, in 2008, Beasley and colleagues, the current study authors, conducted Phase Three of ISAAC, and in the September 20, 2008, issue of The Lancet, they reported that acetaminophen use (paracetamol) in the first year of life was associated with a greater risk for asthma symptoms in children aged 6 to 7 years.

The current study by Beasley and colleagues uses data from ISAAC Phase Three to evaluate whether acetaminophen use is linked with a greater risk for asthma, allergy, or eczema symptoms in children aged 13 to 14 years.

 

Study Highlights

 

  • Data were available for 322,959 children aged 13 to 14 years from 113 centers in 50 countries.
  • Subjects completed a written environmental questionnaire about protective and risk factors including acetaminophen use in the past 12 months; a written questionnaire about current symptoms of asthma, rhinoconjunctivitis, and eczema; and a video questionnaire about asthma symptoms.
  • Exclusion criteria were centers that deleted the acetaminophen use question, centers with less than 70% data for current acetaminophen use, centers with less than 1000 enrolled children, missing data for sex, and missing data for current acetaminophen use.
  • Adjusted and multivariate analyses included 180,887 subjects with complete covariate data or subjects who came from centers with at least 70% covariate data.
  • Current acetaminophen use was considered medium if taken at least once in the past 12 months and high if taken at least once a month in the past 12 months.
  • Current asthma symptoms were defined as reported wheezing or whistling in the chest in the past 12 months.
  • Separate assessment of current wheeze was defined as reported symptoms similar to a video showing wheezing at rest.
  • Current rhinoconjunctivitis symptoms were defined as sneezing, a runny or blocked nose, or itchy watery eyes in the absence of a cold or the flu in the past 12 months.
  • Current eczema symptoms were defined as an itchy rash in the folds of the elbows; behind the knees; in front of the ankles; under the buttocks; or around the neck, ears, or eyes recurring for at least 6 months in the past 12 months.
  • Severe asthma was defined as 4 or more wheezing attacks, 1 or more nights per week of disturbed sleep because of wheezing, or wheezing severe enough to limit speech in the past 12 months.
  • The primary outcome measure was the OR of current asthma symptoms linked with acetaminophen use.
  • Medium acetaminophen use occurred in 73% of participants (range, 41% in China to 92% in Panama).
  • High acetaminophen use occurred in 30% of subjects (range, 2% in Taiwan to 68% in Nigeria).
  • Analysis adjusting for sex, region of the world, language, and gross national income showed that an increased risk for current asthma symptoms was dependent on exposure to acetaminophen use:
    • Medium vs no acetaminophen use (OR, 1.38; 95% CI, 1.31 – 1.46)
    • High vs no acetaminophen use (OR, 2.36; 95% CI, 2.24 – 2.50)
  • Multivariate analysis adjusted for maternal education, current maternal smoking, siblings, and current intake of vegetables and fruit.
  • Multivariate analysis showed that an increased risk for current asthma symptoms was dependent on exposure to acetaminophen use:
    • Medium vs no acetaminophen use (OR, 1.43; 95% CI, 1.33 – 1.53)
    • High vs no acetaminophen use (OR, 2.51; 95% CI, 2.33 – 2.70)
  • In multivariate analysis, there was also an acetaminophen exposure–dependent increased risk for current symptoms of rhinoconjunctivitis:
    • Medium vs no acetaminophen use (OR, 1.38; 95% CI, 1.29 – 1.47)
    • High vs no acetaminophen use (OR, 2.39; 95% CI, 2.24 – 2.55)
  • In multivariate analysis, there was an acetaminophen exposure–dependent increased risk for current symptoms of eczema:
    • Medium vs no acetaminophen use (OR, 1.31; 95% CI, 1.21 – 1.42)
    • High vs no acetaminophen use (OR, 1.99; 95% CI, 1.82 – 2.16)
  • Current acetaminophen use was linked with an exposure-dependent increased risk for current wheeze determined by video questionnaire, severe asthma, current rhinoconjunctivitis, and eczema.
  • After exclusion of subjects with current wheeze, an increased risk for current rhinoconjunctivitis was linked with current acetaminophen use:
    • Medium vs no acetaminophen use (OR, 1.33; 95% CI, 1.25 – 1.42)
    • High vs no acetaminophen use (OR, 2.18; 95% CI, 2.04 – 2.33)
  • After exclusion of subjects with current wheeze, an increased risk for current eczema was linked with current acetaminophen use:
    • Medium vs no acetaminophen use (OR, 1.32; 95% CI, 1.21 – 1.44)
    • High vs no acetaminophen use (OR, 1.87; 95% CI, 1.7 – 2.05)
  • Study limitations include possible confounding and possible increased use of acetaminophen in persons with asthma.

 

Clinical Implications

 

  • Recent acetaminophen use is linked with an exposure-dependent increased risk for asthma symptoms in adolescents.
  • Recent acetaminophen use is linked with an exposure-dependent increased risk for rhinoconjunctivitis and eczema symptoms in adolescents.

fonte: 

 MedscapeCME Clinical Briefs

Read Full Post »

Preeclampsia and IUGR are important causes of maternal and perinatal mortality and morbidity. Preeclampsia affects 2% to 5% of pregnancies, leading to more than 100,000 maternal deaths worldwide each year. Previous studies have indicated a risk reduction of 20% for preeclampsia with low-dose aspirin started any time during pregnancy.

This is a systematic review and meta-analysis of studies examining the use of low-dose aspirin, started at 16 weeks or earlier or later than 16 weeks of gestation, on maternal and neonatal outcomes of preeclampsia or IUGR and other neonatal outcomes in women at risk for preeclampsia.

Study Highlights

  • Included were prospective randomized controlled trials extracted from EMBASE, PubMed, and the Cochrane Central Register of Controlled Trials from 1965 to 2008, which examined the effect of low-dose aspirin on pregnant women at risk for preeclampsia.
  • Excluded were quasi-randomized trials or studies in which 20% or more women were lost to follow-up.
  • Women in the treatment group had to be treated with low-dose aspirin (50 – 150 mg daily, alone or in combination with dipyridamole < 300 mg). The control group had to be allocated to placebo or to no treatment.
  • The primary outcome was the occurrence of preeclampsia.
  • Secondary outcomes included IUGR, severe preeclampsia, gestational hypertension, placental abruption, preterm birth, low birth weight, and gestational age at delivery.
  • Outcomes were stratified by gestational age at which aspirin was started: 16 weeks of gestation or less or more than 16 weeks of gestation.
  • Of 773 articles initially identified, 34 were selected for analysis, including 27 articles for the primary outcome of preeclampsia.
  • 11,348 women were analyzed.
  • 12 studies had women starting aspirin at 16 weeks of gestation or earlier, and 22 studies reported data on women starting aspirin after 16 weeks of gestation.
  • Risk for preeclampsia was defined in different ways, including nulliparity and a history of preeclampsia or other hypertensive disorders.
  • Women who began aspirin at 16 weeks of gestation or less had a significantly reduced risk for preeclampsia (RR, 0.47; prevalence 9.3% vs 21.3% in the control group).
  • They also had a significantly reduced risk for IUGR as defined by the various meta-analysis studies (RR, 0.44; prevalence 7% vs 16.3% in the control group).
  • Low-dose aspirin started at 16 weeks of gestation or earlier was also associated with a reduction in severe preeclampsia (RR, 0.09; prevalence 0.7% vs 15.0% in the control group), gestational hypertension (RR, 0.62; prevalence 16.7% vs 29.7% in the control group), and preterm birth (RR, 0.22; prevalence 3.5% vs 16.9% in the control group).
  • All studies involving starting aspirin at 16 weeks of gestation or earlier included women at moderate or high risk for preeclampsia.
  • The birth weight increase in women starting aspirin at 16 weeks of gestation or earlier was 196 g vs 70 g in women starting aspirin later than 16 weeks.
  • The rate of preterm birth was lower for aspirin started earlier than 16 weeks (weighted mean difference, 1.4 weeks).
  • Starting low-dose aspirin later than 16 weeks of gestation was not associated with a significant reduction in preeclampsia, IUGR, preterm birth, or gestational hypertension.
  • The authors concluded that low-dose aspirin started at 16 weeks of gestation or earlier, but not started at later than 16 weeks, was associated with improved maternal and neonatal outcomes in women at risk for preeclampsia.

Clinical Implications

  • Low-dose aspirin started at 16 weeks of gestation or earlier in women at risk for preeclampsia is associated with a reduction in the risk for preeclampsia, IUGR, preterm birth, low birth weight, and gestational hypertension.
  • Low-dose aspirin started later than 16 weeks of gestation in women at risk for preeclampsia is not associated with a reduction in the risk for preeclampsia, IUGR, preterm birth, and gestational hypertension

Read Full Post »

Pesquisadores acreditam haver uma relação entre a utilização de Insulina e seus análocos, especialmente a insulina Glargina e Câncer, porém, sem mecanismo definido.
Ulf Smith, MD, do Sahlgrenska University Hospital, observa : ” A questão é a seguinte: Isto ocorre devido aos elevados insulina circulante ou é causado por defeitos básicos associados com a obesidade e diabetes tipo 2, ou seja, a resistência à insulina?
Evidências científicas a nível celular e em animais sugerem que resistência à insulina pode ser um fator muito importante, que não podem ser determinados a partir de estudos epidemiológicos”
Porém, outros pesquisadores polemizam o assunto, relatando que não há diferença estatística significativa que aponte para estes resultados, exigindo maiores estudos a respeito.
Fonte: European Association for the Study of Diabetes (EASD) 45th Annual Meeting: Symposium S14. Presented October 1, 2009. MEDSCAPE

Read Full Post »

Geno Merli, MD, FACP, FHM; Alex C. Spyropoulos, MD, FACP, FCCP; Joseph A. Caprini, MD, MS, FACS. Annals of Surgery. 09/08/2009

Objective: A review of clinical data from oral anticoagulant studies in orthopedic/general surgery and extrapolation to actual clinical practice.

Summary Background Data: In all surgical patients, there is a risk of postoperative venous thromboembolism (VTE). Parenteral unfractionated heparin, low-molecular-weight heparin, and fondaparinux are available for VTE prophylaxis. Vitamin K antagonists, the only available oral anticoagulants, are widely used in the United States for thromboprophylaxis in joint replacement surgery in spite of being associated with several disadvantages, limiting their effectiveness in the postoperative setting. The oral direct thrombin inhibitor ximelagatran, briefly approved outside the United States for thromboprophylaxis in orthopedic patients, was discontinued due to severe hepatotoxicity concerns. Recently, the oral factor Xa inhibitors rivaroxaban and apixaban have entered late phase development for VTE thromboprophylaxis and treatment and the oral direct thrombin inhibitor dabigatran has received marketing approval from the European Medicines Agency.

Methods: Review of clinical studies of the oral anticoagulants in VTE prevention in orthopedic surgery and comparison with large observational registries.

Results: Results from Phase II/III studies suggest that new oral anticoagulants may provide an efficacious alternative in VTE prevention in orthopedic surgery. Furthermore, these new oral agents have, so far, shown a good overall safety profile, with no evidence of increased hepatotoxicity. However, comparison with large observational registries reveals differences between real-life patient populations, which make extrapolation of clinical trial data to actual clinical practice difficult. Differences in endpoint definitions also prevent indirect comparison of agents. Specific compliance and postmarketing safety issues (especially liver enzyme monitoring requirements) need to be clarified before these agents are widely accepted into routine clinical practice.

Conclusions: Although new oral anticoagulants appear promising, clinical trial results should be viewed with caution until they can be replicated in routine care settings across a broad spectrum of surgical patients.

Read Full Post »

« Newer Posts - Older Posts »