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TRADUÇÃO MÉDICA 2 Prezadas(os) alunas(os), Que bom tê-las(os) inscritas(os) no Curso de Tradução na Área Médica conduzido integralmente na modalidade online e ao vivo pelo Brasillis, via plataforma Zoom (o link será encaminhado pela secretaria do Brasillis antes da primeira aula). Essa é uma área de grande complexidade para as traduções voltadas para médicos, estudantes de medicina e outras graduações afins e para leigos em geral, e, em razão disso, os organizadores procuraram ser o mais abrangente possível, percorrendo diversas especialidades. Serão dezesseis encontros onde professores e alunos terão a oportunidade de trocar conhecimento em um ambiente de cordialidade e profissionalismo, de modo que todos concluam o curso e sintam-se bastante confortáveis para enfrentar os desafios do mercado de trabalho nas traduções e versões de textos médicos. Para que você possa melhor acompanhar o curso, solicitamos que observe, nos espaços reservados aos dias das aulas, que tipo de trabalho será feito como tradução ou versão de texto(s). Quando não houver indicação da quantidade de palavras a traduzir/verter, a aula abordará as partes relevantes de todo o texto, tal como apresentadas por você durante a aula. Para tanto, é fundamental o estudo prévio de cada texto, para que as dúvidas possam ser debatidas e sanadas no período destinado às respectivas aulas. Caso persistam dúvidas, os assuntos poderão ser levados a debate na aula seguinte, de modo que não fique pergunta sem resposta. Consideramos a sua participação no curso como fundamental para a construção coletiva do conhecimento a ser adquirido. Os professores poderão, conforme o interesse de cada um, inserir e disponibilizar outros textos que possam expandir e/ou complementar um dos temas abordados em cada encontro. Boa sorte e aproveitem ao máximo o Curso de Tradução na Área Médica do Brasillis! 3 TEMAS E TEXTOS Área: Dermatologia Tipo de texto: Artigo publicado em revista especializada Fonte complementar: Surgical & Cosmetic Dermatology Magazine Hyperhidrosis Treatment & Management Medical Care Therapy for hyperhidrosis can be challenging for both the patient and the physician. Both topical and systemic medications have been used in the treatment of hyperhidrosis. Other treatment options for hyperhidrosis include iontophoresis and botulinum toxin injections. Topical agents for hyperhidrosis therapy include topical anticholinergics, boric acid, 2- 5% tannic acid solutions, resorcinol, potassium permanganate, formaldehyde (which may cause sensitization), glutaraldehyde, and methenamine. All of these agents are limited by staining, contact sensitization, irritancy, or limited effectiveness. These agents reduce perspiration by denaturing keratin and thereby occluding the pores of the sweat glands. They have a short-lasting effect. Contact sensitization is increased, especially with formalin. Aldehydes are used to treat the palms and soles; they are not as effective in the axillae. Glutaraldehyde solution 2% is sold as Cidex. It is not as effective but less staining. The 20-50% solution can be diluted to 10% (more effective, especially for feet, but still staining occurs). Because of the limitations of other agents, Drysol (20% aluminum chloride hexahydrate in absolute anhydrous ethyl alcohol) is more commonly used as the first- line topical agent. Drysol should be applied nightly on dry skin with or without occlusion until a positive result is obtained, after which the intervals between applications may be lengthened. To minimize irritation, the remainder of the medication should be washed off when the patient awakes, and the area may be neutralized with the topical application of baking soda. Axillary hyperhidrosis may be treated with aluminium chloride gel, although the gel may cause mild cutaneous irritation.Its antiperspirant action for treatment of palmar hyperhidrosis and its low risk of systemic adverse effects from absorption and accumulation of aluminium in visceral organs are noteworthy. Systemic agents used to treat hyperhidrosis include anticholinergic medications. Anticholinergics such as propantheline bromide, glycopyrrolate, oxybutynin, and benztropine are effective because the preglandular neurotransmitter for sweat secretion is acetylcholine (although the sympathetic nervous system innervates the eccrine sweat glands). The use of anticholinergics may be unappealing because their 4 adverse effect profile includes mydriasis, blurry vision, dry mouth and eyes, difficulty with micturition, and constipation. In addition, other systemic medications, such as sedatives and tranquilizers, indomethacin, and calcium channel blockers, may be beneficial in the treatment of palmoplantar hyperhidrosis. Iontophoresis was introduced in 1952 and consists of passing a direct current across the skin. The mechanism of action remains under debate. In palmoplantar hyperhidrosis, the daily treatment of each palm or sole for 30 minutes at 15-20 mA with tap water iontophoresis is effective. Intact skin can endure 0.2-mA/cm2 galvanic current without negative consequences, and as much as 20-25 mA per palm may be tolerated. Numerous agents have been used to induce hypohidrosis, including tap water and anticholinergics; however, treatment with anticholinergic iontophoresis is more effective than tap water iontophoresis. However, the latter is safe and effective when used on Monday, Wednesday, and Friday for 4 weeks, with continued treatment maintaining the effect. Noncompliance is common with tap water iontophoresis, as it can be time-consuming. This technique merits consideration prior to systemicoraggressive surgical intervention. Botulinum toxin injections are effective because of their anticholinergic effects at the neuromuscular junction and in the postganglionic sympathetic cholinergic nerves in the sweat glands. In palmar hyperhidrosis, 50 subepidermal injections of 2 mouse units per palm (total 100 mouse units per palm) results in anhydrosis lasting 4-12 months. Each injection produces an area of anhydrosis approximately 1.2 cm in diameter. The only adverse effect is mild transient thumb weakness that resolves within 3 weeks. Adverse effects of intradermal injections of botulinum A toxin may result from diffusion into underlying muscles. A substantial increase in the duration of efficacy may be produced by repetitive injections in those with primary palmar hyperhidrosis. = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = Área: Cardiologia 5 Tipo: Informações para pacientes [Tradução] Hypertrophic Cardiomyopathy Overview Hypertrophic cardiomyopathy (HCM) is a disease in which the heart muscle (myocardium) becomes abnormally thick (hypertrophied). The thickened heart muscle can make it harder for the heart to pump blood. Hypertrophic cardiomyopathy often goes undiagnosed because many people with the disease have few, if any, symptoms and can lead normal lives with no significant problems. However, in a small number of people with HCM, the thickened heart muscle can cause shortness of breath, chest pain or problems in the heart's electrical system, resulting in life-threatening abnormal heart rhythms (arrhythmias). Symptoms Signs and symptoms of hypertrophic cardiomyopathy may include one or more of the following: • Shortness of breath, especially during exercise • Chest pain, especially during exercise • Fainting, especially during or just after exercise or exertion • Sensation of rapid, fluttering or pounding heartbeats (palpitations) • Heart murmur, which a doctor might detect while listening to your heart When to see a doctor A number of conditions can cause shortness of breath and heart palpitations. It's important to get a prompt, accurate diagnosis and appropriate care. See your doctor if you experience any symptoms associated with hypertrophic cardiomyopathy. Call 911 or your local emergency number if you experience any of the following symptoms for more than a few minutes: • Rapid or irregular heartbeat • Difficulty breathing • Chest pain Causes 6 Hypertrophic cardiomyopathy is usually caused by abnormal genes (gene mutations) that cause the heart muscle to grow abnormally thick. People with hypertrophic cardiomyopathy also have an abnormal arrangement of heart muscle cells (myofiber disarray). This disarray can contribute to arrhythmia in some people. The severity of hypertrophic cardiomyopathy varies widely. Most people with hypertrophic cardiomyopathy have a form of the disease in which the wall (septum) between the two bottom chambers of the heart (ventricles) becomes enlarged and restricts blood flow out of the heart (obstructive hypertrophic cardiomyopathy). Sometimes hypertrophic cardiomyopathy occurs without significant blocking of blood flow (nonobstructive hypertrophic cardiomyopathy). However, the heart's main pumping chamber (left ventricle) may become stiff, reducing the amount of blood the ventricle can hold and the amount pumped out to the body with each heartbeat. Risk factors Hypertrophic cardiomyopathy is usually inherited. There's a 50 percent chance that the children of a parent with hypertrophic cardiomyopathy will inherit the genetic mutation for the disease. First-degree relatives — parents, children or siblings — of a person with hypertrophic cardiomyopathy should ask their doctors about screening for the disease. Complications Many people with hypertrophic cardiomyopathy (HCM) don't experience significant health problems. But some people experience complications, including: • Atrial fibrillation. Thickened heart muscle, as well as the abnormal structure of heart cells, can disrupt the normal functioning of the heart's electrical system, resulting in fast or irregular heartbeats. Atrial fibrillation can also increase your risk of developing blood clots, which can travel to your brain and cause a stroke. • Sudden cardiac death. Ventricular tachycardia and ventricular fibrillation can cause sudden cardiac death. People with hypertrophic cardiomyopathy have an increased risk of sudden cardiac death, although such deaths are rare. Sudden cardiac death is estimated to occur in about 1 percent of people with HCM each year. Hypertrophic cardiomyopathy can cause heart-related sudden death in people of all ages, but the condition most often causes sudden cardiac death in people under the age of 30. • Obstructed blood flow. In many people, the thickened heart muscle obstructs the blood flow leaving the heart. Obstructed blood flow can cause shortness of breath with exertion, chest pain, dizziness and fainting spells. 7 • Dilated cardiomyopathy. Over time, thickened heart muscle may become weak and ineffective in a very small percentage of people with HCM. The ventricle becomes enlarged (dilated), and its pumping ability becomes less forceful. • Mitral valve problems. The thickened heart muscle can leave a smaller space for blood to flow, causing blood to rush through your heart valves more quickly and forcefully. This increased force can prevent the valve between your heart's left atrium and left ventricle (mitral valve) from closing properly. As a result, blood can leak backward into the left atrium (mitral valve regurgitation), possibly leading to worsening symptoms. • Heart failure. The thickened heart muscle can eventually become too stiff to effectively fill with blood. As a result, your heart can't pump enough blood to meet your body's needs. Prevention Because hypertrophic cardiomyopathy is inherited, it can't be prevented. But it's important to identify the condition as early as possible to guide treatment and prevent complications. Preventing sudden death Implantation of a cardioverter-defibrillator has been shown to help prevent sudden cardiac death, which occurs in about 1 percent of people with hypertrophic cardiomyopathy. Unfortunately, because many people with hypertrophic cardiomyopathy don't realize they have it, there are instances where the first sign of a problem is sudden cardiac death. These cases can happen in seemingly healthy young people, including high school athletes and other young, active adults. News of these types of deaths generates understandable attention because they're so unexpected, but parents should be aware these deaths are quite rare. Still, doctors trained in heart abnormalities generally recommend that people with hypertrophic cardiomyopathy not participate in most competitive sports with the possible exception of some low-intensity sports. Discuss specific recommendations with your cardiologist. = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = 8 Área: Endocrinologia Tipo: Texto para pacientes [Tradução] Alström Syndrome Alström Syndrome is a rare, genetically inherited syndrome which has a number of common features. The key features of Alström syndrome are: • Retinal degeneration: This is often the first feature of Alström Syndrome that is noticed. Children have nystagmus (wobbly eyes) and photophobia (extreme sensitivity to light). Poor vision can be present even in small babies, and gradual vision loss can lead to blindness. • Hearing loss: This is usually noticed before the age of 10. The severity of hearing loss in Alström Syndrome varies considerably. • Cardiomyopathy: This means that the heart doesn’t pump as well as it should. It can improve, although not completely, and it can recur in later life. • Obesity: Children and young people with Alström Syndrome have a lower energy requirement and generally are less active compared with their peer group; as a result they have a higher risk of obesity. This weight gain tends to be less severe in later life. • Type 2 diabetes: In young adulthood, children with Alström Syndrome tend to become resistant to insulin, and can go on to develop Type 2 diabetes. High blood fat levels are also common in people with insulin resistance. • Renal (kidney) failure: This might be acute (happening quickly) or chronic (happening over a long period of time). There are a number of reasons why the kidneys fail; one of these is diabetes. • Orthopaedic and rheumatology problems: People with Alström Syndrome can have problems with their bones and joints. These include curvature of the spine, spondylitis (excessive thickening of the spine), arthritis and short stature. Other problems such as hypogonadism (defects of the reproductive system), undescended testes, low testosterone, polycystic ovaries, underactive thyroid and acanthosis nigricans (dark patches of skin) may also be present. Treating Alström Syndrome There isn’t a cure for Alström Syndrome, but there are treatments for some of the features: sensitivity to bright light can be helped by wearing dark glasses, which may also slow down retinal degeneration as well. Hearing aids can be helpful in managing hearing loss. A number of drugs can be used to treat cardiomyopathy, including digoxin, frusemide and ACE inhibitors. 9 Following a healthy, balanced, low-energy diet and taking regular physical activity are important to keep weight under control and will usually be the first treatment for Type 2 diabetes. Medications such as metformin, sulphonylureas and insulin can be used to treat Type 2 diabetes if weight management and physical activity are unsuccessful. The treatment for renal (kidney) failure depends on how well the kidneys are working, but dialysis and kidney transplants are available should they fail completely. How common is Alström Syndrome? Alström Syndrome is very rare, and estimates suggest there are only around 700 people diagnosed with it worldwide. Alström Syndrome can be diagnosed from the features above, but there is also a genetic test that can be done. Scientists have identified a gene that causes Alström Syndrome which is recessive, which means that the gene must be passed on by both parents. = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = 10 Área: Otorrinolaringologia Tipo de texto: Relato de Caso Metastatic Basal Cell Carcinoma: A Rare Manifestation of a Common Disease 1. Introduction Basal cell carcinoma (BCC) is considered the most common malignancy in Caucasians. It accounts for about 80% of all nonmelanoma skin tumors, characteristically arising in areas of the body exposed to the sun, its most common location is the head and neck, and it is characterized by slow, locally aggressive growth. Despite its high prevalence, the occurrence of metastases is extremely rare, with incidence rates varying from 0.0028% to 0.55%. The metastases are lymphatic or hematogenic, with regional lymph nodes being the most frequent sites, followed by the lungs and bones. Despite the new treatment options recently developed, the prognosis for metastatic disease remains poor. 2. Case Report A 58-year-old male patient presented with a history of basal cell carcinoma on the left nasolabial sulcus for 17 years, having performed three previous excisions with local recurrence. He had a history of intense sun exposure in youth. He did not have primary or acquired immunodeficiency and denied prior radiation therapy or family history of oncology. The patient presented an ulceroinfiltrative lesion of 2.5 cm × 2.0 cm extending through the skin of the maxillary region and the left lateral portion of the nose. There were no palpable cervical masses. Anatomopathological study of the last approach, with deep margin compromised, and computed tomography evidenced infiltration up to periosteum. The patient opted for surgical treatment, so excision of the lesion was performed, with en bloc removal of the maxilla, lateral nasal wall, lateral portion of hard and soft palates on the left, and left neck dissection, levels I to IV. Anatomopathological study confirms the diagnosis of sclerosing basal cell carcinoma, with compromised margin in the region adjacent to the nasal root, perineural carcinomatous invasion, and vascular emboli, and the absence of lymph node metastasis. Posteriorly, he was subjected to adjuvant radiotherapy, presenting clinical remission after treatment. At follow-up, 7 months after surgery, he presented with a painful mass with progressive growth in the left submandibular region, adhered to the mandible. PET-CT has showed hypercaptation of 1.9 cm in the left cervical level I and vertebral body of L5, with pathological fracture (Figures 1 and 2). Then, he was subjected to a new procedure, with modified radical neck dissection and marginal mandibulectomy, 11 whose anatomopathological findings indicated sclerosing basal cell carcinoma compromising the submandibular gland and adjacent soft tissues, a very similar pattern to the primary tumor, with perineural and vascular invasion (Figures 3 and 4). Faced with this, metastatic disease was considered. Concomitant to this, a biopsy of the L5 lesion was performed, evidencing a histological appearance very similar to the primary tumor and submandibular lesion, compatible with bone metastasis (Figure 5). Then, he was subjected to lumbar spine arthrodesis. In postoperative follow-up, a new ulceroinfiltrative lesion was presented in the upper margin of the operative wound, nasal root region, and medial epicanto of the left eye, with induration up to the medial third of the lower eyelid, whose biopsy confirmed local recurrence without surgical proposal. He underwent chemotherapy with paclitaxel and carboplatin, interrupted by toxicity. The patient remains with clinically stable disease 21 months after diagnosis of the first metastasis. 3. Discussion The first case of metastatic basal cell carcinoma (BCC) was reported by Beadles in 1894 [3]. In 1951, Lattes and Kessler described the most widely accepted criteria for the diagnosis of metastatic basal cell carcinoma (mBCC): (a) the primary lesion and metastasis must have histological confirmation and not be predominantly squamous; (b) the primary tumor must originate from the skin and not from salivary glands or mucous membranes; and (c) direct dissemination of the tumor must be excluded [4]. The current basis for understanding mBCC is derived from two major literature reviews. The first review reported 170 cases from 1894 to 1980, and a subsequent review described 194 cases between 1981 and 2011 [5, 6]. To complement these reviews, we performed a search in the PubMed database, using the terms “basal cell” or “basal cell carcinoma”; “metastatic,” “metastases,” or “metastasis”; and “skin,” covering all publications between January 2012 and March 2017. Cases of BCC were defined using the Lattes and Kessler criteria. Thirty cases were identified, of which 6 were excluded (2 were not in the English or Portuguese language, 3 had no histological evidence of metastasis, and 1 had a basal cell nevus syndrome), resulting in 24 cases. Added to these a case reported in the present study, 25 cases were analyzed in total. In our series, the majority were men with a median age of 65 years, indicating a trend of increased incidence in the male population and onset at a higher age [5–7]. The relationship between the size of the primary tumor and the development of metastases is described: lesions smaller than 3 cm with an incidence of 2%, lesions up to 5 cm with 25%, and tumors greater than 10 cm with 50% [8]. The mean size of the primary tumor in our study was 6.1 cm (N = 13, of which two were greater than 10 cm and two were less than 3 cm). In addition to these risk factors, history of previous radiotherapy, local recurrence, location in the central portion of the face or ears, long 12 period of evolution, presence of perineural or perivascular invasion, and possibly immunosuppression are associated with a higher occurrence of metastases. Regarding the location of the primary tumor, the majority were in the head and neck, followed by trunk and extremities, revealing a decrease in the incidence of primary tumors in the head and neck, although this remains the most frequent site [5–7]. The most frequent histological variants were infiltrative, corresponding to 41%, followed by sclerosing, micronodular, and basosquamous/metatypical cell carcinomas in the same proportion, 17% each, and one case of mixed tumor (nodular and infiltrative), corroborating previous studies [2, 12]. The pathways of tumor dissemination described are lymphatic or hematogenic, with the most common site of metastases being lymph nodes, followed by the lungs. Compared with previous studies, there was a decrease in the proportion of lymph node metastases to the detriment of systemic ones [1, 13]. The mean interval between the onset of the tumor and the identification of metastases was approximately 7 years, lower in comparison to the literature, which describes 9 years. [1, 5, 13] Previous studies have indicated a poorer survival, lower in patients with distant metastases when compared to those with only lymph node involvement, estimated at 24 months for the former and 87 months for the latter. Our study does not allow comparisons with these data because of the small proportion of the sample with available prognostic data, that is, only 5 cases [12]. Among the patients analyzed, 92% received some form of treatment, 80% of which underwent surgery, 40% to radiotherapy, and 28% to chemotherapy, of which 60% received combined therapies. Two patients chose not to perform any type of treatment. Only 16% used inhibitors of the Hedgehog signaling pathway, which suggests an underutilization of this new therapeutic modality. 4. Conclusion Basal cell carcinoma represents a very common entity, and the presence of metastasis, although infrequent, must be considered because of the greater morbidity and mortality of this complication. This case shows the importance of diagnosis and early intervention in BCC as the best way to avoid unfavorable outcomes. = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = 13 Área: Pediatria Tipo de texto: Abstract [Tradução] Management of the Child Born Small for Gestational Age through to Adulthood: A Consensus Statement of the International Societies of Pediatric Endocrinology and the Growth Hormone Research Society Abstract Objective: Low birth weight remains a major cause of morbidity and mortality in early infancy and childhood. It is associated with an increased risk of health problems later in life, particularly coronary heart disease and stroke. A meeting was convened to identify the key health issues facing a child born small for gestational age (SGA) and to propose management strategies. Participants: There were 42 participants chosen for their expertise in obstetrics, peri- and neonatal medicine, pediatrics, pediatric and adult endocrinology, epidemiology, and pharmacology. Evidence: Written materials were exchanged, reviewed, revised, and then made available to all. This formed the basis for discussions at the meeting. Where published data were not available or adequate, discussion was based on expert clinical opinions. Consensus Process: Each set of questions was considered by all and then discussed in plenary sessions with consensus and unresolved issues identified. The consensus statement was prepared in plenary sessions and then edited by the group chairs and shared with all participants. Conclusions: The diagnosis of SGA should be based on accurate anthropometry at birth including weight, length, and head circumference. We recommend early surveillance in a growth clinic for those without catch-up. Early neurodevelopment evaluation and interventions are warranted in at-risk children. Endocrine and metabolic disturbances in the SGA child are recognized but infrequent. For the 10% who lack catch-up, GH treatment can increase linear growth. Early intervention with GH for those with severe growth retardation (height SD score, <−2.5; age, 2–4 yr) should be considered at a dose of 35–70 μg/kg·d. Long-term surveillance of treated patients is essential. The associations at a population level between low birth weight, including SGA, and coronary heart disease and stroke in later life are recognized, but there is inadequate evidence to recommend routine health surveillance of all adults born SGA outside of normal clinical practice. = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = 14 Área: Cardiologia Tipo de texto: Artigo [traduzir apenas as partes assinaladas em amarelo] Drug-eluting stents appear superior to bare metal stents for vein-graft PCI in vessels up to a stent diameter of 4 mm Introduction Drug-eluting stents (DES) are now widely used in preference to bare metal stents (BMS) for elective and emergency percutaneous coronary intervention (PCI), with studies demonstrating their superiority to BMS in reducing major adverse cardiac events (MACE) in native coronary artery disease (1-2-3-4). However, the use of DES in saphenous vein graft (SVG) and the long-term MACE outcome has not been yet demonstrated in larger studies over longer follow-up periods. Occlusion rates of SVG over 10 years are 40%, and of those grafts that do not occlude 43% will have significant stenosis (5). Despite the fact that up to 10% of PCIs are done in SVG (6), these lesions have been either poorly represented or excluded from pivotal clinical trials (1, 2). However, the degeneration of SVG appears to be different compared with the progression of coronary artery atherosclerosis in native vessels (7, 8). In native vessels the cause of restenosis is almost exclusively due to neointima proliferation (9) while in SVGs variable degrees of contribution have been reported for thrombus formation, cellular hyperplasia and progression of atherosclerotic process (10). Due to the difference in pathophysiology of vein graft stenosis, the outcome of DES in native coronary artery disease cannot be directly translated to this different clinical setting (11). The question arises as to whether the long-term advantages of DES over BMS in reducing restenosis are offset by increased MACE driven by late stent thrombosis, whether different DES types have different outcomes and whether the size of the stent affects the outcome. To address this we studied a large cohort of consecutive patients undergoing SVG PCI with the aim of comparing long-term outcomes for those treated with DES and BMS. We also investigated the influence of stent diameter on MACE during the follow-up period. Methods This was a retrospective observational cohort study in a high-volume interventional centre of patients with vein graft disease treated with either DES or BMS. The study period was from January 2003 to July 2011. During this period, 15,569 consecutive patients underwent PCI, of whom 13,422 (86%) with complete database records and National Health Service numbers were available for analysis. A total of 657 patients with stable angina, unstable angina or non-ST elevation acute coronary syndrome (NSTEACS) underwent PCI for the treatment of SVG stenosis. Patients undergoing primary PCI were excluded as BMSs were routinely used for the majority of the study period as per local guidelines. 15 Data were prospectively entered into a clinical PCI database at the time of the procedure. Data collected included patient characteristics (age, prior myocardial infarction (MI), PCI and coronary artery bypass grafting (CABG), hypertension, diabetes mellitus, hypercholesterolaemia, peripheral vascular disease (PVD), New York Heart Association class, smoking status, chronic renal impairment (chronic renal failure (CRF): creatinine >200 µmol/l or on renal replacement therapy), left ventricular (LV) function and cardiogenic shock) and procedure-related data (indications for PCI, target vessel, number of diseased vessels, use of intravascular ultrasound (IVUS)/pressure wire, use of DES and glycoprotein (GP) IIb/IIIa inhibitor). Interventional strategy was at the discretion of the operator, including the use of direct stenting, pre/post-dilatation, IVUS, adjunctive antiplatelet therapy and use of ablative devices. Angiographic success was defined as residual stenosis <30% with Thrombolysis In Myocardial Infarction (TIMI) flow grade 3. All patients received aspirin 300 mg and either clopidogrel 300 mg or 600 mg prior to the procedure. All patients were prescribed 75 mg aspirin and 75 mg clopidogrel maintenance therapy. Clopidogrel maintenance therapy was recommended for 1 month in the BMS group, 12 months in the DES group and 12 months for patients treated for NSTEACS. Unfractionated heparin was given during the procedure at a loading dose of 70 u/kg and the activated clotting time was maintained >250 sec. Glycoprotein IIb/IIIa inhibitors were used at the operator’s discretion and according to local guidelines. Procedural complications and MACE were recorded prospectively. MACE was defined as death, MI (new pathologic Q waves in the distribution of the treated coronary artery with an increase of creatine kinase MB to ≥2 times the reference value or significant rise in Troponin T values) and target vessel revascularization (TVR). These MACE rates were adjudicated by three independent physicians who were not involved in the procedure and were unaware of the patient’s stent type. Procedural complications recorded included MI, emergency CABG, arterial complications, aortic/coronary dissection, side branch occlusion and arrhythmia. Procedural complications were recorded at the time of the procedure and in-hospital complications were entered into the database at the time of discharge. Stent thromboses were defined according to the Academic Research Consortium (ARC) definition as angiographic or pathologic confirmation of partial or total thrombotic occlusion within the peri-stent region plus at least one of acute ischaemic symptoms, ischaemic electrocardiogram changes or elevated cardiac biomarkers (12). Repeat PCI rates due to TVR were identified from the PCI database. All-cause mortality data were recorded as of 10 August 2011 and obtained via the British Cardiovascular Intervention Society national database, part of the National Institute of Cardiovascular Outcomes Research. This national database is periodically linked to the UK Office of National Statistics and provides live/death status of treated patients. Only patients who had complete database records and National Health Service unique numbers (allowing live/death status to be assessed) were included in the analysis. A retrospective data quality audit of 100 randomly selected 16 medical records established that 94.8% of data fields, including complications, were entered correctly into the database. Ethics Data were collected as part of a national cardiac audit and all patient-identifiable fields were removed prior to analysis. The local ethics committee advised that formal ethical approval was not required. Statistical analysis Baseline patient, procedural and post-procedural characteristics were compared between the two groups. Categorical data are summarized using absolute values (percentage). Normally distributed, continuous data are presented as mean ± standard deviation or, where skewed, as median (inter-quartile range). Normally distributed continuous variables were compared using Student t-tests, and the Mann–Whitney U test was used to compare non-normally distributed continuous variables. Categorical data were compared using the Pearson chi-squared test. Propensity matching Baseline comorbidity was unbalanced between the DES and BMS groups. A non- parsimonious logistic regression model with stent type as the dependent variable (c- statistic, 0.785) was constructed to adjust for the confounding of baseline comorbidity and surgical complexity. Covariates in the model included age, sex, previous MI, hypertension, previous stroke, PVD, LV ejection fraction, diabetes mellitus, CRF, acute coronary syndrome (ACS) presentation, cardiogenic shock, stent length and GP IIb/IIIa use. To balance comorbidity between the study groups, a greedy matching SPSS macro was used to match the 313 patients who underwent DES insertion with the 344 patients from the BMS group with similar comorbidity. This created a “propensity- matched BMS” population. Midterm survival was described using the Kaplan–Meier method, and comparisons were made using the log-rank statistic. Estimations of risk were calculated using Cox regression analysis. Potential independent predictors of outcome were identified by univariate Cox regression analyses, and all significant univariate predictors (p<0.05) were then entered into the multivariate Cox regression model. Influence of stent diameter and DES type on outcome Subgroup analysis was performed based on the diameter of stent inserted, with patients split into above and below 4 mm with further subgroup analysis based on the type of DES used. 17 Results A total of 657 patients underwent PCI for SVG lesions, 344 patients who underwent PCI with BMS and 313 treated with DES. The DES used was broken down into Taxus 128 (paclitaxel), Cypher (sirolimus) 70, Resolute 20 (zotarolimus), Endeavor 122 (zotarolimus), Promus (everolimus) 37. Baseline characteristics for both groups were similar apart from there being more patients with diabetes in the DES group (31.6% vs. 21.0%, p = 0.007) and more patients with ACS in the BMS group (31.4% vs. 22.0%, p = 0.02). Angiographic success rates were similar for both groups (93.8% vs. 92.8%, p = 0.78). More stents per lesion were used in the DES group (1.5 ± 0.7 vs. 1.3 ± 0.6, p<0.0001), with a longer average length (22.0 ± 5.4 vs. 18.8 ± 3.9, p<0.0001). Average stent width was higher in the BMS group (3.7 ± 0.5 vs. 3.2 ± 0.4, p<0.001). Propensity matched population After propensity matching, all baseline patient and procedural characteristics were balanced between the two groups. MACE after 5 years were less frequent with DES compared with BMS (17.9%, 95% confidence interval (CI) 9.3-14.2% vs. 31.2%, 95% CI 16.9-25.1%, p = 0.017), driven largely by decreased TVR in the DES group (9.9%, 95% CI 6.0-11.5% vs. 18.8%, 95% CI 13.0-22.3%, p = 0.018). Rates of target lesion revascularization were also significantly lower in the DES group (8.3%, 95% CI 5.2-10.1% vs. 17.2%, 95% CI 10.8-19.4%, p = 0.020). There was no difference in death, MI or stroke between the stent types (Fig. 2). Rates of definite/confirmed stent thrombosis were comparable for BMS and DES (3.2%, 95% CI: 1.7-4.6% vs. 3.3%, 95% CI 1.4-4.4%, p = 0.6). There was no difference in the timing of stent thrombosis between the two groups with similar rates of late (1.6% vs. 1.3%) and very late thrombosis (1.6% vs. 1.5%). Procedural characteristics according to stent type are illustrated in Table II. Hazard ratios after multivariate analysis for baseline and procedural characteristics. ACS = acute coronary syndrome; CI = confidence interval; CRF = chronic renal failure; DES = drug-eluting stent; EF = ejection fraction; GP = glycoprotein; MI = myocardial ... Adjusted Cox analysis confirmed a decreased risk of MACE for DES compared with BMS 0.75 (95% CI 0.52-0.94) with no difference in the hazard of all-cause mortality (hazard ratio (HR) 1.08; 95% CI 0.77-1.68). The above Cox proportional hazard model was repeated with the year of procedure included as a categorical variable to allow for improvements in PCI technique and technology over the long study period. This confirmed the association between DES use and improved MACE rates (HR 0.79; 95% CI 0.53-0.96) Table III illustrates the Cox proportional model of univariate and multivariate analysis of predictors of major adverse cardiac events after PCI. 18 Subgroup analysis On subgroup analysis comparing different types of DES there was no significant difference in MACE rates between old- and new-generation DES (198 stents were old- generation DES, and 179 were new-generation DES). Neither stent thrombosis (relative risk (RR) 1.19, 95% CI 0.70-1.80, p = 0.48), restenosis (RR 0.95, 95% CI 0.55-1.49, p = 0.54) nor death (RR 1.13, 95% CI 0.74-1.29, p = 0.44) were statistically significantly improved with new-generation vs. old-generation DES. In the study cohort there were 206 patients who had stent diameters ≥4 mm with the remaining 426 patients having stent diameters <4 mm. The larger diameter (≥4 mm) cohort were split into 101 DES and 105 BMS. In this cohort there were no differences in MACE after 5 years with DES compared with BMS (11.9%, 95% CI 8.1-14.2% vs. 15.2%, 95% CI: 9.4-12.7%, p = 0.317) (Fig. 4A), with no difference in rates of TVR, death, MI or stroke between the stent types. Rates of definite/confirmed stent thrombosis were comparable for BMS and DES in this larger stent cohort (0.6%, 95% CI: 0.2-1.9% vs. 0.9%, 95% CI 0.1-1.7%, p = 0.8). In the smaller stent diameter cohort (<4 mm diameter) MACE after 5 years were significantly less frequent with DES compared with BMS (20.5%, 95% CI 10.8-13.8% vs. 38.2%, 95% CI: 19.9-45.1%, p = 0.0007), driven by decreased TVR in the DES group (14.9%, 95% CI 9.0-16.5% vs. 28.8%, 95% CI 15.0-32.3%, p = 0.0008). There was no difference in death, MI, stent thrombosis or stroke between the stent types in the smaller diameter cohort (Fig. 4B). Discussion This is a large observational study with one of the longest follow-up periods yet reported. Propensity matching is utilized, which is only the case in few other studies (13-14-15). We specifically compared outcomes for patients with SVG disease treated by PCI with drug eluting as compared with BMS. DESs were associated with significantly lower 5-year MACE rates compared with BMSs in both elective and ACS subgroups. This difference was primarily driven by lower rates of repeat TVR by PCI. Rates of late stent thrombosis and subsequent AMI were low, with no difference between the BMS and DES groups. Therefore, the use of DES in the proximal SVG was not associated with an increase in late-stent thrombosis or long-term mortality compared with BMS. Due to the fact that this difference was driven by TVR we also looked into the effect of stent diameter on MACE. Interestingly there was no difference comparing BMS and DES for stents above 4 mm in diameter. The degeneration of SVG appears to be a different phenomenon compared with the progression of coronary artery atherosclerosis in native vessels (7, 8). In native vessels the cause of restenosis is almost exclusively due to neointima proliferation (9), while in SVGs exposed to the arterial circulation variable degrees of contribution have been reported for thrombus formation, cellular hyperplasia and progression of 19 atherosclerotic process (10). Acute thrombosis is the dominant aetiology in the early postoperative period. This is related to the size of the target vessel and distal run-off, size mismatch between the graft and the target vessel, graft ischemia and disruption of the endothelial layer as a result of mechanical trauma and manual distention. Initially intimal hyperplasia is seen, which is caused by the graft’s adaptation to higher arterial pressures and loss of inhibition from the endothelial layer. Later on atherosclerosis becomes the major reason for graft stenosis and occlusion. As in native coronary arteries, vein graft atheromas can rupture and cause thrombotic occlusion of the graft (16). Vein graft atheromas are also more diffuse and concentric. They are less calcified and have poorly developed or absent fibrous caps (17). Vein graft failure is also associated with worse clinical outcomes. A study on 1,243 patients, who previously underwent CABG surgery and were followed up for a median of 6.7 years, reports a significant increase in the composite end point of death, nonfatal MI or revascularization in patients who had critical or occlusive vein graft disease on angiography compared with patients who had noncritical or no vein graft disease. This was primarily driven by TVR (18). Due to the difference in the pathophysiology of vein graft stenosis, investigating the long-term outcomes of these patients is essential. Our finding of better outcomes for DES compared with BMS in a representative PCI population with SVG disease bears comparison with the selected populations included in recent clinical trials of DES vs. BMS. The ISAR-CABG trial, a randomized controlled superiority trial, reported decreased MACE rates for DES compared with BMS in subgroups undergoing SVG stenting after 1 year follow-up (19). Again it was TVR that drove MACE in both groups, although the MACE rates for DES in our study were slightly higher (17.9% DES vs. 31.2% BMS group (p = 0.04) over the 5-year follow-up than with the rate in ISAR-CABG (19) (15% for DES group and 22% for BMS group (p = 0.02)). A recent meta-analysis on 22 studies concluded that DES in vein graft PCI was associated with a decreased reintervention rates and all-cause mortality compared with BMS. There was no difference in the risk of stent thrombosis and MI. No difference in mortality was found in this studyas was the case in the other major studies. The reasons for this are not outrightly apparent, but may be related to case selection and heterogeneity of the studies in the meta-analysis leading to bias. Interestingly, no difference in mortality was reported in randomized controlled trials in the sensitivity analysis (20). A further study investigating newer generation DES reveals no significant difference as compared to early-generation stents over a follow-up period of four years (21), data consistent with our study where no difference between older and newer generation DES was seen. Some safety concerns persist regarding stent thrombosis with DES implantation (1, 22, 23). In contrast to restenosis, which is considered to have a relatively benign clinical course, stent thrombosis is consistently associated with acute MI and the mortality is high (24). We documented low and comparable rates of stent thrombosis for BMS and DES similar to the rates reported in other patient cohorts (23, 25). Importantly, we found no difference in long-term mortality between the DES and BMS groups. Our data 20 show that DES deployment in the SVG is safe and exposes the patient to no greater risk than is associated with BMS deployment. Importantly, the significant difference between the BMS and DES is not evident for stent diameters above 4 mm. This has not been reported in the literature as yet. Operators can therefore consider implanting BMS with large diameter without substantial safety concerns. This is especially important for patients with contraindications to long-term antiplatelet therapy. Strengths and limitations of this study As all patients were treated at a single centre with standardized care protocols and pathways, the effect of bias due to different treatment strategies is limited. Our cohort has large patient numbers. The long-term follow-up based on all-cause mortality and the investigation of both acute and elective cases add to the study strengths. The univariate, multivariate and propensity analysis highlights the quality of the data with well-recognized predictors of mortality associated with adverse outcome in our data set. Although this was not a randomized study the two patient groups appear well matched with respect to baseline and procedural characteristics. There are a number of important limitations common to observational studies of this type. Importantly this study has all the limitations of a registry and all the potential bias and unmeasured confounding associated with non-randomized studies. In addition we cannot exclude the possibility of under-reporting of complications although the tracking of mortality is robust and we only included patients who had definitive mortality data in our study cohort. We cannot account for the effects of residual confounding or of selection bias caused by exclusion of 14% of patients with missing data or no NHS unique number. However, this is unlikely as the distribution of SVG disease and use of DES or BMS was the same in the excluded and analysed cohorts. Conclusions In this long-term observational study of PCI for SVG disease, DES was associated with a lower MACE rate than BMS due to a decreased need for repeat revascularization with no differences in rates of stent thrombosis, MI or all-cause mortality between the groups. However, for stents with a diameter above 4 mm no difference was seen between stent types. This suggests that although DES deployment in SVGs is both safe and clinically more effective than BMS for vessels ≥4 mm, BMSs are a viable alternative. = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = 21 PACKAGE LEAFLET: INFORMATION FOR THE USER Omeprazol XXX 40 mg powder for solution for infusion omeprazole Read all of this leaflet carefully before you start using this medicine. - Keep this leaflet. You may need to read it again. - If you have any further questions, ask your doctor or pharmacist. - This medicine has been prescribed for you. Do not pass it on to others. It may harm them, even if their symptoms are the same as yours. - If any of the side effects gets serious, or if you notice any side effects not listed in this leaflet, please tell your doctor or pharmacist. In this leaflet: 1. What Omeprazol XXX 40 mg powder for solution for infusion is and what it is used for 2. Before you are given Omeprazol XXX 40 mg powder for solution for infusion 3. How Omeprazol XXX 40 mg powder for solution for infusion will be given 4. Possible side effects 5. How to store Omeprazol XXX 40 mg powder for solution for infusion 6. Further information 1. WHAT OMEPRAZOL XXX 40 MG POWDER FOR SOLUTION FOR INFUSION IS AND WHAT IT IS USED FOR Omeprazol XXX 40 mg powder for solution for infusion is a type of drug called a “proton pump inhibitor”. Omeprazole works by reducing the production of acid in your stomach. Each vial is for one infusion. Omeprazol XXX 40 mg powder for solution for infusion is used to treat the following conditions when you are unable to take the medicine by mouth: - Acid from the stomach escaping into the gullet (oesophagus) causing pain, inflammation and heartburn (reflux oesophagitis). - Ulcers in the upper part of the intestine (duodenal ulcer) - Mild and benign (non-cancerous) ulcers in the stomach.. - Excessive acid production in the stomach caused by a condition called Zollinger- Ellison syndrome. 2. BEFORE YOU ARE GIVEN OMEPRAZOL XXX 40 MG POWDER FOR SOLUTION FOR INFUSION Do not use Omeprazol XXX 40 mg powder for solution for infusion if: - you are allergic (hypersensitive) to omeprazole or to any of the other ingredients of omeprazole 22 - you are taking atazanavir (drug used for the treatment of HIV) Omeprazol XXX 40 mg powder for solution for infusion is given to you with special care in case of one of the following conditions: - Tell your doctor if you suffer or have recently suffered from any of the following symptoms: unintentional weight loss, recurrent vomiting or vomiting of blood, or dark stools. He/she may then perform an additional investigation called endoscopy in order to diagnose your condition and/or exclude other more serious conditions. - Treatment with gastric acid inhibitors leads to a slightly increased risk of gastrointestinal infections. Inform your doctor if you suffer from gastrointestinal symptoms like diarrhoea and abdominal pain. - Omeprazole should not be given to children under the age of one. - If you have or have had problems with your liver or kidneys you should tell your doctor. He/she may check how they are working with blood tests especially if you have to take this medicine for a long time. - Blindness and deafness have been reported with the use of Omeprazole, therefore the monitoring of visual and auditory senses may be necessary. - If you suffer from peptic ulcer, the possibility of a bacterial infection caused by Helicobacter pylori should be determined and existing infection should be eliminated prior to omeprazole therapy Ask your doctor for advice if any of the above situations applies to you. Taking other medicines Medicines that are taken concomitantly may influence each other in terms of effect(s) and/or side effect(s). This is called interaction. Interactions may also occur if you have taken medicines recently or will use them in the near future. It is especially important that you tell your doctor if you are taking or have recently taken any medicine which contains: - Atazanavir (drug used for treatment of HIV) - Ketoconazole and itraconazole (medicine used for the treatment of fungal infections) and other medicines whose absorption is influenced by the degree of acidity in the stomach - Digoxin (medicine for heart conditions). - Drugs that are also metabolised by the liver, such as warfarin (a drug to avoid blood coagulation) and phenytoin (a drug for the treatment of epilepsy, for instance) - Disulfiram (medicine to treat alcoholism) - Ciclosporin and tacrolimus (medicines that inhibit the defence mechanism and thus prevents rejection) - Clarithromycin (drug to avoid/fight certain infections) - St. John’s Wort (extract from a medicinal plant, which is often used as a natural antidepressant). - Vitamin B12. 23 - benzodiazepines (drugs with sedative, sleep-inducing and/or muscle-relaxing properties), such as diazepam, triazolam, flurazepam - some drugs used to treat depression, such as citalopram, imipramine and clomipramine - Voriconazole (medicine used for the treatment of fungal infections) If you are taking these types of medicines, you should bear these observations in mind and ask your doctor or pharmacist for advice. Please tell your doctor or pharmacist if you are taking or have recently taken any other medicines, including medicines obtained without a prescription. Pregnancy and breast-feeding Tell your doctor if you are pregnant, think you might be pregnant or plan to become pregnant and also if you are breast-feeding. Your doctor will need to consider any possible risks of you or your child, taking Omeprazol XXX 40 mg powder for solution for infusion. At present, there is insufficient information available to evaluate whether the active substance, omeprazole, has such kind of adverse effects. To date there is no evidence. Driving and using machines There is no evidence of effects on the ability to drive or use machines. It should be remembered that side effects such as drowsiness and visual disturbances may occur and may possibly affect the ability to drive or use machines. Important information about some of the ingredients of Omeprazol XXX 40 mg powder for solution for infusion: This medicinal product contains less than 1 mmol sodium (23 mg) per dose, i.e. essentially “sodium free”. 3. HOW OMEPRAZOL XXX 40 MG POWDER FOR SOLUTION FOR INFUSION WILL BE GIVEN Omeprazol XXX 40 mg powder for solution for infusion is only for adults and should not be given to children under the age of one. Your medicine will be given to you by a health care specialist who will decide how much you need. To start with, this will usually be 100 ml infusion given to you slowly over 20 minutes to half an hour. The reconstituted solution should not be used if particles are present and should be used on one patient during one treatment. If you are givenmore medicine than you should have received: Omeprazole infusion is well tolerated even in high doses. There is no information available on the effects of overdosing. If you suspect that you have been given too much medicine, you may experience some of the possible side effects listed below, please inform your doctor. 24 4. POSSIBLE SIDE EFFECTS Like all medicines, Omeprazole may sometimes cause side effects. These are usually mild and diminish rapidly. The following side effects have been reported at the approximate frequencies shown: Very common (affecting more than one person in 10) Common (affecting fewer than one person in ten but more than one person in 100) Uncommon (affecting fewer than one person in 100 but more than one person in 1,000) Rare (affecting fewer than one person in 1,000 but more than one person in 10,000) Very rare (affecting fewer than one person in 10,000 but more than one person in 100,000) Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness Gastrointestinal disorders: - Common: Diarrhoea, constipation, stomach ache, feeling sick, vomiting, wind. - Rare: Dry mouth, thrush in the mouth or gullet, brownish-black discoloration of the tongue, inflammation of the mouth, inflammation of the pancreas Nervous system disorders: - Common: Headaches, dizziness, light headedness, feeling faint, sleepiness, trouble sleeping - Uncommon: Pins and needles, - Rare: Reversible mental confusion, depression and hallucinations in case of severely ill patients, generally feeling unwell Endocrine disorders: - Rare: Development of breasts in men Blood and lymphatic system disorders: - Rare: Blood disorders (decrease in the number of circulating white blood cells, platelets, or red blood cells in blood) which may lead to frequent infections with symptoms of fever, severe chills, sore throat, mouth ulcers, bleeding or bruising more easily than normal or tiredness Hepatobiliary disorders: - Uncommon: Increase in hepatic enzymes - Rare: Liver disease which may colour your skin and eyes yellow, Liver failure which can lead to brain damage, Musculoskeletal and connective tissues disorders: - Rare: Painful swollen joints, aching muscles or muscle weakness Skin and subcutaneous tissue disorders: - Uncommon. Rash, itching, - Rare: Skin sensitivity to light, severe skin blisters, severe blisters and bleeding in the lips, eyes, mouth, nose and genitals, unusual hair loss or thinning; Other: 25 - Uncommon: Feeling unwell - Rare: Allergic reactions, sometimes very severe, including swelling of the lips, tongue and throat, kidney disease, increased sweating, blurred vision, low blood sodium. If you are very unwell, you may feel confused, nervous, aggressive, depressed and see, feel or hear things that are not there. It is not known whether these side effects are caused directly by Omeprazole. If any of the side effects gets serious, or if you notice any side effects not listed in this leaflet, please tell your doctor or your pharmacist. 5. HOW TO STORE OMEPRAZOL XXX 40 MG POWDER FOR SOLUTION FOR INFUSION Store Omeprazol XXX 40 mg powder for solution for infusion in the original package, in order to protect from light, below 25 °C. When your infusion is made it should be used immediately. Keep out of the reach and sight of children. Do not use this product after the expiry date which is stated on the label after EXP (The expiry date refers to the last day of that month.) Medicines should not be disposed of via wastewater or household waste. Ask your pharmacist how to dispose of medicines no longer required. These measures will help to protect the environment. 6. FURTHER INFORMATION What Omeprazol XXX 40 mg powder for solution for infusion contains - The active ingredient is Omeprazole Each vial of powder for solution for infusion contains 42.6 mg Omeprazole Sodium equivalent to 40 mg Omeprazole. - The other ingredients are sodium hydroxide and disodium edetate What Omeprazol XXX 40 mg powder for solution for infusion looks like and contents of the pack Omeprazol XXX 40 mg powder for solution for infusion is a white to almost white powder. In its dissolved form it is a clear liquid. One package contains 1 or 5 injection vial (s). One injection vial contains 40 mg omeprazole. Marketing Authorisation Holder To be completed nationally Manufacturer To be completed nationally This leaflet was last approved in ………………….. The following information is intended for medical or healthcare professionals only: 26 Indications Gastric antisecretory treatment in severely ill patients where oral therapy is inappropriate with: - Reflux oesophagitis, - Duodenal or benign gastric ulcer - Zollinger-Ellison-Syndrome Posology and method of administration Dosage (adults only) Treatment in patients where oral therapy is inappropriate e.g. in severely ill patients with either reflux oesophagitis, duodenal ulcer or gastric ulcer: Omeprazol XXX 40 mg powder for solution for infusion given as an intravenous infusion once daily is recommended for up to 5 days. The i.v. infusion produces an immediate decrease in intragastric acidity and a mean decrease over 24 hours of approximately 90%. Zollinger-Ellison syndrome: An initial dose of 60 mg of Omeprazol XXX 40 mg powder for solution for infusion in an intravenous infusion is recommended. A higher daily dose may be needed and must be determined individually. If this is more than 60 mg/day the daily dose must be distributed over two administrations. Administration Omeprazol XXX 40 mg powder for solution for infusion is for intravenous administration only and must not be given by any other route. Omeprazol XXX 40 mg powder for solution for infusion should only be dissolved in 100 ml 5% glucose solution for infusion. No other solutions for i.v. infusion should be used (see section 6.6). After reconstitution from a microbiological point of view, use immediately (i.e. within 6 hours) and any unused portion should be discarded. The duration of administration should be 20-30 minutes. For a 20 mg doses half of the reconstituted solution should be used and any unused solution should be discarded. Use in the Elderly: Dosage adjustment is not necessary. Use in Children: There is limited experience of use in children. Omeprazole should not be used in children under 1 year of age since no data are available. The dosage recommendations are as follows: Age Weight Dosage ≥ 1 year of age 10-20 kg 10 mg once daily. The dosage can be increased to 20 mg once daily if needed. ≥ 2 years of age > 20 kg 20 mg once daily. The dosage can be increased to 40 mg once daily if needed. Impaired renal function: Dose adjustment is not required in patients with impaired renal function. 27 Impaired hepatic function: As half-life is increased in patients with impaired hepatic function, the dose requires adjustment and a daily dose of 10mg - 20mg may be sufficient. Contraindications - Known hypersensitivity to omeprazole or to any of the other constituents of the formulation. - Omeprazole should not be administered with atazanavir due to an important reduction in atazanavir exposure (see section 4.5) Special warnings and precautions for use In patients with peptic ulcer disease Helicobacter pylori-status should be determined if relevant. In patients who are shown to be Helicobacter pylori-positive, the elimination of the bacterium by eradication therapy should be aimed wherever possible. When gastric ulcer is suspected the possibility of malignancy should be excluded before treatment with Omeprazol XXX 40 mg powder for solution for infusion is instituted, as treatment may alleviate symptoms and delay diagnosis. The diagnosis of reflux oesophagitis should be confirmed endoscopically. Decreased gastric acidity due to any means including proton-pump inhibitors, increases gastric counts of bacteria normally present in the gastrointestinal tract. Treatment with acid-reducing drugs may lead to a slightly increased risk of gastrointestinal infections, such as Salmonella and Campylobacter. In patients with severe impaired hepatic function, liver enzyme values should be checked periodically during treatment with omeprazole. During combination treatment caution should be exercised in patients with renal or hepatic dysfunction (for dose restriction see section 4.2). Omeprazole should not be used in infants and children under the age of 1 year (see section 4.2). Blindness and deafness have been reported in the use of the injection form of omeprazole; therefore, in severely ill patients the monitoring of visual and auditory senses is recommended. This medicinal product contains less than 1 mmol sodium (23 mg) per dose, i.e. essentially “sodium free Special precautions for disposal and other handling The entire contents of each vial should be dissolved in 100 ml 5% glucose solution for infusion. Omeprazol XXX 40 mg powder for solution for infusion should initially be dissolved in a few ml of fluid. No other solutions for i.v. infusion should be used. Use on one patient during one treatment only. = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = 28 MATERIAL EXTRA Fontes de consulta DICIONÁRIOS www.thefreedictionary.com www.onelook.com Grande Dicionário Ilustrado Inglês-Português de Termos Odontológicos e de Especialidades Médicas – Ana Julia Perrotti-Garcia e Sérgio Jesus-Garcia Dicionário de Substâncias Farmacêuticas Comerciais – PT>EN – Disponível em http://abiquifi.org.br/publicacoes_/dsfc-substancias-df/ Dicionário Stedman (em inglês apenas) – Disponível em http://www.medilexicon.com/dictionary Terminologia da IATE (vários idiomas, português europeu) – Disponível em http://iate.europa.eu/SearchByQueryLoad.do;jsessionid=0GqZsWFRmGypBaxPK1NpdB nmz5uMRYxa97CfdQUgP5dADx-x-fQW!1644451700?method=load Glossários Temáticos do Ministério da Saúde (alguns são bilíngues, nem todos) – Disponíveis em http://bvsms.saude.gov.br/terminologia LINKS https://emedicine.medscape.com/ - A versão em inglês possui uma seção detalhada sobre diversas doenças. A versão em português não é tão rica, trazendo principalmente artigos sobre novidades. http://www.msdmanuals.com/professional - Este site tem uma versão em português: http://www.msdmanuals.com/pt/profissional. Consulte a parte Assuntos Médicos / Medical Topics http://www.ncbi.nlm.nih.gov/pubmed/ http://scielo.br/ Anatomia http://www.thefreedictionary.com/ http://www.onelook.com/ http://abiquifi.org.br/publicacoes_/dsfc-substancias-df/ http://www.medilexicon.com/dictionary http://iate.europa.eu/SearchByQueryLoad.do;jsessionid=0GqZsWFRmGypBaxPK1NpdBnmz5uMRYxa97CfdQUgP5dADx-x-fQW!1644451700?method=load http://iate.europa.eu/SearchByQueryLoad.do;jsessionid=0GqZsWFRmGypBaxPK1NpdBnmz5uMRYxa97CfdQUgP5dADx-x-fQW!1644451700?method=load http://bvsms.saude.gov.br/terminologia https://emedicine.medscape.com/ http://www.msdmanuals.com/professional http://www.msdmanuals.com/pt/profissional http://www.ncbi.nlm.nih.gov/pubmed/ http://scielo.br/ 29 http://www.atlasdocorpohumano.com/ https://www.auladeanatomia.com/novosite/ Classificação Internacional de Doenças – CID 10 Inglês - http://apps.who.int/classifications/icd10/browse/2016/en Português - http://www.medicinanet.com.br/cid10.htm Descritores em 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http://decs.bvs.br/cgi-bin/wxis1660.exe/decsserver/?IsisScript=../cgi-bin/decsserver/decsserver.xis&interface_language=p&previous_page=homepage&previous_task=NULL&task=start 30 MATERIAL EXTRA – Acrônimos de terminologia médica http://www.terminologia.com.br/author/terminologia Acronym Meaning A/G Albumin/Globulin Ratio A&O Alert & Oriented AAA Abdominal Aortic Aneurysm AAD Antibiotic-Associated Diarrhea AAO Alert, Awake, And Oriented AAS Acute Abdominal Series ABD Abdomen ABG Arterial Blood Gas AC Before Eating ACLS Advanced Cardiac Life Support ACTH Adrenocorticotropic Hormone ad lib As Much As Needed ADH Anti-Diuretic Hormone ADR Adverse Drug Reaction. | Acute Dystonic Reaction AED Antiepileptic Drug AF Atrial Fibrillation Or Afebrile AFB Acid-Fast Bacilli AFP Alpha-Fetoprotein AI Aortic Insufficiency AKA Above The Knee Amputation ALD Alcoholic Liver Disease ALL Acute Lymphocytic Leukemia Amb Ambulate AML Acute Myelogenous Leukemia ANA Antinuclear Antibody ANS Autonomic Nervous System AOB Alcohol On Breath AODM Adult Onset Diabetes Mellitus AP Anteroposterior Or Abdominal – Perineal ARDS Acute Respiratory Distress Syndrome ARF Acute Renal Failure AS Aortic Stenosis ASAP As Soon As Possible ASCVD Atherosclerotic Cardiovascular Disease ASD Atrial Septal Defect http://www.terminologia.com.br/author/terminologia 31 ASHD Atherosclerotic Heart Disease AV Atrioventricular A-V Arteriovenous BBB Bundle Branch Block BCAA Branched Chain Amino Acids BE Barium Enema BEE Basal Energy Expenditure bid Twice A Day BKA Below The Knee Amputation BM Bone Marrow Or Bowel Movement BMR Basal Metabolic Rate BOM Bilateral Otitis Media BP Blood Pressure BPH Benign Prostatic Hypertrophy BPM Beats Per Minute BRBPR Bright Red Blood Per Rectum BRP Bathroom Privileges BS Bowel Or Breath Sounds BUN Blood Urea Nitrogen BW Body Weight BX Biopsy c With C/O Complaining Of CA Cancer Ca Calcium CAA Crystalline Amino Acids CABG Coronary Artery Bypass Graft CAD Coronary Artery Disease CAT Computerized Axial Tomography CBC Complete Blood Count CBG Capillary Blood Gas CC Chief Complaint CCU Clean Catch Urine Or Cardiac Care Unit CCV Critical Closing Volume CF Cystic Fibrosis CGL Chronic Granulocytic Leukemia CHF Congestive Heart Failure CHO Carbohydrate CI Cardiac Index CML Chronic Myelogenous Leukemia CMV Cytomegalovirus CN Cranial Nerves CNS Central Nervous System CO Cardiac Output 32 COLD Chronic Obstructive Lung Disease COPD Chronic Obstructive Pulmonary Disease CP Chest Pain Or Cerebral Palsy CPAP Continuous Positive Airway Pressure CPK Creatine Phosphokinase CPR Cardiopulmonary Resuscitation CRCL Creatinine Clearance CRF Chronic Renal Failure CRP C-Reactive Protein CSF Cerebrospinal Fluid CT Computerized Tomography CVA Cerebrovascular Accident Or Costovertebral Angle CVAT Cva Tenderness CVP Central Venous Pressure CXR Chest X-Ray D&C Dilation And Curettage D5W 5% Dextrose In Water DAT Diet As Tolerated DAW Dispense As Written DC Discontinue Or Discharge DDx Differential Diagnosis DI Diabetes Insipidus DIC Disseminated Intravascular Coagulopathy DIP Distal Interphalangeal Joint DJD Degenerative Joint Disease DKA Diabetic Ketoacidosis dL Deciliter DM Diabetes Mellitus DNR Do Not Resuscitate DOA Dead On Arrival DOE Dyspnea On Exertion DPL Diagnostic Peritoneal Lavage DPT Diphtheria, Pertussis, Tetanus DTR Deep Tendon Reflexes DVT Deep Venous Thrombosis DX Diagnosis EAA Essential Amino Acids EBL Estimated Blood Loss ECG Electrocardiogram ECT Electroconvulsive Therapy EFAD Essential Fatty Acid Deficiency EMG Electromyogram EMV Eyes, Motor, Verbal Response (Glasgow Coma Scale) ENT Ears, Nose, And Throat 33 EOM Extraocular Muscles ERCP Endoscopic Retrograde Cholangio -Pancreatography ESR Erythrocyte Sedimentation Rate ET Endotracheal ETOH Ethanol ETT Endotracheal Tube EUA Examination Under Anesthesia FBS Fasting Blood Sugar FEV Forced Expiratory Volume FFP Fresh Frozen Plasma FRC Functional Residual Capacity FTT Failure To Thrive FU Follow-Up FUO Fever Of Unknown Origin FVC Forced Vital Capacity Fx Fracture GC Gonorrhea GETT General By Endotracheal Tube GFR Glomerular Filtration Rate GI Gastrointestinal GTT Glucose Tolerance Test GU Genitourinary H/H Henderson- Hasselbach Equation Or Hemoglobin/ Hematocrit HÁ Headache HAA Hepatitis B Surface Antigen HAV Hepatitis A Virus HBP High Blood Pressure HCG Human Chorionic Gonadotropin HCT Hematocrit HDL High Density Lipoprotein HEENT Head, Eyes, Ears, Nose, Throat Hgb Hemoglobin HIV Human Immunodeficiency Virus HJR Hepatojugular Reflex HLA Histocompatibility Locus Antigen HO History Of HOB Head Of Bed HPF High Power Field HPI History Of Present Illness HR Heart Rate HS At Bedtime HSM Hepatosplenomegaly HSV Herpes Simplex Virus 34 HTN Hypertension Hx History I&O Intake And Output ICS Intercostal Space ICU Intensive Care Unit IDDM Insulin Dependent Diabetes Mellitus IG Immunoglobulin IHSS Idiopathic Hypertropic Subaortic Stenosis IM Intramuscular IMV Intermittent Mandatory Ventilation INF Intravenous Nutritional Fluid IPPB Intermittent Positive Pressure Breathing IRBBB Incomplete Right Bundle Branch Block IRDM Insulin Resistant Diabetes Mellitus IT Interthecal ITP Idiopathic Thrombocytopenic Purpura IV Intravenous IVC Intravenous Cholangiogram | Inferior Vena Cava IVP Intravenous Pyelogram JODM Juvenile Onset Diabetes Mellitus JVD Jugular Venous Distention KOR Keep Open Rate KUB Kidneys, Ureters, Bladder KVO Keep Vein Open L Left LAD Left Axis Deviation Or Left Anterior Descending LAE Left Atrial Enlargement LAHB Left Anterior Hemiblock LAP Left Atrial Pressure Or Leukocyte Alkaline Phosphatase LBBB Left Bundle Branch Block LDH Lactate Dehydrogenase LE Lupus Erythematosus LIH Left Inguinal Hernia LLL Left Lower Lobe LMP Last Menstrual Period LNMP Last Normal Menstrual Period LOC Loss Of Consciousness Or Level Of Consciousness LP Lumbar Puncture LPN Licensed Practical Nurse LUL Left Upper Lobe LUQ Left Upper Quadrant LV Left Ventricle LVEDP Left Ventricular End Diastolic Pressure LVH Left Ventricular Hypertrophy 35 MAO Monoamine Oxidase MAP Mean Arterial Pressure MAST Medical Antishock Trousers MBT Maternal Blood Type MCH Mean Cell Hemoglobin MCHC Mean Cell Hemoglobin Concentration MCV Mean Cell Volume MI Myocardial Infarction Or Mitral Insufficiency mL Milliliter MLE Midline Episiotomy MMEF Maximal Mid Expiratory Flow mmol Millimole MMR Measles, Mumps, Rubella MRI Magnetic Resonance Imaging MRSA Methicillin Resistant Staph Aureus MS Multiple Sclerosis Or Mitral Stenosis, Or Morphine Sulfate MSSA Methicillin-Sensitive Staph Aureus MVA Motor Vehicle Accident MVI Multivitamin Injection MVV Maximum Voluntary Ventilation NAD No Active Disease NAS No Added Salt NCV Nerve Conduction Velocity NED No Evidence Of Recurrent Disease ng Nanogram NG Nasogastric NIDDM Non-Insulin Dependent Diabetes Mellitus NKA No Known Allergies NKDA No Known Drug Allergies NMR Nuclear Magnetic Resonance NPO Nothing By Mouth NRM No Regular Medications NSAID Non-Steroidal Anti- Inflammatory Drugs NSR Normal Sinus Rhythm NT Nasotracheal OB Obstetrics OCG Oral Cholecystogram OD Overdose Or Right Eye OM Otitis Media OOB Out Of Bed OPV Oral Polio Vaccine OR Operating Room OS Left Eye OU Both Eyes 36 P Para P&PD Percussion And Postural Drainage
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