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 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

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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.

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Área: Cardiologia

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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

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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.

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 • 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.

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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.

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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.

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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,

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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

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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.

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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.

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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.

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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

15
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.

16
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.

17
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

18
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

19
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.

=================================================

20
 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

21
- 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.

22
- 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.

23
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:

24
- 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:

25
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.

26
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.
=================================================

27
 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

28
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 Ciências da Saúde

http://decs.bvs.br/cgi-bin/wxis1660.exe/decsserver/?IsisScript=../cgi-
bin/decsserver/decsserver.xis HYPERLINK "http://decs.bvs.br/cgi-
bin/wxis1660.exe/decsserver/?IsisScript=../cgi-
bin/decsserver/decsserver.xis&interface_language=p&previous_page=homepage&pre
vious_task=NULL&task=start"& HYPERLINK "http://decs.bvs.br/cgi-
bin/wxis1660.exe/decsserver/?IsisScript=../cgi-
bin/decsserver/decsserver.xis&interface_language=p&previous_page=homepage&pre
vious_task=NULL&task=start"interface_language=p HYPERLINK "http://decs.bvs.br/cgi-
bin/wxis1660.exe/decsserver/?IsisScript=../cgi-
bin/decsserver/decsserver.xis&interface_language=p&previous_page=homepage&pre
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 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

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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

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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

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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

33
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

34
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

35
P Para
P&PD Percussion And Postural Drainage
PA Posteroanterior
PAC Premature Atrial Contraction
PAO2 Alveolar Oxygen
PaO2 Peripheral Arterial Oxygen Content
PAP Pulmonary Artery Pressure
PAT Paroxysymal Atrial Tachycardia
PC After Eating
PCWP Pulmonary Capillary Wedge Pressure
PDA Patent Ductus Arteriosus
PDR Physicians Desk Reference
PE Pulmonary Embolus, Or Physical Exam Or Pleural Effusion
PEEP Positive End Expiratory Pressure
PFT Pulmonary Function Tests
pg Picogram
PI Pulmonic Insufficiency Disease
PKU Phenylketonuria
PMH Previous Medical History
PMI Point Of Maximal Impulse
PMN Polymorphonuclear Leukocyte (Neutrophil)
PND Paroxysmal Nocturnal Dyspnea
PO By Mouth
POD Post-Op Day
PP Postprandial Or Pulsus Paradoxus
PPD Purified Protein Derivative
PR By Rectum
PRBC Packed Red Blood Cells
PRN As Needed
PS Pulmonic Stenosis
PT Prothrombin Time, Or Physical Therapy
Pt Patient
PTCA Percutaneous Transluminal Coronary Angioplasty
PTH Parathyroid Hormone
PTHC Percutanous Transhepatic Cholangiogram
PTT Partial Thromboplastin Time
PUD Peptic Ulcer Disease
PVC Premature Ventricular Contraction
PVD Peripheral Vascular Disease
PTSD Post Traumatic Stress Disorder
q Every (E.G. Q6H = Every 6 Hours)

q4h, Every 4 Hours, Every 6 Hours Etc.

q6h….

36
qd Every Day
qh Every Hour
qid Four Times A Day
QNS Quantity Not Sufficient
qod Every Other Day
Qs/Qt Shunt Fraction
Qt Total Cardiac Output
R Right
R/O Rule Out
RA Rheumatoid Arthritis Or Right Atrium
RAD Right Atrial Axis Deviation
RAE Right Atrial Enlargement
RAP Right Atrial Pressure
RBBB Right Bundle Branch Block
RBC Red Blood Cell
RBP Retinol-Binding Protein
RCT Randomized Controlled Trial
RDA Recommended Daily Allowance
RDW Red Cell Distribution Width
RIA Radioimmunoassay
RIH Right Inguinal Hernia
RLL Right Lower Lobe
RLQ Right Lower Quadrant
RML Right Middle Lobe
RNA Ribonucleic Acid
ROM Range Of Motion
ROS Review Of Systems
RPG Retrograde Pyelogram
RRR Regular Rate And Rhythm
RT Respiratory Or Radiation Therapy
RTA Renal Tubular Acidosis
RTC Return To Clinic
RU Resin Uptake
RUG Retrograde Urethogram
RUL Right Upper Lobe
RUQ Right Upper Quadrant
RV Residual Volume
RVH Right Ventricular Hyperthrophy
Rx Treatment
s Without | Ss = One-Half
S&E Sugar And Acetone
SA Sinoatrial
SAA Synthetic Amino Acid
SBE Subacute Bacterial Endocarditis

37
SBFT Small Bowel Follow Through
SBS Short Bowel Syndrome
SCr Serum Creatinine
SEM Systolic Ejection Murmur
SG Swan-Ganz
SGA Small For Gestational Age
SGGT Serum Gamma- Glutamyl Transpeptidase
SGOT Serum Glutamic- Oxaloacetic Transaminase
SGPT Serum Glutamic- Pyruvic Transaminase
SIADH Syndrome Of Inappropriate Antidiuretic Hormone
Sig Write On Label
SIMV Synchronous Intermittent Mandatory Ventilation
Sl Sublingual
SLE Systemic Lupus Erythematous
SMO Slips Made Out
SOAP Subjective, Objective, Assessment, Plan
SOB Shortness Of Breath
SQ Subcutaneous
STAT Immediately
SVD Spontaneous Vaginal Delivery
Sx Symptoms
T&C Type And Cross
T&H Type And Hold
TAH Total Abdominal Hysterectomy
TB Tuberculosis
TBG Total Binding Globulin
Td Tetanus-Diphtheria Toxoid
TIA Transient Ischemic Attack
TIBC Total Iron Binding Capacity
Tid Three Times A Day
TIG Tetanus Immune Globulin
TKO To Keep Open
TLC Total Lung Capacity
TMJ Temporo Mandibular Joint
TNTC Too Numerous To Count
TO Telephone Order
TOPV Trivalent Oral Polio Vaccine
TPN Total Parenteral Nutrition
TSH Thyroid Stimulating Hormone
TT Thrombin Time
TTP Thrombotic Thrombocytopenic Purpura
TU Tuberculin Units
TUR Transurethral Resection
TURBT Tur Bladder Tumors

38
TURP Transurethral Resection Of Prostate
TV Tidal Volume
TVH Total Vaginal Hysterectomy
tw Twice A Week
Tx Treatment, Transplant
UA Urinalysis
UAC Uric Acid | Umbilical Artery Catheter
UAO Upper Airway Obstruction
UBD Universal Blood Donor
UC Ulcerative Colitis | Umbilical Cord
ud As Directed
UFH Unfractionated Heparin
UGI Upper Gastrointestinal
URI Upper Respiratory Infection
URQ Upper Right Quadrant
US Ultrasound
UTI Urinary Tract Infection
UUN Urinary Urea Nitrogen
UVA Ultraviolet A Light
V/Q Ventilation – Perfusion
VAD Venous Access Device
VC Vital Capacity
VCT Venous Clotting Time
VCUG Voiding Cysourethrogram
VDRL Venereal Disease Research Laboratory (Test For Syphilis)
VMA Vanillymadelic Acid
VO Verbal Or Voice Order
VRE Vancomycin-Resistant Enterococcus
VSS Vital Signs Stable
VT Ventricular Tachycardia
VV Varicose Veins
VW Vessel Wall
VWD Von Willebrand’S Disease
VZV Varicella Zoster Virus
WB Whole Blood
WBC
WBR Whole Body Radiation
WD Well Developed
WF White Female
WIA Wounded In Action
WID Widow, Widower
WM White Male
WN Well Nourished
WNL Within Normal Limits

39
WO Written Order | Weeks Old | Wide Open.
WOP Without Pain
WPW Wolff-Parkinson-White
W-T-D Wet To Dry
X2d Times 2 Days.
XMM Xeromammography
XOM Extraocular Movements
XS Excessive
XULN Times Upper Limit Of Normal
YF Yellow Fever
YLC Youngest Living Child
yo Years Old
YOB Year Of Birth
yr Year
ytd Year To Date
ZDV Zidovudine
ZE Zollinger-Ellison
Zn Zinc
ZnO Zinc Oxide
ZSB Zero Stools Since Birth

40