jueves, 31 de diciembre de 2009

Pain, Acute, Assessment and Management of (Guideline) [ICSI-NQMC-AHRQ]



Pain, Acute, Assessment and Management of (Guideline)

abrir aquí: [pdf - 59 páginas - 991kb]
http://www.icsi.org/pain_acute/pain__acute__assessment_and_management_of__3.html

Scope and Target Population:
This guideline has been developed for patients of all ages (from infant to very elderly) who have acute pain or may be experiencing acute pain in the future (i.e., planned surgery). This guideline excludes patients with acute cancer pain, labor pain and migraine headache, although many of the guideline's recommendations apply to those groups, as well.

Rather than focus on the cause of the pain (a comprehensive list would fill a textbook) or the setting where the pain is treated (inpatient or outpatient), this guideline focuses on effective treatment based on the physiologic mechanisms of pain transmission (e.g., somatic, visceral, neuropathic). Understanding this should allow clinicians to apply this algorithm to almost any kind of acute pain (no matter what the cause) and in any setting.

We acknowledge that assessments of pain in the preverbal, non-English-speaking and cognitively impaired are challenging. As a result, relevant recommendations will be made in order to enhance assessment of an intervention for all patients. The following definitions are assumed:

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

Acute pain states can be brief, lasting moments or hours, or they can be persistent, lasting weeks or several months until the disease or injury heals.

Chronic pain, is defined as persistent pain, which can be either continuous or recurrent and of sufficient duration and intensity to adversely affect a patient's well-being, level of function, and quality of life. If a patient's pain has persisted for six weeks (or longer than the anticipated healing time), a thorough evaluation for the cause of the chronic pain is warranted.

Clinical Highlights and Recommendations:

Intensity of pain is assessed prior to initiation of appropriate treatment and continually reassessed throughout duration of treatment.

Determine the mechanism of pain (i.e., somatic, visceral, neuropathic) based on the physical examination and detailed history.

Patients often experience more than one type of pain.

Somatic pain is well localized and may be responsive to acetaminophen, cold packs, corticosteroids, localized anesthetic (topical or infiltrate), NSAIDs, opioids and tactile stimulation.

Visceral pain is more generalized and is most responsive to opioid treatment.

Neuropathic pain may be resistant to opioid therapy and consideration should be given to adjuvant therapy such as tricyclic antidepressants and anticonvulsants.

While the emphasis of this guideline is on pharmacologic therapy, multimodal treatment approaches are important to consider because patient satisfaction is high when non-pharmacologic approaches are provided.

Priority Aims:

Improve the assessment and reassessment of all age patients with acute pain by determining the mechanism and intensity of pain.

Improve the treatment of patients (all ages) with acute pain, to include appropriate selection of pharmacologic and/or non-pharmacologic interventions.

Increase the involvement of patients with acute pain of all ages, or their caregiver, in the management of their pain symptoms.

Additional Background:
Rather than focus on the cause of pain (a comprehensive list would fill a text book) or the setting where the pain is treated (inpatient/outpatient), this guideline focuses on effective treatment based on the physiologic mechanisms of pain transmission (e.g., somatic, visceral, neuropathic). Understanding this should allow clinicians to apply this algorithm to almost any kind of acute pain in any setting (this guideline excludes patients with acute cancer pain, labor pain, and migraine headache). We acknowledge that assessments of pain in the preverbal, non-English speaking and cognitively impaired are challenging. As a result, relevant recommendations have been made in order to enhance assessment of an intervention for all patients.

Low Back Pain, Adult (Guideline) [ICSI-NQMC-AHRQ]



Low Back Pain, Adult (Guideline)

abrir aquí: [pdf - 60 páginas - 2MB]
http://www.icsi.org/guidelines_and_more/gl_os_prot/musculo-skeletal/low_back_pain/low_back_pain__adult_5.html

Scope and Target Population:
Adult patients age 18 and over in primary care who have symptoms of low back pain or sciatica. The focus is on acute and chronic management, including indications for medical, non-surgical or surgical referral. For workers' compensation patients, check with state guidelines where the patient resides and where the injury took place: http://www.workerscompensation.com/workers_comp_by_state.php.

Clinical Highlights and Recommendations:

Back pain assessment should include a subjective pain rating, functional status, patient history including notation of presence or absence of "red flags" (Cauda Equina syndrome or other conditions) and psychosocial indicators, assessment of prior treatment and response, employment status, and clinician's objective assessment.

Reduce unnecessary imaging unless “red flag” indicators exist.

A conservative approach should be first-line treatment. Emphasize patient education and conservative home self-care, which includes limited bed rest, early ambulation, postural advice, resumption of light-duty activities, use of ice and heat, anti-inflammatory and analgesic over-the-counter medications, and early return to work or activities.

Patients with acute low back pain should be advised to stay active and continue ordinary daily activity within the limits permitted by the pain. For chronic back pain, there is evidence that exercise therapy is effective.

Consult or refer to surgical spine specialist (neurosurgeon, orthopedic surgeon, or other) or non-surgical spine specialist (physical therapist, chiropractic provider, osteopathic or allopathic physician, or other) if conservative treatment fails.
Priority Aims

Improve the assessment and reassessment of adult patients with low back pain.

Reduce unnecessary imaging with adult patients with low back pain in the absence of “red flag” indicators or progressive symptoms.

Increase the use of recommended conservative approach as first-line treatment, such as activity, self-care and analgesics for adult patients with low back pain.

RARE DISEASES: 5th European Conference on Rare Diseases ECRD 2010


Register to the 5th European Conference on Rare Diseases ECRD 2010 in Krakow now!

May 13, 14 & 15
Jagiellonian University - Auditorium Maximum

Programme and registration: www.rare-diseases.eu

The European Conference on Rare Diseases is the unique platform/forum across all rare diseases, across all European countries, bringing together all stakeholders (academics, health care professionals, industry, policy makers, and patients' representatives).
It covers research, development of new treatments, health care, social care, information, public health and support at European, national and regional levels.

It is a biennial event, providing the state-of-the-art of the rare disease environment, monitoring and benchmarking initiatives.

Special rates if you register before 31 January 2010!

The conference will be interpreted in:
English
French
German
Polish
Spanish

Themes of ECRD 2010

-National strategies and plans for rare diseases
-European Reference Networks and Centres of Expertise for Rare Diseases
-Science from the bench to the bed side
-Information and Medical Education
-The European Committee for Rare Diseases
-Policy scenarii for rare diseases
-Rare diseases in Central/Eastern Europe
-Services to patients, families and carers


Fellowship programme
For patient representatives from Eastern countries who can understand English, the organisers are pleased to announce a fellowship programme that will offer:

Registration fee exemption
Travel (economy class)
Two nights accommodation
To apply to the fellowship programme download the application form and send it by email to :
secretariat@rare-diseases.eu
or by fax to + 33 1 56 53 52 15

Contacts
If you wish information about the conference:
visit the website www.rare-diseases.eu

or contact the secretariat (English only):
secretariat@rare-diseases.eu

I you wish to organise your trip or to visit Krakow and its region after or before the conference, contact the local event organiser office:

Grupa A05
Grupa A-05 Sp. z o.o.
31-101 Krakow, Poland
Pl. Na Groblach 14/2
P. +48 12 429 62 23
F. +48 12 429 62 87
E: a05@a05.pl

Call for abstracts!

You are invited to submit an abstract for the European Conference on Rare Diseases to be presented during the poster session. Posters will be selected by the programme committee.
We are calling for abstracts on "Services to Patients, Families and Carers".

The basic text of your abstracts should not exceed 300 words.
Use the following website: www.rare-diseases.eu/2010/On-line-submission-form

Deadline for Abstract Submission extended to : 31 January 2010

Please also note that your abstract will be included in the scientific programme, if you register before 31 January 2010.

Programme Committee
Cochairs of the programme committee:

Torben Gronnebaek Rare Disorders Denmark
Prof Josep Torrent I Farnell Fundacio Dr. Robert
Other members

Mrs Dorica Dan - Romanian Alliance of Rare Diseases Organisations
Mr Pawel Wojtowicz - Cystic Fibrosis Poland
Mr Rainald von Gizycki - Retina Europe
Mr John Dart - Debra United Kingdom
Mrs Lia van Ginneken - European Myeloma Platform
Dr Ségolène Aymé - Orphanet, RDTF
Prof Tomasz Grodzicki - Faculty of Medicine Krakow
Dr B. Dembowska-Baginska - COMP member, Poland
Dr Frits Lekkerkerker - Dutch Steering Committee on Orphan Drugs WGM
Dr Kerstin Westermark - COMP Chair, EMEA
Mr Jakub Adamski - Ministry of Health, Poland

Contact us!
The project leader is Yann Le Cam, Eurordis CEO.

Please contact the project coordination:
François Houÿez
Eurordis - Plateforme Maladies Rares - 102 rue Didot - 75014 Paris, France
Tel: + 331 56 53 52 18
email: kasia.peala@eurordis.org

Sincerely,
The Polka team

miércoles, 30 de diciembre de 2009

FELIZ AÑO 2010 a todos los lectores

 

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Cardiovascular Guidelines: 10 clinical guidelines [ICSI] NQMC - AHRQ



Cardiovascular Guidelines

1. * ACS: Chest Pain and Acute Coronary Syndrome, Diagnosis and Treatment of (Guideline - 70 pages)

open here:
http://www.icsi.org/acs_acute_coronary_syndrome/acute_coronary_syndrome_and_chest_pain__diagnosis_and_treatment_of_2.html

Scope and Target Population:
Adults greater than age 18 years presenting with past or present symptoms of chest pain/discomfort and/or indications of acute coronary syndrome.

Clinical Highlights and Recommendations:

On initial contact with the health care system, high-risk patients need to be identified quickly and referred to an emergency department via the 911 system.

Patients whose chest pain symptoms are suggestive of serious illness need immediate assessment in a monitored area of the emergency department and early therapy to include an immediate EKG, intravenous access, oxygen, aspirin and other appropriate medical therapies.

Triage and management of patients with chest pain and unstable angina should be based on a validated risk assessment systems and clinical findings.

Patients with low-risk symptoms could be evaluated as outpatients.

Patients with high-risk features need to be identified quickly and treatment instituted in a timely fashion.

Thrombolysis should be instituted within 30 to 60 minutes of arrival, or angiogram/primary percutaneous coronary intervention should be performed within 90 minutes of arrival, with a target of less than 60 minutes.

Recommend use of the following medications: aspirin and clopidogrel (or clopidogrel alone if aspirin allergic) at admission. Avoid clopidogrel if cardiac surgery is anticipated. Use beta-blockers whenever possible and/or ACE inhibitors/angiotensin receptor blockers at 24 hours if stable, nitrates (when indicated), and statins whenever possible. Once the issue of surgery is clarified, consider the early use of a thienopyridine for those in whom percutaneous coronary intervention is planned.

Recommend appropriate use of cardiac rehabilitation postdischarge.
Priority Aims:
Increase the success of emergency intervention for patients with high-risk chest pain.

Minimize the delay in administering thrombolytics or percutaneous coronary intervention to patients with acute myocardial infarction.

Increase the timely initiation of treatment to reduce postinfarction mortality in patients with acute myocardial infarction.

Increase the percentage of patients with acute myocardial infarction who have used tobacco products within the past year who receive tobacco cessation advice and counseling during the hospital stay (The Joint Commission).

Increase the percentage of patients with acute myocardial infarction using appropriate cardiac rehabilitation postdischarge.
---------------

2. *Antithrombotic Therapy Supplement (Guideline - 71 pages)

open here:
http://www.icsi.org/antithrombotic_therapy_supplement__guideline__14045/antithrombotic_therapy_supplement__guideline_.html

Scope and Target Population:
This guideline supplement is targeted for any patient receiving antithrombotic therapy. Please refer to related ICSI guidelines for specific target populations.

Clinical Highlights and Recommendations:

There are no circumstances under which patients absolutely should or should not receive anticoagulation therapy. Clinicians must consider the risks and benefits of anticoagulation therapy for a patient based upon the individual's risk for thrombosis if not treated weighed against the risk of bleeding if treated.

In the initial phase of treatment for patients with active thrombosis (such as acute deep vein thrombosis [DVT]) or high risk of thrombosis, immediate-acting anticoagulant agents (UFH/LMWH/fondaparinux) should be used concomitant with warfarin.

Loading doses of warfarin should be avoided.

Many prescription medications and over-the-counter remedies, including dietary supplements and herbs, may alter the effectiveness of warfarin or vitamin K antagonists (detected by the INR) and/or reduce the effectiveness of platelets (not detected by the INR).

Vitamin K may be used to reverse supratherapeutic anticoagulation with warfarin. The dose of vitamin K depends upon the degree of international/normalized ratio (INR) elevation and/or signs and symptoms of bleeding. Vitamin K can lead to warfarin resistance and subsequently to an increased risk of thromboembolism.

Regardless of the anticoagulant used, it is important that patients know they must always inform their physician and other health care providers that they are on anticoagulation therapy, especially if they are undergoing an invasive procedure.

Patients should be encouraged and empowered to play an active role in the self-management of their treatment. Self-management is best initiated and sustained through active involvement of patients and family members with their multidisciplinary health care team. This educational partnership should be encouraged to decrease potential risks and improve understanding of the importance of patient adherence to their treatment regimen.

Patients with mechanical heart valves who are pregnant have complex anticoagulation needs and should be managed by an anticoagulation expert.

Priority Aims:
The Antithrombotic Therapy Supplement does not contain priority aims or suggested measures. These components are addressed in the related guidelines.

Additional Background:
The ICSI Antithrombotic Therapy Supplement has been developed as a resource for the use of antithrombotic drugs. This is a supplemental document that brings about consistency in recommendations that are common to the scope of related ICSI guidelines. See related ICSI scientific documents: Atrial Fibrillation, Heart Failure in Adults, Diagnosis and Initial Treatment of Ischemic Stroke, Diagnosis and Treatment of Chest Pain and Acute Coronary Syndrome (ACS), Venous Thromboembolism Diagnosis and Treatment and Venous Thromboembolism Prophylaxis.

Antithrombotic drugs are used to decrease the risk of thrombosis by interfering with the homeostatic clotting mechanism. The major side effect of these drugs is bleeding either from supratherapeutic effect or by accentuating the blood loss of patients with an existing source of bleeding.

There are few absolute contraindications to antithrombotic therapy. The decision to treat a patient with antithrombotic drugs takes into account an individual patient's risk for thrombosis if not treated weighed against the risk of bleeding while on antithrombotic drug therapy.
This supplement and related guidelines should help physicians to make that risk-benefit treatment decision. This supplement is also meant to serve as a tool to use for patients treated with antithrombotic.

A glossary of abbreviations used throughout this guideline is in Appendix F, "Glossary of Abbreviations."
---------------

3. * Atrial Fibrillation (Guideline - 63 pages)

open here:
http://www.icsi.org/atrial_fibrillation__guideline_/atrial_fibrillation__guideline__38782.html

Scope and Target Population:
This guideline addresses first detected episode and recurrent (paroxysmal, persistent and permanent) atrial fibrillation and atrial flutter in the adult population that present in primary care, emergency room, and the inpatient settings. The scope includes stabilization, assessment, labeling (classification), treatment and patient education.

This document is not intended to replace the comprehensive ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation, which the interested provider is encouraged to review.

Clinical Highlights and Recommendations:
There are five key steps in the management of patients with atrial fibrillation or atrial flutter (SALT-E): stabilize, assess, label, treat and educate.

After confirming the diagnosis of atrial fibrillation or atrial flutter with a 12-lead electrocardiogram:


Stabilize

Assess for hemodynamic instability (hypotension, myocardial ischemia, uncompensated congestive heart failure, altered mental status or end-organ dysfunction).

Treat hemodynamic instability with emergent direct current cardioversion and obtain an emergent cardiology or internal medicine consult.

Establish adequate rate control.

Assess

Assess for potentially reversible causes and for comorbidities of atrial fibrillation/atrial flutter.

Hypertension is one of the most common causes of atrial fibrillation. In addition, hypertension is one of the most common risk factors for thromboembolic complications associated with atrial fibrillation. Treatment for hypertension should be initiated early.

Label

Label (classify) patients into one of three categories:

First Detected Episode, Duration Known greater than or equal to 48° or Duration Unknown

Recurrent atrial fibrillation

Paroxysmal

Persistent

Permanent

Recurrent atrial flutter
Treatment options are determined by these three categories.

Treat
First Detected Episode, Duration Known > 48 hours or Duration Unknown

Patients with stable atrial fibrillation or atrial flutter with duration greater than 48 hours or duration unknown require appropriate anticoagulation (international normalized ratio greater than or equal to 2.0) for three weeks prior to electrical cardioversion or use of antiarrhythmics/chemical cardioversion.
Recurrent atrial fibrillation

Patients with paroxysmal, persistent or permanent atrial fibrillation require assessment for chronic anticoagulation (risk of thromboembolism compared with risk of bleeding) and adequate rate control.

Patients with persistent symptoms despite adequate rate control may require intermittent cardioversion, antiarrhythmic agents and/or electrophysiology consultation.

Recurrent atrial flutter

Patients with recurrent atrial flutter should be referred for an electrophysiology consultation.

Educate
Patient education is a critical component in the management of all patients with atrial fibrillation/atrial flutter. Patients who have experienced one or more episodes of atrial fibrillation should be taught to periodically monitor their pulse and have a plan for treatment if they detect an irregular pulse.

Priority Aims

Increase the percentage of adult patients (age 18 years and older) who are accurately diagnosed with atrial fibrillation/flutter.

Improve the consistency of anticoagulation therapy in adult patients (age 18 years and older) with non-valvular paroxysmal, persistent or permanent atrial fibrillation/flutter.

Improve rate control in adult patients (age 18 years and older) with permanent atrial fibrillation.

Increase the percentage of adult patients (age 18 years and older) with a confirmed diagnosis of atrial fibrillation/atrial flutter who, along with their family, have received education around atrial fibrillation/flutter and anticoagulation therapy.

Reduce the percentage of patient harm associated with the use of anticoagulation therapy.

Increase the percentage of adult patients (age 18 years and older) with a confirmed diagnosis of atrial fibrillation/flutter, receiving dietary monitoring.

Increase the percentage of adult patients (age 18 years and older) with a confirmed diagnosis of atrial fibrillation/flutter who have a medication communication/reconciliation plan throughout the continuum of care.

Additional Background
This guideline follows closely the American College of Cardiology and the American Academy of Family Physician guidelines. Areas of divergence from other clinical practice guidelines are TEE and rhythm vs. rate control. The purpose of this guideline is to provide primary care with a guideline that outlines areas for systems improvement for the diagnosis and treatment of atrial fibrillation in primary care.

A Fib is a common arrhythmia and an important independent risk factor for stroke. The prevalence of A Fib increases from 0.5% for the 50- to 59-year-old age group to 8.8% in the 80- to 89-year-old age group. Symptoms vary from none to severe disabling palpitations, dyspnea and syncope. Patients with A Fib have a mortality rate double that of control subjects. The attributable risk of embolic stroke from A Fib increases from 1.5% per year for the 50- to 59-year-old age group to nearly 30% per year for the 80- to 89-year-old age group, and increases substantially in the presence of other cardiovascular conditions.
---------------

4. * Coronary Artery Disease, Stable (Guideline - 42 pages)

open here:
http://www.icsi.org/coronary_artery_disease/coronary_artery_disease__stable_.html

Scope and Target Population:
Adults aged 18 and over who meet the stated guideline criteria as identified in Annotation #1, "Patient with Stable Coronary Artery Disease."Adults who have a diagnosis of stable coronary artery disease. The criteria, as noted on the Main algorithm, includes patient presenting with:

previously diagnosed coronary artery disease without angina, or symptom complex that has remained stable for at least 60 days;

no change in frequency, duration, precipitating causes or ease of relief of angina for at least 60 days; and

no evidence of recent myocardial damage.

Clinical Highlights and Recommendations

Prescribe aspirin in patients with stable coronary artery disease if there are no medical contraindications.

Evaluate and treat the modifiable risk factors, which include smoking, sedentary activity level, stress, hyperlipidemia, obesity, hypertension and diabetes.

Patients with chronic stable coronary artery disease should be on statin therapy regardless of their lipid levels unless contraindicated.

Perform prognostic testing in patients whose risk determination remains unclear. This may precede or follow an initial course of pharmacologic therapy.

Refer the patient for cardiovascular consultation when clinical assessment indicates the patient is at high risk for adverse events, the non-invasive imaging study or electrocardiography indicates the patient is at high risk for an adverse event, or medical treatment is ineffective.

For relief of angina, prescribe beta-blockers as first-line medication. If beta-blockers are contraindicated, nitrates are the preferred alternative. Calcium channel blockers may be an alternative medication if the patient is unable to take beta-blockers or nitrates.

Priority Aims

Increase the percentage of appropriate patients with an appropriate diagnosis of stable coronary artery disease (SCAD), who are prescribed aspirin and antianginal medications.

Improve education/understanding around the management of stable coronary artery disease.

Increase the percentage of patients with stable coronary artery disease who receive an intervention for modifiable risk factors.

Improve the assessment of patients with a diagnosis of stable coronary artery disease who present with angina symptoms.

Increase the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBS) in patients with coronary artery disease, including those patients with a diagnosis of diabetes, chronic kidney disease, and hypertension.

Increase the percentage of patients with a diagnosis of stable coronary artery disease who receive education around nutritional supplement therapy.

Increase prognostic testing for patients whose risk determination remains unclear.

---------------
5. * Heart Failure in Adults (Guideline - 120 pages)

open here:
http://www.icsi.org/heart_failure_2/heart_failure_in_adults_.html

Scope and Target Population:
The management of adult patients age 18 and older with suspected heart failure and heart failure requiring hospitalization.

Clinical Highlights and Recommendations:

Evaluate patients presenting with heart failure for exacerbating and underlying causes, including coronary artery disease, hypertension, valvular disease and other cardiac and non-cardiac causes.

Studies show that the distinction between systolic dysfunction and preserved systolic function is important, because the choice of therapy may be quite different and some therapies for systolic dysfunction may be detrimental if used to treat preserved systolic function.

After evaluation, diagnosis and initiation of pharmacologic and non-pharmacologic management of heart failure, follow-up in the ambulatory setting should focus on optimizing pharmacologic and non-pharmacologic therapy and preventing heart failure exacerbations. Patient education is central in this effort.

Daily weights are critical for managing heart failure and early detection of increases in fluid retention. Patients should call their provider about a two-pound or greater weight gain overnight or a five-pound or greater weight gain in a week.

Unless specific contraindications exist, treat all patients, including Class IV patients, with beta-blockers, starting with a low dose and titrating upward. Do not unnecessarily reduce or discontinue beta-blockers in severe or decompensated heart failure. After fluid overload and hypotension are corrected and when only one drug can be initiated, beta-blockers are preferred.

Treat all patients with left ventricular systolic dysfunction with ACE inhibitors (or ARBs if intolerant) unless specific contraindications exist, such as intolerance or adverse reactions to ACE inhibitors, serum potassium greater than 5.5 mEq/L, symptomatic hypotension, severe renal artery stenosis or pregnancy. Gradually titrate dose up over a two- to three-month period.

Consider treatment with aldosterone antagonists for Class III and IV heart failure patients with appropriate follow-up.

Consider early specialty referral for patients with ischemia or those who are refractory despite optimal medical therapy.

Brain natriuretic peptide (BNP) and proBNP is useful in the diagnosis and prognosis of heart failure in patients with dyspnea of unknown etiology.

Priority Aims:

Decrease the readmission rate within 30 days of discharge following hospitalization for heart failure.

Optimize the pharmacologic treatment of adult patients with heart failure.

Improve the use of diagnostic testing in order to identify and then appropriately treat adult patients with heart failure.

Improve care of adult heart failure patients by assuring comprehensive patient education and follow-up care.

Additional Background:
Facts about congestive heart failure:

3,000,000 patients in the United States have HF.

15,000,000 patients worldwide have HF.

Approximately 400,000 are diagnosed with HF each year in the United States.

It is the most common discharge diagnosis in patients age 65 and older.

Approximately 200,000 HF-related deaths occur each year in the United States.

Population demographics suggest these figures will continue to increase.

The guideline follows closely the Agency for Health Care Policy and Research (AHCPR) Heart Failure guideline. The only significant deviation is we recommend assessment of left/ventricular (LV) function earlier.
---------------

6. * Hypertension Diagnosis and Treatment (Guideline - 60 pages)

open here:
http://www.icsi.org/hypertension_4/hypertension_diagnosis_and_treatment_4.html

Scope and Target Population:
Adults age 18 or older.

Clinical Highlights and Recommendations:

Confirmation of hypertension is based on the initial visit, plus two follow-up visits with at least two blood pressure measures at each visit.

Standardized blood pressure measurement techniques (including out-of-office or home blood pressure measurements) should be employed when confirming an initially elevated blood pressure and for all subsequent measures during follow-up and treatment for hypertension.

A thiazide-type diuretic should be considered as initial therapy in most patients with uncomplicated hypertension.

Physician reluctance to initiate and intensify treatment is a major obstacle to achieving treatment goals.

Systolic blood pressure level should be the major factor for the detection, evaluation and treatment of hypertension, especially in adults 50 years and older.

Fewer than 50% of patients with hypertension will be controlled with a single drug.

Priority Aims

Increase the percentage of adult patients in blood pressure control.

Improve the assessment of adult patients with hypertension.

Increase the percentage of adult patients with hypertension who receive patient education, with a focus on the use of non-pharmacological treatments.

Increase the percentage of adult patients not in blood pressure control who have a care plan.

Increase the percentage of adult patients not at blood pressure goal who have a change in subsequent therapy.
---------------

7. * Lipid Management in Adults (Guideline - 73 pages)

open here:
http://www.icsi.org/lipid_management_3/lipid_management_in_adults_4.html

Scope and Target Population:
This guideline describes the treatment of adults age 20 and older who are dyslipidemic.

Clinical Highlights and Recommendations:

Initiate a statin with patients who have a history of CHD or CHD risk equivalent.

Establish lipid goals based on risk level.

Instruct patients on healthy lifestyle and adjunctive measures.

Patient adherence with recommended therapy should be reinforced during scheduled follow-up.

LDL goal less than 70 can be considered for patients with established CAD, non-cardiac atherosclerosis or coronary artery disease equivalent.
Priority Aims:

Increase the percentage of patients with CHD or whose 10-year risk is greater than 20% who are on a statin.

Improve the percentage of patients with or without CHD who meet their lipid treatment goals.

Increase adherence with adjunctive treatment of patients with CHD or CHD risk equivalent through education.

Improve the percentage of patients on lipid-lowering medication who receive regular follow-up care for lipid disorder.

Increase the percent of patients on lipid-lowering therapy who remain on therapy.

Additional Background:
The guideline is a natural follow-up to the ICSI Preventive Services for Adults Guideline. Management of lipid disorder in adults is an area of practice variability among providers. The condition is relatively common in the adult population and treatment costs can be significant. The guideline incorporates recommendations from the National Cholesterol Education Program (NCEP-ATP III) and research studies which include: the Framingham Study, WOSCOPS, TexCAPS, 4S, Helsinki Heart Study, HITS Trial, The LIPID Study, and HERS.
---------------

8. * Stroke, Ischemic, Diagnosis and Initial Treatment of (Guideline - 64 pages)

open here:
http://www.icsi.org/stroke/diagnosis_and_initial_treatment_of_ischemic_stroke___pdf_.html

Scope and Target Population:
The scope of the following guideline is the 48 hours beginning when a patient age 18 years or older presents to a provider with symptoms of ischemic stroke or transient ischemic attack. For most stroke patients who are hospitalized, the guideline's temporal scope will expire before discharge. The guideline work group on Diagnosis and Initial Treatment of Ischemic Stroke recognizes that two time frames are critically important in the overall outcome, and fall outside the defined scope. They are prehospital care, and continuing care of stroke patients after 48 hours, which includes the development of a long term secondary prevention strategy. While the group has not itself performed a systematic review of the primary evidence on these matters, we recommend the following guidelines from the American Heart Association/American Stroke Association.

Clinical Highlights and Recommendations:
Patients presenting with signs and symptoms of TIA should be evaluated for risk of immediate future events using the ABCD score.

Patients who present in time to be candidates for treatment with intravenous tissue plasminogen activator (tPA) should be evaluated by a physician within 10 minutes, undergo a CT scan within 25 minutes of arrival in the ED, and have CT interpreted within 20 minutes of test completion.

tPA, if given, should be administered within three hours (4.5 hours in selected patients; see Annotation #18, "Consider IV Tissue Plasminogen Activator [tPA]/See Stroke Code Algorithm") of stroke onset and less than 60 minutes of arrival at the ED.

Patients presenting with stroke onset who are not candidates for intravenous tPA should promptly be given aspirin, after exclusion of hemorrhage on CT scan.

Education regarding early stroke symptoms, risk factors, diagnostic procedures, and treatment options should be offered to the patient and family. This should be documented in the patient chart.

Medical management for prevention of complications within the initial 24-48 hours of diagnosis and initial treatment of ischemic stroke include:
- continue appropriate blood pressure management;
- continue to treat hyperthermia;
- continue to treat hypo- or hyperglycemia;
- continue IV fluids;
- initiate deep vein thrombosis prophylaxis;
- perform swallow evaluation;
- initiate early rehabilitation; and
- perform nutritional status assessment.


Priority Aims:
1. Increase the percentage of patients presenting within three hours of stroke onset who are evaluated within 10 minutes of arriving in the ED.

2. Increase the percentage of patients presenting with TIA symptoms within 24 hours at high risk for stroke who are admitted to the hospital.

3. Increase the percentage of patients receiving appropriate thrombolytic and antithrombotic therapy for ischemic stroke (use of tPA and aspirin).

4. Increase the percentage of non-tPA recipients who have hypertension appropriately managed in the first 48 hours of hospitalization or until neurologically stable.

5. Increase the percentage of patients who receive appropriate medical management for prevention of complications within the initial 24-48 hours of diagnosis:

.Continue to treat hypoglycemia and hyperglycemia

.Continue to treat hyperthermia

.Continue IV fluids

.Continue to treat hypoxia

.Initiate deep vein thrombosis prophylaxis

.Perform swallow

.Initiate early rehabilitation (early mobilization)

.Perform nutritional status assessment
6. Improve patient and family education of patients with ischemic stroke in both the ED and the admitting hospital unit.
---------------

9. * Venous Thromboembolism Diagnosis and Treatment (Guideline 80 pages)

open here:
http://www.icsi.org/venous_thromboembolism/venous_thromboembolism_4.html

Scope and Target Population:
Adult patients age 18 and over with venous thromboembolism (VTE).

Clinicians Highlights and Recommendations:

A clinical pretest probability assessment should be completed in patients with suspected venous thromboembolism.

D-dimer can be used as a negative predictor to eliminate need for further testing.

Confirm diagnosis of DVT with imaging study, preferably duplex ultrasound (with compression).

In patients with a high clinical pretest probability for PE, begin anticoagulation without delay.

Computed tomographic angiography combined with clinical pretest probability scoring and D-dimer testing has the predictive value to safely diagnose or rule out pulmonary embolism in patients. Additional diagnostic testing is necessary only when clinical symptoms persist or progress.

Achieve rapid effective anticoagulation with LMWH/fondaparinux.

In patients with acute VTE, heparin (UFH or LMWH/fondaparinux) should be given for at least four days and until the INR is 2.0 for two consecutive days.

Arrange for home therapy in appropriate patients.

Graded compression stockings help prevent post-phlebotic syndrome. All patients should be assessed for the need for compression graded stockings (not Teds).

Patient to be treated three to six months for acute thrombosis followed by
re-evaluation of ongoing risks to determine the need for ongoing anticoagulation therapy to prevent recurrent events.


Priority Aims:

Prevent progression or recurrence of thromboembolic disease.

Reduce the risk of complications from anticoagulation therapy.

Improve the safety of using medications by reducing the likelihood of patient harm associated with the use of anticoagulation therapy.

Improve accurate diagnosis and treatment of venous thromboembolism (VTE).

Increase the percentage of patients who are evaluated upon change in level of care, and/or upon discharge.
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10. * Venous Thromboembolism Prophylaxis (Guideline - 30 pages)

open here:
http://www.icsi.org/venous_thromboembolism_prophylaxis__2__guideline_/venous_thromboembolism_prophylaxis__guideline__47057.html

Scope and Target Population:
This guideline addresses risk assessment for venous thromboembolism, risk assessment for bleeding, and mechanical and pharmacologic therapies to reduce the occurrence of venous thromboembolism in adult hospitalized patients.

Clinical Highlights and Recommendations:

All patients should be evaluated for venous thromboembolism risk upon hospital admission, change in level of care, change in providers, and prior to discharge.

All patients should receive proper education regarding venous thromboembolism risk, signs and symptoms of venous thromboembolism, and mechanical prophylaxis methods available.

Early and frequent ambulation should be encouraged when possible in all patient groups.

All medical and surgical/trauma patients who have a high or very high risk for venous thromboembolism should receive anticoagulation prophylaxis unless contraindicated.

Aspirin alone is not recommended for routine venous thromboembolism prophylaxis following hip/knee arthroplasty but may be considered in combination with mechanical prophylaxis methods in patients without additional risk factors. Further study is needed.

For all patients receiving spinal or epidural anesthesia, precautions should be taken when using anticoagulant prophylaxis to reduce the risk of epidural perispinal hematoma.

Risk of venous thromboembolism development continues beyond hospitalization, and the need for postdischarge anticoagulation should be assessed.

Priority Aims:
Increase the percentage of hospitalized adult patients (18 years and older) who are appropriately assessed for venous thromboembolism risk within 24 hours of admission.

Increase the percentage of adult patients (18 years and older) who are evaluated for venous prophylaxis upon change in level of care, change in providers, and/or upon discharge.

Increase the percentage of hospitalized adult patients (18 years and older) who are at risk for venous thromboembolism who have received education within 24 hours of admission for venous thromboembolism that includes venous thromboembolism risk, signs and symptoms, and treatment/prophylaxis methods.

Improve the safety of using medications by reducing the likelihood of patient harm associated with the use of anticoagulation therapy.

Increase the percentage of hospitalized adult patients who begin early and frequent ambulation.

Increase the percentage of hospitalized adult patients (18 years and older) receiving appropriate pharmacological and/or mechanical prophylaxis treatment within 24 hours of admission.

Reduce the risk of complications from pharmacologic prophylaxis.

Increase the percentage of surgery patients who receive appropriate venous thromboembolism prophylaxis within 24 hours prior to surgery to 24 hours after surgery.
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Displacement of Dengue Virus Type 1 by Type 4 | CDC EID




EID Journal Home > Volume 16, Number 1–January 2010

Volume 16, Number 1–January 2010
Dispatch
Rapid Displacement of Dengue Virus Type 1 by Type 4, Pacific Region, 2007–2009
Dong-sheng Li, Wen Liu, Aurélie Guigon, Candice Mostyn, Richard Grant, and John Aaskov
Author affiliations: Queensland University of Technology, Brisbane, Queensland, Australia (D. Li, J. Aaskov); Australian Army Malaria Institute, Brisbane (W. Liu, C. Mostyn, R. Grant, J. Aaskov); and Institut Pasteur, Noumea, New Caledonia (A. Guigon)


Suggested citation for this article

Abstract
Since 2000–2001, dengue virus type 1 has circulated in the Pacific region. However, in 2007, type 4 reemerged and has almost completely displaced the strains of type 1. If only 1 serotype circulates at any time and is replaced approximately every 5 years, DENV-3 may reappear in 2012.

During the past 10–15 years in the Pacific island nation states, sustained transmission of only 1 serotype of dengue virus (DENV) has occurred at any given time (1). This single serotype is in marked contrast to all 4 serotypes that cocirculate in many countries in Southeast Asia where dengue is endemic. During 1997–2000 in the Pacific region, the serotype recovered from patients was almost exclusively DENV-2, but during 2000–2001, <1 year, DENV-2 was displaced by multiple genotypes of DENV-1 (2). We describe rapid replacement of DENV-1 by DENV-4 during 2008.

The Study
Figure 1

Figure 1. Island nation states of the Pacific region.


Figure 2

Figure 2. Phylogenetic relationships between the envelope (E) protein genes of dengue type 4 viruses recovered from patients from Pacific island nation states during 2007–2009 outbreaks...

In May 2008, an outbreak of a dengue-like illness began on the island of Tarawa in Kiribati (Figure 1). Immunochromatographic and ELISA assays (PanBio, Brisbane, Queensland, Australia) detected anti–dengue virus immunoglobulin (Ig) M or high titers (>1,280) of anti–dengue virus IgG in serum from 5 of 18 patients. DENV-4 transmission had not been reported in the Pacific region for >1 decade; however, after serum was cultured with Aedes albopictus C6/36 cells, DENV-4 was recovered from 5 of the 13 serum samples from patients who had no detectable anti-DENV IgG or IgM (2).

In July 2008, a similar outbreak began in Samoa. Serum from 87 of 469 patients with suspected dengue contained anti-DENV IgM or high titers of anti-DENV IgG (ELISA; PanBio). Serum from 7 of the 87 patients with anti-DENV IgM contained no detectable anti-DENV IgG, suggesting a primary infection. DENV-4 was recovered from 42 of the 382 seronegative patients when serum was cultured with C6/36 cells.

From June 2007 through February 2008 in Tonga, small numbers of dengue cases, confirmed by ELISA, had been reported; the only DENV isolates recovered from these patients were 4 isolates of DENV-1 (J. Aaskov, unpub. data). However, in December 2008 and January 2009, only 4 DENV-4 isolates were recovered from 55 serum samples collected from patients with suspected dengue in Tonga.

In November 2008 in New Caledonia, DENV-4 transmission was detected after the virus had been introduced by residents returning from Vanuatu; and in February 2009, DENV-4 transmission was detected in French Polynesia after it had been introduced there by travelers from New Caledonia. In June 2009, DENV-1 and DENV-4 were cocirculating in New Caledonia and French Polynesia.

DENV-4 was reportedly recovered from a traveler returning to Taiwan from the Solomon Islands in 2007 (3) and from a resident of the Solomon Islands in April 2008 (Alyssa Pyke, pers. comm.). DENV-1 had been circulating in the Solomon Islands until at least 2002, preceding the 2003 arrival of a multinational peacekeeping force composed of persons from Australia, Papua New Guinea, New Zealand, Fiji, and Tonga. The chronology of these and other reports of dengue outbreaks involving DENV-4 are shown in the Table.

During some of these outbreaks, the envelope (E) protein genes of DENV-4 recovered from patients were amplified by reverse transcription–PCR (2) by using forward primer 5´-GGATTCGCTCTCTTGGCAGGATTTATG-3´ and reverse primer 5´- GCTTCCACACTTCAATTCTTTCCCACTCCA-3´, corresponding to regions in the premembrane and nonstructural protein gene 1, respectively, and the consensus nucleotide sequences of the resultant cDNA determined by Dye Terminator Cycle Sequencing on an automated sequencer (ABI Prism, Australian Genome Research Facility, Brisbane, Queensland, Australia). Sequencing was performed by using the primers above as well as 5´-AACACAGCATGGGACAACAGT-3´ and 5´-GACTCAAACATCTTACCAATGGAG-3´. Sequences were analyzed by using ClustalW, Seqboot, DNADist, Kitsch, and Consense software (www.angis.org.au) from the Australian National Genome Information Service of the University of Sydney. Phylogenetic analyses (Human Research Ethics Approval QUT-0700000910) of the nucleotide sequences of the E genes of DENV-4 that we recovered from patients in Kiribati, Samoa, and Tonga and those of strains of DENV-4 recovered by others showed that all isolates from this recent outbreak in the Pacific were closely related but distinct from other DENV-4 isolates for which sequences were available (Figure 2), including isolates recovered in the Pacific region during the 1970s and 1980s.

The chronology of the recovery of DENV-4 from patients in the region and the phylogenetic analyses suggest that DENV-4 was introduced from Indonesia/Malaysia into the Pacific region, possibly into the Solomon Islands, sometime before 2007. The 3 genotypes of DENV-1 responsible for the earlier outbreak also originated in Southeast Asia (Philippines, Malaysia, Myanmar/Thailand) (2). The relative genetic homogeneity of the DENV-4 recovered during this most recent outbreak in the Pacific region (24 variable nucleotide sites in the E genes of 20 isolates resulting in 9 variable amino acid sites) suggests introduction of a single genotype rather than introduction of multiple genotypes and to different locations, as was the case with DENV-1 (2). The E proteins of all recent DENV-4 isolates from the Pacific region had isoleucine at position E365 rather than the threonine that was found at this position in earlier DENV-4 isolates. All Pacific region isolates except DENV4 Kiribati08.278 also had isoleucine at E335 rather than valine, which was found at this position in most earlier isolates. These 2 aa changes occurred in a region of domain III of the E protein of flaviviruses rich in epitopes recognized by serum from dengue patients and by neutralizing monoclonal antibodies (4–6); they occurred adjacent to the change at E390 in DENV-2, which was associated with the appearance of dengue hemorrhagic fever in South America (7).

Conclusions
Outbreaks of dengue in the Pacific region are initiated by the introduction of DENV, usually from Southeast Asia, but the populations of most Pacific island nation states are too small to sustain transmission of a single DENV serotype for >4–5 years. The interisland mobility of the human population in this region ensures rapid spread of any newly introduced viruses.

That the spread of dengue virus serotypes through the Pacific should be so synchronized is remarkable. This synchronization may reflect the relatively small populations of most island states (≈250,000 residents), high attack rates, and a high birth rate (≈30% of the population is <14 years of age). If only 1 DENV serotype circulates at any time, and serotype replacement occurs approximately every 5 years, these data suggest that ≈30% (75,000) of 250,000 susceptible hosts are sufficient in these settings to support a serotype replacement and that DENV-3 may reappear in the Pacific island states in ≈2012.

At this stage of study, data are insufficient for drawing conclusions about a role for the amino acid changes at E335 and E365 in the reemergence of DENV-4 in the Pacific region. There may be value in delineating the factors that appear to enable multiple DENV serotypes to circulate in urban areas of more developed Pacific nations (e.g., French Polynesia, New Caledonia, Australia) but that appear to prevent cocirculation of DENV serotypes in nations that are less developed but rapidly becoming urbanized. Such a study, however, would require more robust and comprehensive dengue surveillance programs than exist in many of these nations.

Acknowledgments
We thank staff from ministries of health in Pacific island nation states, who assisted in the provision of diagnostic material and data, and laboratory staff at the Institute Pasteur, New Caledonia, who provided technical support.

This study was supported by the National Health and Medical Research Council of Australia.

Dr Li has worked in several virology research programs, most recently at the Institute of Health and Biomedical Innovation at the Queensland University of Technology. His research focuses on molecular epidemiology of flaviviruses and how the evolution of theses viruses affects their structure and function.

References
Singh N, Kiedrzynski T, Lepers C, Benyon E. Dengue in the Pacific—an update of the current situation. Pac Health Dialog. 2005;12:111–9.
A-Nuegoonpipat A, Berlioz-Arthaud A, Chow V, Endy T, Lowry K, Mai L, et al. Sustained transmission of dengue virus type 1 in the Pacific due to repeated introductions of different Asian strains. Virology. 2004;329:505–12.
Shu P-Y, Su C-L, Liao T-L, Fang C-F, Chang S-F, Lin C-C, et al. Molecular characterisation of dengue viruses imported into Taiwan during 2003–2007: geographic distribution and genotype shift. Am J Trop Med Hyg. 2009;80:1039–46.
Aaskov JG, Geysen HM, Mason TJ. Serologically defined epitopes in the envelope protein of dengue 2 (Jamaica strain 1409). Arch Virol. 1989;105:209–21. PubMed DOI
Trirawatanapong TB, Chandran R, Putnak R, Padmanabhan R. Mapping of a region of dengue virus type 2 glycoprotein required for binding by a neutralising monoclonal antibody. Gene. 1992;116:139–50. PubMed DOI
Sukupolvi-Petty S, Austin SK, Purtha WE, Oliphant T, Nybakken GE, Schlesinger JJ, et al. Type- and subcomplex-specific neutralising antibodies against domain III of dengue virus type 2 envelope protein recognise adjacent epitopes. J Virol. 2007;81:12816–26. PubMed DOI
Leitmeyer KC, Vaughn DW, Watts DM, Salas R, Villalobos I, de Chacon RC, et al. Dengue virus structural differences that correlate with pathogenesis. J Virol. 1999;73:4738–47.
Figures
Figure 1. Island nation states of the Pacific region.
Figure 2. Phylogenetic relationships between the envelope (E) protein genes of dengue type 4 viruses recovered from patients from Pacific island nation states during 2007–2009 outbreaks...

Table
Table. Chronology of appearance of dengue virus type 4, Pacific region

Suggested Citation for this Article
Li D, Liu W, Guigon A, Mostyn C, Grant R, Aaskov J. Rapid displacement of dengue virus type 1 by type 4, Pacific region, 2007–2009. Emerg Infect Dis [serial on the Internet]. 2010 Jan [date cited]. Available from http://www.cdc.gov/EID/content/16/1/123.htm

DOI: 10.3201/eid1601.091275

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Displacement of Dengue Virus Type 1 by Type 4 | CDC EID

Human Herpesvirus 8 in Healthy Blood Donors, Argentina | CDC EID




EID Journal Home > Volume 16, Number 1–January 2010

Volume 16, Number 1–January 2010
Letter
Human Herpesvirus 8 in Healthy Blood Donors, Argentina
Celeste L. Pérez, Mónica I. Tous, Norma Zala, and Sofía Camino
Author affiliations: Administración Nacional de Laboratorios e Institutos de Salud, Buenos Aires, Argentina (C.L. Perez, M.I. Tous); and Hospital de Enfermedades Infecciosas "Francisco J Muñiz," Buenos Aires (N. Zala, S. Camino)


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To the Editor: Human herpesvirus 8 (HHV-8), or Kaposi sarcoma–associated herpesvirus, is associated with malignant disorders such as Kaposi sarcoma, primary effusion lymphoma, and multicentric Castleman disease. Although HHV-8 does not necessarily cause life-threatening infection in healthy persons, it causes more severe infection in those who are immunocompromised, such as organ recipients and HIV-infected persons.

HHV-8 has been found in a number of clinical specimens (blood, saliva, and semen) from persons with HHV-8 related diseases (1,2). Identification of infectious virus in lymphocytes from a healthy blood donor and evidence that HHV-8 might be transmitted by blood has raised concern about the safety of the blood supply (3,4). Few studies have detected viral DNA in blood samples of blood donors from areas with low HHV-8 prevalence (5–7). During January 2000 and December 2002, the Virology Department, National Institute of Infectious Diseases, Administración Nacional de Laboratorios e Institutos de Salud, "Dr C G. Malbrán" conducted an HHV-8 serosurvey of 6 blood banks from 5 South American regions and found overall seroprevalence to be 3.7% (range 1.9%–6.7%). The 6.7% seroprevalence from a blood bank in Buenos Aires city was substantially higher than that of other blood banks (8).

From July 2004 through January 2005, to look for the virus in blood and saliva, we conducted the study reported here, an HHV-8 survey at the same blood bank. A total of 577 volunteer blood donors (431 men and 146 women), mean age 39 years (range 17–76 years), were enrolled at the Hemotherapy Service, Hospital of Infectious Diseases "Francisco Javier Muñiz." The protocol was approved by the Teaching and Research Committee.

Serum and whole blood were collected from all 577 donors, and paired blood–saliva samples were obtained from 394. Serum samples were routinely tested for hepatitis B and C viruses, HIV, human T-lymphotropic viruses I and II, Treponema pallidum, Brucella spp., and Trypanosoma cruzi; results were used to determine associations between HHV-8 and these agents. Specimens were stored at –20°C until serologic and molecular investigation at the Virology Department, National Institute of Infectious Diseases.

Serologic screening for HHV-8 infection was performed by indirect immunofluorescence assay by using lytically induced cells; serum samples were diluted 1:40 (8). Then 45 blood and 39 paired blood–saliva samples from HHV-8-seroreactive donors were investigated for viral genome by open reading frame 26 nested PCR. DNA was purified from 0.3 mL of whole blood by using FlexiGene DNA Kit (QIAGEN, Gmbh, Hilden, Germany); concentrations and quality were measured with a UV spectrophotometer, and 1 μg was used for PCR. The QIAamp DNA Mini Kit (QIAGEN, Gmbh,) was used to obtain DNA from 0.2-mL saliva samples. Crude pellets were resuspended in 20 μL of Tris EDTA, pH 8, then 5 μL were added to the PCR. Quality of DNA isolated from negative PCR samples was tested by amplifying the human housekeeping gene β-globin. In addition, inhibitors were investigated by adding the minimum viral DNA amount detected by our nested PCR, previously assessed by 10-fold serial dilutions of DNA from body cavity–based lymphoma 1 cells. The results are expressed as percentages, 95% confidence intervals (CIs), and proportions (positive/total). When necessary, the associations between variables were tested by means of χ2 or logistic regression. Significance was defined as p<0.05. Data were analyzed by using the Epidat 3.0 program, available from www.paho.org.

Positive immunofluorescence assay results were obtained for 45 (7.79%) of the 577 blood donors; seroprevalence was independent of gender (p = 0.8) and increased with age (odds ratio 1.04, 95% CI 1.01–1.07, p = 0.028). No association was found between HHV-8 and seroreactivity to the infectious agents tested (p = 0.3438). HHV-8 DNA was found in 3 seroreactive blood donors: 1 in saliva only and 2 in blood and saliva. Of the 45 HHV-8 seropositive samples, 38 were nonreactive to any infectious agents tested in the blood bank. One donor was seroreactive for hepatitis B.

In summary, we found HHV-8 in blood and saliva of blood donors even in an area where the virus is not endemic. Seroprevalence for HHV-8 was similar to that previously reported (8). Also, low viral loads might be undetectable by PCR but high enough to cause an infection with usual volumes of blood used in transfusions (9), especially when the hemoderivatives are given to immunocompromised recipients. This study was done in a blood bank from a hospital for infectious diseases in which the recipient population consisted of numerous HIV patients (10). It is a concern that these patients could have received blood infected with HHV-8. The fact that saliva samples were also positive is consistent with previously reported findings (1,2) and might indicate that the virus is active at a site from which samples are easier to obtain and in which the virus easier to detect than the bloodstream. This study provides further evidence that blood transfusion carries a potential risk for HHV-8 infection, even in areas where its prevalence is low.

Acknowledgment
We thank Sara Vladimirsky for statistical support.

References
Edelman DC. Human herpesvirus 8—a novel human pathogen. Virol J. 2005;2:78. PubMed DOI
Pica F, Volpi A. Transmission of human herpesvirus 8: an update. Curr Opin Infect Dis. 2007;20:152–6. PubMed DOI
Blackbourn DJ, Ambroziak J, Lennette E, Adams M, Ramachandran B, Levy JA. Infectious human herpesvirus 8 in a healthy North American blood donor. Lancet. 1997;349:609–11. PubMed DOI
Hladik W, Dollard SC, Mermin J, Fowlkes AL, Downing R, Amin MM, et al. Transmission of human herpesvirus 8 by blood transfusion. N Engl J Med. 2006;355:1331–8. PubMed DOI
Pellet C, Kerob D, Dupuy A, Carmagnat MV, Mourah S, Podgorniak MP, et al. Kaposi's sarcoma–associated herpesvirus viremia is associated with the progression of classic and endemic Kaposi's sarcoma. J Invest Dermatol. 2006;126:621–7. PubMed DOI
Kumar N, McLean K, Inoue N, Moles DR, Scully C, Porter SR, et al. Human herpesvirus 8 genoprevalence in populations at disparate risks of Kaposi's sarcoma. J Med Virol. 2007;79:52–9. PubMed DOI
Nishiwaki M, Fujimuro M, Teishikata Y, Inoue H, Sasajima H, Nakaso K, et al. Epidemiology of Epstein-Barr virus, cytomegalovirus, and Kaposi's sarcoma–associated herpesvirus infections in peripheral blood leukocytes revealed by a multiplex PCR assay. J Med Virol. 2006;78:1635–42. PubMed DOI
Perez C, Tous M, Gallego S, Zala N, Rabinovich O, Garbiero S, et al. Seroprevalence of human herpesvirus-8 in blood donors from different geographical regions of Argentina, Brazil, and Chile. J Med Virol. 2004;72:661–7. PubMed DOI
Dollard SC, Nelson KE, Ness PM, Stambolis V, Kuehnert MJ, Pellett PE, et al. Possible transmission of human herpesvirus-8 by blood transfusion in a historical United States cohort. Transfusion. 2005;45:500–3. PubMed DOI
Perez C, Tous M, Benetucci J, Gomez J. Correlations between synthetic peptide–based enzyme immunoassays and immunofluorescence assay for detection of human herpesvirus 8 antibodies in different Argentine populations. J Med Virol. 2006;78:806–13. PubMed DOI
Suggested Citation for this Article
Pérez CL, Tous MI, Zala N, Camino S. Human herpesvirus 8 in healthy blood donors, Argentina. Emerg Infect Dis [serial on the Internet]. 2010 Jan [date cited]. Available from http://www.cdc.gov/EID/content/16/1/150.htm

DOI: 10.3201/eid1601.090893

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Human Herpesvirus 8 in Healthy Blood Donors, Argentina | CDC EID