Sunday, August 30, 2009

Higher Diastolic, Not Systolic, Blood Pressure Linked to Impaired Cognition

From Medscape Medical News
Deborah Brauser

August 25, 2009 — Higher diastolic blood pressure (DBP) levels, but not systolic blood pressure (SBP) levels, can impair cognitive status in individuals without prior history of stroke or transient ischemic attack, according to the results of a large study reported in the August 25 issue of Neurology.

"Althugh both higher [pulse pressure] and SBP values were related to cognitive impairment in unadjusted analyses, these associations were no longer significant after accounting for demographics, health behaviors, and vascular risk factors," write Georgios Tsivgoulis, MD, from the Comprehensive Stroke Center at the University of Alabama in Birmingham, and colleagues.

"The present study indicates that elevated [DBP] levels are linearly and cross-sectionally associated with a higher likelihood of impaired cognitive status. If this association is causally established in future longitudinal studies, than reducing elevated BP levels may result in reducing the incidence of dementia," Dr. Tsivgoulis told Medscape Neurology.

Background

The study authors write that the prevalence of dementia is estimated at approximately 8% and the prevalence of hypertension approximately 65% among individuals aged 65 years or older. Although the relationship among BP, cognitive function, and dementia has received a lot of attention in recent years, the findings have varied greatly.

In this study, the investigators sought to evaluate the cross-sectional relationship of BP components (SBP, DBP, and pulse pressure) with cognitive impairment after adjusting for potential confounders.

Dr. Tsivgoulis and colleagues looked at data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a national, population-based, longitudinal cohort study evaluating stroke risk in 30,228 black and white men and women aged 45 years or older.

From REGARDS, the investigators selected 19,836 participants (mean age, 64.6 years; 57.7% white, 60.8% female), who were enrolled from December 2003 to March 2007, had no prior history of stroke or transient ischemic attack, and completed baseline home physical evaluations.

During the in-home visit, BP measurements were taken as the average of 2 measurements using a standard aneroid sphygmomanometer.

The participants also completed the 6-Item Screener, which was administered either in-person or by telephone, to assess cognitive status, as well as the Center for Epidemiologic Studies-Depression 4-Item version to evaluate depressive symptoms.

Incremental logistic models were used to examine baseline relationships among SBP, DBP, and pulse pressure with impaired cognitive status.

Intriguing Findings

At the end of the study, results showed that higher DBP levels were associated with impaired cognitive status after adjusting for demographic and environmental characteristics, risk factors, depressive symptoms, and antihypertensive medications. An increment of 10 mm Hg in DBP was associated with 7% (95% confidence interval [CI], 1% – 14%; P = .0275) higher odds of cognitive impairment.

However, no independent association was identified between impaired cognitive status and SBP (odds ratio [OR], 1.02; 95% CI, 0.99 – 1.06) or pulse pressure (OR, 0.99; 95% CI, 0.95 – 1.04).

"We were surprised by the fact that DBP and not SBP or [pulse pressure] was related to cognitive impairment after adjusting for potential confounders," said Dr. Tsivgoulis. "We attributed these intriguing findings to a potential association between diastolic hypertension and accelerated stiffening of cerebral small vessels that are profoundly affected by DBP."

"These vascular changes...result in a reduction of luminal diameter, which in turn causes increased resistance to flow and decline in cerebral perfusion. Such hypoperfusion may produce discrete regions of small cerebral infarctions and diffuse ischemic changes in the periventricular and deep white matter (leukoaraiosis), causing vascular cognitive impairment and also contributing to the pathogenesis of Alzheimer's disease by destabilizing neurons and synapses," the authors write.

The results showed no evidence of nonlinear relationships between any of the BP components and impaired cognitive status and no interaction between age and the relationship of impaired cognitive status with SBP (P = .827), DBP (P = .1333), or pulse pressure (P = .827) levels. Also, no interaction was identified between race and the relationship of impaired cognitive status with SBP (P = .899), DBP (P = .966), or pulse pressure (P = .858) levels.

"Our study showed that higher DBP levels were independently related to a higher likelihood of impaired cognitive status in a large national sample that was nearly balanced with respect to race and gender," said Dr. Tsivgoulis. However, he added, the linear, cross-sectional association needs to be confirmed in a longitudinal analysis.

Laying the Groundwork

"This is a good study," said John Hart, Jr, MD, professor of behavioral and brain sciences and medical science director at the Center for BrainHealth at the University of Texas in Dallas in an interview with Medscape Neurology. Dr. Hart was not involved with the study.

"It's another step in laying the groundwork for some things we're noticing about the vascular effects on cognitive decline with aging," Dr. Hart continued. "It's not necessarily saying we have a definitive answer here. But it is saying that in a large study like this, there appears to be an effect of diastolic BP."

However, he added that the study also has some weaknesses, including its cross-sectional design. In addition, the investigators "report diastolic BP versus cognitive impairment based on only a 6-point test, and from a cognitive point of view, that's pretty minimalistic. Calling someone impaired based just on this test really gives a rudimentary picture of their cognitive status."

In the future, Dr. Hart said that he would like to see a big, definitive, prospective, longitudinal study "with a rich set of cognitive measures and some neuroimaging to correlate with the findings."

"I think this study reaffirms the fact that you want to do your best to screen and treat for vascular risk factors in individuals, not just in what people normally think of (heart disease), but also factors such as strokes or vascular changes that might affect cognition in the brain. It just adds another piece of evidence that says that we should all be treating these risk factors aggressively to prevent long-term effects down the road. That's such a straightforward easy thing to do and it lets you see real differences at the end of the game."

Several of the study authors disclosed financial relationships that are listed at the end of the original article. Dr. Hart has disclosed no relevant financial relationships.

Neurology. 2009;73:589–595.

Friday, August 14, 2009

Elevated Cholesterol in Midlife May Increase Dementia Risk

From Medscape Medical News
Janis Kelly

August 11, 2009 — Even moderately elevated cholesterol levels in midlife are strongly associated with later risk for Alzheimer's disease (AD) and vascular dementia (VaD), new research suggests.

Lead author Alina Solomon, MD, from the University of Kuopio, Finland, used data from the Kaiser Permanente Northern California Medical Group to investigate the relationship between midlife cholesterol and dementia and found that even cholesterol levels of 200 to 239 mg/dL increase risk.

"Both physicians and patients need to know that elevated cholesterol increases the risk not only for heart disease but also for dementia," Dr. Solomon told Medscape Psychiatry. "The most important finding was that even moderately elevated cholesterol at midlife can increase the risk of both AD and VaD later in life," she added. "This emphasizes the fact that AD and VaD may have more in common than was previously thought. Several studies have pointed out that there is a degree of overlap between the 2 dementia types in terms of risk factors, clinical symptoms, and neuropathology. Vascular factors can be associated with AD as well — not just with vascular forms of dementia."

The study is published in the August issue of Dementia and Geriatric Cognitive Disorders.

More than 9000 Subjects

Performed in collaboration with Rachel A. Whitmer, PhD, from Kaiser Permanente in Oakland, California, the study included 9844 subjects who had undergone detailed health evaluations during 1964 to 1973, when they were 40 to 45 years old.

Data from 1994 showed that 469 participants had AD, and 127 had VaD. The researchers adjusted for age, education, race/ethnic group, sex, midlife diabetes, hypertension, body mass index, and late-life stroke. They used cholesterol levels lower than 200 mg/dL as a reference point.

The analysis showed AD hazard ratios of 1.23 for midlife borderline cholesterol (200 – 239 mg/dL) and 1.57 for high cholesterol (≥240 mg/dL). Quartile analysis showed that hazard ratios were 1.31 for cholesterol levels of 221 to 238 mg/dL and 1.58 for levels of 249 to 500 mg/dL.

VaD hazard ratios were 1.50 for borderline cholesterol and 1.26 for high cholesterol.

Dr. Solomon said that the results were not entirely surprising, as previous studies have shown a link between high cholesterol and dementia risk. However, she added, this study is the largest to date, includes a heterogeneous population, and considers VaD as well as AD as an outcome.

Unanswered questions for future investigations include the roles of different cholesterol types, the significance of cholesterol changes after midlife in relation to dementia risk, and the effect of lipid-lowering treatment on dementia risk.

According to Dr. Solomon, the mechanisms behind the cholesterol-dementia association are not entirely clear.

"Our results remained significant even after taking into account several vascular-related factors and conditions, so other mechanisms may be involved as well. The brain is the most cholesterol-rich organ in the human body, but compared to serum cholesterol, far less is known about brain cholesterol and the interactions between the 2 cholesterol pools," she said.

What Is Bad for the Heart Is Bad for the Brain

Robert Stewart, MD, head of epidemiology at the Institute of Psychiatry, King's College London, United Kingdom, told Medscape Psychiatry that the Solomon study data are "convincing" and "consistent with those from other studies which have screened community populations for this disorder."

"In general, there is now a large body of evidence which indicates that what is bad for the heart is bad for the brain — that is, that that the well-known risk factors for coronary heart disease and stroke are also risk factors for dementia (whether this is classified as AD or VaD)," Dr. Stewart said.

"So the real message for clinicians is not to do anything differently, but to be aware that what they should be doing already — identifying and treating high cholesterol, high blood pressure, [and] diabetes and promoting healthy diet and active lifestyles — is likely to have more benefits than originally envisaged and should reduce risk of dementia as well as reducing risk of cardiovascular disease."

The authors have disclosed no relevant financial relationships.

Dement Geriatr Cogn Disord. 2009;28:75–80.

Tuesday, August 11, 2009

H1N1 EVERYTHING U NEED TO KNOW

Everything you wanted to know about swine flu

TNN 10 August 2009, Indian Medical Association
The spread of swine flu is fast emerging as No 1 healthcare emergency not just in the country but the world over. Despite the issue being in the media for a long time, there continue to be ignorance and mis-information about the disease and how to handle it. Indian Medical Association, Nagpur Centre, has come up with a information dossier on the subject. We reproduce it here for the benefit of our readers.

What is H1N1 (swine) flu?
H1N1 (referred to as "swine flu" early on) is a new influenza virus causing illness in people. This new virus was first detected in people in the United States in April 2009. Other countries, including Mexico and Canada, have also reported people sick with this new virus. This virus is spreading from person-to-person, probably in much the same way that regular seasonal influenza viruses spread.

In late March and early April 2009, cases of human infection with swine influenza A (H1N1) viruses were first reported in Southern California and near San Antonio, Texas.

In the beginning it was difficult to predict the effect of this virus on general population. In seasonal flu, there are certain people who are at higher risk of serious flu-related complications. This includes people with 65 years of more age, children below five years, pregnant women, and people of any age with chronic medical conditions.

This virus is contagious but, at this time, it not known how easily the virus spreads between people. The symptoms of H1N1 swine flu in people are similar to the symptoms of regular human flu and include fever, cough, sore throat, body aches, headache, chills and fatigue. Some people have reported diarrhoea and vomiting associated with H1N1 swine flu. Severe illness (pneumonia and respiratory failure) and even deaths have been reported with H1N1 swine flu infection. Like seasonal flu, H1N1 swine flu may cause a worsening of underlying chronic diseases.

In children, emergency warning signs that need urgent medical attention include:
* Fast breathing or difficulty in breathing
* Bluish or gray skin colour
* Not drinking enough fluids
* Severe or persistent vomiting
* Not waking up or not interacting
* Being so irritable that the child does not want to be held
* Flu-like symptoms improve but then return with fever and worse cough

In adults, emergency warning signs that need urgent medical attention include:
* Difficulty in breathing or shortness of breath
* Pain or pressure in the chest or abdomen
* Sudden dizziness
* Confusion
* Severe or persistent vomiting
* Flu-like symptoms improve but then return with fever and worse cough

How do you catch H1N1 (swine) flu?
Spread of H1N1 (swine) flu can occur in two ways:

H1N1 virus appears to be transmitted the same way that seasonal flu spreads. Flu viruses are spread mainly from person to person through coughing or sneezing by people with influenza. Sometimes people may become infected by touching something with flu viruses on it and then touching their mouth or nose.

How can someone with the flu infect someone else?

Infected people can infect others right from day one even before they themselves develop any symptoms up to seven or more days after becoming sick. That means that one can pass on the infection to someone else before he/she even knows that he/she is sick, as well as while one is sick.

What can I do to protect myself from getting sick?

There is no vaccine available right now to protect against H1N1 (swine) flu. There are everyday actions that can help prevent the spread of germs that cause respiratory illnesses like influenza. Take these everyday steps to protect your health:

* Cover your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the trash after you use it.

* Wash your hands often with soap and water, especially after you cough or sneeze. Alcohol-based hand cleaners are also effective.

* Avoid touching your eyes, nose or mouth. Germs spread this way.

* Try to avoid close contact with sick people.

* If you get sick with influenza, you should stay at home and not go for work or school and limit contact with others to prevent them from getting infecting by you.

* Reduce the time spent in the crowded settings.

* Improve airflow in the living space by opening the windows and proper ventilation.

* Practice good health habits including adequate sleep, eating nutritious food, and keeping physically active.

How long can influenza virus remain viable on objects (such as books and doorknobs)?

Studies have shown that influenza virus can survive on environmental surfaces and can infect a person for up to 2-8 hours after being deposited on the surface.

Germs can be spread when a person touches something that is contaminated with germs and then touches his or her eyes, nose, or mouth. Droplets from a cough or sneeze of an infected person move through the air. Germs can be spread when a person touches respiratory droplets from another person on a surface like a desk, for example, and then touches his own eyes, mouth or nose before washing hands.

Are there medicines to treat H1N1 (swine) flu?

Yes, use of oseltamivir (brand name Tamiflu?) or zanamivir (brand name Relenza ?) for the treatment and/or prevention of infection with these H1N1 (swine) influenza viruses. Antiviral drugs are prescription medicines (pills, liquid or an inhaler) that fight against the flu by keeping flu viruses from reproducing in your body. If you get sick, antiviral drugs can make your illness milder and make you feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within two days of symptoms).

Follow the advice of your local public health department regarding school closures, avoiding crowds and other measures to reduce flu transmission. These measures will continue to be important after a novel H1N1 vaccine is available because they can prevent the spread of other viruses that cause respiratory infections.

What should I do if I get sick?

If you live in areas where people have been identified with new H1N1 flu and become ill with influenza-like symptoms, including fever, body aches, runny or stuffy nose, sore throat, nausea, or vomiting or diarrhoea, you should stay home and avoid contact with other people, except to seek medical care. If you have severe illness or you are at high risk for flu complications, contact your health care provider or seek medical care. Your health care provider will determine whether flu testing or treatment is needed.

Antiviral drugs may reduce the symptoms and duration of illness, just as they do for seasonal influenza. They also may contribute to preventing severe disease and death. WHO is in touch with public health authorities and clinicians in affected countries and is gathering information about how effective the drugs are.

What about using a mask? What does WHO recommend?

If you are not sick you do not have to wear a mask. If you are caring for a sick person, you can wear a mask when you are in close contact with the ill person and dispose of it immediately after contact, and clean your hands thoroughly afterwards.

If you are sick and have to travel or be around others, cover your mouth and nose.

Using a mask correctly in all situations is essential. Incorrect use actually increases the chance of spreading infection.

How do I know if I have influenza A (H1N1)?

You will not be able to tell the difference between seasonal flu and influenza A (H1N1) without medical help. Typical symptoms to watch for are similar to seasonal viruses and include fever, cough, headache, body aches, sore throat and runny nose. Only your medical practitioner and local health authority can confirm a case of influenza A (H1N1). If they suspect any symptoms they will send your blood sample, throat swab and nasopharyngeal (nose to mouth) for testing to laboratories. Presently this facility is available only at certain

Sunday, August 9, 2009

Gender Gap, Inflammation and Acute Coronary Disease: Are Women Resistant to Atheroma Growth? Observations at Autopsy

From The Journal of Invasive Cardiology
Richard J. Frink, MD

Abstract
Background: Gender differences that exist in patients with acute coronary disease (ACD) are unexplained. We sought to determine if these differences could be related to differences in the pathologic substrate found in the coronary arteries at the time of death.

Methods: The hearts of 83 patients (64 men and 19 women) who died of ACD were obtained fresh and uncut at the autopsy table. The coronary arteries were injected with a colored barium gelatin mass. After formalin fixation, the epicardial arteries were dissected intact, decalcified and cut at 2-3 mm intervals, with all segments mounted for histologic study. The severity of luminal stenosis and the frequency of adventitial inflammation, intimal calcification and atheromas were determined microscopically for each segment. Plaque burden was determined histologically by assessing the severity of luminal stenosis for each coronary segment. The number of plaque ruptures (PRs), with and without luminal thrombosis, were tabulated for each heart in the study. These results were compared with 22 control patients who died of noncoronary disease.

Results: There are gender similarities as well as significant differences in the pathologic substrate of patients who die of ACD. Active, inflammatory atherosclerosis and associated ACDs develop earlier in life in men than in women, and are associated with death at an earlier age, producing a "gender gap." There were no significant gender differences in the frequency of PRs. The women were significantly older than the men and had more extensive active disease, but had the same overall plaque burden as men, suggesting women may be resistant to plaque growth, particularly atheroma growth.
Conclusions: Gender gap appears to be related to factors peculiar to women who resist atheroma growth, delaying PR and the onset of ACD.

Introduction
The gender differences that exist in patients with acute coronary disease (ACD) remain largely unexplained and may reflect anatomic, biologic or pathophysiologic differences.[1,2]
Women who develop ACD are often older than men, typically die at an older age and have a worse prognosis following acute myocardial infarction (AMI), or after interventions such as coronary bypass graft surgery (CABG) or percutaneous coronary intervention (PCI).[2-6]
These differences, often referred to as "gender gap", are consistently present in all countries and cultures where coronary artery disease exists.[1]

The low frequency of ACD in premenopausal women suggests they are "protected" or resistant in some way to developing atherosclerosis and subsequent ACD,[1,2,7-9] but the mechanism of such resistance is unknown.
The protective factor(s) appear to be powerful and are not found to operate through lipid-related mechanisms.[9] Additionally, levels of known common risk factors do not explain gender gap.[1,9] Even women with heterozygous familial hyperlipidemia appear to be protected.[10]
A sudden increase in ACD does not occur at the time of menopause,[1] as might be expected if this resistance were related to female hormones.
In fact, the administration of female hormones to the postmenopausal woman is associated with increased risk of ACD.[11]
The presence or absence of female hormones does not explain gender gap.[1,9,12]

Saturday, August 8, 2009

Low-Carb or Low-Fat Diet May Similarly Affect Weight, A1C in Patients With Type 2 Diabetes CME

From Medscape Medical News CME
Laurie Barclay, MD
Désirée Lie, MD, MSEd

July 21, 2009 — A low-carbohydrate diet may have effects similar to those of a low-fat diet on weight and hemoglobin A1C (A1C) levels in patients with type 2 diabetes, but patients following the low-carbohydrate diet have a greater increase in high-density lipoprotein (HDL) cholesterol levels after 1 year, according to the results of a randomized clinical trial reported in the July issue of Diabetes Care.

"Optimal weight loss strategies in patients with type 2 diabetes continue to be debated, and the best dietary strategy to achieve both weight loss and glycemic control in type 2 diabetes is unclear," write Nichola J. Davis, MD, MS, from the Albert Einstein College of Medicine of Yeshiva University, Bronx, New York, and colleagues. "Prior studies, done primarily in patients without diabetes, demonstrated weight loss outcomes with low carbohydrate diets comparable to that with other diets. Based on the effectiveness of low-carbohydrate diets for weight loss, recent guidelines from the American Diabetes Association state that for short-term weight loss either a low carbohydrate or low-fat calorie-restricted diet may be effective."

The goal of this study was to compare the effects during 1 year of a low-carbohydrate diet and a low-fat diet on weight loss and glycemic control in 105 overweight adults with type 2 diabetes. The main endpoints of the study were weight and A1C levels, and secondary endpoints were blood pressure and lipid profile, measured at 3, 6, and 12 months.

Weight loss occurred faster in the low-carbohydrate group vs the low-fat group (P = .005), with the greatest decrease in weight and A1C levels occurring during the first 3 months. However, both dietary groups had a similar 3.4% weight loss at 1 year, and neither group had a significant change in A1C levels at this time point. Blood pressure was unaffected. Compared with the low-fat dietary group, the low-carbohydrate group had a greater increase in HDL cholesterol levels (P = .002).

"The most relevant point is that there were increases in HDL cholesterol with the low carbohydrate diet," Maria-Luz Fernandez, PhD, a professor of nutritional sciences at the University of Connecticut, told Medscape Diabetes & Endocrinology when asked for independent comment. "This is a very consistent finding in low-carb interventions. HDL cholesterol is most of the time very low in diabetic people so this is a very important clinical implication."

Limitations of this study include greater baseline weight in the low-fat group vs the low-carbohydrate group, possible bias caused by use of single-day dietary recall or a single-day food record to evaluate dietary intake, and lack of objective measures of physical activity.

"Among overweight patients with type 2 diabetes, there was no significant difference in the weight or A1C change in participants after a low carbohydrate compared with a low-fat diet for 12 months," the study authors write. "Participants in both arms achieved an average 3.4% weight reduction but did not reduce A1C. Differences in the short-term effects of each diet were not sustained."

When asked about clinical caveats or recommendations regarding low-carbohydrate diets, Dr. Fernandez said: "Low-carb diets are difficult to follow if the carbohydrate is very low, but a 25% carbohydrate diet is not difficult to follow and it can be very useful for diabetic patients."

In additional research, Dr. Fernandez recommends studies to evaluate whether there are sex responses or if the responses vary depending on low HDL cholesterol levels at baseline.

Diabetes Care. 2009;32:1147-1152.

Reducing Salt Intake May Reduce Blood Pressure in 3 Ethnic Groups

Laurie Barclay, MD
Charles P. Vega, MD
From Medscape Medical News

July 27, 2009 — Modestly reducing salt intake is associated with significant decreases in blood pressure in blacks, Asians and whites, according to the results of a randomized, double-blind, crossover trial reported online in the July 20 issue of Hypertension. Most previous trials were in whites, with few in blacks and Asians.

"A lower salt intake, in the long-term, could play an important role in the prevention of cardiovascular disease, renal disease and osteoporosis," lead author Feng J. He, PhD, from St. George's, University of London, United Kingdom, said in a news release. "Our study provides further support for the current public health recommendations to reduce salt intake to less than 6 grams per day."

In this crossover trial, 71 whites, 69 blacks, and 29 Asians with untreated, mildly raised blood pressure underwent salt restriction with slow sodium or placebo, each for 6 weeks. Reduction in urinary sodium levels from slow sodium to placebo was from 165 ± 58 mmol/24 hours to 110 ± 49 mmol/24 hours (9.7 - 6.5 g/day salt).

This reduction in salt intake was associated with reductions in the following measures:

•blood pressure from 146 ± 13/91 ± 8 mm Hg to 141 ± 12/88 ± 9 mm Hg (P < .001),
•urinary albumin from 10.2 (interquartile range [IQR], 6.8 - 18.9) mg/24 hours to 9.1 (IQR, 6.6 - 14.0) mg/24 hours (P < .001),
•albumin/creatinine ratio from 0.81 (IQR, 0.47 - 1.43) mg/mmol to 0.66 (IQR, 0.44 - 1.22) mg/mmol (P < .001), and
•carotid-femoral pulse wave velocity from 11.5 ± 2.3 meters/second to 11.1 ± 1.9 meters/second (P < .01).
All 3 ethnic groups had significant decreases in blood pressure and urinary albumin/creatinine ratio with salt restriction, according to subgroup analysis. However, only blacks had a significant decrease in pulse wave velocity.

Based on the findings, the investigators concluded that a modest reduction in salt intake, comparable with the current public health recommendations, could cause significant reduction in blood pressure and urinary albumin levels in all 3 ethnic groups and could improve large-artery compliance.

"About 80 percent of salt intake in developed countries comes from sodium added by the food industry," said senior author Graham A. MacGregor, MD, also from St. George. "The best strategy to reduce salt intake in the population is to persuade the food industry to make a gradual and sustained reduction in the amount of salt added to food in a structured program across the whole of the food industry. This is now happening in the United Kingdom and the average salt intake has already fallen from 9.5 to 8.6 grams per day, and will continue to fall as more salt is taken out of all foods, with the saving of many lives."

Limitations of this study include relatively small sample size, particularly regarding Asians.

"Even a small reduction in blood pressure in the whole population would have a large impact on reducing the number of people suffering and/or dying from strokes, heart attacks and heart failure," Dr. MacGregor concluded.

•The World Health Organization recommends a daily salt intake of less than 5 g/day among adults.
•The current study finds that reduced salt intake improves blood pressure and urinary albumin excretion among whites, blacks, and Asians.

FDA Approves Hydrocortisone/Acyclovir Cream for Treating Cold Sores

From Medscape Medical News
Yael Waknine

August 6, 2009 — The US Food and Drug Administration (FDA) has approved a hydrocortisone plus acyclovir cream (Lipsovir, Medivir AB) for the early treatment of recurrent herpes labialis — cold sores — to reduce the likelihood of ulcerative cold sores and to shorten the lesion healing time. Treatment is approved for adults and children aged 12 years and older.

The approval was based on data from a clinical phase 3 program showing that 42% of patients using hydrocortisone/acyclovir cream did not develop cold sores with blisters, ulcers, and crusting compared with 26% of those receiving placebo.

For those patients who developed cold sores, healing time was significantly decreased, being lowered by 1.5 days in the active treatment group vs in the placebo group.

"No product currently marketed for the treatment of cold sores has a corresponding label or has been shown to prevent an outbreak with early treatment," the company noted in a news release.

Penicillin Allergy Skin Testing Practical in ED;

Many Who Say They Have Allergy Don't
From Reuters Health Information

NEW YORK (Reuters Health) Aug 05 - Penicillin skin prick and cutaneous testing provides prompt results in emergency department patients with self-reported allergy. In most cases, that gives doctors more treatment options, according to researchers, because many of those who believe they are allergic to the antibiotic actually are not.

"It is feasible to determine if patients are truly allergic to penicillin in an emergency department setting," senior investigator Dr. Joseph J. Moellman told Reuters Health.

"Many patients that say they have an allergy," he added, "in actuality really do not when formally tested."

As reported in the July issue of the Annals of Emergency Medicine, Dr. Moellman of the University of Cincinnati College of Medicine, Ohio, and colleagues studied 150 patients with self-reported penicillin allergy.

Either of two physicians initially conducted skin tests in the patients, and if negative, intracutaneous testing was then employed. Total testing time was about 30 minutes.

The penicillin skin test result was negative in 137 of the patients, giving a false-positive rate for self-reported penicillin allergy of 91.3%. There were no adverse reactions associated with the testing.

"The clinical ramification of this study," continued Dr. Moellman, "is that many of these patients who might require penicillin to treat a specific infection would be able to receive penicillin if they tested negative to this skin test."

"This," he concluded, "would allow clinicians to avoid more costly alternative antibiotics and ultimately decrease drug resistance."

Ann Emerg Med 2009;54:72-77.

Thursday, August 6, 2009

A(H1N1) flu: Updates on 10 FAQs

Thursday August 6, 2009

by Dr David KL Quek

1) Can we distinguish between regular and H1N1 flu, without a lab test?

No, the flu is the flu, but there are variations in presentation. Some symptoms such as cough, runny nose, fever, body aches, fatigue, vomiting, diarrhoea occur more or less in every flu patient, but may present differently by different people. Some infected people have very mild symptoms, some in between, and a small minority, probably less than 10 per cent, have severe features including the dangerous pneumonia.

However, from sentinel testing and surveillance by the Ministry of Health the last few weeks have shown that almost 95 per cent of all flu-like illness are now caused by the H1N1 virus. Earlier some months ago, seasonal flu variants caused by the B and other A virus were the main causes, the bug causing most flu these few days is the A(H1N1). This appears to be the case also in neighbouring countries, meaning that the new virus is causing more havoc and symptomatic illness than previous types of flu (which are still in the community).

Because almost every flu-like illness (influenza-like illness or ILI) is due to H1N1, the MOH is now recommending that no testing to confirm this H1N1 will now be offered.

Treat as if this is H1N1 for ILI — symptom relief for mild symptoms (paracetamol, hydration, cough medicines, etc) and self-quarantine, social distancing, be alert for complications.

Most (70 per cent) do not need any anti-viral medications such as Tamiflu or Relenza. Only severe cases need to be referred to hospital for further treatment.

2) How should doctors decide if a person be given further specific treatment for H1N1?

If after 2-3 days, fever and cough symptoms do not improve, a recheck with the doctor is recommended, especially if there are features of difficulty breathing, severe weakness and giddiness, or, if the following risk factors are present:

1. obesity (fatter patients seem to have poorer outcome and more complications)

2. those with underlying diabetes, heart disease

3. those with asthma, or chronic lung disease

4. pregnant women

5. those with reduced immunity, cancer patients, etc

6. those with obvious pneumonia features

3) Many anxious people with flu-like symptoms want to be tested or treated for suspected H1N1, but are kept waiting or sent home, without being tested. Is this practice right?

There is no right or wrong practice as this outbreak is extensive and is stretching our resources to the limit. This is also the case not just here in Malaysia, but also elsewhere around the entire world!

The recommendation is now not to spend too much time and effort trying to get tested at designated hospitals or clinics — there is probably no need to do so. I have been informed that as many as 1,000 patients queue anxiously at Sungai Buloh Hospital for testing, due to fear of the H1N1 flu.

So the message must be made clear: Most flu illness do not require confirmatory testing, and are mild and self-limiting. More than 90 per cent will get better on their own, with symptomatic treatment — just watch out for possible complications, and risk factors as mentioned above.

Our resources are limited especially for testing. This is not just for Malaysia, but globally as well. The global demand for test kits and reagents for the H1N1 (PCR) is overextended and are rationed due to this extreme demand.

Some 200 million test kits have been deployed worldwide, but this supply is critically short because of excessive demand, so most countries have to ration testing to confirm only the worst cases, so as to monitor the pandemic better.

4) Are doctors confused as to what to do in this outbreak, especially when they do not have ready access to confirmatory lab tests?

Not really. Earlier on there was some confusion as to what to do next and who to test or who to refer for further testing and admission. Now the rules are clearer.

There is no need to do any testing to confirm the H1N1 virus for any ILI — just assume that this is the case in the majority of cases. Treat symptomatically when symptoms are mild, reassure the patients and ensure that these infected patients practice good personal hygiene, impose self-quarantine and social distancing, wear masks if their coughing or sneezing become troublesome, and keep a watchful eye on whether the infection is getting better or worse.

If there is difficulty breathing and gross weakness, then patients should quickly present themselves for admission. Understandably this phase of worsening is not always clear or easily understood by everyone... But there is not much more that we can do — otherwise we will be admitting too many patients and this will totally overwhelm our health services.

But prudent caution would help to determine which seriously ill patients need more attention and more intensive care. Unfortunately however, there will be that odd patient who will progress unusually quickly and collapse even before anything can be planned — hopefully these will be few and far between.

A more important note is that all doctors and nursing personnel should be very aware that they too have to take precautions, and employ barrier contact practices, if there are patients with cough and cold during this period of H1N1 outbreak, which is expected to last a year or two. Carelessness can result in the physician or nurse or nurse-aide becoming infected!

5) Are there sufficient guidelines from the Ministry of Health to address this situation?

I think there are sufficient guidelines from the MOH. Although some politicians have blamed the MOH and the minister for being inept at handling this pandemic — in truth this is not the case.

It is useful to remember that this is an entirely new or novel virus, which no one previously had encountered before — thus its infectivity and contagiousness is quite high and almost no one is immune to this virus.

Perhaps, there will come a time when all the resources from both public and private sectors can be put to more efficient use. Some logistic problems will invariably occur, because human beings differ in their capacity to understand or follow directives, whatever the source or authority.

Also patient demands have been extraordinarily high and at times very difficult to meet — every patient necessarily feels that his flu is potentially the worst possible type and therefore requires the most stringent measures and testing...

Doctors are also unsure as to the seriousness or severity of this new ailment — and we are only now beginning to understand this better — so our less than reassuring style when encountering this new H1N1 flu is sometimes detected by an equally anxious patient and/or their relatives.

But there is only so much that we can do under such a pressure cooker of an outbreak which is spreading like wildfire! But nevertheless we should not panic, and remember that most (more than 90 per cent) of infected people will recover with very little after-effects. Possibly only one in 10 patients develop more serious problems which necessitate hospitalisation.

6) Is limiting H1N1 testing only to those who have been admitted to hospital justifiable?

I have explained the worldwide shortage of such testing kits and reagents. Also it is near impossible to test everyone, the world over. Besides, knowing now that almost all the flu-like illness in the country is due to H1N1 makes it a moot point to want to test for this, especially when most are mild.

The rationale for testing only those who need hospitalisation is to ensure that we are dealing with the true virus, and also help to isolate possible changes or mutations to this viral strain. The MOH is also constantly doing sentinel surveillance (random spot-testing at various sites around the country to determine more accurately the various virus types and spread that are causing ILI).

7) Are we short of anti-virul drugs (Tamiflu, Relenza)? Should I take Tamiflu?

These antiviral drugs were available to most doctors during the earlier scare of the bird flu virus, but now are severely restricted, although some orders are still entertained from individual doctors, clinics or hospitals. Remember that these have been block-booked by more than 167 countries which have been shown to have been penetrated by the H1N1 flu bug.

Our MOH has actually stockpiled some two million doses of the Tamiflu or its generic form. In the last inter-ministerial pandemic influenza task force meeting, this stockpile will be bumped up to 5.5 million doses to cover some possible 20 per cent of the population.

Right now there is no shortage in the country. It is just that it is not readily available on demand for anyone just yet. The MOH is still of the opinion that this antiviral drug be used prudently and would like to register every patient given this drug.

The private sector on the other hand would like to have a looser control over the use of this drug — but we acknowledge that we should be meticulously prudent in its use. There is a genuine fear that resistant strains to this drug may develop with indiscriminate and unnecessary use — then we will all be in trouble with a drug-resistant H1N1 virus run amok!

Drug-resistant strains have been detected in Mexico, border-towns in the US, Vietnam, Britain, Australia even. So we have to be vigilant and closely monitor the situation. Right now, the very limited usage of Tamiflu gives us good reason to be optimistic.

However, because of some unusual patterns of seemingly well people dying or having very critical infections, some people and doctors are wondering if these new strains have already reached our shores... or have we been too late in instituting proper treatment...?

The rising number of deaths to 14 now is quite worrisome, but our health authorities are watching this development very closely and are also checking the virus strain to see if this has mutated. We can only hope that this is not the case, for now.

8) What are some of the problems faced by doctors in dealing with the H1N1 problem?

It would be good if every medical practitioner keeps a close tab on the H1N1 pandemic, and remain fully aware of the developments and changes, which are evolving daily. Every doctor has to be learning on the trot, so to speak, to keep up with the progress of this outbreak and its management, so that we can serve our patients better.

Logging in to the Internet regularly for more updated information will certainly help, instead of lamenting that not enough is being disseminated via the media thus far... Every doctor has to be more proactive and practice more responsible and cautious medicine during this trying period which is expected to run into at least one to two years. Importantly, look out for lung complications, and the above stated higher risk profiles, and refer these patients quickly for further care.

Easier access to antiviral drugs and their responsible use and monitoring would help allay public fears of delay in treatment, but this should be tempered with care and not over-exuberance to dish out to one and all, the precious antiviral drug, just for prevention — this may be a very bad move which can inadvertently create a worse outcome of drug-resistant bugs.

However, in the light of the very quick deterioration of some young patients who have died, it might be prudent to use antiviral treatment earlier and more aggressively.

We look forward to the specific H1N1 vaccine, when it does come our way, probably towards the end of the year. In the meantime, encouraging those in the front-line, heart or lung patients and frequent travellers to have the seasonal flu vaccination is a useful adjunct to help stem the usual problems from other flu types.

9) Are we doing everything that should or needs to be done?

Yes, if you check what other nations are doing, we are doing relatively well. We are not overstating the dangers and we have been quite transparent on the possibilities of this pandemic. Earlier, many agencies and even the public and doctors have accused us of exaggerating the pandemic, and our response was dismissed as being too much, even over the top! Unfortunately, it was only when some deaths occur that many are now decrying that we have done too little!

Also if you are quite honest about it, just compare with the countries globally, and you will notice that no one health or government authority has got this right, spot on.

We are all learning about this novel flu pandemic, and each country's response is coloured by its past experiences. In Hong Kong, China, Vietnam, Singapore and Malaysia we have had the SARS outbreak, so we are necessarily more paranoid! Also here the experience is that flu does not usually cause death in our community, unlike the west where seasonal flu kills some hundreds of thousands every year!

So the fear factor for this H1N1 flu is not nearly as great in the West, although it is slowly sinking in that its contagiousness and infectivity is far greater, and fears of its reassortment to a more virulent mutant form are growing, into the so-called second and/or third wave of this pandemic, but we will not know until a year or so down the line.

10) Is the public in general doing enough to help in controlling the outbreak?

I think the public is now reasonably well-informed as to this H1N1 pandemic. Perhaps, they are too well-informed, that they have a fearful approach to this virus. But the proper thing is not too over-react and to panic, although I know this does sound easier said than done.

It is almost a certainty that this flu will spread within the community — in schools, universities, academies, factories, work places, offices, etc. WHO has projected that possibly some 20-30 per cent of the population worldwide will become infected by this novel flu bug, after studying various models of spread of past infections — the huge and very rapid spread worldwide is mainly due to air travel. While older flu pandemics took six months to extend to so many countries, this H1N1 flu did so in less than six weeks!

In the worst-case scenarios of course, this outbreak will be alarming — hospitalisations may be required for 100,000 up to 500,000 Malaysians, with perhaps as many as 5,000 to 27,000 infected patients (depending on the case fatality rate or either 0.1 to 0.5 per cent) succumbing to this illness.

But because we have been monitoring closely and containing the outbreak thus far, with heightened awareness and greater social responsibility, it is possible to ameliorate the infectivity, spread and fatality that will unfortunately accompany this pandemic... Just how successful we will be in limiting these adverse outcomes remains to be seen, but we can be hopeful.

How can the public help? First learn and acquire good personal hygiene. If sick, please be responsible and stay at home, even in your own room where possible, wear a face mask (a cheap three-ply surgical mask will do, because large droplet spread is the main danger). Do not go out, practice what is now known as social distancing (about three metres from anyone), and be socially responsible, don't go to public places and infect others — for young people this would be hard, but absolutely necessary — the spread is most rampant in this age group between 16 and 25 years.

When the illness does not go away after a few days or when you are deteriorating, get to the nearest hospital. Most importantly, be very aware and responsible!

Finally, keep abreast of all new developments, because these are evolving all the time. With keen awareness, prudent care, early detection and social responsibility, correct and prompt use of antiviral and other support medical care, and later mass specific vaccination, we can overcome this novel H1N1 flu! But it will take time, patience, public cooperation, much concerted effort and consume great resources.

Dr David KL Quek is president the Malaysian Medical Association.