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Acne-Treating Antibiotic Cuts Catheter Infections in Dialysis Patients

Newswise — Washington, DC (August 19, 2011) — Antibiotics
can help ward off serious bacterial infections in kidney disease
patients who use tubes called catheters for their dialysis treatments.
But if antibiotics are used too often, “super bugs” may crop up that are
resistant to the drugs.

A new randomized controlled clinical
trial has shown that using an antibiotic that is not usually used to
treat other serious infections may be a safe way to prevent bacterial
infections in dialysis patients. The study, which included approximately
200 dialysis patients,was conducted by Rodrigo Peixoto Campos, MD
(Pontifícia Universidade Católica do Paraná, in Curitiba, Brazil) and
colleagues, and appears in an upcoming issue of the Journal of the American Society Nephrology (JASN), a publication of the American Society of Nephrology.

Between
dialysis treatments, a catheter is “locked” to prevent blood clots from
forming within the device. A lock is usually made by injecting the
blood thinner heparin into the catheter. In this study, researchers
compared heparin use with a solution made up of the antibiotic
minocycline and the chemical EDTA. Minocycline is routinely used only to
treat acne, and EDTA improves the action of antibiotics, fights fungal
infections, and prevents blood clots. Half of patients in the study had
catheter locks containing this combination while the other half had
catheter locks containing only heparin.

Among the major findings:
•Patients were less likely to get a bacterial infection with minocycline-EDTA locks compared to heparin locks.
•During
a 90 day period, bacterial infections developed in the catheters of 19
patients in the heparin group compared with only five patients in the
minocycline-EDTA group.
•The catheters in the two groups functioned similarly well.

“When
a dialysis clinic cannot achieve lower rates of catheter-related
bacterial infections with routine catheter care protocols, the use of a
catheter lock solution of minocycline-EDTA may be the next step to
reduce this major complication, without the apprehension of developing
bacterial resistance to systemic antibiotics,” said Dr. Campos.

Study
co-authors include Marcelo Mazza do Nascimento, MD, PhD (Hospital
Universitário Evangélico de Curitiba, in Curitiba, Brazil); Domingos
Candiota Chula, MD (Clínica de Doenças Renais do Novo Mundo, in
Curitiba, Brazil); and Miguel Carlos Riella, MD, PhD, FACP (Pontifícia
Universidade Católica do Paraná and Hospital Universitário Evangélico de
Curitiba, in Curitiba, Brazil).

Disclosures: The authors reported no financial disclosures.

The
article, entitled “Hemodialysis Catheter-Related Bacteremia Prevention
Using a Locking Solution of Minocycline-EDTA,” will appear online at http://jasn.asnjournals.org/ doi #10.1681/ASN.2010121306

The
content of this article does not reflect the views or opinions of The
American Society of Nephrology (ASN). Responsibility for the information
and views expressed therein lies entirely with the author(s). ASN does
not offer medical advice. All content in ASN publications is for
informational purposes only, and is not intended to cover all possible
uses, directions, precautions, drug interactions, or adverse effects.
This content should not be used during a medical emergency or for the
diagnosis or treatment of any medical condition. Please consult your
doctor or other qualified health care provider if you have any questions
about a medical condition, or before taking any drug, changing your
diet or commencing or discontinuing any course of treatment. Do not
ignore or delay obtaining professional medical advice because of
information accessed through ASN. Call 911 or your doctor for all
medical emergencies

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Cholesterol Drugs can Reduce Stroke Risk, but Aren't for Everyone

Newswise — MAYWOOD, Ill. -- For many patients,
cholesterol-lowering statin drugs can reduce the risk of strokes as well
as heart attacks.

But in a review article, Loyola University
Health System neurologists caution that statins may not be appropriate
for certain categories of patients who are at-risk for stroke.

The article, by Dr. Murray Flaster and colleagues, appears in the August issue of the journal Expert Review of Neurotherapeutics.

A landmark 2006 study known as SPARCL, published in the New England Journal of Medicine,
found that in patients who have experienced strokes or transient
ischemic attacks (mini strokes), statins reduced the risk of subsequent
strokes by 16 percent.

But this benefit generally applies only to
patients who have experienced ischemic strokes, which are caused by
blood clots in brain vessels. About 85 percent of strokes are ischemic.

And
even among ischemic stroke patients, there is a small subgroup that
should be placed on statin therapy only "with circumspection," the
researchers write. These patients are those who have had strokes in
small blood vessels, have poorly controlled high blood pressure and
consume more than one drink of alcohol per day.

The picture is
more varied for the 15 percent of stroke patients who have had
hemorrhagic strokes (caused by bleeding on or in the brain). There are
two types of hemorrhagic stroke: aneurysmal subarachnoid hemorrhage
(SAH) and intracranial hemorrhage (ICH). A SAH stroke involves bleeding
over the surface of the brain, while an ICH stroke involves bleeding
inside the brain.

Statins have been postulated to help recovery in
patients with SAH. While the jury is still out, "the overall evidence
slightly favors a benefit," researchers wrote.

But high-dose
statin therapy "should be avoided as routine therapy in ICH patients
until the competing risks and benefits are better understood," the
researchers wrote.
Complicating matters further, if a patient who is
on statins experiences a SAH or ICH stroke, he or she should remain on
the drugs in the short run. "Reassessment of continuing statin utility
in these patients should be considered immediately after recovery,"
researchers write.
Flaster and colleagues write that more research is needed:
"Clearly,
the potential influences of statins are so broad and mixed and the
potential for effects and counter-effects so likely that both careful
science and detailed clinical investigation, especially well-designed
clinical trials, will be needed to realize and document effective and
safe therapeutic intervention.

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Kidney Drugs Hampered by High Blood Phosphate Levels


Newswise — Washington, DC (August 18, 2011) — High blood phosphate levels can set chronic kidney disease (CKD) patients on a rapid path to kidney failure, according to a study appearing in an upcoming issue of the Journal of the American Society Nephrology (JASN). To make matters worse, phosphate appears to interfere with the effectiveness of important kidney medications.

The kidneys of patients with CKD cannot efficiently get rid of wastes such as excess phosphate in the blood. As a result, the kidneys become overloaded with phosphate. Carmine Zoccali, MD (CNR-IBIM, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension of Reggio Calabria, Italy) and his colleagues wondered how this phosphate overload affects the kidneys of patients with CKD. They also wondered whether phosphate overload alters the effects of ramipril, a drug prescribed to slow the progression of kidney disease. (The use of ramipril and other drugs in its class represents the current standard of care for patients with CKD.)

The researchers studied health information from 331 CKD patients, dividing patients into four groups based on their phosphate levels.

Among the major findings:
•Even though their blood phosphate was still normal or near normal, patients in the two highest phosphate groups progressed more quickly to serious kidney dysfunction or kidney failure than patients with lower phosphate levels.
•Higher phosphate levels blunted ramipril’s benefits.

These results suggest that phosphate levels can predict which CKD patients are in serious trouble of developing kidney failure. They also show that high phosphate levels block the beneficial effects of important kidney medications.

Future studies should test whether reducing phosphate improves kidney health and optimizes patients’ medications. “Our study opens the exciting possibility that reducing phosphate, either by diet or drug treatment, may enhance CKD patients’ response to certain drugs,” said Dr. Zoccali. “If our findings are replicated in a new clinical trial, interventions aimed at reducing phosphate will be a relevant step forward in the fight against these dangerous kidney diseases,” he added.

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Nasal Administration May Enhance Response to Pain Medications

Intranasal Technique Shows Direct Effect of Morphine on Central Nervous System

Newswise
— San Francisco, CA. (August 22, 2011) – A simple new approach to nasal
drug administration may allow morphine and other strong pain
medications to be targeted directly to the central nervous system (CNS),
reports an experimental study in the September issue of Anesthesia & Analgesia, official journal of the International Anesthesia Research Society (IARS).

John
D. Hoekman, Ph.D., and Rodney J.Y. Ho, Ph/D., of University of
Washington, Seattle, developed and tested a new "pressurized olfactory
device" (POD) in experimental animals.  A similar technique used in
humans might provide an effective, noninvasive technique for opioid drug
administration, with the potential for excellent pain control with
fewer side effects and a faster onset of action.

'POD' Shows Direct CNS Effect of Morphine
Drs.
Hoekman and Ho designed the POD to deliver morphine (or other drugs)
with pinpoint precision directly to the olfactory region of the nasal
cavity.  The olfactory region is small and difficult to reach—it makes
up no more than ten percent of the surface area of the human nasal
cavity, and can only be accessed through a one- to two-millimeter slit
in the back of the nasal cavity.  However, its location between the nose
and the brain makes the olfactory region an attractive target for drugs
targeting the CNS. 

Experiments in rats showed significantly
enhanced effects of morphine delivered through the POD.  Unlike other
methods of drug administration, the POD showed evidence of a direct
"nose-to-CNS" transport mechanism.

With POD injection, 38 to 55
percent of the total morphine dose was directly transported to the CNS.
This provided a greater pain-relieving effect, without increasing the
morphine concentration in the blood. 

Experiments also showed
promising results with POD delivery of another powerful analgesic  drug
called fentanyl.  Administered via the POD, fentanyl achieved a faster
and more intense pain-relieving effect, compared to a simple nasal
spray.

Opioid drugs such as morphine and fentanyl are widely
used for pain control—for example, after surgery or for treatment of
severe cancer pain.  Although very effective, these drugs have some
potential side effects and other disadvantages.  For example, morphine
can cause problems with constipation, while fentanyl may act too slowly
for optimal treatment of "breakthrough" cancer pain.

It's not a
new discovery that delivering drugs to the olfactory region can have a
direct "nose-to-CNS" effect.  However, this method of administration is
infrequently used—largely because there's no simple and convenient way
to administer medications directly to the olfactory region.

So
far, the POD is just a preliminary concept—it has yet to be tested in
humans.  However, the promising results suggest that a similar device
for direct "nose-to-CNS" drug delivery might provide a simple new
approach to maximizing the response to morphine and fentanyl, while
avoiding disadvantages like side effects and delays to pain relief.

"Intranasal
delivery of drugs to the CNS bypasses the barrier of the systemic
circulation as well as the blood-brain barrier," comments Dr. Steven L.
Shafer of Columbia University, Editor-in-Chief of Anesthesia &
Analgesia. 
'There may be benefits of administering opioids
intranasally, but the rapid pain relief has to be balanced against the
risks inherit with a rapid onset of respiratory depression."

Although
the POD concept is relatively simple, it could lead to the development
of new types of pain medications, Dr. Shafer believes.  "This technology
is particularly exciting with molecules such as small peptides and
biologic agents, which are so rapidly destroyed in the blood that they
are ineffective if given orally or intravenously.  Intranasal delivery
may create an opportunity for the introduction of entirely new classes
of pain killers that could not be effectively administered by
traditional methods."

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Cholesterol-Lowering Drug May Help to Prevent Surgery-Related Spinal Cord Damage

Could Statins Help to Reduce Paraplegia Risk after Aortic Surgery?

Newswise
— San Francisco, CA. (August 22, 2011) – The cholesterol-lowering drug
simvastatin appears to reduce spinal cord injury caused by oxygen
deprivation in experimental animals, according to a study in the
September issue of Anesthesia & Analgesia, official journal of the International Anesthesia Research Society (IARS).

With
further research, treatment with statin drugs might provide a new
approach to lowering the risk of paraplegia as a complication of surgery
involving the aorta, the new research suggests.  The experimental study
was led by Takeshi Saito, Ph.D., of Nigata University Graduate School
of Medical and Dental Sciences, Japan.

Simvastatin Reduces Spinal Cord Damage from Ischemia/Reperfusion Injury
The
researchers used a standard technique to produce spinal cord damage due
to oxygen deprivation in laboratory rats.  This technique simulates a
serious complication that can occur in patients undergoing major surgery
involving the aorta, such as surgery to repair an aortic aneurysm.  In
this situation, temporary interruption of blood supply
(ischemia/reperfusion injury) can lead to spinal cord injury and
paraplegia.

In the experiments, rats received either simvastatin
or an inactive treatment for one week before interruption of blood
supply to the spinal cord, plus an additional dose 24 hours after blood
flow was restored.  Signs of spinal cord damage and paraplegia were
compared between the two groups.

After 24 and 48 hours, movement
of the rear limbs was significantly better in rats treated with
simvastatin.  The limb motion abnormality caused by ischemia/reperfusion
injury was reduced by about half in statin-treated animals, compared to
those receiving inactive treatment.

Follow-up examination of spinal cord specimens showed less cellular damage in the simvastatin group.

Spinal
cord damage resulting in paraplegia is a potential risk of aortic
surgery.  Several different strategies have been tried to prevent this
devastating complication, with limited success.

Recent studies
have suggested that statin drugs —widely used to lower cholesterol
levels—can protect the brain from damage caused by oxygen deprivation. 
This raises the possibility that statins might have a similar
"neuroprotective" effect against spinal cord damage caused by
ischemia/reperfusion injury.

The new experiments suggest that
simvastatin protects against spinal cord damage caused by
ischemia/reperfusion injury in rats, in a situation similar to that
caused by aortic surgery in humans.  It's unclear exactly how
simvastatin exerts its neuroprotective effect—possibly through
suppression of harmful substances released in response to oxygen
deprivation.  More research will be needed to see if statin drugs have
any protective effect against spinal cord injury and paraplegia in
patients undergoing aortic surgery.

"Spinal cord injury is among
the most devastating complications of major vascular surgery," comments
Dr. Steven L. Shafer of Columbia University, Editor-in-Chief of
Anesthesia & Analgesia.  "Although this result is very preliminary,
it opens up a new approach to cord protection. If the result is
reproducible in larger animals, then clinical trials should be conducted
to establish safety and efficacy for patients undergoing aortic
repair."

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Could a Tumor Suppressor also Fight Obesity?

Newswise — PHILADELPHIA—The hormone receptor guanylyl
cyclase C (GCC) has been established as a suppressor of colorectal
cancer tumors, but new evidence from Thomas Jefferson University suggests it may also help fight one of the country’s biggest pandemics: obesity.

Reporting in the August 25 online issue of the Journal of Clinical Investigation, Scott Waldman, M.D., Ph.D., chairman of the Department of Pharmacology and Experimental Therapeutics
at Jefferson, and colleagues found that silencing GCC affected appetite
in mice, disrupting satiation and inducing obesity. Conversely, mice
who expressed the hormone receptor knew when to call it quits at
mealtime.

Revealing a never-before-shown endocrine axis between
the intestine and hypothalamus, the research could provide novel
therapeutic targets to control appetite, obesity and the metabolic
syndrome, a promising notion, given that one-third of the U.S.
population is considered obese.

Until now, the role of GCC outside
the gut has remained elusive. Dr. Waldman and his team have previously
shown its role as a tumor suppressor and biomarker that reveals occult
metastases in lymph nodes. But its role in appetite is new and
surprising territory.

“We were working with GCC-deficient mice to
look at its role in tumorigenesis in the intestine,” said Dr. Waldman. 
“Then the mice grew up, and we noticed something: They got fatter.

“We
couldn’t understand why it was happening, because GCC is expressed
predominantly in intestine, and there was no indication that it
regulated any function that had to do with metabolism and nutrient
uptake.”

To investigate this, Dr. Waldman, who also leads the Gastrointestinal Malignancies Program at the Kimmel Cancer Center
at Jefferson. and his colleagues raised both GCC mice and GCC deficient
mice, tracking their weight, satiation responses, hepatic and serum
triglyceride measurements, hormone receptor expression, and physical
activity.

When food was digested by the mice, they found, the gut
released hormones into the blood stream, not just within the
intestines, and up into the brain, where the hormone receptors were
triggered. Mice with GCC knew when to stop, but hormone
receptor-deficient mice never got the message that their stomachs were
full. They simply kept eating and became obese.

“They got to be
diabetic and developed the metabolic syndrome, fatty livers, etc.” Dr.
Waldman said. “We ruled out usual suspects: gastroenterology function
was normal. They weren’t more sedentary than wild type mice. And they
did not have abnormal metabolism. We realized they just have a different
appetite.”

The research offers up a new neural-gut axis that
explains appetite more, but it still begs some questions: Do obese
people possess little to no GCC? And if so, does that mean obese people
have a genetic disposition to gain weight?

It’s possible, said
Dr. Waldman, but it’s still unclear. There is the possibility that obese
people do not have the receptor or they do not release enough hormones
to trigger the receptor. More studies are needed to better explain this,
he added.

“Obesity could be biological, and not behavioral,” said
Dr. Waldman. “But there is no evidence here that confirms that;
however, knowing this new information opens that possibility.”

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Dendritic Cells in Liver Protect Against Acetaminophen Toxicity

Newswise — NYU School of Medicine researchers have discovered that dendritic cells in the liver have a protective role against the toxicity of acetaminophen, the widely used over-the-counter pain reliever and fever reducer for adults and children. The study’s findings are published in the September issue of the journal Hepatology.

The liver is the organ that plays a central role in transforming and filtering chemicals from the body.
High-doses of acetaminophen can cause hepatotoxicity, chemical driven liver damage. In fact, accidental and intentional acetaminophen overdose are the most frequent causes of acute liver failure (ALF) in the United States. Acetaminophen related liver failure by intentional or accidental overdose causes 56,000 emergency room visits, 2,600 hospital visits and 450 deaths annually. As a result, this year the FDA mandated drug manufacturers to start limiting the amount of acetaminophen in combination drug products and is currently exploring adding safer dosing instructions to children’s acetaminophen products.

In the new study, researchers found an abundance of dendritic cells in the liver can protect the organ from acetaminophen damage while low levels of dendritic cells in the liver are associated with exacerbated liver damage, liver cell and tissue death, known as centrilobular hepatic necrosis, and acute liver failure from acetaminophen.

“Our research results confirm a central role for dendritic cells and their powerful regulation of acetaminophen’s toxicity,” said George Miller, MD, senior author of study and assistant professor, Departments of Surgery and Cell Biology at NYU Langone Medical Center. “High levels of dendritic cells have a novel, critical and innate protective role in acetaminophen hepatotoxicity. We now have greater insight into the liver’s tolerance of acetaminophen toxicity and dendritic cell regulation of these toxins.”

In the study, researchers used acetaminophen-induced hepatic injured mice models to closely examine the protective role of dendritic cells. Dendritic cells are the main antigens in the liver that trigger an immune response and control the liver’s tolerance to high doses of invading toxins like acetaminophen. In the experiment all mice were injected with acetaminophen but some mice models were first depleted of dendritic liver cells using a diphtheria toxin while others had their dendritic cell levels bolstered with Flt3L, a protein in the blood previously shown to increase proliferation of dendritic cell levels.

Researchers discovered dendritic cell depletion exacerbates acetaminophen’s damage to the liver. The acetaminophen treated mice with depleted dendritic cells had more extensive liver cell and tissue death compared to other mice. Also, these mice died within 48 hours of acetaminophen challenge- whereas death was rare in other mice without dendritic cell depletion. In addition, the study shows dendritic cell expansion successfully diminished the hepatotoxic effects of acetaminophen protecting the liver from damage.

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Bananas Vs. Asthma

Newswise — Going bananas may help kids breathe easier. Children who ate just one banana a day had a 34% less chance of developing asthmatic symptoms, according to new British research.

The Imperial College of London collected dietary information from 2,640 children, ages 5 to 10, and found that banana-eaters were one-third less likely to encounter breathing problems like wheezing. Children who drank apple juice daily experienced a 47% reduction. Other research suggests that children with low fiber intake are more vulnerable to the respiratory problems associated with secondhand smoke. The pineapple enzyme, bromelain, also appeared to reduce the inflammation associated with asthma in one animal trial.

These results offer yet more proof of the potential of food to affect asthma symptoms for better...or for worse. As previously reported in this space, kids who eat even one burger a week are more likely to suffer from asthma.

Banana Bonus: Early banana consumption may also be associated with lower risk of childhood leukemia. Bananas' fiber, potassium, vitamin C and B6 content support heart health. Bananas also contain tryptophan, an amino acid which may play a role in preserving your memory and boosting your mood. To get the health benefits of bananas try this issue's featured recipe.

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What are Antioxidants and Why Do You Need Them?


Newswise — IFT Member Claudia Fajardo-Lira, PhD, Professor of Food Science and Nutrition at California State University-Northridge, explains the facts about antioxidants:

Q: What are antioxidants?

A: Antioxidants play an important role in overall health. They are natural compounds found in some foods that help neutralize free radicals in our bodies. Free radicals are substances that occur naturally in our bodies but attack the fats, protein and the DNA in our cells, which can cause different types of diseases and accelerate the aging process.

Q: What foods are the best sources for antioxidants?

A: The best antioxidant sources are fruits and vegetables, as well as products derived from plants. Some good choices include blueberries, raspberries, apples, broccoli, cabbage, spinach, eggplant, and legumes like red kidney beans or black beans. They’re also found in green tea, black tea, red wine and dark chocolate. Usually, the presence of color indicates there is a specific antioxidant in that food.

The keyword here is variety. Try to get as many fruits and vegetables with different colors when you plan your meals and go to the grocery store. An array of color in your diet will give you the widest range of beneficial antioxidants.

Q: Does it matter whether the produce is cooked or consumed raw?

A: Depending on the particular food, cooking temperatures and methods can sometimes increase or decrease antioxidant levels. The important thing is that you eat antioxidant-rich foods, so go with your personal preference for preparation—as long as it's not deep frying!

Q: Are added antioxidants as effective as those that occur naturally?

A: Yes, vitamins such as C, A and E can be added to foods – and they often are, such as in orange juice. One of the things those additives do is act as antioxidants in the body. There is no significant physiological difference between the added antioxidants and the ones occurring naturally in the food source. However, there’s also no evidence that taking antioxidant dietary supplements work as well as the antioxidants found in food products. It’s important not to overdo it on supplements because there can be too much of a good thing. With food products, it would be extremely difficult to consume an excessive amount of antioxidants.

Q: Is there a specific amount of antioxidants consumers should aim for each day?

A: There is not a set recommended daily allowance (RDA) for antioxidants, but the new MyPlate tool based on the Dietary Guidelines for Americans recommends that you make half your plate fruits and vegetables. If you aim to do that at most meals, you can be sure to get the antioxidants you need.

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الأنسولين يساعد في علاج الزهايمر

يعكف فريق من الباحثين على إجراء المزيد من البحوث على الأنسولين كعلاج محتمل لمرض الزهايمر بعد أن بينت دراسة أولية أن للدواء المستخدم لمرضى السكرى نتائج واعدة.

وقالت الدراسة التي نشرت في دورية أرشيف علم الأعصاب إن تناول الإنسولين عبر الأنف قد يساعد في زيادة الإدراك بين المرضى ممن يعانون درجات متفاوتة من العته من حالات معتدلة أو أكثر حدة بيد أنها شددت على أنه من السابق لأوانه النظر للأنسولين كعلاج للزهايمر لمحدودية البحث الذي شمل 104 مرضى فقط.

وقال القائمون على البحث إنه بحاجة للمزيد من التمحيص والمزيد من الاختبارات حوله بتضمين عدد أكبر من المشاركين لتحديد مدى فعالية الأنسولين رغم أنها مهدت الطريق للمزيد من الأبحاث السريرية الواسعة.

وأوضحت سوزن كرافت أستاذة طب النفس بجامعة واشنطن إن الأنسولين يلعب دوراً مهماً في عدد من وظائف المخ فإلى جانب تنظيمه معدل السكر بالدم فإنه يحفز على تجديد الخلايا وخلايا المنشأ ويدعو للاعتقاد بأنه قد يعدل مسار مرض الزهايمر.

وخلال الدراسة قام الباحثون بإجراء اختبارات على مرضى الزهايمر في مراحله الأولية وآخرين يعانون من نسبة متوسطة من العته باستخدام جهاز صمم لنقل الأنسولين من الأنف إلى المخ وتفادي ضخ الكثير منه إلى الدم وذلك بمحاولة إمداد وتطبيع معدلاته في المخ دون التأثير على نسبته في بقية الجسم.

وأشار الباحثون الى أن المرضى ممن ضخت إليهم جرعات من الأنسولين عبر المخ تحسنت بينهم القدرة على تذكر المعلومات بواقع 20 بالمئة كما أنه عزز أيضاً الجلوكوز في بعض مناطق الدماغ.

وقالت كرافت ان للعلاج بالأنسولين عبر الأنف أعراضا جانبية بسيطة كالإصابة أحياناً بنوبات صداع طفيف وسيلان الأنف إلا أنها أكدت سلامة العلاج إجمالاً.