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Thursday 24, Nov 2011

  Brain development affected by steroids in premature babies

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A study has confirmed that powerful steroids can affect brain development in premature babies.

Researcher Emily Tam, MD, of the University of California-San Francisco explains that animal studies found that the steroids called glucocorticoids affect a certain part of the brain.

From Voanews.com:

“The cerebellum is particularly targeted, resulting in cell death and decreased cell growth,” Tam says. “And so, the question then is, is this same thing happening in humans?”

The cerebellum is involved in motor control and some cognitive functions, among other things, so it plays a critical role in an infant’s first years.

In a study, which was published in Science Translational Medicine, 172 premature babies born in the United States and Canada got MRI scans to measure their cerebellums. Tam says researchers found no adverse affects from steroids given to the pregnant mothers before birth.

“On the other hand,” Tam says, “we did find that when hydrocortisone and dexamethasone were given after the child was born, this was associated with decreased growth of cerebellum. So by term age, the cerebellum was 10 percent smaller that it should have been.”

Tuesday 08, Nov 2011

  Harm to brain when steroids are given to premature infants

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Preterm infants who are treated with glucocorticoids could be at a growing risk for damage to the cerebellum in the brain, according to a recent study by scientists from the University of California.

Glucocorticoids are usually administered to premature infants to facilitate lung maturation and normalization of breathing and blood pressure.

From Healthjockey.com:

Emily Tam, MD, a child neurologist in the Neurological Intensive Care Nursery at the UCSF Benioff Children’s Hospital and lead author of the study, remarked, “This study provides new evidence that these drugs, even at low doses, are associated with impaired cerebellar development when given to babies after birth.”

Initial studies have linked smaller cerebellum volumes of premature children to cognitive and motor disorders as they reach young adulthood. In order to test the effects of glucocorticoids, nearly 172 premature babies were examined. Around 85% of them had received betamethasone before birth and almost 20% of them were given hydrocortisone or dexamethasone after birth.

The study, ‘Preterm Cerebellar Growth Impairment After Postnatal Exposure to Glucocorticoids’, is published in the journal Science Translational Medicine.

Thursday 28, Oct 2010

  Potential treatment option for osteonecrosis discovered

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Potential treatment for osteonecrosis identifiedResearchers from Mount Sinai School of Medicine have been able to identify a potential treatment for the death of bone tissue or osteonecrosis.

The health complication is noticed among people administered with steroids to treat different medical conditions; there is no treatment option, at present, to provide relief to patients afflicted with this complication.

From Sciencedaily.com:

Glucocorticoids cause reduced blood flow to bone cells in the hip, resulting in cell death, and ACTH reduces these devastating side effects. However, research indicates that osteonecrosis is not significant in people in which steroid levels are high in the blood. Dr. Zaidi’s team knew that these tumors produce excess ACTH, and this spurred the team to evaluate the ACTH’s potential therapeutic effect.

The researchers injected one group of rabbits with depomedrol, a type of steroid, and another group with depomedrol plus ACTH. Osteonecrosis was dramatically reduced in the rabbits that were treated with ACTH. Dr. Zaidi’s team found that ACTH stimulates the vascular endothelial growth factor (VEGF), a protein that signals for the growth of new blood vessels. The stimulation of VEGF results in increased blood flow to the bone cells, preventing cell death.

“The results confirm that ACTH may be of value as a drug to prevent osteonecrosis,” said Dr. Zaidi. “While more research is required, we hope to someday evaluate the efficacy of ACTH in treating osteoporosis as well.”

The research was published in the April 27 issue of Proceedings of the National Academy of Sciences.

Saturday 21, Aug 2010

  Obese asthmatic patients fail to benefit from steroids

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Obese asthmatic patients fail to benefit from steroidsThe primary controller medication for asthma, glucocorticoids, is 40 percent less effective in obese and overweight asthmatic patients when compared to patients with normal weight, according to researchers at National Jewish Health.

A long-term study was initiated by Dr. Sutherland and his colleagues for evaluating the clinical effects of steroid resistance among overweight and obese asthma patients and further clarifying the signaling pathways involved.

From Sciencedaily.com:

The study at National Jewish Health sought to understand why glucocorticoids, commonly called steroids, might be less effective in overweight and obese asthma patients. Dr. Sutherland and his colleagues enrolled 45 nonsmoking adults, 33 of whom had asthma, and measured the response of cells in the blood and the lungs to the steroid dexamethasone.

Steroids interfere with inflammatory signaling pathways by raising the level of a molecule known as MAP kinase phosphatase-1 (MKP-1). When the researchers applied the steroid dexamethasone to cultures of the participants’ blood cells, they found that steroids did not increase MKP-1 as effectively in overweight and obese asthmatics when compared to lean asthmatics. Dexamethasone increased the levels of MKP-1 by 5.27 times in cultured blood cells from lean asthma patients, whereas MKP-1 levels in overweight and obese asthmatics increased by only 3.11 times, a 41 percent smaller response. The heavier a person was the less their cells were likely to respond to dexamethasone. This negative relationship between weight and response to steroids did not occur in participants who did not have asthma.

The study by Associate Professor of Medicine E. Rand Sutherland, MD, MPH and his colleagues at National Jewish Health, appeared in an issue of the American Journal of Respiratory and Critical Care Medicine.

Friday 20, Aug 2010

  Potential bone death treatment in the hip from osteonecrosis

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Potential bone death treatment in the hip from osteonecrosisA potential treatment for the death of bone tissue or osteonecrosis has been identified by researchers at Mount Sinai School of Medicine.

This complication is seen in people administered with steroids for varying medical conditions and there is no treatment option at present to deal with this debilitating disease.

From Sciencedaily.com:

Glucocorticoids cause reduced blood flow to bone cells in the hip, resulting in cell death, and ACTH reduces these devastating side effects. However, research indicates that osteonecrosis is not significant in people in which steroid levels are high in the blood. Dr. Zaidi’s team knew that these tumors produce excess ACTH, and this spurred the team to evaluate the ACTH’s potential therapeutic effect.

The researchers injected one group of rabbits with depomedrol, a type of steroid, and another group with depomedrol plus ACTH. Osteonecrosis was dramatically reduced in the rabbits that were treated with ACTH. Dr. Zaidi’s team found that ACTH stimulates the vascular endothelial growth factor (VEGF), a protein that signals for the growth of new blood vessels. The stimulation of VEGF results in increased blood flow to the bone cells, preventing cell death.

“The results confirm that ACTH may be of value as a drug to prevent osteonecrosis,” said Dr. Zaidi. “While more research is required, we hope to someday evaluate the efficacy of ACTH in treating osteoporosis as well.”

The research was published in the April 27 issue of Proceedings of the National Academy of Sciences.

Saturday 29, May 2010

  Obese asthmatic patients do not benefit from steroids like others

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Obese asthmatic patients do not benefit from steroids like othersGlucocorticoids, the primary controller medication for asthma, are 40 percent less effective in obese and overweight asthma patients than in asthmatic patients with normal weight. This finding was disclosed by researchers at National Jewish Health.

The study, by Associate Professor of Medicine E. Rand Sutherland, MD, MPH and his colleagues at National Jewish Health, appeared in an issue of the American Journal of Respiratory and Critical Care Medicine.

From Medicalnewstoday.com:

The study at National Jewish Health sought to understand why glucocorticoids, commonly called steroids, might be less effective in overweight and obese asthma patients. Dr. Sutherland and his colleagues enrolled 45 nonsmoking adults, 33 of whom had asthma, and measured the response of cells in the blood and the lungs to the steroid dexamethasone.

Steroids interfere with inflammatory signaling pathways by raising the level of a molecule known as MAP kinase phosphatase-1 (MKP-1). When the researchers applied the steroid dexamethasone to cultures of the participants’ blood cells, they found that steroids did not increase MKP-1 as effectively in overweight and obese asthmatics when compared to lean asthmatics. Dexamethasone increased the levels of MKP-1 by 5.27 times in cultured blood cells from lean asthma patients, whereas MKP-1 levels in overweight and obese asthmatics increased by only 3.11 times, a 41 percent smaller response. The heavier a person was the less their cells were likely to respond to dexamethasone. This negative relationship between weight and response to steroids did not occur in participants who did not have asthma.

Steroids were clearly less effective in overweight and obese asthma patients,” said Dr. Sutherland. “Previous studies have suggested a link between weight and response to steroids in patients, and this study suggests a potential mechanism by which this occurs. It also suggests that future research should be directed specifically to understanding how asthma medications work in overweight and obese asthmatics.

It was remarked that inhaled steroids are still effective in treating overweight and obese asthmatics.

Tuesday 18, May 2010

  Potential treatment for osteonecrosis identified

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Potential treatment for osteonecrosis identifiedA potential new treatment for death of bone tissue or osteonecrosis has been identified by researchers at Mount Sinai School of Medicine. This form of treatment is in context to individuals who are treated with steroids for different common medical disorders.

Presently, there are no treatment options for people affected with this debilitating disease.

From Sciencedaily.com:

Osteonecrosis is a very painful condition that has the potential to affect hundreds of thousands of Americans who are treated with steroids, with no treatment option until now except hip replacement,” said Dr. Zaidi. “Our research is the first to show the therapeutic benefit of ACTH in experimental osteonecrosis, providing the first treatment option for these patients.”

Glucocorticoids cause reduced blood flow to bone cells in the hip, resulting in cell death, and ACTH reduces these devastating side effects. However, research indicates that osteonecrosis is not significant in people in which steroid levels are high in the blood. Dr. Zaidi’s team knew that these tumors produce excess ACTH, and this spurred the team to evaluate the ACTH’s potential therapeutic effect.

The researchers injected one group of rabbits with depomedrol, a type of steroid, and another group with depomedrol plus ACTH. Osteonecrosis was dramatically reduced in the rabbits that were treated with ACTH. Dr. Zaidi’s team found that ACTH stimulates the vascular endothelial growth factor (VEGF), a protein that signals for the growth of new blood vessels. The stimulation of VEGF results in increased blood flow to the bone cells, preventing cell death.

“The results confirm that ACTH may be of value as a drug to prevent osteonecrosis,” said Dr. Zaidi. “While more research is required, we hope to someday evaluate the efficacy of ACTH in treating osteoporosis as well.”

The research was published in the April 27 issue of Proceedings of the National Academy of Sciences.

Sunday 02, May 2010

  Intravenous Immunoglobulin minimizes insensitivity to steroids

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Intravenous Immunoglobulin minimizes insensitivity to steroidsPeople suffering from severe asthma and insensitive to steroids require less of the medication and spend less time in the hospital when compared with those using intravenous immunoglobulin (IVIG) in conjunction with steroids. This finding was disclosed by a research published in the Journal of Allergy and Clinical Immunology.

Researchers were of the view that IVIG increases the sensitivity of the lungs to steroids in part by minimizing lung inflammation.

From Sciencedaily.com:

While steroid-insensitive patients must take higher doses to achieve minimal control of their disease, they also may become dependent on the medication to breathe normally. Researchers found that by taking IVIG in conjunction with glucocorticoids, patients could use less glucocorticoids more efficiently.

Long-term use of glucocorticoids can stunt growth in children or cause osteoporosis, while IVIG has few side effects. “Compared to steroids, IVIG is not toxic at all,” Dr. Gelfand said. “In addition, lowering the amount of steroids a patient takes reduces side effects and the patient’s quality of life improves dramatically.”

IVIG treatments cost several thousand dollars each month for people with severe asthma, but many health insurance companies cover the cost because, as this study shows, IVIG lowers emergency room and hospital use by patients with severe asthma. Glucocorticoids reduce inflammation in the lungs. IVIG is an antibody that is removed from the plasma portion of blood and is concentrated for use as a medication. IVIG can regulate the immune/inflammatory system and has been shown to reduce inflammation in the lungs.

Erwin Gelfand, M.D., a pediatric immunology and asthma specialist and chair of the Department of Pediatrics at National Jewish Medical and Research Center, said he has noticed asthmatic patients who required high doses of steroids in order to control the disease.

Friday 23, Apr 2010

  Interference with vagal nerve activity prevents hypertension and diabetes in mice

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Interference with vagal nerve activity prevents hypertension and diabetes in mice  According to scientists at Washington University School of Medicine in St. Louis, diabetes and hypertension in mice can be prevented by interrupting nerve signals to the liver. The finding was reported in an issue of the journal Cell Metabolism.

Clay F. Semenkovich, M.D., professor of medicine and of cell biology and physiology, said that interrupting vagal nerve signaling can prevent the development of hypertension and diabetes at least in mice.

From Sciencedaily.com:

Previously, the research team had shown that a nuclear receptor called PPAR-alpha (Ppara) was necessary for the induction of both diabetes and hypertension when mice were treated with glucocorticoids, also known as steroids.

“Mice that can’t make Ppara don’t develop diabetes or hypertension in response to glucocorticoids,” says Semenkovich, who also is chief of the Division of Endocrinology, Metabolism and Lipid Research. “The use of steroids is very common in medicine. People with asthma, arthritis, organ transplants and others rely on those steroid drugs, and many of them go on to develop insulin resistance that can advance to diabetes and hypertension.”

But in these most recent experiments, the researchers showed that both Ppara and the vagus nerve seem to play important roles in the development of these disorders.

“If the vagus nerve has been surgically removed, the mice won’t develop diabetes or hypertension in response to glucocorticoids, even if they have Ppara,” says first author Carlos Bernal-Mizrachi, M.D., an assistant professor of medicine in the Division of Endocrinology, Metabolism and Lipid Research. “The process seems to be mediated by communication between the liver cells, the liver branch of the vagus nerve and its signals to the brain.”

Semenkovich remarked that he is not sure as of now if this works for humans but expect that alteration of vagal nerve activity can offer a novel approach to treat the common metabolic disorders.

Thursday 22, Apr 2010

  Post-traumatic stress reversible with steroids

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Post-traumatic stress reversible with steroidsHuman body’s own natural stress hormone can help in reducing the fearful response associated with reliving a traumatic memory, according to researchers at UT Southwestern Medical Center, working with mice.

Dr. Craig Powell, senior author and assistant professor of neurology and psychiatry at UT Southwestern, said corticosterone tends to enhance new memories that compete with the fearful memory to reduce its negative emotional significance.

From Sciencedaily.com:

“We’re not erasing memories,” said Dr. Robert Greene, professor of psychiatry at UT Southwestern and another author of the study. “What the steroid does is attenuate the fear memory by helping the mice to learn that these contexts should no longer be perceived as dangerous.”

The study is being published online and in the Sept. 13 issue of the Journal of Neuroscience.

While other researchers have tested such steroids clinically with some success for patients with disorders of emotional memories such as post-traumatic stress disorder (PTSD) and phobias, those studies did not control for a number of variables and were not designed to address the mechanism of the drug’s action, Dr. Greene said.

This study focused on a mechanism called extinction, in which a memory gradually diminishes, but can be re-established by a small reminder of the original event.

“Our studies show that glucocorticoids work specifically to enhance the extinction of fear memory, as opposed to other mechanisms affecting recall, such as eliminating the memory entirely,” said Dr. Greene. “This provides a proof of principle, and is an essential step in advancing this therapeutic approach.”

The work was supported by the National Institute of Mental Health, the Conte Center, the National Alliance for Research on Schizophrenia and Depression, and the Department of Veterans Affairs.

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