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Experts reflect on the past, present and future of diabetes

Over r the past 50 years, treatment and outcomes for diabetes have changed dramatically. At a recent symposium, experts looked back at how lives have changed over the past 5 decades and what remains to be addressed over the next 5.

The symposium was held at the American Diabetes Association's (ADA) 75th Scientific Sessions.

"There are things that have happened over the past 50 years that clearly make life a lot better for people," says Dr. Fred Whitehouse, of the Henry Ford Health System in Detroit, MI. "There's been a lot of change, most of it for the better, but what people want is a cure and we don't have that yet."

Dr. Whitehouse has overseen many changes in how people with diabetes have been treated. When he first started treating people with the condition, the only form of treatment was the injection of animal insulin, obtained from cows or pigs, which could sometimes cause adverse reactions.

Nowadays, human insulin is used, produced by microorganisms and delivered through a variety of different systems including insulin pumps. There are now fewer adverse reactions and no fear of supplies running out, Dr. Whitehouse says, with methods of delivery that are more accurate than ever before.

Glucose levels can also be tracked more accurately. Previously, diabetes control could only be assessed by analyzing the levels of sugar in urine. There are many more options available to patients now, including the noninvasive A1C test that measures average levels over 3 months, "showing whether a person is on the right road or not," states Dr. Whitehouse.

As methods for treating and tracking the disorder have improved for patients, so too has the collective understanding of diabetes shared by researchers and clinicians. It takes a long time for research to make a clinical impact and recent years have seen the results of 50 years of hard work.

Dr. Daniel Porte, Jr., a professor at the University of California-San Diego, describes one of the most recent discoveries in the field:

"This year, amazingly enough to me, it was discovered that insulin sent to the central nervous system not only feeds back to the brain, it also affects glucose production. It regulates the islet cells, so there is a complete integration of the endocrine system and the nervous system. It took 40 years to discover this."

Originally, the endocrine and nervous systems were believed to function completely independently of each other, with glucose the sole regular of insulin.

In 50 years, 'complications of diabetes should become historical memories'

Dr. Porte states that with diabetes research, it is crucial to be patient. "For example, the drugs we use now to treat diabetes were first studied 30 to 40 years ago. And there are many more than the one or two that were being used back in the 1970s."

Such research not only leads to an improved understanding of diabetes but of other conditions as well. "We now believe that perhaps impaired insulin action in the central nervous system leads to the behavioral changes we see in Alzheimer's patients," Dr. Porte explains.

Dr. Michael Brownlee, associate director for biomedical sciences at the Albert Einstein College of Medicine's Diabetes Research Center in New York City, NY, states that diabetes is such a serious health problem due to its complications. His research on the mechanisms that cause complications such as eye and kidney disease has led to great change.

"Prior to the Diabetes Control and Complications Trial (DCCT) study that was published [in 1993], the general dogma was that diabetes caused both metabolic changes and complications, which had nothing to do with each other. They were just two parallel manifestations of the disease," he says.

"Now it's known that prolonged high glucose levels increase the risk for eye and kidney complications associated with diabetes, and maintaining tighter control of blood glucose levels reduces that risk."

Although the landscape of diabetes treatment and research has changed radically over the past 50 years, physicians are still only able to manage the disease rather than cure it. Dr. Robert Ratner, chief scientific & medical officer for the ADA, outlines what needs to be done:

"The next 50 years must elucidate the mechanisms by which both type 1 and type 2 diabetes occur, along with those critical steps at which we might intervene to prevent disease. Treatments must provide optimal glucose and metabolic control, without the risk of hypoglycemia, and complications of diabetes should become historical memories."

If research and treatment can progress at the same rate over the next 5 decades as it has over the past 5, who is to say what can be accomplished?

Tomado de McIntosh, J. (2015, June 8). "Experts reflect on the past, present and future of diabetes." Medical News Today. Retrieved from

http://www.medicalnewstoday.com/articles/295011.php.

Teen cannabis users have poor long-term memory in adulthood

Teens who were heavy marijuana users -- smoking it daily for about three years -- had an abnormally shaped hippocampus and performed poorly on long-term memory tasks, reports a new study. The hippocampus is important to long-term memory, which is the ability to remember life events. The brain abnormalities and memory problems were observed during the individuals' early twenties, two years after they stopped smoking marijuana.

Teens who were heavy marijuana users -- smoking it daily for about three years -- had an abnormally shaped hippocampus and performed poorly on long-term memory tasks, reports a new Northwestern Medicine study.

The hippocampus is important to long-term memory (also known as episodic memory), which is the ability to remember autobiographical or life events.

The brain abnormalities and memory problems were observed during the individuals' early twenties, two years after they stopped smoking marijuana.

Young adults who abused cannabis as teens performed about 18 percent worse on long-term memory tests than young adults who never abused cannabis.

"The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said senior author Dr. John Csernansky, the Lizzie Gilman professor and chair of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine and Northwestern Memorial Hospital.

The study will be published March 12 in the journal Hippocampus.

The study is among the first to say the hippocampus is shaped differently in heavy marijuana smokers and the different looking shape is directly related to poor long-term memory performance. Previous studies of cannabis users have shown either the oddly shaped hippocampus or poor long-term memory but none have linked them.

Previous research by the same Northwestern team showed poor short-term and working memory performance and abnormal shapes of brain structures in the sub-cortex including the striatum, globus pallidus and thalamus.

"Both our recent studies link the chronic use of marijuana during adolescence to these differences in the shape of brain regions that are critical to memory and that appear to last for at least a few years after people stop using it," said lead study author Matthew Smith, assistant professor of psychiatry and behavioral sciences at the Feinberg School of Medicine.

The longer the individuals were chronically using marijuana, the more abnormal the shape of their hippocampus, the study reports. The findings suggest that these regions related to memory may be more susceptible to the effects of the drug the longer the abuse occurs.

The abnormal shape likely reflects damage to the hippocampus and could include the structure's neurons, axons or their supportive environments.

"Advanced brain mapping tools allowed us to examine detailed and sometimes subtle changes in small brain structures, including the hippocampus," said Lei Wang, also a senior study author and an assistant professor of psychiatry and behavioral sciences at Feinberg. The scientists used computerized programs they developed with collaborators that performed fine mappings between structural MRIs of different individuals' brains.

Subjects took a narrative memory test in which they listened to a series of stories for about one minute, then were asked to recall as much content as possible 20 to 30 minutes later. The test assessed their ability to encode, store, and recall details from the stories.

The groups in the study started using marijuana daily between 16 to 17 years of age for about three years. At the time of the study, they had been marijuana free for about two years. A total of 97 subjects participated, including matched groups of healthy controls, subjects with a marijuana use disorder, schizophrenia subjects with no history of substance use disorders, and schizophrenia subjects with a marijuana use disorder. The subjects who used marijuana did not abuse other drugs.

The study also found that young adults with schizophrenia who abused cannabis as teens performed about 26 percent more poorly on memory tests than young adults with schizophrenia who never abused cannabis.

In the U.S., marijuana is the most commonly used illicit drug, and young adults have the highest -- and growing -- prevalence of use. Decriminalization of the drug may lead to greater use. Four states have legalized marijuana for recreational use, and 23 states plus Washington D.C. have legalized it for medical use.

Because the study results examined one point in time, a longitudinal study is needed to definitively show if marijuana is responsible for the observed differences in the brain and memory impairment, Smith said.

"It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Smith said. "But evidence that the longer the participants were abusing marijuana, the greater the differences in hippocampus shape suggests marijuana may be the cause."

Other Northwestern authors include senior author Hans C. Breiter and coauthors Derin J. Cobia, James L. Reilly, Andrea G. Roberts and Kathryn I. Alpert.

The study was funded by the National Institute of Mental Health of the National Institutes of Health, grants R01 MH056584 and P50 MH071616.

Tomado de:Northwestern University. (2015, March 12). Teen cannabis users have poor long-term memory in adulthood. ScienceDaily. Retrieved May 19, 2015 from www.sciencedaily.com/releases/2015/03/150312082906.htm

LUPUS ESRITEMATOSO SISTEMICO

CLASE LUPUS ERITEMATOSO SISTEMICO
COAGULACION Y ALTERACIONES VASCULARES
ROTACION PATOLOGIA CLINICA
ABRIL 2015

La risa disminuye los niveles de hormonas asociadas con el estrés

Según un estudio de la Universidad de Maryland, las personas que han padecido un infarto del miocardio ríen hasta un 40% menos que las personas sin ese antecedente.

La risa, al igual que el llanto, es un acto involuntario para la mayoría de las personas. Su mecanismo de funcionamiento reside en la respiración, y se produce mediante interrupciones de la exhalación del aliento. Este proceso activa, además del sistema respiratorio, otros sistemas de nuestro organismo, como son el neurológico y el cardiovascular., según recuerda la Fundación Española del Corazón (FEC).

El efecto de la risa en nuestro sistema cardiovascular es vasodilatador; la risa genera  endorfinas, que producen un estado de bienestar psicológico, de tal manera que ésta ayuda a proteger el aparato cardiovascular. Cuando reímos, el endotelio  se relaja, mejorando así la circulación de la sangre y disminuyendo la presión arterial.

El Dr. José Luis Palma Gámiz, vicepresidente de la FEC, afirma que "la risa y la actitud positiva frente a la vida son beneficiosas para la salud cardiovascular. Por el contrario, los estados de estrés producen alteraciones en la pared vascular y favorecen la aparición de arteriosclerosis". El doctor Palma añade que “el estrés permanente condiciona la presencia de sustancias  vasoconstrictoras que afectan al endotelio y facilitan  que  el colesterol, penetren en la pared interior de los vasos sanguíneos, dando lugar a distintas enfermedades cardiovasculares”.

Reír también ayuda a aumentar el HDL  y potencia la actividad de los linfocitos. Reír reduce, además, el nivel de hormonas asociadas al estrés y aumenta el nivel de óxido nítrico, por lo que mejora la circulación, reduce la inflamación  y previene la formación de placas de colesterol.

Según explica el Dr.Palma, “el óxido nítrico es el vasodilatador natural más potente que se conoce. Cuando actúan conjuntamente sustancias como la serotonina y el óxido nítrico se producen las condiciones óptimas para una mayor vasodilatación, especialmente en los pequeños vasos sanguíneos, y, por tanto, disminuye la posibilidad de que se produzca una alteración del endotelio”.

Diferencia diametrial arterial

Son varios los estudios que han constatado beneficios de la risa en nuestro sistema cardiovascular. uno de ellos, realizado por la Unidad de Cardiología Preventiva del Centro Médico de la Universidad de Maryland, demostró que las personas que han sufrido un infarto agudo de miocardio ríen hasta un 40% menos que las personas que no han sufrido ningún tipo de enfermedad cardiovascular.

Este mismo centro realizó otro estudio en el que sometió a los participantes a situaciones cómicas y estresantes a través del visionado de películas. Tras analizar su reacción fisiológica, se comprobó que la diferencia diametral arterial entre estas dos situaciones opuestas oscilaba entre un 30% y un 50%. Así, en el caso de las películas estresantes, las arterias se contraían dificultando el aporte sanguíneo y aumentando el riesgo de sufrir problemas cardiovasculares, mientras que en situaciones cómicas, se dilataban, mejorando así la circulación de la sangre.

El Dr. Palma recuerda, por último, que “estar en paz con uno mismo y con su entorno y tener una actitud positiva frente a la vida, viendo los aspectos buenos, ayuda a prevenir las enfermedades cardiovasculares".

Tomado de: Jano.es

CLASE TRASTORNOS DE LA HEMOSTASIA EN HEPATOPATIAS

CLASE TRASTORNOS DE LA HEMOSTASIA EN HEPATOPATIAS

ROTACIONPATOLOGIA CLINICA

ABRIL 2015

NEW STUDY INDICATES THAT EXERCISE IMPROVES NON-ALCOHOLIC FATTY LIVER DISEASE

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the western world. A new study published in the Journal of Hepatology shows that exercise, regardless of frequency or intensity, benefits obese and overweight adults with NAFLD.

NAFLD is considered the hepatic manifestation of metabolic syndrome and is commonly associated with obesity and diabetes. There are no approved drug treatments for NAFLD, but lifestyle interventions such as diet, exercise, and the resulting weight loss have been shown to help improve NAFLD. In particular, these interventions can improve some features of non-alcoholic steatohepatitis (NASH), which is the progressive form of NAFLD.

Weight loss is the commonly recommended strategy for all obese and overweight patients with NAFLD. Both aerobic and resistance training-based exercise regimens reduce liver fat as well as visceral fat. However, the exact role of the amount and the intensity of aerobic exercise that would be needed to reverse or improve NAFLD (or NASH) had not been systematically assessed.

In the new study published in the Journal of Hepatology, investigators examined the effect of various aerobic exercise regimens in improving liver and visceral fat in overweight and obese people who had sedentary lifestyles. Using a randomized, placebo-controlled clinical trial (RCT) design, they randomized 48 participants into four equal groups of 12 people: low-to-moderate intensity, high-volume aerobic exercise (LO:HI); high-intensity, low-volume aerobic exercise (HI:LO); low-to-moderate intensity, low-volume aerobic exercise (LO:LO); and placebo (PLA) for an eight-week period. Change in liver fat was assessed by magnetic resonance spectroscopy (MRS).

All three groups, irrespective of the exercise regimen, showed improvement in liver fat of about 18-29% from the average baseline 7.5%, compared with the placebo group in which liver fat increased by an average of 14%. The improvement was independent of weight loss. There were no significant differences between the various aerobic exercise regimens in reducing liver fat over an eight-week period. However, the investigators conducted additional exploratory analyses and proposed that there was a trend towards greater reduction in liver fat and visceral fat in the two groups that utilized either high intensity with low volume (HI:LO) or low intensity with high volume (LO:HI) aerobic exercise.

“The results from our study show that all exercise doses, irrespective of volume or intensity, were efficacious in reducing liver fat and visceral fat by an amount that was clinically significant, in previously inactive, overweight, or obese adults compared with placebo. These changes were observed without clinically significant weight loss,” explained lead investigator Dr. Nathan Johnson, PhD, Senior Lecturer at the University of Sydney, Australia. “We found no difference between exercise regimens for these benefits,” added Jacob George, PhD, MBBS, Professor of Hepatic Medicine at the University of Sydney, Australia, and Head of the Department of Gastroenterology and Hepatology at Westmead Hospital and University of Sydney.

In an editorial in the same issue, Rohit Loomba, MD, MHSc, of the Division of Gastroenterology and Epidemiology at the University of California, San Diego, and Helena Cortez-Pinto, MD, PhD, of the Gastroenterology Service, Hospital de Santa Maria, Lisbon, Portugal, observed that “There is good quality evidence to support that regular exercise is beneficial in reducing the risk of NAFLD. In addition, both aerobic and resistance training regimens are equally effective in reducing liver fat in individuals with NAFLD even in the absence of weight loss.

They suggest that duration of exercise and intensity of exercise are both important and one could perhaps personalize the exercise regimen based upon a participant’s choice and still achieve similar results. “There are, however, no data to support that exercise alone without weight loss can improve or reverse NASH. There is preliminary evidence that vigorous exercise may be associated with a decreased risk of having NASH,” added Dr. Loomba and Dr. Cortez-Pinto. “The individual and joint effect of dose and intensity of exercise and their association with improvement in liver fat and other histologic features that are associated with NASH is a key research priority. In our expert opinion, a more stringent exercise-regimen than the U.S. Department of Health and Human Services recommends, coupled with dietary interventions, may be needed to induce improvement in liver histologic features associated with NASH.”

Tomado de:http://www.easl.eu/.  JOURNAL OF HEPATOLOGY - EASL APRIL 08,2015

CRITERIOS DIAGNOSTICOS DE ADA PARA DIABETES MELLITUS 2015

Classification and Diagnosis of Diabetes 2015

CLASE PURPURA DE HENOCH

CLASE : PURPURA DE HENOCH

ROTACION PATOLOGIA CLINICA

MODULO MEDICINA INTERNA

ABRIL 2015

Los fumadores subestiman su propio riesgo

Los fumadores tienden a subestimar su propio riesgo de padecer una enfermedad (especialmente si solo consumen unos pocos cigarrillos al día). Este es el resultado de una encuesta realizada en Francia y presentada en la Conferencia Europea sobre Cáncer de Pulmón (European Lung Cancer Conference, ELCC) celebrada en Ginebra (Suiza).

Investigadores del Hospital Nord de Marsella (Francia) analizaron datos de una encuesta representativa de 1602 franceses de edades comprendidas entre los 40 y 75 años. La encuesta incluyó a 1463 personas sin antecedentes de cáncer, de las que 481 eran exfumadoras y 330 fumadoras (un promedio de 14,2 cigarrillos al día).

Los resultados fueron un tanto alarmantes para los médicos. Solo la mitad de los participantes respondió que no existe una cantidad “segura” de cigarrillos que uno pueda fumar al día. El 34 % consideró, erróneamente, que fumar hasta diez cigarrillos al día no está relacionado con el riesgo de padecer cáncer de pulmón. Según el responsable del estudio, Laurent Greillier, “Este hallazgo es especialmente llamativo y peligroso. Demuestra que el consumo de cigarrillos relativamente bajo es considerado ‘seguro’ por muchas personas”.

Los encuestados también subestimaron su propio riesgo de cáncer. Solo aproximadamente la mitad de los fumadores afirmaron que tenían un riesgo superior al de la población corriente. Únicamente el 40 % de los encuestados era consciente de que la probabilidad mayor no desaparece tras dejar de fumar.

“Parece que las personas son conscientes de los peligros del tabaco para la salud, pero podrían pensar que los riesgos no son para ellos, sino solo para los demás. La negación es aún muy prevalente. Por tanto, las campañas contra el tabaquismo y la labor educativa sobre los riesgos deben ser constantes”, enfatizaba Greillier.

Tomado de Univadis.com

The placebome: Where genetics and the placebo effect meet

Placebos have helped to ease symptoms of illness for centuries and have been a fundamental component of clinical research to test new drug therapies for more than 70 years. But why some people respond to placebos and others do not remains under debate.

With the advent of genomics, researchers are learning that placebo responses are modified by a person's genetics, a discovery that raises important new questions regarding the role of the placebo in patient care and in drug development: How many genetic biomarkers exist? Can the medical field harness the placebo response to enhance personalized medical treatment? What might be the impact of placebo-drug interactions? And what will this new information mean for randomized clinical trials, which depend on placebo controls to test the efficacy of new drug candidates? Should a "no-treatment" control be added to future trials?

Researchers from the Program in Placebo Studies (PiPS) at Beth Israel Deaconess Medical Center (BIDMC) and from the Department of Medicine at Brigham and Women's Hospital (BWH) explore these provocative issues in a review of evidence from placebo studies and randomized clinical trials. Published online today in Trends in Molecular Medicine, the article introduces the concept of "the placebome,"and identifies a network of genes that could significantly influence medicine and clinical trial design -- suggesting that placebos play a larger role in health care than previously recognized.

"Genetic sequencing is revealing that the placebo response is, in fact, a complex phenotype with an unfolding physiology," says corresponding author Kathryn T. Hall, PhD, MPH, a PiPS Research Fellow in the Division of General Medicine and Primary Care at BIDMC and Harvard Medical School. "The study of genomic effects on the placebo response -- what we call 'the placebome' -- is in its infancy, but there is already ample evidence that genetic variations in the brain's neurotransmitter pathways modify placebo effects. As a result, placebo responses are emerging as a legitimate series of biological reactions that must be rigorously characterized for efficient pharmaceutical development and optimal patient care."

The article focuses on several key concepts for future research and discussion regarding the role of the placebome in health care.

The Role of the Neurotransmitter in the Placebo Effect

The placebo effect occurs when patients show improvement from treatments that contain no active ingredients. Scientists initially used behavioral instruments, such as personality measures, to predict which patients would respond to placebos, but over the past decade, the development of sophisticated neuroimaging technologies illuminated the activation of the brain's neurotransmitter pathways in response to placebos. "Because they are the chemical messengers that either excite or inhibit nerve function in the brain, many neurotransmitters play key roles in reward and pain," explains Hall. "We hypothesized that genetic variation in the genes that encode the proteins in these neurotransmitter pathways might also modify placebo responses."

In 2012, Hall identified the first placebo biomarker, the catechol-O-methyltransferase (COMT) gene, reporting that genetic variations in COMT -- which influence the brain's levels of the neurotransmitter dopamine -- also determined the extent of an individual's placebo response.

A review of the scientific literature over the last 10 years provided the authors with further confirmation that, beyond the COMT gene, there is evidence for genetic variation in other neurotransmitter pathways that modify placebo response. These include the opioid, endocannabinoid and serotonin pathways -- suggesting the potential existence of a placebome or "network" of genes.

Possibility of Placebo-Drug Interactions

Knowing that neurotransmitter pathways are involved in placebo responses now raises a new consideration for both patient care and clinical research, say the authors: What if placebo responses and drug responses share the same brain pathways?

"We're discovering that the placebo is not the only component in the placebo effect," explains the paper's coauthor Ted Kaptchuk, Director of the PiPS at BIDMC and Professor of Medicine at Harvard Medical School. "These neurotransmitter pathways, which are modified by genetics, are pathways that both drugs and the placebo act on. This now suggests that a drug could change a placebo response and a placebo response could modify a drug response."

The authors add that the potential overlap between placebo, drug treatment and disease adds to the complexity of the placebome and underscores the importance of understanding how it fits into larger more complex networks.

No-Treatment Arms in Clinical Trials

"The possibility that there could be a placebo-drug interaction as a result of genetic variation in placebo pathway genes suggests that we need to refine and recalibrate the assumptions of placebo controls in randomized clinical trials," the authors write. "An important next step in describing the placebome would be to include a no-treatment control in placebo-controlled randomized clinical trials. This approach might be cost effective and allow for a broad view of placebo response genes and other molecules across varying conditions and treatments."

As the "gold standard" for pharmaceutical research, randomized clinical trials include a "placebo arm," which is designed to control for the non-specific, non-pharmacological effects that are part of the administration and receipt of clinical treatment (i.e. the way a doctor is dressed, the way he or she describes what to expect from a drug, even the physical appearance of the doctor's office). But in order to properly study the placebo response, the authors propose that a "no -treatment" control needs to be incorporated into the trials.

"The best control for a drug is a placebo, but if you want to study placebos you need a no-treatment control," says Hall. "This is one of the major limitations in the scientific literature, but we believe that this could be addressed prospectively by including such an arm in future clinical trials.

"Knowledge of the placebome has the potential to guide development of novel strategies for both identifying placebo responders and clinical trial design," she adds. "The field of pharmacogenomics and our health care system's focus on precision medicine both call for the right treatment in the right place at the right time, and incorporating the placebome into this overall strategy could help lead to cost effective treatments and improved patient care. The placebome now let's us consider the placebo in a serious biological manner."

Tomado de: www.sciencedaily.com

Beth Israel Deaconess Medical Center. (2015, April 13). The placebome: Where genetics and the placebo effect meet. ScienceDaily. Retrieved April 15, 2015 

Tango dancing benefits Parkinson's patients

Dancing the Argentine tango could have potential benefits for people at certain stages in the development of Parkinson's disease (PD), according to findings in a new study by researchers at the Montreal Neurological Institute and Hospital -The Neuro, McGill University and the Research Institute of the McGill University Health Centre. The study looked at changes in patients' motor abilities following a 12-week tango course, and is also the first study to assess the effect that tango has on non-motor symptoms.

The study looked at whether a social and physical activity linked to music, such as tango, could have possible therapeutic value for PD patients who characteristically suffer from motor dysfunctions -- tremor, rigidity, gait dysfunction -- as well as from non-motor symptoms, such as depression, fatigue and cognitive degeneration. Forty men and women with idiopathic Parkinson's disease participated in the study, which involved studio classes with two professional dance teachers. Patients were from the Movement Disorders Clinics of the McGill University Health Centre.

"There's accumulating evidence that habitual physical activity is associated with a lower risk of developing PD, which suggests a potential slowing of PD progression," says Dr. Silvia Rios Romenets, lead researcher in the study with a special interest in Parkinson's disease and dance therapy. Dr. Rios Romenets is a clinical research fellow at the Movement Disorders Clinics at The Neuro and Montreal General Hospital. "In the study, we found the tango was helpful in significantly improving balance and functional mobility, and seemed to encourage patients to appreciate their general course of therapy. We also found modest benefits in terms of patients' cognitive functions and in reducing fatigue. No significant changes were detected in overall motor functions."

Argentine tango may be particularly helpful for improving balance and functional mobility in patients with PD. Tango requires specific steps that involve rhythmically walking forward and backward. This may be particularly helpful for walking difficulties especially for freezing of gait and to prevent backward falls. In addition, tango requires working memory, control of attention, and multitasking to incorporate newly learned and previously learned dance elements, to stay in rhythm with the music, and maneuver around others on the dance floor.

Many PD patients find traditional exercise programs unappealing. Over half of PD patients fail to get their recommended daily dose of physical activity. There is however, a connection between music and the dopamine systems in the brain -- which are pivotal for establishing and maintaining behavior. So, combining music with exercise in dance such as the tango, can increase accessibility, enjoyability, and motivation, as well as improving mood and stimulating cognition. Also, the social interaction and social support involved in tango have positive results on mood and compliance.

Tomado de www.sciencedaily.com

McGill University. (2015, April 13). Tango dancing benefits Parkinson's patients.ScienceDaily. Retrieved April 15, 2015 

Coffee consumption and coronary artery calcium in young and middle-aged asymptomatic adults

RESUMEN:

Objective To investigate the association between regular coffee consumption and the prevalence of coronary artery calcium (CAC) in a large sample of young and middle-aged asymptomatic men and women.

Methods This cross-sectional study included 25 138 men and women (mean age 41.3 years) without clinically evident cardiovascular disease who underwent a health screening examination that included a validated food frequency questionnaire and a multidetector CT to determine CAC scores. We used robust Tobit regression analyses to estimate the CAC score ratios associated with different levels of coffee consumption compared with no coffee consumption and adjusted for potential confounders.

Results The prevalence of detectable CAC (CAC score mayor a 0) was 13.4% (n=3364), including 11.3% prevalence for CAC scores 1–100 (n=2832), and 2.1% prevalence for CAC scores mayor to 100 (n=532). The mean ±SD consumption of coffee was 1.8±1.5 cups/day. The multivariate-adjusted CAC score ratios (95% CIs) comparing coffee drinkers of menor to 1, 1– menor que 3, 3– menor que5, and mayor o igual que 5 cups/day to non-coffee drinkers were 0.77 (0.49 to 1.19), 0.66 (0.43 to 1.02), 0.59 (0.38 to 0.93), and 0.81 (0.46 to 1.43), respectively (p for quadratic trend=0.02). The association was similar in subgroups defined by age, sex, smoking status, alcohol consumption, status of obesity, diabetes, hypertension, and hypercholesterolaemia.

Conclusions In this large sample of men and women apparently free of clinically evident cardiovascular disease, moderate coffee consumption was associated with a lower prevalence of subclinical coronary atherosclerosis.

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TOMADO DE :heart.bmj.com/

HEPATITIS B

CLASE DIAGNOSTICO DE HEPATITIS B
ROTACION PATOLOGIA CLINICA
FEBRERO 2015

HIGADO GRASO

CLASE HIGADO GRASO
ROTACION PATOLOGIA CLINICA
FEBRERO 2015

ICTERICIA

CLASE ICTERICIA
ROTACION PATOLOGIA CLINICA
FEBRERO 2015

PURPURA TROMBOCITOPENICA TROMBOTICA

Diet, exercise alone not sufficient obesity treatment for most

Researchers suggest that obesity is a chronic disease with a number of biological causes that make it impossible to be cured with diet and exercise alone in a recently published comment in The Lancet Diabetes & Endocrinology.

Eighty percent to 95% of people with obesity who lose weight eventually regain it. Several biological systems are triggered when caloric intake is reduced, which drives people to eat more high-calorie foods and, in turn, gain or regain weight. According to the researchers lifestyle changes are not enough to override the fat-loss defense for most individuals with sustained obesity.

“Although lifestyle modifications may result in lasing weight loss in individuals who are overweight, in those with sustained obesity, bodyweight seems to become biologically ‘stamped in’ and defended,” Christopher N. Ochner, PhD, assistant professor of pediatrics and psychiatry at Icahn School of Medicine at Mount Sinai and a research associate at the New York Obesity Nutrition Research Center at Columbia University Medical Center, said in a press release. “Therefore, the current advice to eat less and exercise more may be no more effective for most individuals with obesity than a recommendation to avoid sharp objects for someone bleeding profusely.”

Biological adaptations that occur with the development of obesity and undermine health weight loss effors can persist even in people who were are formerly obese and achieve a healthy bodyweight through dieting.

“Few individuals ever truly recover from obesity; rather they suffer from ‘obesity in remission,’” Ochner said in the press release. “They are biologically very different from individuals of the same age, sex and bodyweight who never had obesity.”

The researchers suggest that biological factors should be addressed to help sustain long-term weight loss, but current biologically-based interventions are limited to antiobesity drugs, weight loss surgery and intra-abdominal vagal nerve block. According to the researchers these interventions do not permanently correct the biological factors adaptations undermine healthy weight loss efforts. However, during use, the interventions alter neural or hormonal signaling associated with appetite, which can yield a 4% to 10% reduction in weight.

“Many clinicians are not aware of the reasons individuals with obesity struggle to achieve and maintain weight loss,” Ochner said. “Obesity should be recognized as a chronic and often treatment-resistant disease with both biological and behavioral causes that may require biologically-based interventions, such as pharmacotherapy or surgery, in addition to lifestyle modification. Ignoring the biological adaptations that undermine healthy weight loss efforts and continuing to rely solely on behavioral modification will surely result in the continued inability to treat obesity effectively and the premature deaths of millions of individuals each year.” 

Tomado de:Halo.org

Ochner CN, et al. Lancet Diabetes Endocrinol. 2015;doi:10.1016/S2213-8587(15)70010.

Cannabis: A new frontier in therapeutics

Wile debate about recreational marijuana use continues, researchers are investigating the effectiveness of cannabis for treating pain, spasticity, and a host of other medical problems. In a symposium organized by the McGill University Health Centre (MUHC) as part of the 2015 American Association for the Advancement of Science Annual Meeting held this week in San Jose, California,  experts from North America and the U.K. share their perspectives on the therapeutic potential of medical cannabis and explore the emerging science behind it.

"We need to advance our understanding of the role of cannabinoids in health and disease through research and education for patients, physicians and policy-makers," says Dr. Mark Ware, director of clinical research at the Alan Edwards Pain Management Unit at the MUHC, in Canada.

As a pain specialist Dr. Ware regularly sees patients with severe chronic pain at his clinic in Montreal, and for some of them, marijuana appears to be a credible option. "I don't think that every physician should prescribe medical cannabis, or that every patient can benefit but it's time to enhance our scientific knowledge base and have informed discussions with patients."

Increasing numbers of jurisdictions worldwide are allowing access to herbal cannabis, and a range of policy initiatives are emerging to regulate its production, distribution, and authorization. It is widely believed that there is little evidence to support the consideration of cannabis as a therapeutic agent. However, several medicines based on tetrahydrocannabinol (THC), the psychoactive ingredient of cannabis, have been approved as pharmaceutical drugs.

Leading British cannabis researcher Professor Roger Pertwee, who co-discovered the presence of tetrahydrocannabivarin (THCV) in cannabis in the 70's, recently published with collaborators some findings of potential therapeutic relevance in the British Journal of Pharmacology. "We observed that THCV, the non-psychoactive component of cannabis, produces anti-schizophrenic effects in a preclinical model of schizophrenia," says Pertwee, professor of Neuropharmacology at Aberdeen University. "This finding has revealed a new potential therapeutic use for this compound."

Neuropsychiatrist and Director of the Center for Medicinal Cannabis Research (CMCR) at the University of California, San Diego Dr. Igor Grant is interested in the short and long-term neuropsychiatric effects of marijuana use. The CMCR has overseen some of the most extensive research on the therapeutic effects of medical marijuana in the U.S. "Despite a commonly held view that cannabis use results in brain damage, meta analyses of extensive neurocognitive studies fail to demonstrate meaningful cognitive declines among recreational users," says Dr. Grant. "Bain imaging has produced variable results, with the best designed studies showing null findings."

Dr. Grant adds that while it is plausible to hypothesize that cannabis exposure in children and adolescents could impair brain development or predispose to mental illness, data from properly designed prospective studies is lacking.

Tomado de sciencedaily.com

FUente: McGill University Health Centre. (2015, February 15). Cannabis: A new frontier in therapeutics. ScienceDaily. Retrieved February 16, 2015 from www.sciencedaily.com/releases/2015/02/150215070209.htm

El efecto placebo es más eficaz si el fármaco tiene un precio elevado

Un estudio en 12 personas con párkinson prueba que los medicamentos caros generan más expectativas de mejora que los baratos'.

Los medicamentos crean expectativas de curación en los pacientes. En numerosas ocasiones, estas esperanzas producen una mejoría similar o mayor a la que producen los fármacos, lo que se conoce como efecto placebo. Ahora, un estudio llevado a cabo por investigadores de la Academia Estadounidense de Neurología con enfermos con párkinson, indica que este efecto es mayor cuando el precio de los remedios es elevado. El artículo ha sido publicado en American Academy of Neurology.

"Las expectativas desempeñan un papel importante en la eficacia de los tratamientos, sobre todo en personas con enfermedad de párkinson", explica el venezolano Alberto J. Espay, investigador en neurología de la Universidad de Cincinnati, Estados Unidos, y autor principal del artículo.

La investigación se llevó a cabo en 12 pacientes con esta patología. Los científicos administraron a cada uno de ellos dos dosis de placebo ­–una solución salina–, indicándoles que se trataba de dos medicamentos diferentes, igualmente efectivos, pero de diferente precio, unos 90 y 1.300 euros, respectivamente. Antes y después de cada toma, los participantes pasaron varias pruebas para medir sus habilidades motoras y se sometieron a escáneres para medir la actividad cerebral.

Al tomar el fármaco etiquetado como caro, los pacientes mejoraron en un 28% sus habilidades motoras en comparación a cuando tomaban el barato. Este efecto fue particularmente notable cuando el que creían más costoso se recibía primero. Los resultados de la resonancia magnética también mostraron una diferencia a favor del medicamento de mayor valor económico. "Si aprovechamos la respuesta al placebo para mejorar los beneficios de los tratamientos, podríamos reducir las dosis y, posiblemente, los efectos secundarios", indica Espay.

Para Peter A. LeWitt, investigador del departamento de Neurología del Hospital Henry Ford en Michigan, Estados Unidos, y autor del editorial sobre el estudio, “asumir que se obtienen los mejores resultados con los medicamentos más caros puede ser una mala noticia para el control de costes médicos”.

El poder de la expectativa

La enfermedad de párkinson disminuye la cantidad de dopamina que genera el cerebro de las personas afectadas. Esta hormona afecta el movimiento, pero también a la anticipación, la motivación y la respuesta a nuevos estímulos. "La respuesta ante el tratamiento se asocia con la liberación de dopamina en el cerebro”, señala Espay.

Cuando se informó a los participantes de la naturaleza del estudio, los pacientes mostraron asombro por la gran diferencia que habían notado. “Las personas que admitieron tener más expectativas con el fármaco caro fueron las que más mejoría notaron al tomarlo, mientras que aquellos a los que el precio no les pareció determinante percibieron menos diferencias”, indica.

Una de las limitaciones del estudio es la diferente percepción en los precios que puedan existir según los estratos económicos en la sociedad. “Sería interesante reconocer en qué casos un medicamento de 90 euros es considerado o no como un medicamento barato”, concluye, por su parte, LeWitt.

Tomado de Jano.es

American Academy of Neurology (2015); doi: 10.1212/WNL.0000000000001294

Obesity experts recommend weight loss drugs, surgery as supplement to lifestyle interventions

The  Endocrine Society today issued a Clinical Practice Guideline (CPG) on strategies for prescribing drugs to manage obesity and promote weight loss

The CPG, entitled "Pharmacological Management of Obesity: An Endocrine Society Clinical Practice Guideline," was published online and will appear in the February 2015 print issue of the Journal of Clinical Endocrinology and Metabolism (JCEM), a publication of the Endocrine Society.

Obesity is a worsening public health problem. According to the 2012 National Health and Nutrition Examination Survey, about 33.9 percent of adults ages 19-79 were overweight, 13.4 percent were obese and 6.4 were extremely obese.

The Food and Drug Administration has approved four new anti-obesity drugs -- lorcaserin, phentermine/topiramate, naltrexone/bupropion and liraglutide -- in the past two years. Medications like these can be used in combination with diet and exercise to help people lose weight.

"Lifestyle changes should always be a central part of any weight loss strategy," said Caroline M. Apovian, MD, of Boston University School of Medicine and Boston Medical Center, and chair of the task force that authored the guideline. "Medications do not work by themselves, but they can help people maintain a healthy diet by reducing the appetite. Adding a medication to a lifestyle modification program is likely to result in greater weight loss."

In the CPG, the Endocrine Society recommends that diet, exercise and behavioral modifications be part of all obesity management approaches. Other tools such as weight loss medications and bariatric surgery can be combined with behavioral changes to reduce food intake and increase physical activity. Patients who have been unable to successfully lose weight and maintain a goal weight may be candidates for prescription medication if they meet the criteria on the drug's label.

Other recommendations from the CPG include:

• If a patient responds well to a weight loss medication and loses 5 percent or more of their body weight after three months, the medication should be continued. If the medication is ineffective or the patient experiences side effects, the prescription should be stopped and an alternative medication or approach considered.

• Since some diabetes medications are associated with weight gain, people with diabetes who are obese or overweight should be given medications that promote weight loss or have no effect on weight as first- and second-line treatments. Doctors should discuss medications' potential effects on weight with patients.

• Certain types of medication -- angiotensin converting enzyme inhibitors, angiotensin receptor blockers and calcium channel blockers -- should be used as a first-line treatment for high blood pressure in obese people with Type 2 diabetes. These are effective blood pressure treatments that are less likely to contribute to weight gain than the alternative medication, beta-adrenergic blockers.

• When patients need medications that can have an impact on weight such as antidepressants, antipsychotic drugs and medications for treating epilepsy, they should be fully informed and provided with estimates of each option's anticipated effect on weight. Doctors and patients should engage in a shared-decision making process to evaluate the options.

• In patients with uncontrolled high blood pressure or a history of heart disease, the medications phentermine and diethylpropion should not be used.

The Hormone Health Network offers resources on weight and health at

http://www.hormone.org/diseases-and-conditions/weight-and-health.

Tomado de: sciencedaily.com

Journal Reference: Caroline M. Apovian, Louis J. Aronne, Daniel H. Bessesen, Marie E. McDonnell, M. Hassan Murad, Uberto Pagotto, Donna H. Ryan, Christopher D. Still.Pharmacological Management of Obesity: An Endocrine Society Clinical Practice Guideline. The Journal of Clinical Endocrinology & Metabolism, 2015; jc.2014-3415 DOI: 10.1210/jc.2014-3415

How Much Do We Know About HDL Cholesterol?

As levels of HDL cholesterol increase, rates of heart disease go down. It’s this fact that has given HDL its reputation as the “good cholesterol,” serving a crucial role in reverse cholesterol transport. According to our models, HDL ferries cholesterol away from our arteries – where its buildup leads to heart disease and stroke – and back towards our liver, safely out of harm’s way. The epidemiology backs this up: people with higher levels of HDL tend to have a lower risk of heart disease.[1] But why don’t pharmacologic efforts to raise HDL cholesterol reduce morbidity and mortality from heart disease the same way that statins do? As more data on HDL-raising efforts are published, both scientists and the popular press [3] are beginning to eulogize the end of the HDL hypothesis. So how can we reconcile these discordant pieces of evidence? To answer that question, we must take a look at what the data tell us on the role of HDL in heart disease.

CETP Inhibitors

Cholesterylester transfer protein (CETP) transfers cholesterol from HDL to the atherogenic particles of VLDL and LDL, making it a promising target for drug development. Indeed, the initial studies on CETP inhibitors showed that their administration raised HDL cholesterol while simultaneously lowering LDL cholesterol. On paper, it sounded like a win-win. And then the medical world was shocked in 2006 when Pfizer was forced to halt phase III trials of torcetrapib, a CETP inhibitor, after it was shown to increase mortality by 60% when prescribed in conjunction with atorvastatin, compared to atorvastatin alone. [5] Pfizer spent over $800 million on their failed HDL raising attempt. [6] Some suggested that the mortality increase was due to adverse effects such as raising blood pressure. However, subsequent data analysis found that torcetrapib also failed to stop the progression of carotid intima media thickness, [7] further confirming its lack of efficacy in halting or reversing atherosclerosis. Another CETP inhibitor, dalcetrapib, was tested in the dal-OUTCOMES study and found to have no reduction in cardiovascular events despite earlier trials confirming its seemingly positive impact on HDL and LDL cholesterol levels. [8]  The previous failures of CETP inhibitors on improving cardiovascular outcomes have not deterred pharmaceutical companies from pursuing this mechanism of disease prevention, as both Merck and Lilly are both optimistic that their own medications in this class will lead to better outcomes. [9]

Niacin

Nicotinic acid, also known as vitamin B3 or niacin, raises HDL by as much as 35% by reducing cholesterol transfer from HDL to VLDL and by delaying HDL clearance. [10]  Several trials have evaluated the effect of niacin on cardiovascular outcomes. The HATS trial evaluated the effect of simvastatin plus niacin and found not only a rise in HDL levels but a regression of atherosclerotic lesions as well as reduced incidence of coronary events. [11] This trial did not compare niacin plus a statin to statin alone, however, so the marginal benefit of raising HDL could not be tested. The ARBITER 6-HALTS study looked at statin plus niacin versus statin plus ezetimibe and found regression of carotid intimal media thickness for patients taking niacin plus statin versus progression for the other group. [12] Similar to HATS, the marginal benefit of raising HDL on top of statin use could not be evaluated. In addition, this was an open label trial, so blinding was not preserved. The AIM-HIGH trial, published in 2011, aimed to settle some of the questions about isolated HDL raising therapy on top of patients who were already receiving statins. This study investigated the effect of niacin versus placebo on patients already taking statins. [13] AIM-HIGH was terminated after finding no incremental benefit for raising HDL with niacin on top of statin therapy.[14] And recently, the HPS2-THRIVE study found no benefit when adding extended release niacin plus laropiprant to background statin therapy. [15] The evidence for niacin is clearly mixed, but it should be noted that no study has shown an additional outcome benefit from the addition of niacin to statin therapy. It’s interesting to note that while niacin may increase HDL cholesterol levels, it does not improve the functioning of HDL particles. [16] If adding niacin to therapy does not increase cholesterol efflux from the vessels, it makes intuitive sense that there would be no disease modifying benefit from its addition. This research also suggests that there may be more to the HDL story than simply increasing the amount of cholesterol it carries.

Given the paucity of evidence that pharmacologic HDL raising treatments have any clinical benefit, many have asked the question of whether high HDL is actually protective against heart disease or whether it is simply a marker for some other mechanism of decreased risk. In 2012, Voight et al published a Mendelian randomization paper in the Lancet that investigated whether genetic polymorphisms that raise HDL also protect against heart disease. The authors found that the genetic mechanisms that raise HDL do not seem to protect against heart disease. [17] When you synthesize the results of this study with the previously discussed data, it calls the currently proposed mechanisms of HDL’s protective effect into question.

HDL Hypothesis, revisited

In a previous Clinical Correlations post, [18] the benefit of measuring lipoproteins instead of cholesterol as a means of assessing heart disease risk was discussed. It appears that measuring apolipoprotein B is a better measure of cardiac risk than simply measuring LDL. The reason for this has to do with the mechanism of heart disease: atherosclerosis is the result of subendothelial penetration of an apoB containing particle that stimulates inflammatory cell recruitment and oxidation/phagocytosis of the offending particle. The reason measuring apoB is a better assessment of risk is that LDL is simply a measurement of the amount of cholesterol contained in the particles – it says nothing about how many particles there are. However, since HDL doesn’t always have 1 apolipoprotein per particle like LDL, VLDL, and Lp(a), measuring apolipoproteins isn’t a simple solution. In addition, the protective role of HDL is not just measured by the number of HDL particles: the smaller the HDL particle (i.e. the less cholesterol it contains), the better its anti-atherogenic activity. We should also note that HDL does more to fight atherosclerosis than simply participate in reverse cholesterol transport. HDL protects against LDL oxidation, it is anti-inflammatory, [20] it promotes maintenance of endothelial function, and it may even interfere with thrombosis. [21] And a higher number of smaller HDL particles does seem to be protective against cardiovascular disease. [22,23] Investigation into a apoA1-Milano, a mutated variant of the apolipoprotein in HDL found in some Italians has further complicated our understanding of HDL’s role in atherosclerosis. Patients with this variant of apoA1 tend to have lower risk of coronary disease even though they have lower HDL-C and higher triglycerides. [24] And testing the intravenous administration of apoA-1 Milano into post ACS patients found regression of coronary plaques after five weeks. As the role of HDL in heart disease is further investigated, it becomes clear that assessing its role is more complicated than can be measured by simple HDL cholesterol measurement.

The research we have on the pharmacologic manipulation of HDL raises more questions than it answers. There are several areas to investigate before we should move on from attempting therapeutic intervention on HDL. How do these interventions affect HDL particle size and, perhaps more importantly, HDL particle function? What impact do these interventions have on HDL particle number? Are CETP inhibitors and niacin simply increasing the amount of cholesterol carried by HDL, and thus confounding our efforts to measure their effect? Investigating methods of simply raising the cholesterol carried by HDL particles may well be barking up the wrong tree. It’s clear from epidemiological data that high HDL is protective against heart disease. It’s also likely that both HDL particle number and particle function are better markers of this protective effect than the cholesterol carried by these particles. But there is much research to be done before we are able to provide our patients with a real benefit from intervening on their low HDL numbers. We advocate that investigators in this area not hang their “HATS” on the research to date and “AIM-HIGH” for a possible therapeutic intervention that increases HDL particles or improves their functioning.

By Gregory Katz, MD

Tomado de: www.clinicalcorrelations.org