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Donde acaba la dudaacaba la ciencia

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How the Brain Puts the Brakes On Negative Impact of Cocaine

ScienceDaily (Jan. 11, 2012) — Research published by Cell Press in the January 12 issue of the journal Neuron provides fascinating insight into a newly discovered brain mechanism that limits the rewarding impact of cocaine. The study describes protective delayed mechanism that turns off the genes that support the development of addiction-related behaviors. The findings may lead to a better understanding of vulnerability to addiction and as well as new strategies for treatment.


Drug addiction is associated with persistent and abnormal changes in the reward circuitry of the brain, and drug-induced changes in gene expression are thought to contribute to addiction behaviors. Recent research with rodent models of addiction has implicated histone deacetylases (HDACs), which are modulators of gene expression, in the regulation of cocaine-induced behaviors. However, how cocaine regulates the function of HDACs and whether this regulation can modify addiction-related behaviors was not known.

"HDAC5 in the nucleus accumbens, a key brain region involved in drug abuse, limits the rewarding impact of cocaine and the long-lasting memory of places where the drug was taken, particularly after prior cocaine exposure," explains senior study author Dr. Christopher W. Cowan from the University of Texas Southwestern Medical Center. "However, it was not clear whether this was a passive role for HDAC5 or whether drugs of abuse might regulate its function after drug exposure." In the current study, Dr. Cowan and colleagues explored how cocaine might regulate HDAC5 and the development of drug reward-associated behaviors.

Using a rodent model, the researchers discovered that cocaine triggered a novel signaling pathway that caused HDAC5 to move to the cell nucleus, where gene expression occurs, and they found that this process was essential for HDAC5 to limit the development of cocaine reward-associated behaviors. "Our findings reveal a new molecular mechanism by which cocaine regulates HDAC5 function to antagonize the rewarding impact of cocaine, likely by putting a brake on drug-stimulated genes that would normally support drug-induced behavioral changes," concludes Dr. Cowan. "Deficits in this process may contribute to the development of maladaptive behaviors associated with addiction following repeated drug use in humans and may help to explain why some people are more vulnerable to addiction than others."




Makoto Taniguchi, Maria B. Carreira, Laura N. Smith, Benjamin C. Zirlin, Rachael L. Neve, Christopher W. Cowan. Histone Deacetylase 5 Limits Cocaine Reward through cAMP-Induced Nuclear Import. Neuron, 2012; 73 (1): 108 DOI: 10.1016/j.neuron.2011.10.032

Diet Counts: Iron Intake in Teen Years Can Impact Brain in Later Life

ScienceDaily (Jan. 12, 2012) — Iron is a popular topic in health news. Doctors prescribe it for medical reasons, and it's available over the counter as a dietary supplement. And while it's known that too little iron can result in cognitive problems, it's also known that too much promotes neurodegenerative diseases.

Iron-related gene HFE and the brain. (Credit: Image courtesy of University of California - Los Angeles)


Now, researchers at UCLA have found that in addition to causing cognitive problems, a lack of iron early in life can affect the brain's physical structure as well.

UCLA neurology professor Paul Thompson and his colleagues measured levels of transferrin, a protein that transports iron throughout the body and brain, in adolescents and discovered that these transferrin levels were related to detectable differences in both the brain's macro-structure and micro-structure when the adolescents reached young adulthood.

The researchers also identified a common set of genes that influences both transferrin levels and brain structure. The discovery may shed light on the neural mechanisms by which iron affects cognition, neurodevelopment and neurodegeneration, they said.

Their findings appear in the current online edition of the journal Proceedings of the National Academy of Sciences.

Iron and the proteins that transport it are critically important for brain function. Iron deficiency is the most common nutritional deficiency worldwide, causing poor cognitive achievement in school-aged children. Yet later in life, iron overload is associated with damage to the brain, and abnormally high iron concentrations have been found in the brains of patients with Alzheimer's, Parkinson's and Huntington diseases.

Since both a deficiency and an excess of iron can negatively impact brain function, the body's regulation of iron transport to the brain is crucial. When iron levels are low, the liver produces more transferrin for increased iron transport. The researchers wanted to know whether brain structure in healthy adults was also dependent on transferrin levels.

"We found that healthy brain wiring in adults depended on having good iron levels in your teenage years," said Thompson, a member of UCLA's Laboratory of Neuro Imaging. "This connection was a lot stronger than we expected, especially as we were looking at people who were young and healthy -- none of them would be considered iron-deficient.

"We also found a connection with a gene that explains why this is so. The gene itself seems to affect brain wiring, which was a big surprise," he said.

To assess brain volume and integrity, Thompson's team collected brain MRI scans on 615 healthy young-adult twins and siblings, who had an average age of 23. Of these subjects, 574 were also scanned with a type of MRI called a "diffusion scan," which maps the brain's myelin connections and their strength, or integrity. Myelin is the fatty sheath that coats the brain's nerve axons, allowing for efficient conduction of nerve impulses, and iron plays a key role in myelin production.

Eight to 12 years before the current imaging study, researchers measured the subjects' blood transferrin levels. They hoped to determine whether iron availability in the developmentally crucial period of adolescence impacted the organization of the brain later in life.

"Adolescence is a period of high vulnerability to brain insults, and the brain is still very actively developing," Thompson said.

By averaging the subjects' transferrin levels, which had been assessed repeatedly -- at 12, 14 and 16 years of age -- the researchers estimated iron availability to the brain during adolescence, he said.

The team discovered that subjects who had elevated transferrin levels -- a common sign of poor iron levels in a person's diet -- had structural changes in brain regions that are vulnerable to neurodegeneration. And further analyses of the twins in the study revealed that a common set of genes influences both transferrin levels and brain structure.

One of the genetic links -- a specific variation in a gene called HFE, which is known to influence blood transferrin levels -- was associated with reduced brain-fiber integrity, although subjects carrying this gene variant did not yet show any symptoms of disease or cognitive impairment.

"So this is one of the deep secrets of the brain," Thompson said. "You wouldn't think the iron in our diet would affect the brain so much in our teen years. But it turns out that it matters very much. Because myelin speeds your brain's communications, and iron is vital for making myelin, poor iron levels in childhood erode your brain reserves which you need later in life to protect against aging and Alzheimer's.

"This is remarkable, as we were not studying iron deficient people, just around 600 normal healthy people. It underscores the need for a balanced diet in the teenage years, when your brain's command center is still actively maturing. "

The findings, he said, may aid future studies of how iron transport affects brain function, development and the risk of neurodegeneration.

The research was supported by the National Institute of Child Health and Human Development; Australia's National Health and Medical Research Council; the Achievement Rewards for College Scientists Foundation; the National Institute of Mental Health; and the Australian Research Council Future Fellowship.




N. Jahanshad, O. Kohannim, D. P. Hibar, J. L. Stein, K. L. McMahon, G. I. de Zubicaray, S. E. Medland, G. W. Montgomery, J. B. Whitfield, N. G. Martin, M. J. Wright, A. W. Toga, P. M. Thompson. PNAS Plus: Brain structure in healthy adults is related to serum transferrin and the H63D polymorphism in the HFE gene. Proceedings of the National Academy of Sciences, 2012; DOI: 10.1073/pnas.1105543109

Master Controller of Memory Identified

ScienceDaily (Jan. 6, 2012) — When you experience a new event, your brain encodes a memory of it by altering the connections between neurons. This requires turning on many genes in those neurons. Now, MIT neuroscientists have identified what may be a master gene that controls this complex process.

Yingxi Lin, a member of the McGovern Institute for Brain Research and the the Frederick and Carole Middleton Career Development Assistant Professor of Brain and Cognitive Sciences. (Credit: Photo courtesy Kent Dayton)


The findings, described in the Dec. 23 issue of Science, not only reveal some of the molecular underpinnings of memory formation -- they may also help neuroscientists pinpoint the exact locations of memories in the brain.

The research team, led by Yingxi Lin, a member of the McGovern Institute for Brain Research at MIT, focused on the Npas4 gene, which previous studies have shown is turned on immediately following new experiences. The gene is particularly active in the hippocampus, a brain structure known to be critical in forming long-term memories.

Lin and her colleagues found that Npas4 turns on a series of other genes that modify the brain's internal wiring by adjusting the strength of synapses, or connections between neurons. "This is a gene that can connect from experience to the eventual changing of the circuit," says Lin, the Frederick and Carole Middleton Career Development Assistant Professor of Brain and Cognitive Sciences.

To investigate the genetic mechanisms of memory formation, the researchers studied a type of learning known as contextual fear conditioning: Mice receive a mild electric shock when they enter a specific chamber. Within minutes, the mice learn to fear the chamber, and the next time they enter it, they freeze.

The researchers showed that Npas4 is turned on very early during this conditioning. "This sets Npas4 apart from many other activity-regulated genes," Lin says. "A lot of them are ubiquitously induced by all these different kinds of stimulations; they are not really learning-specific."

Furthermore, Npas4 activation occurs primarily in the CA3 region of the hippocampus, which is already known to be required for fast learning.

"We think of Npas4 as the initial trigger that comes on, and then in turn, in the right spot in the brain, it activates all these other downstream targets. Eventually they're going to modify synapses in a way that's likely changing synaptic inhibition or some other process that we're trying to figure out," says Kartik Ramamoorthi, a graduate student in Lin's lab and lead author of the paper.

Genetic regulation

So far, the researchers have identified only a few of the genes regulated by Npas4, but they suspect there could be hundreds more. Npas4 is a transcription factor, meaning it controls the copying of other genes into messenger RNA -- the genetic material that carries protein-building instructions from the nucleus to the rest of the cell. The MIT experiments showed that Npas4 binds to the activation sites of specific genes and directs an enzyme called RNA polymerase II to start copying them.

"Npas4 is providing this instructive signal," Ramamoorthi says. "It's telling the polymerase to land at certain genes, and without it, the polymerase doesn't know where to go. It's just floating around in the nucleus."

When the researchers knocked out the gene for Npas4, they found that mice could not remember their fearful conditioning. They also found that this effect could be produced by knocking out the gene just in the CA3 region of the hippocampus. Knocking it out in other parts of the hippocampus, however, had no effect. Though they focused on contextual fear conditioning, the researchers believe that Npas4 will also prove critical for other types of learning.

Gleb Shumyatsky, an assistant professor of genetics at Rutgers University, says that an important next step is to identify more of the genes controlled by Npas4, which should reveal more of its role in memory formation. "It's definitely one of the major players," says Shumyatsky, who was not involved in this research. "Future experiments will show how major a player it is."

The MIT team also plans to investigate whether the same neurons that turn on Npas4 when memories are formed also turn it on when memories are retrieved. This could help them pinpoint the exact neurons that are storing particular memories.

"We're hunting for the memory, and we think we can use Npas4 to mark where it is," Ramamoorthi says. "That's because it's turned on specifically and now we can label the cells and maybe fish out where in the brain the memory is sitting."


K. Ramamoorthi, R. Fropf, G. M. Belfort, H. L. Fitzmaurice, R. M. McKinney, R. L. Neve, T. Otto, Y. Lin. Npas4 Regulates a Transcriptional Program in CA3 Required for Contextual Memory Formation. Science, 2011; 334 (6063): 1669 DOI: 10.1126/science.1208049

Why Coffee Drinking Reduces the Risk of Type 2 Diabetes

ScienceDaily (Jan. 11, 2012) — Why do heavy coffee drinkers have a lower risk of developing Type 2 diabetes, a disease on the increase around the world that can lead to serious health problems? Scientists are offering a new solution to that long-standing mystery in a report in ACS' Journal of Agricultural & Food Chemistry.


Ling Zheng, Kun Huang and colleagues explain that previous studies show that coffee drinkers are at a lower risk for developing Type 2 diabetes, which accounts for 90-95 percent of diabetes cases in the world. Those studies show that people who drink four or more cups of coffee daily have a 50 percent lower risk of Type 2 diabetes. And every additional cup of coffee brings another decrease in risk of almost 7 percent. Scientists have implicated the misfolding of a substance called human islet amyloid polypeptide (hIAPP) in causing Type 2 diabetes, and some are seeking ways to block that process. Zheng and Huang decided to see if coffee's beneficial effects might be due to substances that block hIAPP.

Indeed, they identified two categories of compounds in coffee that significantly inhibited hIAPP. They suggest that this effect explains why coffee drinkers show a lower risk for developing diabetes. "A beneficial effect may thus be expected for a regular coffee drinker," the researchers conclude.

The authors acknowledge funding from the National Natural Science Foundation of China, the National Basic Research Program of China and the Chinese Ministry of Education.

Why do heavy coffee drinkers have a lower risk of developing Type 2 diabetes? (Credit: © Marco Mayer / Fotolia)


Biao Cheng, Xinran Liu, Hao Gong, Lianqi Huang, Hong Chen, Xin Zhang, Chuanzhou Li, Muyang Yang, Bingjun Ma, Lihua Jiao, Ling Zheng, Kun Huang. Coffee Components Inhibit Amyloid Formation of Human Islet Amyloid Polypeptide in Vitro: Possible Link between Coffee Consumption and Diabetes Mellitus. Journal of Agricultural and Food Chemistry, 2011; 59 (24): 13147 DOI: 10.1021/jf201702h

Scientists Shed New Light On Link Between 'Killer Cells' and Diabetes

ScienceDaily (Jan. 15, 2012) — Killer T-cells in the human body which help protect us from disease can inadvertently destroy cells that produce insulin, new research has uncovered.


The study provides the first evidence of this mechanism in action and could offer new understanding of the cause of Type 1 diabetes.

Professor Andy Sewell, an expert in human T-cells from Cardiff University's School of Medicine worked alongside diabetes experts from King's College London to better understand the role of T-cells in the development of Type 1 diabetes.

The team isolated a T-cell from a patient with Type 1 diabetes to view a unique molecular interaction which results in the killing of insulin-producing cells in the pancreas.

"Type 1 diabetes is a result of the body's own immune system attacking and destroying the cells in the pancreas that manufacture the hormone insulin. Insulin controls blood sugar levels and a lack of insulin is fatal if untreated," said Professor Sewell.

"The mechanism by which the body attacks its own insulin producing cells in the pancreas is not fully understood. Our findings show how killer T-cells might play an important role in autoimmune diseases like diabetes and we've secured the first ever glimpse of the mechanism by which killer T-cells can attack our own body cells to cause disease," he added.

Co-author of the study, Professor Mark Peakman from the National Institute for Health Research (NIHR) Biomedical Research Centre at King's College London and Guy's and St Thomas' NHS Foundation Trust said: "This first sight of how killer T-cells make contact with the cells that make insulin is very enlightening, and increases our understanding of how Type 1 diabetes may arise.

"This knowledge will be used in the future to help us predict who might get the disease and also to develop new approaches to prevent it. Our aim is to catch the disease early before too many insulin-producing cells have been damaged."

The team now hope that by gaining a better understanding of this process it will put them in a much stronger position to devise new ways to prevent or even halt the disease.

The study, funded by the UK Biotechnology and Biological Sciences Research Council (BBSRC), the Juvenile Diabetes Research Foundation (JDRF) using facilities at Diamond Light Source and published in Nature Immunology, shows that the killer T-cell receptor utilises an abnormal mode of binding in order to recognise cells producing insulin.

"The results of Dr Sewell's work provide key novel insights into T1D pathogenesis" said Teodora Staeva, Director of JDRF's Immune Therapies Program. "JDRF is pleased to support this kind of research that will accelerate the development of biomarkers and preventive therapies for Type 1 diabetes."

This unusual binding is thought to allow the T-cell to survive the culling process designed to rid the body of autoreactive T-cells.

The structure of the killer T-cell receptor bound to the insulin peptide shows that the interaction is highly focused on just a small part of the molecule.

In a further study published in the Journal of Biological Chemistry the same Cardiff and King's team has shown that this focused binding mode allows this T-cell receptor to respond to over 1.3 million other peptides of different molecular shape.

This ability to bind peptides with a multitude of different shapes may provide a clue as to how autoimmune diseases are initiated. It is possible that this T-cell was raised to fight an infection via one of the other 1.3 million peptides it can recognise but then inadvertently also recognised insulin once it had been put on 'red alert' by this infection.

Diabetes describes diseases where a person has high blood sugar. Treatment of diabetes and its complications represents a major health burden and accounts for over 10% of the National Health Service's annual budget.



L. Wooldridge, J. Ekeruche-Makinde, H. A. van den Berg, A. Skowera, J. J. Miles, M. P. Tan, G. Dolton, M. Clement, S. Llewellyn-Lacey, D. A. Price, M. Peakman, A. K. Sewell. A Single Autoimmune T Cell Receptor Recognizes More Than a Million Different Peptides. Journal of Biological Chemistry, 2011; 287 (2): 1168 DOI: 10.1074/jbc.M111.289488




·       LEBEN-CELTICS capsulas

·       LINDEZA capsulas PISA

·       REDUSTAT capsulas LIOMONT

·       XENICAL capsulas ROCHE



Cada capsula contiene orlistat 120 mg

Excipiente c.b.p. 1 capsula


Orlistat esta indicado como tratamiento farmacológico para producir una perdida de persona en personas con sobrepeso u obesidad y en aquellos pacientes en los que estas condiciones se acompañan con factores de riesgo asociados. También puede ser utilizado como terapia de mantenimiento a corto y largo plazo para mantener un peso adecuado una vez se obtiene el peso deseado, lo encontramos indicado como coadyuvante en el manejo de pacientes con síndrome metabólico o alguna de sus manifestaciones como son hipercolesterolemia, hiperinsulinemia, intolerancia a la glucosa, diabetes mellitus, e hipertensión arterial y para disminuir la grasa visceral.

Por otro lado lo tenemos indicado para mejorar el control de la glicemia en paciente con DM2 con sobrepeso y obesidad, independientemente del control de glicemia, manejándose con dieta y ejercicio, hipoglucemiantes orales o insulina. Es posible lograr control del peso adecuado a largo plazo favoreciendo la reducción del peso, el mantenimiento de peso una vez lograda la reducción y la prevención del aumento de peso.




Esta contraindicado en pacientes con hipersensibilidad conocida al activo, paciente con síndrome de malabsorción crónica y pacientes con colestasis.


Aun cuando los estudios realizados con orlistat demostraron que la mayoría delos pacientes tratado hasta por dos años mantuvieron sus niveles normales de vitaminas A,DE,K y B-carotenos podría ser considerado el administrar un suplemento multivitamínico, en cuyo caso deberá administrarse por lo menos 2 horas después de la administración de orlistat a pacientes que reciben una dieta alta en grasas puede aumentar la posibilidad de presentar efectos secundarios gastrointestinales. Debido a que la perdida de peso obtenida con el uso de Orlistat en paciente con DM2 puede mejorar el control metabólico y disminuir los niveles de glucosa, podría ser necesario reducir la dosis de hipoglucemiante que se este utilizando.

En pacientes bajo tratamiento con ciclosporina a los que se les administre orlistat, podría observarse una disminución de los niveles plasmáticos de ciclosporina por lo que se recomienda un monitoreo estricto.

Igualmente en los pacientes en que se administre simultáneamente orlistat y anticoagulantes orales deben monitorearse estrechamente los parámetros de coagulación.


Hasta la fecha no se ha establecido la seguridad de uso de orlistat durante el embarazo por lo que no deberá ser utilizado en mujeres embarazadas. Tampoco se ha investigado si orlistat se secreta por la leche materna por lo que tampoco se recomienda su uso durante el periodo de lactancia.


Tomando en consideración que orlistat se absorbe en un mínimo porcentaje, las reacciones secundarias y adversas que se han reportado mayormente se limitan al tracto gastrointestinal y habitualmente son leves y transitorias, presentan al inicio del tratamiento e incluyen heces blandas o liquidas aumentadas en frecuencia, urgencia fecal, manchas de grasa, heces grasosas, incontinencia fecal, goteo grasos de ano, flatulencia, dolor abdominal , nauseas y vomito.

Mientras mayor sea el contenido de grasa en la dieta existe mayor posibilidad de presentar estos efectos secundarios lo que es recomendable aconsejar al paciente que lleve una dieta con poco contenido engrasas.

Adicionalmente a los efectos secundarios gastrointestinales en pacientes con DM2 han reportado algunos casos de hipoglicemia posiblemente debido al mejor control metabólico que se obtiene con orlistat. También han sido algunas casos de infecciones del tracto respiratorio, infecciones urinarias,. Influenza, ansiedad, fatiga, cefalea por irregularidades menstruales y casos muy raros de hipersensibilidad manifestados principalmente por prurito urticaria, exantema, Angioedema, anafilaxias. También han sido reportados casos muy raros de erupción bulosa y hepatitis que pueden ser grave. Hasta el momento no se ha establecido ninguna relación causal entre la hepatitis y terapia con orlistat.


Orlistat no tiene ningún tipo de interacción con el alcohol, metformina, estatinas, anticonceptivos orales, nifedipino y digoxina.

En pacientes bajo tratamiento con ciclosporina a los que se administre orlistat, podría observarse una disminución de los niveles plasmáticos de ciclosporina por lo que se recomienda un monitoreo mas estricto de lo habitual.

Igualmente en los pacientes que se administre simultáneamente orlistat o anticoagulantes orales debe monitorearse estrechamente los parámetros de coagulación.


En los estudios de reproducción realizados en animales no se observaron efectos teratógenos ni embriotoxicos con el orlistat. Tampoco se observo un efecto carcinogénico ni se vio afectado el curso normal del embarazo ni la viabilidad embriológica y/o fetal. Sin embargo en ausencia de datos clínicos no se recomienda el uso durante el embarazo.


La dosis recomendada es una capsula de 120 mg administrada con el primer bocado del desayuno, otra con el primer bocado de la comida y otra con el primer bocado de la cena. En caso de que alguno de estos tres alimentos no contenga grasa o contenga una muy pequeña cantidad de grasas puede omitirse la toma.

No es necesario ajustar la dosificación en ancianos ni en paciente con insuficiencia hepática o renal

Puede administrarse en paciente con sobrepeso u obesidad desde los 12 años de edad en adelante, las mismas dosis del adulto.

Las dosis mayores a 120 mg tres veces al día no mostraron ningún beneficio adicional

El efecto terapéutico benéfico de orlistat en cuanto ala reducción del peso y la mejoría de los factores de riesgo se mantiene con la administración a largo plazo.


Tomando en consideración que la absorción de orlistat es mínima, no es de esperarse que existan manifestaciones  adversas con la sobredosificación de orlistat.

Se han evaluado dosis únicas de 800mg y dosis múltiples de 400 mg tres veces al día durante 15 días así como dosis de 240 mg cada 8 horas durante 6 meses sin haber encontrado manifestaciones adversas significativas. Sin embargo si un paciente que tuvo una sobredosificación con orlistat presenta alguna manifestación adversa, deberán tomarse las medidas de sostén adecuadas para este caso


Consérvese a temperatura ambiente a no mas de 25 grados Celsius y en un lugar seco.









Cada gragea contiene bromuro de butilhioscina 10.00 mg

Excipiente c.b.p. 1 tableta


Espasmos del tracto gastrointestinal, espasmo y desinencias de vías biliares, espasmos genito urinarios (litiasis renal, dismenorrea) síndrome de colon irritable.


Es un fármaco derivado semi sintético de la escopolamina encontrada en la corteza de las plantas solanáceas.

El amino cuaternario bromuro de n-bitilhioscina no posee efecto anticolinérgico central, por lo tanto no ocurren reacciones adversas anticolinérgicas a nivel central. La acción anticolinérgica resulta del bloqueo ganglionar en las paredes viscerales, así como por su actividad antimuscarinica.

Farmacocinética: bromuro de n-butilhioscina como un amonio cuaternario, el bromuro de n-butilhioscina es altamente polar y por ende solo se absorbe parcialmente después de una administración oral (8%) o rectal (3%). La disponibilidad sistémica es menor al 1%, sin embargo, a pesar de los bajos niveles plasmáticos, se logran concentraciones locales relativamente altas, medidas por radioisopos de n-butilhioscina y/o metabolitos, en el sitio d acción: tracto gastrointestinal, vesícula biliar, conductos biliares, hígado y riñones.

El bromuro de n-butilhioscina no atraviesa la barrera hematoencefalica y la unión a proteínas plasmáticas es baja. La eliminación total después de una dosis determinada IV, es de 1.2 lt/min, la mitad de la eliminación es renal. Los principales metabolitos encontrados en la orina, se une pobremente a los receptores muscarinicos.


Esta contraindicado en casos de glaucoma e hipertrofia prostática, insuficiencia renal.

Hipersensibilidad al principio activo


Debido al riesgo potencial de complicaciones anticolinérgicas debe utilizarse con cuidado en pacientes con glaucoma de Angulo cerrado, así como pacientes susceptibles de desarrollar obstrucción intestinal o urinaria y en aquellos con tendencias a taquiarritmias.


Efectos secundarios anticolinérgicos como xerostomía, dishidrosis, taquicardia y potencial retención urinaria, pueden ocurrir a niveles moderados y auolimitados. En casos muy raros se han presentado reacciones cutáneas. En casos aislados reacciones anafilácticas con episodios de disnea y choque.


No se han presentado a las dosis recomendadas.


No se han reportado


Vía de administración: oral

Adultos y niños mayores a 6 años: 1 a 2 grageas cada 6 a 8 horas. Las grageas deben ingerirse sin masticar con un poco de liquido. No debe excederse la dosis diaria de 6 grageas al día.


En el caso de sobredosis pueden ocurrir síntomas anticolinérgicos como: retención urinaria, boca seca, rubicundez en la piel, taquicardia, inhibición de la motilidad gastrointestinal y alteraciones visuales transitorias. Tratamiento: se puede utilizar fármacos parasimpaticometicos se debe consultar en calidad de urgencia en casos de glaucoma

En caso de paro respiratorio: intubación y apoyo respiratorio, en caso de retención urinaria se puede requerir cateterismo.


Consérvese a temperatura ambiente a no mas de 30 grados Celsius y en un lugar seco.


Naproxeno sodico



  • Alebrem - tabletas - ALPHARMA
  • defloxen - tabletas - LIOMONT
  • Deflamox- suspension, tabletas - HORMONA
  • Flavoxen - Tabletas- ALPHARMA



Cada tablta contiene: naproxeno sodico 275 y 550 mg

excipiente c.b.p. 1 tableta


Por sus propiedades inflamatorias y analgésicas esta indicado para el alivio de molestias y dolores moderados debidos a resfriados, dolor de garganta, traumatismos, dismenorrea primaria, extracciones dentales primarias, artritis reumatoide, osteoartritis, artritis juvenil, espondilitis anquilosante, tendinitis y bursitis. para el control del dolor e inflamación producido por el ataque de gota aguda.


naproxeno y naproxeno sódico se absorben fácilmente en el tubo digestivo. Se alcanzan concentraciones plasmáticas máximas aproximadamente al cabo de 1 a 3 horas de la ingestión del naprxeno sódico y de 2 a 4 horas en el naproxeno. Los alimentos reducen la velocidad pero no el grado de absorción.

El naproxeno y naproxeno sódico también se absorbe tras su administración rectal, aunque se aborse aun mas lento que por vía oral. A concentraciones terapéuticas el naproxeno no se halla unido en mas de 99% de las proteínas plasmáticas. Las concentraciones plasmáticas de naproxeno aumentan porporcionalmente a la dosis hasta 500mg/dia; a dosis mas elevadas, aumenta su aclaramiento por saturación de proteínas plasmáticas. El naproxeno difunde el liquido sinovial; atravisa la barrera placentaria y aparece en pequeñas cantidades en la leche materna. El naproxeno tiene una vida media de eliminación de 13 horas. Aproximadamente el 95% de la dosis se elimina por la orina en forma de naproxino y 6-0-demetilnaproxeno y sus conjugados. En las heces se recuperan menos de 5% de la dosis.

Naproxeno, un fármaco no esteroide con propiedades antiinflamatorias y analgésicas, derivado del acido propionico, como todos los fármacos antiinflamatorios de su tipo, inhibe la actividad de la enzima ciclixigenasa disminuyendo la formación de los precursores de prostaglandinas y tromboxanos a partir del acido araquidónico.

El resultado de esta acción sobre varios tejidos puede ser responsable de muchas de sus acciones terapéuticas, asi como de sus efectos indeseables.

Como antiinflamatorio su mecanismo de acción exacto no ha sido determinado. Sin embargo, se piensa que puede actuar reduciendo la actividad de prostaglandinas en tejidos inhibiendo la síntesis Y/O la acción de enzimas lisosomicas, que pueden estar implicadas en otras acciones como son procesos celulares e inmunológicos en el tejido mesenquimatosos y conjuntivo.


el uso de naproxeno sódico esta contraindicado en paciente con antecedentes de hipersensibilidad al principio activo, pólipos nasales asociados a broncoespasmo, angioedema o anafilaxia, reacciones alérgicas inducidas por el acido acetilsalicílico y otro antiinflamatorios analgésicos no esteroides.

De la misma manera, naproxeno sodico no debe ser sado en caso de alcoholismo activo, ulcera péptica activa, colitis ulcerativas y antecedentes de enfermedad acido péptica o sangrado del tubo digestivo superior, pacientes con hemofilia o trastornos de coagulación plaquetario, su empleo en la insuficiencia renal esta contraindicado. De la misma manera en paciente con lupus eritematosos sistémico ya que puede disponer a efectos indeseables sobre SNC y riñones.


En pacientes con anemia o asma debe valorarse el riesgo-beneficio debido a la retención de líquidos que puede originarse. También en pacientes con predisposición a retención de líquidos como insuficiencia cardiaca e hipertensión. En la insuficiencia cardiaca, diabetes mellitus, edema preexistente, depleción de volumen y sepsis las concentraciones de naproxeno libre aumentan en la cirrosis hepática alcohol nutricional, por lo que debe usarse dosis mínima y el paciente debe ser monitoreado. Puede inducir estomatitis y debe tomarse en cuenta su posible asociación con discrasias sanguíneas que pueden estar enmascaradas



las reacciones de hipersensibilidad pueden ser similares a las reportadas para el acido acetilsalicílico, por ejemplo:

·       Rinosinusitis

·       Asma

·       Angioedema

·       Urticaria

Se han reportado reacciones anafilácticas tanto en pacientes sensibles al acido acetilsalicílico como aquellos sin antecedentes de hipersensibilidad.

Sus acciones antiinflamatoria y analgésica pueden enmascarar síntomas de presencia de infecciones severas. La sobredosis con cualquier derivado del acido propionico puede ocasionar pocos síntomas o ser relativamente leves en el SNC apareciendo letargo, vértigo ,etc.

El sodio que contiene el naproxeno sódico de tomarse en cuanto cuando se administre en pacientes con necesidad de restringir su ingestión de sodio.


El naproxeno puede interferir co la determinación urinaria del acido 5 hidroxiindolacetico

También puede presentar falsos resultados en las determinaciones urinarias de 17 cetosteroides y se recomienda suspenderlo hasta 72 horas antes de cualquier prueba de función suprarrenal.

El tiempo de sangrado puede ser prolongado hasta 4 días con el uso de naproxeno, también puede presentarse aumento sérico de los niveles de nitrógeno ureico, creatinina, potasio y sodio pueden estar disminuidos. La actividad de la transaminasas puede estar elevada en las pruebas de función hepática por lo que debe toarse en cuenta cuando se este usado naproxeno.


ORAL. Siempre debe recordarse el contenido de sodio antes de su administración en pacientes que este con dieta estricta sin sodio. Se aconseja reducir la dosis al 50% en pacientes con mas de 70 años de edad, sin embargo si es bien tolerado puede conservarse la dosis normal del adulto.

Se recomienda que las tabletas se administren con un vaso de agua completo (250 ml) con lo que se disminuye la posible irritación esofágica, se sugiere administración inmediatamente después de alimentos.

En la dismenorrea se recomienda su uso inmediatamente después del inicio de la menstruación. En el tratamiento profiláctico, iniciar su administración 2 a 3 días antes del inicio de la menstruación.

Adultos: la dosis oral habitual inicialmente es de 550 mg, seguido de 275 cada 6 a 8 horas.

En dismenorrea: por vía oral inicialmente 550 mg seguido de 275 mg cada 6 a 8 horas. El limite máximo de la dosis habitual para el adulto es de 1375 g al día.


La sobredosis puede estar caracterizada por vértigo, sensación de quemadura retro esternal, nauseas o vomito.

Algunos pacientes han experimentado convulsiones pero no se ha comprobado si este síntoma esta relacionado al medicamento. La dosis letal media es de 543 mg/kg en ratas, 1234 mg/kg en ratones 4,110 mg/kg en cobayos y mas de 1,000 mg/kg en perros.

Si el paciente ingiere una dosis alta ya sea accidentalmente o de forma voluntaria, el estomago debe vaciarse por lavado gástrico para tratar de retirar la mayor cantidad posible de fármaco antes de que se absorba e instalar medidas generales de sostén.

En animales el uso de 0.5 mg/kg del peso del carbón activado ha sido útil para disminuir los niveles plasmáticos de naproxeno por su elevada unión a proteínas.


Consérvese a temperatura ambiente a no mas de 30 grados Celsius y en un lugar seco



articulo de revision bibliografica - importancia clinica de la digestion de carbohidratos


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