lunes, 28 de junio de 2010
domingo, 27 de junio de 2010
LA RELACION ENTRE LA DIETA Y EL ACNE
La relación entre la dieta y el acné ha sido formulada y reformulada con el paso de los años, y hoy es revisitada de la mano de estudios que sugieren que los alimentos con alto índice glucémico (con mucha azúcar en poco espacio) podrían favorecer la aparición del acné.
"Entre 1930 y 1960, a los pacientes se les desaconsejaba comer una amplia selección de alimentos, como chocolates, grasas, dulces. Pero luego de una serie de estudios criticos, esa asociación se desvaneció", recuerda una revisión del asunto publicada recientemente en la revista de la Academia Estadounidense de Dermatología.
Sin embargo, continúa la publicación, "la pregunta por la relación entre dieta y acné ha vuelto a ser formulada. Existe evidencia razonablemente convincente de que las dietas con alto índice glucémico pueden exacerbar el acné".
"Los alimentos con grandes cantidades de azúcar incrementan la producción del llamado factor de crecimiento de insulina, que al unirse en receptores de los queratinocitos producen su proliferación excesiva", explicó la dermatóloga francesa Brigitte Dréno.
La proliferación excesiva de esas células cutáneas colabora con el taponamiento de los poros, que es la lesión inicial del acné.
"La relación entre el acné y la alimentación va cambiando permanentemente y por eso, por el momento, no se recomienda ninguna dieta restrictiva ni se hace mucho hincapié en lo alimentario -comentó la doctora María Valeria Angles, del Servicio de Dermatología del Hospital Italiano-. De todos modos, si uno observa que en un paciente un alimento determinado produce más lesiones de acné, la decisión es suspender ese alimento."
En el taller que Angles coordina en el Italiano, también se tratan otros mitos del acné, como por ejemplo, que el sol lo mejora, cuando, en realidad, hace que la enfermedad reaparezca con más fuerza, o que el acné está relacionado con la suciedad, "lo que hace que muchos se laven obsesivamente la cara -dijo-. Eso irrita la piel y vuelve intolerable el tratamiento".
"Entre 1930 y 1960, a los pacientes se les desaconsejaba comer una amplia selección de alimentos, como chocolates, grasas, dulces. Pero luego de una serie de estudios criticos, esa asociación se desvaneció", recuerda una revisión del asunto publicada recientemente en la revista de la Academia Estadounidense de Dermatología.
Sin embargo, continúa la publicación, "la pregunta por la relación entre dieta y acné ha vuelto a ser formulada. Existe evidencia razonablemente convincente de que las dietas con alto índice glucémico pueden exacerbar el acné".
"Los alimentos con grandes cantidades de azúcar incrementan la producción del llamado factor de crecimiento de insulina, que al unirse en receptores de los queratinocitos producen su proliferación excesiva", explicó la dermatóloga francesa Brigitte Dréno.
La proliferación excesiva de esas células cutáneas colabora con el taponamiento de los poros, que es la lesión inicial del acné.
"La relación entre el acné y la alimentación va cambiando permanentemente y por eso, por el momento, no se recomienda ninguna dieta restrictiva ni se hace mucho hincapié en lo alimentario -comentó la doctora María Valeria Angles, del Servicio de Dermatología del Hospital Italiano-. De todos modos, si uno observa que en un paciente un alimento determinado produce más lesiones de acné, la decisión es suspender ese alimento."
En el taller que Angles coordina en el Italiano, también se tratan otros mitos del acné, como por ejemplo, que el sol lo mejora, cuando, en realidad, hace que la enfermedad reaparezca con más fuerza, o que el acné está relacionado con la suciedad, "lo que hace que muchos se laven obsesivamente la cara -dijo-. Eso irrita la piel y vuelve intolerable el tratamiento".
sábado, 26 de junio de 2010
Curiosidades de este Mundial
Camerun tiene un jugador llamado (Webo).
Brasil tiene dos uno llamado (Elano) y otro (Kaka).
Eslovaquia tiene a (Kucka).
Menos mal NO juegan el en el mismo equipo...!
Te imaginas una sustitucion entre ellos...??
Webo entra por Kucka y sale Kaka por Elano...
Brasil tiene dos uno llamado (Elano) y otro (Kaka).
Eslovaquia tiene a (Kucka).
Menos mal NO juegan el en el mismo equipo...!
Te imaginas una sustitucion entre ellos...??
Webo entra por Kucka y sale Kaka por Elano...
martes, 15 de junio de 2010
lunes, 14 de junio de 2010
Poder versus pasión
El dinero es secundario con respecto al país y a la tradición cuando se proyectan los ganadores de la Copa Mundial de Fútbol. ¿Quiénes son los favoritos para Sudáfrica 2010? Lo anticipa PwC.
“Brasil es el favorito para ganar la Copa Mundial 2010. Inglaterra se daría por bien servido si pasara de los cuartos de final. Los equipos africanos deberían beneficiarse de la ventaja de ser locales”. Estas son algunas de las definiciones conocidas ayer del informe “¿Qué puede decirnos la econometría sobre el desempeño de la Copa Mundial?”, elaborado por la oficina británica de PricewaterhouseCoopers LLP (PwC).
Los países más ricos generalmente no superan a sus oponentes más pobres en el fútbol, de acuerdo al reporte de PwC.
Brasil es el favorito estadísticamente en el torneo de la Copa Mundial de este año, mientras Inglaterra debería darse por bien servido al pasar de los cuartos de final, basados tanto en las clasificaciones mundiales de la FIFA como en el desempeño histórico de la Copa Mundial.
El documento de PwC encuentra que no hay un enlace significativo entre los niveles de ingreso promedio (PIB per cápita) y el éxito en el torneo. Países latinoamericanos con un ingreso relativamente bajo frecuentemente igualaban o superaban a sus rivales europeos más acomodados, particularmente cuando jugaban en su región como locales.
El tamaño de la población tiene algún efecto en el desempeño en la Copa Mundial, pero no es tan significativo estadísticamente. Argentina, por ejemplo, ha alcanzado a Brasil en algunas ocasiones, aunque tenga solamente una quinta parte de su población.
Países relativamente pequeños como Uruguay, Suecia y Croacia también han peleado por arriba de su peso, particularmente cuando juegan en casa o cerca de ella.La ventaja de jugar en casa y la fuerza de las tradiciones futbolísticas históricas pueden resultar determinantes en el éxito de la Copa Mundial.
John Hawksworth, director de macroeconomía de PricewaterhouseCoopers LLP, dijo:
“Nuestro análisis demuestra que los niveles de ingresos de promedio bajo no son un impedimento para el éxito en la Copa Mundial, como tampoco el tamaño de la población es un factor tan crítico como lo suponen. David bien puede ganarle a Goliat en el campo de fútbol”.
“Aquellos países con una cultura arraigada en el fútbol y un seguimiento nacional apasionado pueden superar a las potencias de la economía mundial”.
Por ejemplo, el desempeño del equipo de fútbol de Estados Unidos es inferior a las expectativas basadas en el tamaño de su economía o población, si lo relacionamos, por ejemplo, con Brasil.
Esto refleja la ascendencia del fútbol en Brasil en contraste con la mayor popularidad de deportes tales como el fútbol americano y béisbol en Estados Unidos. China e India son ejemplos aún más dramáticos de bajos niveles de éxito en la Copa Mundial relativo a poblaciones de más de mil millones y economías rápidamente crecientes.
India prefiere enfocarse al críquet, mientras que China se ha concentrado en deportes que maximizaron su éxito en medallas de oro en los Juegos Olímpicos de Beijing 2008.
Hawksworth, continuó: “Si un país tiene una fuerte tradición futbolística, entonces encontrar 11 jugadores de clase mundial no debería ser tan difícil, aun con una población de tan solo unos pocos millones”.
Además, el estudio no encontró una correlación significativa entre el PIB per cápita y las clasificaciones actuales de la FIFA o el desempeño histórico en la Copa Mundial.
“Esto puede reflejar que el hecho de que las habilidades básicas de fútbol pueden ser perfeccionadas fácilmente tanto en los callejones como en un caro centro deportivo. Además, el fútbol puede representar una de las formas más llamativas para que los jóvenes salgan de la pobreza en países con ingresos más bajos”, explicó Hawksworth.
¿En casa o afuera?
Estos descubrimientos de fútbol difieren de investigaciones anteriores de PwC que demostraban que la población y el promedio de niveles de ingresos impactaban las medallas ganadas en los Juegos Olímpicos.
Sin embargo, la ventaja de jugar en casa es un factor que es sumamente importante estadísticamente al momento de explicar el éxito tanto en la Copa Mundial de la FIFA como en los Juegos Olímpicos. El país anfitrión ha ganado 6 de 18 Copas Mundiales y aún cuando no ganaron, los países anfitriones han tenido generalmente fuertes campañas.
Inglaterra y Francia solo ganaron la Copa Mundial cuando jugaron en casa, mientras que países más pequeños como Uruguay (el cual ganó en casa en la primera Copa Mundial en 1930), Suecia (la cual llegó a la final jugando en casa en 1958) y Corea del Sur (que le ganó a Italia y luego llegó a las semifinales en 2002) han todos superado las expectativas de desempeño cuando fueron anfitriones de la Copa Mundial. El desempeño relativamente modesto de España al ser anfitriones de la competencia en 1982 fue una de las comparativamente raras excepciones a esta regla. También hay un claro efecto de la región anfitriona que puede ser asociado con un fuerte apoyo de la multitud y condiciones climáticas familiares.
Los países europeos han ganado la Copa Mundial únicamente cuando se ha llevado a cabo en Europa, mientras que los equipos latinoamericanos han ganado todas las Copas Mundiales llevadas a cabo en las Américas.
Camerún y Nigeria deben, por ende, tener el potencial de quedar bien este año, mientras que a Sudáfrica debería irle mucho mejor que lo que sugiere su baja clasificación de 90 de la FIFA. John Hawksworth, director de macroeconomía de PricewaterhouseCoopers LLP, concluyó: “Brasil permanece como el favorito para alzar la Copa Mundial este verano como el país futbolero clasificado número uno y el único que ha ganado el torneo fuera de su región”.
“Inglaterra aparenta ser una apuesta razonable para que alcance los cuartos de final basados en su clasificación mundial actual de la FIFA y en su desempeño en la Copa Mundial pasada, pero se daría por bien servido si pasara de ese punto, que nunca ha alcanzado anteriormente jugando fuera de Europa”.
Mejores países según su desempeño histórico
en la Copa Mundial y Clasificación actual de la FIFA
Total de puntos de Copas Mundiales alcanzados (1930-2006)
Clasificación mundial de la FIFA actual (28 de abril de 2010)
Clasificación País Puntos* Clasificación País Puntos
1 Brasil 206 1 Brasil 1611
2 Alemania 184 2 España 1565
3 Italia 151 3 Portugal 1249
4 Argentina 112 4 Holanda 1221
5 Inglaterra 92 5 Italia 1184
6 Francia 85 6 Alemania 1107
7 España 78 7 Argentina 1084
8 Suecia 61 8 Inglaterra 1068
9 Holanda 58 9 Croacia 1052
10 Rusia 57 10 Francia 1044
11 Serbia/Yugoslavia 56 11 Rusia 1003
12 Uruguay 55 12 Grecia 968
13 Polonia 50 13 Egipto 967
14 Hungría 48 14 EEUU 950
15 México 45 15 Chile 948
16 Republica Checa** 41 16 Serbia 944
17 Austria 40 17 México 936
18 Bélgica 39 18 Uruguay 902
19 Portugal 34 19 Camerún 887
20 Rumania 29 20 Nigeria 883
*Solo juegos finales de la Copa Mundial: 3 puntos por ganar, 1 punto por empatar, 0 por perder. **Incluye los resultados de la antigua Checoslovaquia. Igualmente para Rusia/USSR y Serbia/Yugoslavia
Por: PricewaterhouseCoopers*,
sábado, 12 de junio de 2010
What is the best treatment of recurrent aphthous ulcers?
Evidence-Based Answer:Amlexanox 5% paste significantly reduces ulcer size and duration of pain, and increases speed of healing. (SOR A, based on multiple randomized controlled trials [RCTs].) Topical silver nitrate and corticosteroids reduce pain. (SOR B, based on multiple RCTs.) Chlorhexidine mouthwash reduces overall ulcer burden. (SOR B, based on heterogeneous RCTs.) "Magic mouthwash" is as effective as saline baking soda washes. (SOR B, based on a single RCT.) Nonpharmacologic interventions include avoiding trauma, avoidance of acidic foods/beverages, and minimizing stress. (SOR C, based on expert opinion.)
Artículo completo: http://www.globalfamilydoctor.com/search/GFDSearch.asp?itemNum=11439&ContType=HDA
Artículo completo: http://www.globalfamilydoctor.com/search/GFDSearch.asp?itemNum=11439&ContType=HDA
Diagnosis and Management of H pylori Infection CME/CE
May 4, 2010 — A clinical review in the April 29 issue of the New England Journal of Medicine provides information on how to detect, diagnose, treat, and manage Helicobacter pylori infection.
"Infection with H. pylori is a cofactor in the development of three important upper gastrointestinal diseases: duodenal or gastric ulcers (reported to develop in 1 to 10% of infected patients), gastric cancer (in 0.1 to 3%), and gastric mucosa-associated lymphoid-tissue (MALT) lymphoma (in <0.01%)," writes Kenneth E. L. McColl, MD, from the Division of Cardiovascular and Medical Sciences, University of Glasgow, Gardiner Institute, Glasgow, United Kingdom.
"The risk of these disease outcomes in infected patients varies widely among populations. The great majority of patients with H. pylori infection will not have any clinically significant complications."
Methods of Testing
Routine testing for H pylori infection is not recommended because the vast majority of patients with this infection do not have any associated clinical disease. However, confirmed gastric or duodenal ulcers and gastric MALT lymphoma are definite indications for detecting and treating H pylori infection. After surgical removal of early gastric cancers, it may also be reasonable to test for and eradicate H pylori infection.
For younger patients with upper gastrointestinal tract symptoms but without alarm symptoms such as weight loss, persistent vomiting, or gastrointestinal tract bleeding, it is reasonable to use a noninvasive test-and-treat strategy for H pylori infection. Options for noninvasive testing include the urea breath test, fecal antigen test, and serologic test. Of these options, the least accurate is the serologic test. Patients with positive test results should undergo eradication therapy.
For patients with alarm symptoms, or for older patients with new-onset dyspepsia, endoscopy is recommended. Depending on the specific set of guidelines used, older patients are defined as those 45 years or older or 55 years or older. Because nonsteroidal anti-inflammatory drugs can cause ulcers in the absence of H pylori infection, endoscopy is warranted for patients with dyspepsia associated with use of these drugs.
Treatments
Unless there is a high local rate of resistance to clarithromycin, appropriate first-line treatment is triple therapy using a proton-pump inhibitor plus clarithromycin and amoxicillin, each given twice per day for 7 to 14 days. Patients with a penicillin allergy should receive metronidazole instead of amoxicillin. When the prevalence of clarithromycin-resistant H pylori infection exceeds 20%, an alternative initial treatment regimen is quadruple therapy with a proton-pump inhibitor, tetracycline, metronidazole, and a bismuth salt for 10 to 14 days. However, bismuth salts are not available in the United States and in some other countries.
Another option is 10-day sequential therapy with a proton-pump inhibitor plus amoxicillin for 5 days, followed by a proton-pump inhibitor plus clarithromycin and tinidazole for 5 more days. However, the efficacy of this regimen needs to be confirmed before it is widely used.
"Data are lacking to inform the optimal management of recurrent or persistent dyspepsia after noninvasive testing and treatment of H. pylori infection," Dr. McColl writes. "Options include symptomatic acid-inhibitory therapy, endoscopy to check for underlying ulcer or another cause of symptoms, and repeat of the H. pylori test-and-treat strategy; other potential reasons for the symptoms should also be reconsidered."
After Eradication Therapy: What Next?
When gastrointestinal tract symptoms recur or persist after eradication therapy without first testing for H pylori, the most likely explanation is that the symptoms are unrelated to H pylori infection, rather than treatment failure. Unless persistent H pylori infection is confirmed, further eradication therapy should not be considered.
Eradication of H pylori infection should be confirmed in patients who have had an H pylori–associated ulcer or gastric MALT lymphoma or who have undergone resection for early gastric cancer. Tests for eradication may include a urea breath test or fecal antigen test performed at least 4 weeks after treatment is completed, so that false-negative results from suppression of H pylori are avoided. For patients requiring endoscopy, eradication can also be confirmed by testing during this procedure.
When treatment fails to eradicate H pylori infection, therapeutic options include empiric acid-inhibitory therapy, endoscopy to detect underlying ulcer or another cause of symptoms, and subsequent use of the noninvasive test-and-treat strategy. Clinicians should also consider another cause for the symptoms, such as biliary tract, pancreatic, musculoskeletal, or cardiac disease or psychosocial stress. Poor compliance with initial treatment may also be implicated and mandates adherence to the second treatment regimen.
Treatment failure may be caused by H pylori resistance to clarithromycin or metronidazole, or both. Bismuth-based quadruple therapy is often used as second-line therapy if initial treatment did not include a bismuth salt. In patients previously treated with a proton-pump inhibitor, amoxicillin, and clarithromycin, a proton-pump inhibitor used in combination with metronidazole and either amoxicillin or tetracycline is recommended.
"Data from randomized trials are lacking to guide the care of patients whose symptoms persist after completion of H. pylori eradication therapy for uninvestigated dyspepsia," Dr. McColl concludes. "The effect of eradication of H. pylori infection on the risk of gastric cancer is unclear but is currently under study."
N Engl J Med. 2010;362:1597-1604
Artículo completo: http://cme.medscape.com/viewarticle/721198?src=cmenews&uac=85318MZ
"Infection with H. pylori is a cofactor in the development of three important upper gastrointestinal diseases: duodenal or gastric ulcers (reported to develop in 1 to 10% of infected patients), gastric cancer (in 0.1 to 3%), and gastric mucosa-associated lymphoid-tissue (MALT) lymphoma (in <0.01%)," writes Kenneth E. L. McColl, MD, from the Division of Cardiovascular and Medical Sciences, University of Glasgow, Gardiner Institute, Glasgow, United Kingdom.
"The risk of these disease outcomes in infected patients varies widely among populations. The great majority of patients with H. pylori infection will not have any clinically significant complications."
Methods of Testing
Routine testing for H pylori infection is not recommended because the vast majority of patients with this infection do not have any associated clinical disease. However, confirmed gastric or duodenal ulcers and gastric MALT lymphoma are definite indications for detecting and treating H pylori infection. After surgical removal of early gastric cancers, it may also be reasonable to test for and eradicate H pylori infection.
For younger patients with upper gastrointestinal tract symptoms but without alarm symptoms such as weight loss, persistent vomiting, or gastrointestinal tract bleeding, it is reasonable to use a noninvasive test-and-treat strategy for H pylori infection. Options for noninvasive testing include the urea breath test, fecal antigen test, and serologic test. Of these options, the least accurate is the serologic test. Patients with positive test results should undergo eradication therapy.
For patients with alarm symptoms, or for older patients with new-onset dyspepsia, endoscopy is recommended. Depending on the specific set of guidelines used, older patients are defined as those 45 years or older or 55 years or older. Because nonsteroidal anti-inflammatory drugs can cause ulcers in the absence of H pylori infection, endoscopy is warranted for patients with dyspepsia associated with use of these drugs.
Treatments
Unless there is a high local rate of resistance to clarithromycin, appropriate first-line treatment is triple therapy using a proton-pump inhibitor plus clarithromycin and amoxicillin, each given twice per day for 7 to 14 days. Patients with a penicillin allergy should receive metronidazole instead of amoxicillin. When the prevalence of clarithromycin-resistant H pylori infection exceeds 20%, an alternative initial treatment regimen is quadruple therapy with a proton-pump inhibitor, tetracycline, metronidazole, and a bismuth salt for 10 to 14 days. However, bismuth salts are not available in the United States and in some other countries.
Another option is 10-day sequential therapy with a proton-pump inhibitor plus amoxicillin for 5 days, followed by a proton-pump inhibitor plus clarithromycin and tinidazole for 5 more days. However, the efficacy of this regimen needs to be confirmed before it is widely used.
"Data are lacking to inform the optimal management of recurrent or persistent dyspepsia after noninvasive testing and treatment of H. pylori infection," Dr. McColl writes. "Options include symptomatic acid-inhibitory therapy, endoscopy to check for underlying ulcer or another cause of symptoms, and repeat of the H. pylori test-and-treat strategy; other potential reasons for the symptoms should also be reconsidered."
After Eradication Therapy: What Next?
When gastrointestinal tract symptoms recur or persist after eradication therapy without first testing for H pylori, the most likely explanation is that the symptoms are unrelated to H pylori infection, rather than treatment failure. Unless persistent H pylori infection is confirmed, further eradication therapy should not be considered.
Eradication of H pylori infection should be confirmed in patients who have had an H pylori–associated ulcer or gastric MALT lymphoma or who have undergone resection for early gastric cancer. Tests for eradication may include a urea breath test or fecal antigen test performed at least 4 weeks after treatment is completed, so that false-negative results from suppression of H pylori are avoided. For patients requiring endoscopy, eradication can also be confirmed by testing during this procedure.
When treatment fails to eradicate H pylori infection, therapeutic options include empiric acid-inhibitory therapy, endoscopy to detect underlying ulcer or another cause of symptoms, and subsequent use of the noninvasive test-and-treat strategy. Clinicians should also consider another cause for the symptoms, such as biliary tract, pancreatic, musculoskeletal, or cardiac disease or psychosocial stress. Poor compliance with initial treatment may also be implicated and mandates adherence to the second treatment regimen.
Treatment failure may be caused by H pylori resistance to clarithromycin or metronidazole, or both. Bismuth-based quadruple therapy is often used as second-line therapy if initial treatment did not include a bismuth salt. In patients previously treated with a proton-pump inhibitor, amoxicillin, and clarithromycin, a proton-pump inhibitor used in combination with metronidazole and either amoxicillin or tetracycline is recommended.
"Data from randomized trials are lacking to guide the care of patients whose symptoms persist after completion of H. pylori eradication therapy for uninvestigated dyspepsia," Dr. McColl concludes. "The effect of eradication of H. pylori infection on the risk of gastric cancer is unclear but is currently under study."
N Engl J Med. 2010;362:1597-1604
Artículo completo: http://cme.medscape.com/viewarticle/721198?src=cmenews&uac=85318MZ
'La Sirvienta Bruta'
Aprovechando la ausencia de su esposa e hijos que pasan un fin de semana en la playa, Don Luis se encuentra insistiéndole a la nueva y muy bonita sirvienta, que le abra la puerta de su dormitorio.
- Anda, María, abre la puerta que no te va a pasar nada malo. Sólo vamos a gozar mucho.
- No, siñor, tese quieto!.
- Mira, María, si abres te aumento el sueldo...
- ¿Y, luego quí li dicimos a la patrona?
- Pues nada, ella no tiene porque enterarse de nada.
- Ta bueno, patrón, pero pase por dibajo di la puerta su cirtificado de que no tienes SIDA.
Don Luis recuerda el chequeo médico que se acaba de practicar y le pasa hasta su acta de nacimiento, ante lo cual la sirvienta por fin cede y Don Luis se da el gustazo. Al rato ya calmado y disfrutando de un buen tabaco, le dice Don Luis a sirvienta:
-¡Caramba, María, no sabes leer ni escribir, pero, que bien estas enterada de las cuestiones de salud!
- Si, patroncito, yo seré disnorante, muy disnorante, rete disnorante,pero esto del Sida no me lo pegan dos veces!
- Anda, María, abre la puerta que no te va a pasar nada malo. Sólo vamos a gozar mucho.
- No, siñor, tese quieto!.
- Mira, María, si abres te aumento el sueldo...
- ¿Y, luego quí li dicimos a la patrona?
- Pues nada, ella no tiene porque enterarse de nada.
- Ta bueno, patrón, pero pase por dibajo di la puerta su cirtificado de que no tienes SIDA.
Don Luis recuerda el chequeo médico que se acaba de practicar y le pasa hasta su acta de nacimiento, ante lo cual la sirvienta por fin cede y Don Luis se da el gustazo. Al rato ya calmado y disfrutando de un buen tabaco, le dice Don Luis a sirvienta:
-¡Caramba, María, no sabes leer ni escribir, pero, que bien estas enterada de las cuestiones de salud!
- Si, patroncito, yo seré disnorante, muy disnorante, rete disnorante,pero esto del Sida no me lo pegan dos veces!
Long term treatment of depression with selective serotonin reuptake inhibitors and newer antidepressants
Depression is commonly a recurrent illness: over half of people with a diagnosis of major depression will go on to have a further episode, and the risk of future relapse rises, with 80% of those having a second episode going on to have a third.
Most clinical guidelines recommend that treatment with antidepressants should be continued for four to six months after recovery to reduce the risk of relapse (re-emergence of original symptoms) and recurrence (new episode of depression).
However, the benefits of long term or maintenance treatment are considered, particularly by clinicians, to be less certain. A systematic review included 31 randomised trials (4410 participants) investigating whether continuing treatment with antidepressants (of all classes, although most included either a tricyclic antidepressant or an SSRI) reduced the risk of relapse.
These trials were mainly discontinuation studies in which participants with depressive disorders who had responded to acute treatment were randomly assigned to continue drug treatment or receive a placebo.
Pooled results found that, compared with placebo, continuing antidepressant treatment after recovery markedly reduced the proportion of patients who relapsed over one to three years (pooled odds ratio for relapse 0.30; 95% confidence interval 0.22 to 0.38).
A re-analysis of these data, summarises the rates of relapse by length of follow-up. While the absolute risk reduction progressively increased from six to 36 months of follow-up, the relative risk reduction was stable (from 60% at six months to 58% at 36 months), suggesting that continuing antidepressant treatment more than halved the average relapse rate regardless of the duration of treatment. The absolute risk reduction was similar at six and 12 months, although the larger sample size at 12 months provides a more precise estimate. On average four patients required antidepressant treatment to prevent one additional relapse. Further systematic reviews, restricted to data on SSRIs and newer antidepressants (bupropion, mirtazapine, nefazodone, and venlafaxine), produced similar findings: a risk reduction in the proportion of patients relapsing of about 50%.
These trials also indicate that the reduction in relapse rates with prophylactic antidepressants is greater for patients with single episodes (odds ratio for relapse 0.12; 0.06 to 0.26) than for those with recurrent episodes (0.37; 0.31 to 0.44).
An evidence based approach to long term treatment with SSRIs and newer antidepressants
In adults with depression who have benefited from treatment with an antidepressant good evidence exists that they are at high risk of relapse, particularly in the first six months after recovery. Good evidence also exists that continuing antidepressant treatment reduces the absolute risk of relapse by about 50%.
The trials on which guidelines are based come predominantly from secondary care settings with follow-up limited to three years. Longer term studies that include patients from primary care with less severe illness would inform clinical practice.
Psychological treatments may augment the prophylactic effect of antidepressants, but much of the evidence for this has been inconclusive. Several studies have found that cognitive behavioural therapy combined with maintenance drug treatment significantly reduces rates of relapse compared with antidepressants alone, although whether this additional benefit is due to non-specific therapeutic effects is not clear.
In summary, after a single depressive episode in the absence of specific risk factors for relapse (see the box on risk factors) people should be advised to continue treatment with antidepressants for 12 months after recovery. Treatment should be regularly re-evaluated, with the frequency determined by the severity of the episode. Individuals with risk factors for relapse, in particular those with several previous episodes or two episodes in the recent past, should be advised to continue with treatment for at least 12 months and consider long term maintenance treatment. With long term antidepressant treatment, regular reviews should take into consideration the social consequences of relapse for the individual, concurrent physical health problems, and the development of adverse effects, as well as patient preference.
BMJ 2010;340:c1468
Steven Reid, consultant psychiatrist1, Corrado Barbui, lecturer in psychiatry2 1 Department of Liaison Psychiatry, St Mary’s Hospital, London W2 1PF, 2 Department of Medicine and Public Health, Section of Psychiatry and Clinical Psychology, University of Verona, 37134 Verona, Italy Correspondence to: S Reid steve.reid@nhs.net
Most clinical guidelines recommend that treatment with antidepressants should be continued for four to six months after recovery to reduce the risk of relapse (re-emergence of original symptoms) and recurrence (new episode of depression).
However, the benefits of long term or maintenance treatment are considered, particularly by clinicians, to be less certain. A systematic review included 31 randomised trials (4410 participants) investigating whether continuing treatment with antidepressants (of all classes, although most included either a tricyclic antidepressant or an SSRI) reduced the risk of relapse.
These trials were mainly discontinuation studies in which participants with depressive disorders who had responded to acute treatment were randomly assigned to continue drug treatment or receive a placebo.
Pooled results found that, compared with placebo, continuing antidepressant treatment after recovery markedly reduced the proportion of patients who relapsed over one to three years (pooled odds ratio for relapse 0.30; 95% confidence interval 0.22 to 0.38).
A re-analysis of these data, summarises the rates of relapse by length of follow-up. While the absolute risk reduction progressively increased from six to 36 months of follow-up, the relative risk reduction was stable (from 60% at six months to 58% at 36 months), suggesting that continuing antidepressant treatment more than halved the average relapse rate regardless of the duration of treatment. The absolute risk reduction was similar at six and 12 months, although the larger sample size at 12 months provides a more precise estimate. On average four patients required antidepressant treatment to prevent one additional relapse. Further systematic reviews, restricted to data on SSRIs and newer antidepressants (bupropion, mirtazapine, nefazodone, and venlafaxine), produced similar findings: a risk reduction in the proportion of patients relapsing of about 50%.
These trials also indicate that the reduction in relapse rates with prophylactic antidepressants is greater for patients with single episodes (odds ratio for relapse 0.12; 0.06 to 0.26) than for those with recurrent episodes (0.37; 0.31 to 0.44).
An evidence based approach to long term treatment with SSRIs and newer antidepressants
In adults with depression who have benefited from treatment with an antidepressant good evidence exists that they are at high risk of relapse, particularly in the first six months after recovery. Good evidence also exists that continuing antidepressant treatment reduces the absolute risk of relapse by about 50%.
The trials on which guidelines are based come predominantly from secondary care settings with follow-up limited to three years. Longer term studies that include patients from primary care with less severe illness would inform clinical practice.
Psychological treatments may augment the prophylactic effect of antidepressants, but much of the evidence for this has been inconclusive. Several studies have found that cognitive behavioural therapy combined with maintenance drug treatment significantly reduces rates of relapse compared with antidepressants alone, although whether this additional benefit is due to non-specific therapeutic effects is not clear.
In summary, after a single depressive episode in the absence of specific risk factors for relapse (see the box on risk factors) people should be advised to continue treatment with antidepressants for 12 months after recovery. Treatment should be regularly re-evaluated, with the frequency determined by the severity of the episode. Individuals with risk factors for relapse, in particular those with several previous episodes or two episodes in the recent past, should be advised to continue with treatment for at least 12 months and consider long term maintenance treatment. With long term antidepressant treatment, regular reviews should take into consideration the social consequences of relapse for the individual, concurrent physical health problems, and the development of adverse effects, as well as patient preference.
BMJ 2010;340:c1468
Steven Reid, consultant psychiatrist1, Corrado Barbui, lecturer in psychiatry2 1 Department of Liaison Psychiatry, St Mary’s Hospital, London W2 1PF, 2 Department of Medicine and Public Health, Section of Psychiatry and Clinical Psychology, University of Verona, 37134 Verona, Italy Correspondence to: S Reid steve.reid@nhs.net
