Monday, January 21, 2013

Lance Armstrong’s Dope: Why EPO?

Photo-Gallery-Lance-Armstrong Lance Armstrong, winner of 7 consecutive Tour de France bicycle race titles, ultimately admitted that his victory was fuelled by drugs i.e.EPO, steroid and even blood transfusion. His career is ended now and all his trophies were stripped, but curiosity might drive us question how that “EPO” makes him an infamous cyclist nobody can beat.

EPO?

EPO, short of Erythropoietin, is a hormone produced mostly by kidney to ultimately create red blood cells (RBC) in red bone marrow, in response to tissue hypoxia (low oxygen in tissue), blood loss or iron therapy (in those who have iron deficiency). It is normally-occurring hormone that keeps our RBC produced. However, EPO, as was used by Lance Armstrong, was artificially harvested, or we can say “Drug”. That EPO drug is epoetin alfa (under trade name Procrit® or Epogen®) which is used therapeutically for people with low red blood counts (such as those received chemotherapy or anemia). On the other hand, EPO comes at a price. Because EPO excessively increases the number of RBC, it could raise viscosity of blood, thus makes it hard for heart to pump (due to high resistance to blood flow), and eventually stroke.

So why does EPO relate to winning?

red-blood-cells

Running, cycling or weight lifting is sport requires strong endurance. Therefore, oxygen delivery to muscle mass is an important key to success, yet it is a limited factor in normal individual. So, to increase athlete’s performance in sport, they need to increase their blood oxygen-carrying capability. But how?

One among other answers to this question lies inside red blood cells. Since RBC transport oxygen, athletes have tried to increase their red blood cell counts known as “Blood Doping” or “Artificially Induced Polycythemia”, as was done by Lance Armstrong. As explained above that EPO might lead to stroke, evidence pointed out that 15 cyclists had died from EPO-related stroke or heart attack in 1980s, which ultimately drove International Olympic Committee to ban the use of epoetin alfa in sport.

EPO, one among other banned substances Lance Armstrong used, was an indicator that his winning was of no meaning but cheat. Additionally, that might give an implication that Lance had not physically pushed himself to the limit, instead he relied on drug that makes no sense to the beautiful definition of “Sport”.

Kenyans are *always* marathon running gold-medalists

Have you ever wondered why those Kenyans always place themselves on top of the list in marathon winner? Of course, their endurance is so strong, and that might explain how they possibly run kilometers non-stop. So, the way we explain it is the way we look at their training ground. Kenya is an African country with highland, specifically more than 2 000 meters above sea level. Because high altitude is scarce of oxygen, their body produces natural EPO to increase their RBCs and even more when they greatly exercise (our body needs more oxygen when exercise). Therefore, their performance and endurance were boosted when they compete in lower land i.e. in Phnom Penh, because their EPO level was higher than athletes trained at lower altitude. Thus, many athletes around the world now become attracted to set up their training camp in Kenya as well.

As epotin alfa is banned, however, it is difficult to detect (high reticulocytes counts) as it is identical to natural Erythropoietin.

Tuesday, January 8, 2013

Reflux Gastro-oesophagienne

Definition

Reflux gastro-oesophagienne est le mouvement de contenu gastrique dans l’œsophage distal.

Pathogenie

- Mécanisme anti-reflux normale : sphincter d’œsophage inferieur (LES), diaphragme crural, anatomie de jonction gastro-œsophagienne.
- Reflux est provoqué par la perte de gradient de pression entre LES et l’estomac.
Cause de l’hypotonie de LES :
- Sans causes apparentes
- Secondaire à myopathie associée avec pseudo-obstruction intestinal chronique, grossesse, tabac, médicament anticholinergique, relaxante de muscle lisse, atteinte chirurgical de LES et œsophagite.
Autre causes :
- Volume gastrique augmentée (post-repas, obstruction de pylore, stase gastrique)
- Contenu gastrique près de jonction gastro-œsophagienne (courber, coucher, hernie hiatale)
- Pression gastrique augmentée (obésité, grossesse, ascite, vêtement serré)
Exposition de l’œsophage à contenu de reflex dépende aux épisodes de reflux, fréquences de reflux, taux de clairance œsophagienne par pesanteur et contraction péristaltisme. La salive aussi joue un rôle dans la neutralisation de l’acidité. Donc, la perturbation de péristaltisme et de salive augmente l’exposition de l’œsophage à l’acidité de contenu de reflux.
Si la contenu gastrique passe à l’œsophage cervicale ou traverse le sphincter supérieur, elle peut entrer le pharynx, larynx, trachée.

Clinique

- Asymptomatique
- Retard (traiter à domicile)
- Pyrosis et régurgitation de contenu gastrique aigre dans la bouche. (plus courant)
- Douleur pseudo-angine ou thoracique
- Dysphagie, perte de poids (à noter l’œsophage de Barrett)
- Manifestation extra-œsophagienne : toux, laryngite, pharyngite…

Diagnostic

- Évidemment clinique
- Documentation de l’atteinte muqueuse :
o Lavement baryté : Plutôt normale. Chercher l’ulcère.
o Œsophagoscopie : chercher l’érosion, ulcère, œsophage de Barrett, adénocarcinome…
o Biopsie muqueuse : chercher l’œsophagite.
o Bernstein test : chercher l’œsophagite.
o Extra-œsophagienne : examen ORL et thoracique
- Quantifier le reflux
o pH métrie : BRAVO. (seulement reflux acidique)

Traitement

- Objective :
o Calmer les symptômes
o Traiter l’œsophagite. (si l’existe)
o Prévenir la complication
1- Modification la mode de vie : pour réduire l’incident de reflux
- Elever tête du lit
- Éviter le repas ou boisson avant se coucher
- Éviter le repas épicé ou graisseux
- Éviter l’alcool et tabac
- Réduire le poids
- Antacide ou inhibiteur H2
2- Symptômes persistés
Sans oesophagite · Antacide.
o (Gaviscon), 10mL 30min après repas et avant de s’endormir
· Médicament promotilité
o Cisapride 10mg. 4f/j
o Metoclopramide 10mg. 4f/j
· Inhibiteur H2
o Cimetidine, 400mg 2f/j
o Ranitidine, 150mg 2/j
o Famotidine, 20mg 2/j
o Nizatidine, 150mg 2/j








Avec oesophagite · Inhibiteur H2 (dose habituelle ou doublée selon la sévérité)
· Inhibiteur H2 + Promotilité
· IPP
o Oméprazole 20mg. Matin
o Lansoprazole 30mg. Matin




- Reflux alkaline ou légèrement acidique : cholestyramine, aluminum hydroxide, ou sucralfate.
3- Chirurgie : Fondoplicature

Complication

- L’oesophagite, ulceration, œsophage de Barrette.

Référence

Fauci, Braunwald et al., Harrison’s Principles of Internal Medicine (Ed. 18, 2012), McGraw-Hill
Robert C. Lowe, M. Michael Wolfe, Cecil Essential of Medicine (Ed. 6th), Elsevier.