![]() ![]() Congress ![]() ![]() ![]() Sponsors màj 23/07/98 |
Introduction/Welcome address
First of all, I would like to say my pleasure to welcome you all to Montpellier. You know that our medical school is one of the oldest in the world, thanks to its hippocratic tradition, and because it is placed inside the umbilical cord between North and South, East and West Europe. This medical cord, which was in the past, the road for Hannibal's elephants and roman legions, is also today a corridor, with sixty thousand vehicles by day today, hundred thousand tomorrow, and will increase the levels of nitrogen dioxide, ozone and diesel exhausts during the summer months. I would like then to thank my friend Pascal Chanez, who has organized this meeting, working with Isabelle Vachier, Jean Bousquet and Philippe Godard, with financial support of Merck-Sharp and Dhome - particularly Mrs Doctor Fouchard - and then, to congratulate my friend Steve Holgate, the ENFUMOSA general secretary. |
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1. Asthma 2000 !
Year two thousand is today, is upon us, is finished. The dawn of a new century is always a challenging era and we have long been involved into making predictions, of what that dawn will bring. For a long time, we have sung the refrain "When we reach the year 2000....!" But that future now, is today and we perfectly know what will be the extent of our knowledge, and the limits of our understanding in the year 2000.
We can state with pride that only "Yesterday", we had already formulated some important ideas. Trousseau who had suffered an asthmatic attack on catching his valet stealing the horses' oats from the granary, demonstrated, perhaps albeit unwillingly, that the inhalation of allergen led to the onset of an asthmatic attack. But between the allergenic protein and the dyspnoea, remained a baffling impenetrable fog. In "Hygiene of asthmatics" which was published in eighteen ninety six, Brissaud pointed out the polymorphism of asthma, and confirmed that it developed from the superposition of spasmodic factors and vasomotor and secretory factors which is still held to be the case today.
In the nineteen fifties, the Pasteur-Vallery-Radot group in Paris carried out the first endoscopies in asthmatics, and described in fascinating details, the endobronchial lesions found in asthma. Unfortunately, at this time photographic and filming techniques were not sufficiently advanced, and the authors were limited to drawings of what they could see ; the consequence of this being that their work, did not achieve the success it merited.
2. What are the challenges for Asthma 2010 ?
Epidemiology, genetics and
pathophysiology
Are we well enough
informed on the epidemiology and genetics of the disease ?
When we consider the results of epidemiological studies which are now world-wide and scientifically credible, we see without discussion that bronchial asthma is increasing, everywhere in the world, but there are also differences between, for example, Finland (very low) and New Zealand (extremely high). These differences are probably due to geographical factors. What is the role of genetic factors in this situation ? After being told that they were linked to ONE chromosome for asthma and allergy, we now know that there are 20 chromosomic sites corresponding to numerous genotypes (see the attached table by clicking here).
If we are willing to implicate pollution for the increase in the frequency of asthma, a direct link remains to be fully and unequivocally delineated. There remains much to be discovered as we step into the 21st century.
What type of asthma are we going to
talk about ?
We are very pleased with our
classifications (mild, intermittent, severe asthma etc...) and
international consensus, but can we be sure that these are
sufficient to cover all the asthmatics which we see daily in the
clinic ? Could it be that the box, so to speak, into which we
place our severe asthmatics contains a puzzle with too many
pieces.
Where are we with regard to
treatment ?
From the Datura
leaves powder inhalation of Marcel Proust, to the long acting
§-mimetics on one hand and the powerful inhaled glucocorticoids
on the other, together with the anti-leukotrienes which are now
available, we have run a fantastic way allowing us to control the
majority of asthmatics and to give them a quality of life which
is close to normal.
But here are the new challenges :
| Les
gènes liés à l'asthme et aux phénotypes associés (hyperréactivité bronchique- HRB - et atopie) |
|||
| Régions chromosomiques | Gènes candidats | Phénotypes associés | Equipes/années |
| 1q21.23 | Fce Rla g | IgE totales, HRB | Holgate 1996 |
| 4 | HRB | Cookson 1996 | |
| 5q31.1-q33 | IL4 | IgE totales | Marsh 1994 |
| IL9, IL4 | IgE totales | Holgate 1996 | |
| Asthme | Meyers 1994 | ||
| HRB | Postma 1995 | ||
| 6p21.3 | HLA-D | IgE spécifiques | Marsh 1981 |
| TNFa | IgE totales, HRB | Holgate 1996 | |
| IgE totales | Cookson 1996 | ||
| 7 | IgE totales, atopie | Cookson 1996 | |
| 9q22 | IFNa | IgE totales, HRB | Holgate 1996 |
| 11q13 | Fce Rlb | IgE totales, HRB | Holgate 1996 |
| Fce Rlb | Atopie | Cookson 1994 | |
| Fce Rlb | Asthme, HRB | Van Herwerden 1995 | |
| 12q22.24 | IFNg | IgE totales, HRB | Holgate 1996 |
| IFNg | IgE totales, Asthme | Marsh 1996 | |
| 13 | IgE totales, atopie | Cookson 1996 | |
| 14q11.1 | TCRa | IgE spécifiques | Cookson 1994 |
| 16p12.1-12.2 | IL4R | IgE totales, HRB | Holgate 1996 |
| IgE totales, HRB | Cookson 1996 | ||
| 19q13.3 | FceRII | IgE totales, HRB | Holgate 1996 |
| 19q13.3-13.4 | IL11 | IgE totales, HRB | Holgate 1996 |
| 22q13 | IL2R | IgE totales, HRB | Holgate 1996 |
En italiques figurent les résultats qui demandent confirmation
.
Enfumosa
Congrès Conçue et réalisée par: Michel Godard (at)
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Date de création: 1er Mars 1998 -Dernière mise à jour: 23/07/98
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