{"id":32,"date":"2010-04-22T10:01:34","date_gmt":"2010-04-22T10:01:34","guid":{"rendered":"http:\/\/www.pjh.fr\/wordpress\/?page_id=32"},"modified":"2010-07-06T23:04:04","modified_gmt":"2010-07-06T21:04:04","slug":"maladie-de-waldenstrom-diagnostic","status":"publish","type":"page","link":"http:\/\/www.pjh.fr\/wordpress\/?page_id=32","title":{"rendered":"Diagnostic et pr\u00e9sentation"},"content":{"rendered":"<div class=\"pni-navigation pni-navigtion\"><a name=\"pni-top0\"><\/a><ol><li><a href=\"#introduction\">Introduction<\/a><\/li><li><a href=\"#pr%c3%a9sentation-clinique\">Pr\u00e9sentation clinique<\/a><ol><li><a href=\"#a-manifestations-li%c3%a9es-%c3%a0-linfiltration-tumorale\">A. Manifestations li\u00e9es \u00e0 l&rsquo;infiltration tumorale<\/a><\/li><li><a href=\"#b-complications-li%c3%a9es-%c3%a0-limmunoglobuline\">B. Complications li\u00e9es \u00e0 l&rsquo;immunoglobuline <\/a><ol><li><a href=\"#waldenstr%c3%b6m-et-cryoglobulin%c3%a9mie\">Waldenstr\u00f6m et cryoglobulin\u00e9mie\n<\/a><\/li><li><a href=\"#waldenstr%c3%b6m-et-amylose\">Waldenstr\u00f6m et amylose<\/a><\/li><\/ol><\/li><\/li><\/ol><\/li><li><a href=\"#diagnostic\">Diagnostic<\/a><ol><li><a href=\"#a-ant%c3%a9c%c3%a9dents-importants-car-20-%de-formes-familiales\">A. Ant\u00e9c\u00e9dents : importants car 20 %de formes familiales !!!<\/a><\/li><li><a href=\"#b-crit%c3%a8res-diagnostiques-de-maladie-de-waldenstr%c3%b6m-2002\">B. Crit\u00e8res diagnostiques de maladie de Waldenstr\u00f6m (2002)<\/a><\/li><li><a href=\"#c-les-examens-diagnostiques\">C. Les examens diagnostiques :<\/a><\/li><\/ol><\/li><\/ol><\/div><div class=\"pni-content\">\n<table border=\"1\" cellspacing=\"0\" cellpadding=\"2\">\n<tbody>\n<tr>\n<td style=\"background-color: #dddddd;\"><strong>R\u00e9sum\u00e9<br \/>\n<\/strong><\/td>\n<\/tr>\n<tr>\n<td>\n<ul>\n<li>syndrome lymphoprolif\u00e9ratif B avec prolif\u00e9ration m\u00e9dullaire de cellules lymphoplasmocytaires s\u00e9cr\u00e9tant une IgM<\/li>\n<li>pr\u00e9disposition familiale dans 20% des cas<\/li>\n<li>Pr\u00e9sentation clinique et biologique :\n<ul>\n<li>Homme (H\/F = 1.5)<\/li>\n<li>65 ans<\/li>\n<li>syndrome tumoral moins fr\u00e9quent que dans les autres lymphomes de bas grade<\/li>\n<li>cytop\u00e9nies<\/li>\n<li>complications li\u00e9e \u00e0 l&rsquo;Ig : hyperviscosit\u00e9, neuropathie, agglutinines froides, cryoglobulin\u00e9mie, amylose<\/li>\n<\/ul>\n<\/li>\n<li>Diagnostic :\n<ul>\n<li>pr\u00e9sence d&rsquo;une IgM monoclonale (EPP + IF)<\/li>\n<li>infiltration m\u00e9dullaire par de petits lymphocytes pr\u00e9sentant une diff\u00e9renciation plasmacyto\u00efde\/plasmocytaire<\/li>\n<li>ph\u00e9notype B CD20+ (g\u00e9n\u00e9ralement CD5-)<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p><strong><a href=\"#introduction\"><br \/>\n<\/a><a href=\"#diagnostic\"><\/a><\/strong><\/p>\n<h2><a name=\"introduction\"><\/a>Introduction<a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h2>\n<blockquote><p>La maladie de Waldenstr\u00f6m est un <strong>syndrome lymphoprolif\u00e9ratif B<\/strong> r\u00e9sultant de l&rsquo;accumulation, principalement au niveau de la moelle osseuse, de cellules clonales <strong>lymphoplasmocytaires<\/strong> s\u00e9cr\u00e9tant une <strong>Ig M<\/strong>. Cette entit\u00e9 fait partie des <strong>lymphomes lymphoplasmocytaires (LPL)<\/strong> dans la classification OMS : plus de 95 % des LPL sont des maladies de Waldenstr\u00f6m (moins de 5 % s\u00e9cr\u00e8tent une autre Ig ou sont non s\u00e9cr\u00e9tant).<\/p>\n<p>La maladie de Waldenstr\u00f6m a \u00e9t\u00e9 d\u00e9crite initialement en 1944 par Jan Waldenstr\u00f6m.<\/p>\n<p>On retrouve une <strong>pr\u00e9disposition familiale<\/strong> chez 20% des patients.<\/p><\/blockquote>\n<h2><a name=\"pr%c3%a9sentation-clinique\"><\/a>Pr\u00e9sentation clinique<a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h2>\n<ul>\n<li>Plus fr\u00e9quent chez l&rsquo;<strong>homme <\/strong>(Sex ratio = 1.5)<\/li>\n<li>\u00e2ge moyen au diagnostic : <strong>65 ans<\/strong><\/li>\n<li><strong>Spl\u00e9nom\u00e9galie et <\/strong><strong>ad\u00e9nopathies plus rares<\/strong> que dans les autres lymphomes de bas grade (&lt; 15%-30%)<\/li>\n<\/ul>\n<ul>\n<li>Les manifestations cliniques sont li\u00e9es \u00e0 <strong>l&rsquo;infiltration tumorale<\/strong> et\/ou aux complications li\u00e9es \u00e0 la s\u00e9cr\u00e9tion de l&rsquo;<strong>immunogloubline <\/strong>(cf. Tableau 1)<\/li>\n<\/ul>\n<h3><a name=\"a-manifestations-li%c3%a9es-%c3%a0-linfiltration-tumorale\"><\/a>A. <span style=\"text-decoration: underline;\">Manifestations li\u00e9es \u00e0 l&rsquo;infiltration tumorale<\/span><a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h3>\n<ul>\n<li>Infiltration m\u00e9dullaire (quasi-constante) : <strong>cytop\u00e9nies<\/strong><\/li>\n<li>1\/3 des patients : <strong>ad\u00e9nopathies<\/strong>, <strong>spl\u00e9nom\u00e9galie <\/strong>ou <strong>h\u00e9patom\u00e9galie<\/strong><\/li>\n<\/ul>\n<ul>\n<li>Les atteintes d&rsquo;<strong>autres organes sont plus rares<\/strong> mais tout organe peut \u00eatre virtuellement infiltr\u00e9 :\n<ul>\n<li>3-5% d&rsquo;atteinte pulmonaire (infiltrats, nodules, masses, \u00e9panchements pleuraux)<\/li>\n<li>quelques cas d&rsquo;infiltration gastrique<\/li>\n<li>infiltration r\u00e9nale \/ masses r\u00e9nales ou p\u00e9ri-r\u00e9nales<\/li>\n<li>infiltration du derme (l\u00e9sions maculo-papuleuses, plaques, nodules)<\/li>\n<li>atteinte orbitaire (r\u00e9tro-orbitaire, glandes lacrymales, infiltration de la conjonctive voire uv\u00e9ite)<\/li>\n<li>infiltration du SNC rare<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<blockquote><p><strong>Syndrome de Bing-Neel<\/strong><br \/>\nCliniquement : confusion, pertes de m\u00e9moire, d\u00e9sorientation, d\u00e9ficits moteurs voire coma<br \/>\nUne hyperviscosit\u00e9 prolong\u00e9e est responsable d&rsquo;alt\u00e9ration de la perm\u00e9abilit\u00e9 vasculaire et<br \/>\npermet une infiltration p\u00e9rivasculaire par les cellules malignes au niveau c\u00e9r\u00e9bral.<br \/>\nenviron 35 cas publi\u00e9s<\/p><\/blockquote>\n<h3><a name=\"b-complications-li%c3%a9es-%c3%a0-limmunoglobuline\"><\/a>B. <span style=\"text-decoration: underline;\">Complications li\u00e9es \u00e0 l&rsquo;immunoglobuline <\/span><a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h3>\n<div><strong>Tableau 1 : Morbidities mediated by the monoclonal IgM protein in WM<\/strong><\/div>\n<div><a href=\"index.php?option=com_jombib&amp;task=showbib&amp;id=8&amp;return=index.php%3Foption%3Dcom_jombib%26amp%3Bcatid%3D54&amp;Itemid=69\">Treon, S. P. (2009), \u00ab\u00a0How I treat Waldenstrom macroglobulinemia\u00a0\u00bb, <em>Blood<\/em>, <strong>114<\/strong>, <strong>12<\/strong>: 2375-85.<\/a><\/div>\n<div><strong> <\/strong><\/p>\n<table border=\"1\" cellspacing=\"0\" cellpadding=\"2\">\n<tbody>\n<tr>\n<td>Propri\u00e9t\u00e9 de l&rsquo;IgM monoclonale<\/td>\n<td>Circonstances diagnostiques<\/td>\n<td>Manifestations cliniques<\/td>\n<\/tr>\n<tr>\n<td>Structure pentam\u00e9rique<\/td>\n<td>Hyperviscosit\u00e9<\/td>\n<td>C\u00e9phal\u00e9es, vision floue, \u00e9pistaxis, h\u00e9morragies r\u00e9tiniennes, crampes,  ralentissement psychomoteur, h\u00e9morragies intracr\u00e2niennes<\/td>\n<\/tr>\n<tr>\n<td>Pr\u00e9cipitation \u00e0 froid<\/td>\n<td>Cryoglobulin\u00e9mie<br \/>\n(type I)<\/td>\n<td>Ph\u00e9nom\u00e8nes de Raynaud, acrocyanose, ulc\u00e8res, purpura, urticaire au froid<\/td>\n<\/tr>\n<tr>\n<td>Autoantibody activity to myelin-associated glycoprotein (MAG),  ganglioside M1 (GM1), sulfatide moieties on peripheral nerve sheaths<\/td>\n<td>Neuropathies  p\u00e9riph\u00e9riques<\/td>\n<td>Neuropathies sensitivo-motrices, neuropathies douloureuses, marche  ataxique<\/td>\n<\/tr>\n<tr>\n<td>Auto-anticorps \u00e0 activit\u00e9 anti IgG<\/td>\n<td>Cryoglobulinemia<br \/>\n(type II)<\/td>\n<td>Purpura, arthralgies, insuffisance r\u00e9nale, neuropathies   sensitivo-motrices<\/td>\n<\/tr>\n<tr>\n<td>Auto-anticorps dirig\u00e9s contre les antig\u00e8nes \u00e9rythrocytaires<\/td>\n<td>Agglutinines froides<\/td>\n<td>Anemie h\u00e9molytique, Ph\u00e9nom\u00e8nes de Raynaud, acrocyanose, livedo reticularis<\/td>\n<\/tr>\n<tr>\n<td>D\u00e9p\u00f4ts tissulaires de substance amorphe<\/td>\n<td>Dysfonctions d&rsquo;organe<\/td>\n<td>peau : maladie bulleuse, papules : \u00ab\u00a0macroglobulinemia cutis\u00a0\u00bb, syndrome de Schnitzler<br \/>\nTube digestif : diarrh\u00e9es, malabsorption, saignements<br \/>\nRein : prot\u00e9inurie non s\u00e9lective, insuffisance r\u00e9nale<\/td>\n<\/tr>\n<tr>\n<td>D\u00e9p\u00f4ts de tissus amylo\u00efdes (cha\u00eenes l\u00e9g\u00e8res le + souvent)<\/td>\n<td>Dysfonctions d&rsquo;organe<\/td>\n<td>Fatigue, perte de poids, oed\u00e8me, h\u00e9patom\u00e9galie, macroglossie, dysfonction d&rsquo;organe : coeur, reins, foie, syst\u00e8me nerveux sensitif et autonome<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p><strong> <\/strong><\/p>\n<\/div>\n<h4><a name=\"waldenstr%c3%b6m-et-cryoglobulin%c3%a9mie\"><\/a><strong>Waldenstr\u00f6m et cryoglobulin\u00e9mie<br \/>\n<\/strong><a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h4>\n<p>Jusqu&rsquo;\u00e0 20 % des patients pr\u00e9sentent une IgM ayant tendance \u00e0 pr\u00e9cipiter \u00e0 froid et pouvant se comporter comme une cryoglobulin\u00e9mie de type I.  N\u00e9anmoins, les manifestations cliniques de cryoglobulin\u00e9mie (Raynaud, ulc\u00e8res cutan\u00e9s, n\u00e9croses, urticaire \u00e0 froid&#8230;) ne sont retrouv\u00e9s que dans moins de 5% des cas.<\/p>\n<h4><a name=\"waldenstr%c3%b6m-et-amylose\"><\/a>Waldenstr\u00f6m et amylose<a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h4>\n<p>L&rsquo;amylose (AL) est une complication rare de la maladie de Waldenstr\u00f6m. Dans une large s\u00e9rie de la Mayo Clinic de patients pr\u00e9sentant des pics monoclonaux IgM (<em><strong>J Clin Oncol 11:914-920, 1993<\/strong><\/em>), seulement 2% des patients ayant un pic IgM ont pr\u00e9sent\u00e9 une amylose, parmi eux, 21% avaient une maladie de Waldenstr\u00f6m. Les organes atteints sont le coeur (44%), le syst\u00e8me nerveux p\u00e9riph\u00e9rique (38%), les reins (32%), les tissus mous (18%), le foie (14%) et les poumons (10%). L&rsquo;incidence des atteintes cardiaque et pulmonaire semble \u00eatre plus fr\u00e9quente avec les amylose associ\u00e9e \u00e0 une IgM qu&rsquo;avec les autres Ig. Le diagnostic peut \u00eatre en g\u00e9n\u00e9ral fait soit sur une biopsie de la graisse sous-cutan\u00e9e abdominale ou la BOM.<br \/>\nL&rsquo;amylose est plus souvent responsable du d\u00e9c\u00e8s que la maladie de Waldenstr\u00f6m sous-jacente, la majorit\u00e9 des d\u00e9c\u00e8s \u00e9tant attribuable \u00e0 l&rsquo;<strong>atteinte cardiaque<\/strong>.<\/p>\n<h2><a name=\"diagnostic\"><\/a>Diagnostic<a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h2>\n<h3><a name=\"a-ant%c3%a9c%c3%a9dents-importants-car-20-%de-formes-familiales\"><\/a>A. Ant\u00e9c\u00e9dents : importants car 20 %de formes familiales !!!<a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h3>\n<ul>\n<li><strong>Familiaux :<\/strong> Indispensables \u00e0 r\u00e9cup\u00e9rer car on retrouve jusqu&rsquo;\u00e0 20% de formes familiales =&gt; <strong>arbre g\u00e9n\u00e9alogique<\/strong> +++<\/li>\n<li><strong>Personnels : <\/strong>exposition \u00e0 l&rsquo;h\u00e9patite C ??? (discut\u00e9)<\/li>\n<\/ul>\n<h3><a name=\"b-crit%c3%a8res-diagnostiques-de-maladie-de-waldenstr%c3%b6m-2002\"><\/a>B. Crit\u00e8res diagnostiques de maladie de Waldenstr\u00f6m (2002)<a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h3>\n<table border=\"1\" cellspacing=\"0\" cellpadding=\"2\">\n<tbody>\n<tr>\n<td><strong>Crit\u00e8res<br \/>\n(Second International Workshop on Waldenstrom&rsquo;s Macroglobulinemia, 2002)<\/strong><\/td>\n<\/tr>\n<tr>\n<td>IgM monoclonale quelque soit sa concentration<\/td>\n<\/tr>\n<tr>\n<td>Infiltration m\u00e9dullaire par de petits lymphocytes pr\u00e9sentant une diff\u00e9renciation plasmacyto\u00efde\/plasmocytaire<\/td>\n<\/tr>\n<tr>\n<td>Infiltration m\u00e9dullaire intertrab\u00e9culaire*<\/td>\n<\/tr>\n<tr>\n<td>Surface IgM+, CD5\u00b1, CD10\u2013, CD19+, CD20+, CD22+, CD23\u2013, CD25+, CD27+, FMC7+, CD103\u2013, CD138 immunophenotype*<\/td>\n<\/tr>\n<tr>\n<td>* en faveur mais non n\u00e9cessaire au diagnostic<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<h3><a name=\"c-les-examens-diagnostiques\"><\/a>C. Les examens diagnostiques :<a href=\"#pni-top0\" class=\"toplink\">^<\/a><\/h3>\n<table style=\"background-color: #f3f3f3; width: 90%;\" border=\"1\" cellspacing=\"0\" cellpadding=\"4\">\n<tbody>\n<tr>\n<td>La<strong> Biopsie ost\u00e9o-m\u00e9dullaire et\/ou le my\u00e9logramme coupl\u00e9 \u00e0 un  immunoph\u00e9notypage<br \/>\nL&rsquo;\u00e9lectrophor\u00e8se des protides + Immunofixation<\/strong><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<blockquote><p><strong>NB : le pic est mieux \u00e9valu\u00e9 \u00e0 l&rsquo;\u00e9lectrophor\u00e8se des protides qu&rsquo;au dosage pond\u00e9ral des Ig, on utilise l&rsquo;EPP pour suivre la maladie.<\/strong><\/p><\/blockquote>\n<p>Le <strong>niveau du pic d&rsquo;IgM<\/strong> a en g\u00e9n\u00e9ral une bonne corr\u00e9lation avec la masse tumorale avec quelques exceptions :<\/p>\n<ul>\n<li>cryoglobulin\u00e9mie<\/li>\n<li>traitements par rituximab (effet <strong>flare <\/strong>=&gt; majoration du pic monoclonal) ou par bort\u00e9zomib 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