{"id":29022,"date":"2025-06-11T10:26:12","date_gmt":"2025-06-11T08:26:12","guid":{"rendered":"https:\/\/www.neolifesalud.com\/blog\/sin-categorizar\/terapies-emergents-contra-la-lipoproteina-a\/"},"modified":"2025-06-11T10:26:12","modified_gmt":"2025-06-11T08:26:12","slug":"terapies-emergents-contra-la-lipoproteina-a","status":"publish","type":"post","link":"https:\/\/www.neolifesalud.com\/ca\/blog\/prevencio-i-antiaging\/terapies-emergents-contra-la-lipoproteina-a\/","title":{"rendered":"Ter\u00e0pies emergents contra la Lipoprote\u00efna (a)"},"content":{"rendered":"
\n

En els darrers anys, un nom poc conegut est\u00e0 guanyant protagonisme al m\u00f3n de la salut del cor: Lipoprote\u00efna(a) o Lp(a). La lipoprote\u00efna (a) es consolida com un biomarcador i objectiu terap\u00e8utic emergent en la prevenci\u00f3 cardiovascular. <\/h1>\n

La seva elevaci\u00f3 s’associa de forma independent amb m\u00e9s risc de malaltia cardiovascular ateroscler\u00f2tica, fins i tot en persones amb colesterol LDL controlat. Encara que no hi ha un tractament aprovat espec\u00edficament repassarem en aquest bloc quin \u00e9s l’arsenal terap\u00e8utic m\u00e9s recent amb qu\u00e8 comptem. <\/p>\n

Dra. Cristina Minguito – Equip M\u00e8dic Neolife <\/em><\/p>\n

\n
Qu\u00e9 \u00e9s la Lp(a)?<\/strong><\/h5>\n

La Lp(a) \u00e9s una part\u00edcula complexa que circula al plasma sanguini i est\u00e0 composta per una lipoprote\u00efna de baixa densitat (LDL), <\/strong>que cont\u00e9 apolipoprote\u00efna B-100 (apoB-100), unida covalentment a una apolipoprote\u00efna(a),<\/strong> que estructuralment \u00e9s similar al plasmin\u00f3.<\/p>\n

\"Lp(a)\"<\/p>\n

La cantidad de<\/strong> Lp(a)<\/strong> en sangre est\u00e1 determinada principalmente por el gen LPA<\/strong>, que codifica la apolipoprote\u00edna(a). Este gen presenta gran variabilidad, especialmente en el n\u00famero de repeticiones del dominio kringle IV tipo 2<\/strong>, lo que genera diferentes isoformas de Lp(a). Esta variabilidad gen\u00e9tica explica por qu\u00e9 las concentraciones de Lp(a) pueden variar m\u00e1s de 1000 veces entre individuos y por qu\u00e9 los niveles son pr\u00e1cticamente independientes del estilo de vida.<\/strong> <\/p>\n

En termes d’aterogenicitat, Lp(a) \u00e9s de 5 a 6 vegades m\u00e9s perjudicial que les LDL (lipoprote\u00efnes de baixa densitat), cosa que la converteix en un objectiu crucial per a la prevenci\u00f3 infarts, ictus i altres esdeveniments cardiovasculars.<\/p>\n

S’estima que m\u00e9s del 20% de la poblaci\u00f3 general t\u00e9 nivells elevats de Lp(a), fet que est\u00e0 associat causalment amb la malaltia cardiovascular <\/strong>ateroscler\u00f2tica i la malaltia de la v\u00e0lvula a\u00f2rtica calcificada<\/p>\n

\"Lp(a)\"<\/p>\n

*Valors >180 mg\/dl<\/em> equivalen en risc a la hipercolesterol\u00e8mia familiar.<\/strong><\/p>\n

\u00bfC\u00f3m act\u00faa la Lp(a) en el cos?<\/strong><\/h5>\n

La Lp(a) <\/strong>penetra les parets dels vasos sanguinis i facilita l’acumulaci\u00f3 de fosfol\u00edpids rovellats, promovent inflamaci\u00f3 i calcificaci\u00f3 arterial. Tamb\u00e9 interfereix amb la fibrin\u00f2lisi mitjan\u00e7ant la inhibici\u00f3 competitiva del plasminogen, afavorint la trombosi. <\/p>\n

    \n
  • Inflamaci\u00f3: afavoreix la formaci\u00f3 de plaques en les arteries.<\/li>\n
  • Trombosi: activa les plaquetes (interacci\u00f3 amb el receptor PAR-1 de les plaquetes), augmentant l’activaci\u00f3 i agregaci\u00f3 plaquet\u00e0ria, per tant, augmentant el risc de co\u00e0guls.<\/li>\n
  • Calcificaci\u00f3 a\u00f2rtica: accelera el dany (indueix la diferenciaci\u00f3 osteocl\u00e0stica, contribuint a l’estenosi a\u00f2rtica) a les v\u00e0lvules del cor.<\/li>\n
  • Fibrin\u00f2lisi redu\u00efda: dificulta la dissoluci\u00f3 natural de co\u00e0guls en competir amb el plasminogen.<\/li>\n<\/ul>\n

    \"Lp(a)\"<\/p>\n

    \u00bfC\u00f3m es medeix?<\/strong><\/h5>\n

    El mesurament de Lp(a) <\/strong>no \u00e9s com\u00fa en les an\u00e0lisis de sang rutin\u00e0ries, per\u00f2 es pot fer amb una an\u00e0lisi espec\u00edfica. No cal estar en dej\u00fa, i es pot fer en qualsevol moment, encara que es recomana evitar fer-ho durant malalties agudes. <\/p>\n

    Important: avui dia no hi ha un \u00fanic m\u00e8tode universal per mesurar-la i els resultats poden variar entre laboratoris. A m\u00e9s, hi ha dues maneres d’expressar-la: en mg\/dL i en nmol\/L, cosa que pot generar confusi\u00f3. <\/p>\n

    \u00bfQui hauria de medir-se la Lp(a)?<\/strong><\/h5>\n

    Segons les guies internacionals recomanen que els pacients amb un risc intermedi, moderat o alt es mesurin els seus nivells de Lp(a)<\/strong> aix\u00ed com aquells amb:<\/p>\n

      \n
    • Enfermetat cardiovascular prematura<\/li>\n
    • Hipercolesterolemia familiar<\/li>\n
    • Antecedents familiars d enfermetat cardiovascular prematura<\/li>\n
    • Antecedents familiars de Lp(a) elevada<\/li>\n
    • Enfermetat cardiovascular recurrent malgrat el tractament m\u00e8dic \u00f3ptim<\/li>\n
    • Estenosis valvular a\u00f3rtica calcificada.<\/li>\n<\/ul>\n
      \u00bfQu\u00e9 fer si tinc Lp(a) alta?<\/strong><\/h5>\n

      Encara que encara no existeix un tractament aprovat exclusivament per reduir Lp(a), s\u00ed que existeixen estrat\u00e8gies cl\u00edniques recomenades<\/p>\n

        \n
      1. Redu\u00efr el colesterol LDL per sota de 70 mg\/dl (o incl\u00fas < 40 mg\/dl en alto riesgo).<\/li>\n
      2. Controlar tots els factors de risc: pressi\u00f3 glucosa, tabaquisme, pes.<\/li>\n
      3. Considerar inhibidors de PCSK9 (com evolocumab o alirocumab), que poden reduir Lp(a) en un 25\u201330% i millorar el pron\u00f2stic cardiovascular.<\/li>\n
      4. Nous tractaments prometedors en investigaci\u00f3 que podrien canviar el panorama terap\u00e8utic en pocs anys.<\/li>\n<\/ol>\n
        Tractaments en desenvolupament per reduir la Lp(a)<\/strong><\/h5>\n

        Actualment, no existeix un tractament aprovat espec\u00edficament per les ag\u00e8ncies regulat\u00f2ries (com la FDA o EMA) per a la reducci\u00f3 selectiva de la lipoprote\u00efna(a)<\/strong>, malgrat la seva associaci\u00f3 clara amb el risc cardiovascular. Tanmateix, el creixent reconeixement del seu paper com a factor de risc independent ha motivat una intensa investigaci\u00f3 en m\u00faltiples l\u00ednies terap\u00e8utiques <\/p>\n

        1. Anticossos Monoclonals (Alirocumab i Evolocumab)<\/p>\n

        Aquests medicaments s\u00f3n inhibidors de PCSK9, inicialment dissenyats per reduir el colesterol LDL.<\/strong> S\u00b4ha observat que, a m\u00e9s del seu potent efecte hipolipidant (reduccions de c-LDL de fins a 60%), tamb\u00e9 aconsegueixen disminuir la Lp(a<\/strong>) en un 25%-30%. <\/p>\n

          \n
        • Mecanisme possible: encara que el mecanisme exacte no est\u00e0 completament aclarit, es creu que podria ser degut a un augment de l’expressi\u00f3 del receptor LDL al fetge, que tamb\u00e9 eliminaria part\u00edcules que contenen Lp(a), o una reducci\u00f3 indirecta de la seva producci\u00f3.<\/li>\n
        • Evid\u00e8ncia: en estudis com FOURIER i ODYSSEY OUTCOMES, aquesta reducci\u00f3 es va associar amb una disminuci\u00f3 d’esdeveniments cardiovasculars, especialment en pacients amb Lp(a) elevada.<\/li>\n<\/ul>\n

          2. Interfer\u00e8ncia d’ ARN (siRNA)<\/p>\n

          La interfer\u00e8ncia per ARN \u00e9s una tecnologia avan\u00e7ada que utilitza petites mol\u00e8cules d’ARN interferent (siRNA) per silenciar l’expressi\u00f3 de gens espec\u00edfics. En aquest cas, l’ARN del gen LPA <\/strong>que codifica l’apolipoprote\u00efna(a). <\/p>\n

            \n
          • F\u00e0rmacs en estudi: Olpasiran, Zerlasiran, Lepodisiran.<\/li>\n
          • Reducci\u00f3 de Lp(a): fins un 97%, el que representa el major efecte conegut fins la data.<\/li>\n
          • Administraci\u00f3: S’ administren per v\u00eda subcut\u00e1nea, generalment de forma trimestral, el que facilita la adher\u00e8ncia.<\/li>\n
          • Avantatge: Alta efic\u00e0cia, pocs efectes adversos fins ara, i potencial de reduir significativament esdeveniments cardiovasculars (tot i que els resultats finals encara estan en fase de recerca).<\/li>\n
          • Assajos cl\u00ednics: OCEAN(a)-Outcomes (olpasiran), ACCLAIM-Lp(a) (lepodisiran).<\/li>\n<\/ul>\n

            3. Oligonucle\u00f3tidos Antisentido (Pelacarsen)<\/p>\n

            Pelacarsen (anteriorment conegut com TQJ230) \u00e9s un oligonucle\u00f2tid antisentit que s’uneix a l’ARN missatger de l’apolipoprote\u00efna(a)<\/strong> al fetge, bloquejant-ne la traducci\u00f3 i reduint aix\u00ed la s\u00edntesi de Lp(a).<\/strong><\/p>\n

              \n
            • Reducci\u00f3: aproximadament 80% de los nivells plasm\u00e0tics de Lp(a).<\/strong><\/li>\n
            • Administraci\u00f3: subcut\u00e0nea, de forma mensual.<\/li>\n
            • Assaig cl\u00ednic principal: Lp(a)-HORIZON, actualment en fase 3, cerca demostrar la seva efic\u00e0cia en la reducci\u00f3 d’esdeveniments cardiovasculars com a infart o ictus.<\/li>\n
            • Ventaja: reducci\u00f3 profunda i sostinguda de Lp(a), amb resultats preliminare prometedors.<\/li>\n<\/ul>\n

              4. Petites Mol\u00b7l\u00e8cules Orals (Muvalaplin)<\/p>\n

              Muvalaplin representa una nova classe terap\u00e8utica: petites mol\u00e8cules orals capaces d’interrompre la uni\u00f3 entre apo(a) i apoB100, un pas clau en la formaci\u00f3 de la part\u00edcula Lp(a).<\/strong><\/p>\n

                \n
              • Mecanisme: en impedir l’acoblament de Lp(a), evita la seva formaci\u00f3 sense afectar altres lipoprote\u00efnes.<\/li>\n
              • Reducci\u00f3 estimada: fins un 65% en estudis de fase 1.<\/li>\n
              • Avantatge cl\u00ednic: administraci\u00f3 oral di\u00e0ria, cosa que millora la comoditat i l’adher\u00e8ncia del pacient.<\/li>\n
              • Estat actual: en desenvolupament cl\u00ednic primerenc (fase 1-2).<\/li>\n<\/ul>\n

                5. Edici\u00f3 gen\u00e8tica (CRISPR\/Cas9)<\/p>\n

                L’edici\u00f3 gen\u00e8tica mitjan\u00e7ant CRISPR\/Cas9 representa una cura definitiva potencial. S’ha utilitzat amb \u00e8xit en models precl\u00ednics per editar el gen LPA, responsable de la producci\u00f3 d’apolipoprote\u00efna(a), <\/strong>cosa que ha resultat en reduccions de m\u00e9s del 90% dels nivells de Lp(a).<\/strong> <\/p>\n

                  \n
                • Estat actual: en fase precl\u00ednica, amb proves en animals i cultius cel\u00b7lulars.<\/li>\n
                • Avantatge futur: soluci\u00f3 \u00fanica, de per vida, amb una sola intervenci\u00f3.<\/li>\n
                • Desafiaments: seguretat, efic\u00e0cia sostinguda i q\u00fcestions \u00e8tiques relacionades amb l’edici\u00f3 gen\u00e8tica en humans.<\/li>\n<\/ul>\n
                  Terapies emergents contra la Lp(a)<\/strong><\/h5>\n

                  \"Lp(a)\"<\/p>\n

                  En resum:<\/strong><\/h5>\n

                  La lipoprote\u00efna(a)<\/strong> es consolida com un biomarcador i objectiu terap\u00e8utic emergent en la prevenci\u00f3<\/strong> cardiovascular. La seva elevaci\u00f3 s’associa de forma independent amb m\u00e9s risc de malaltia cardiovascular ateroscler\u00f2tica, fins i tot en persones amb colesterol LDL controlat. Encara que actualment no hi ha tractaments espec\u00edfics aprovats per a la seva reducci\u00f3, l’aven\u00e7 de noves ter\u00e0pies dirigides \u2014com els siRNA, oligonucle\u00f2tids antisentit i anticossos monoclonals\u2014 ofereix perspectives molt prometedores. Paral\u00b7lelament, la identificaci\u00f3 preco\u00e7 de nivells elevats de Lp(a) <\/strong>mitjan\u00e7ant cribratge pot permetre una millor estratificaci\u00f3 del risc, optimitzaci\u00f3 del tractament d’altres factors modificables i detecci\u00f3 d’individus candidats a estudis cl\u00ednics. La integraci\u00f3 rutin\u00e0ria del seu mesurament a la pr\u00e0ctica cl\u00ednica i l’enfocament preventiu personalitzat podrien canviar de manera substancial el paradigma en el maneig del risc cardiovascular en els propers anys. <\/p>\n

                  \n

                  BIBLIOGRAFIA<\/p>\n

                  (1) Greco A, Finocchiaro S, Spagnolo M, Faro DC, Mauro MS, Raffo C, et al.<\/p>\n

                  (2) Lipoprotein(a) as a pharmacological target: Premises, promises, and prospects.<\/p>\n

                  (3) Circulation<\/em>. 2025 Feb 11;151(6):400\u2013415. <\/p>\n

                  \n","protected":false},"excerpt":{"rendered":"

                  En els darrers anys, un nom poc conegut est\u00e0 guanyant protagonisme al m\u00f3n de la salut del cor: Lipoprote\u00efna(a) o Lp(a). La lipoprote\u00efna (a) es consolida com un biomarcador i objectiu terap\u00e8utic emergent en la prevenci\u00f3 cardiovascular. La seva elevaci\u00f3 s’associa de forma independent amb m\u00e9s risc de malaltia cardiovascular ateroscler\u00f2tica, fins i tot en […]<\/p>\n","protected":false},"author":31,"featured_media":28928,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"footnotes":""},"categories":[5139],"tags":[5154,5152,5153,5151,5155],"class_list":["post-29022","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-prevencio-i-antiaging","tag-apolipoproteinaa-ca","tag-colesterol-ldl-ca","tag-lipoproteina-de-baixa-densitat-ldl","tag-malaltia-cardiovascular","tag-prevencio-cardiovascular"],"acf":[],"yoast_head":"\nTer\u00e0pies emergents contra la Lipoprote\u00efna (a)<\/title>\n<meta name=\"description\" content=\"En els darrers anys, un nom poc conegut est\u00e0 guanyant protagonisme al m\u00f3n de la salut del cor: Lipoprote\u00efna(a) o Lp(a). 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