{"id":53219,"date":"2020-04-01T17:00:01","date_gmt":"2020-04-01T16:00:01","guid":{"rendered":"https:\/\/fjala.info\/?p=53219"},"modified":"2020-04-01T18:05:35","modified_gmt":"2020-04-01T17:05:35","slug":"covid-19-ndikimi-nga-antihipertoniket","status":"publish","type":"post","link":"https:\/\/jehonashqiptare.al\/fjala\/covid-19-ndikimi-nga-antihipertoniket\/","title":{"rendered":"COVID-19: Ndikimi nga Antihipertonik\u00ebt"},"content":{"rendered":"

Koronavirusi SARS-CoV-2 lidhet me receptorin ACE-2 (blu) t\u00eb qeliz\u00ebs njer\u00ebzore me an\u00eb t\u00eb protein\u00ebs spike (t\u00eb kuqe). Foto: selvanegra\/iStock<\/em><\/span><\/p>\n

RAPORT MJEK\u00cbSOR<\/p>\n

– P\u00ebrktheu nga gjermanishtja Arben<\/strong> & Dr. Dashamir \u00c7okaj<\/strong><\/em><\/p><\/blockquote>\n

Deutsche Arzteblatt<\/a> 2020; 117(13): A-664 \/ B-565<\/span>
\nWendt, Ralph; Beige, Joachim; L\u00fcbbert, Christoph<\/p>\n

Virusi SARS-CoV-2 p\u00ebrdor receptorin ACE-2 p\u00ebr t\u00eb “infiltruar” trupin. \u00cbsht\u00eb e diskutueshme n\u00ebse frenuesit e sistemit renin-angiotensin – si\u00e7 jan\u00eb frenuesit ACE, ose bllokuesit e receptor\u00ebve AT2 – jan\u00eb terapeutikisht t\u00eb dobish\u00ebm apo t\u00eb d\u00ebmsh\u00ebm.<\/p><\/blockquote>\n

Bota \u00ebsht\u00eb kapur nga efektet e p\u00ebrhapjes pandemike t\u00eb koronavirusit t\u00eb ri SARS-CoV-2<\/strong>. Ky virus shoq\u00ebrohet me nj\u00eb vdekshm\u00ebri duksh\u00ebm m\u00eb t\u00eb lart\u00eb sesa gripi sezonal (1<\/a>). Koh\u00ebt e fundit ka pasur raporte dhe lajm\u00ebrime, q\u00eb agjent\u00eb antihipertensiv\u00eb t\u00eb p\u00ebrshkruar gjer\u00ebsisht (si\u00e7 jan\u00eb frenuesit ACE dhe bllokuesit e receptor\u00ebve AT2) ndikojn\u00eb n\u00eb frekuenc\u00ebn dhe ashp\u00ebrsin\u00eb e s\u00ebmundjes COVID-19 (2<\/a>). Shqet\u00ebsimet korresponduese u diskutuan edhe n\u00eb revistat speciale (3<\/a>, 4<\/a>).<\/p>\n

Si p\u00ebrmbledhje, konstatohet se n\u00eb t\u00eb dh\u00ebnat klinike t\u00eb disponueshme deri m\u00eb tani n\u00eb COVID-19 nga Republika Popullore e Kin\u00ebs, pacient\u00ebt me diabet mellitus<\/em>, hipertension<\/em> dhe komorbiditete <\/em>4.1<\/a> t\u00eb tjera kardiovaskulare kishin nj\u00eb rezultat m\u00eb t\u00eb dob\u00ebt, ve\u00e7an\u00ebrisht nj\u00eb vdekshm\u00ebri m\u00eb t\u00eb lart\u00eb (tabela).<\/p>\n

\"\"Tabela<\/strong><\/span>
\nStudimi i t\u00eb dh\u00ebnave nga PRC (VR Kina) me informacion mbi shpesht\u00ebsin\u00eb e pacient\u00ebve me hipertension arterial (aHT) si komorbiditet dhe shoq\u00ebrimin e tyre me rezultatin klinik (sipas [15])<\/em><\/span><\/p>\n

Nga ky v\u00ebzhgim, \u00ebsht\u00eb sugjeruar q\u00eb popullatat e p\u00ebrmendura se pacient\u00ebt me vdekshm\u00ebri m\u00eb t\u00eb lart\u00eb kishin shum\u00eb t\u00eb ngjar\u00eb t\u00eb kishin nj\u00eb indikacion m\u00eb t\u00eb shpesht\u00eb, p\u00ebr p\u00ebrdorimin e frenuesit t\u00eb sistemit renin-angiotensin (RAS), n\u00eb ve\u00e7anti frenuesit ACE, dhe se ky grup ila\u00e7esh mund t\u00eb jet\u00eb dometh\u00ebn\u00ebs n\u00eb kontributin e rezultatit m\u00eb t\u00eb keq t\u00eb vrojtuar. Kjo marr\u00ebdh\u00ebnie \u00ebsht\u00eb teknikisht e kuptueshme, por ende nuk \u00ebsht\u00eb v\u00ebrtetuar nga t\u00eb dh\u00ebna konkrete.<\/p>\n

Sfondi p\u00ebr k\u00ebt\u00eb \u00ebsht\u00eb v\u00ebzhgimi se receptori p\u00ebr hyrjen e SARS-CoV-2 n\u00eb qelizat e sistemit t\u00eb frym\u00ebmarrjes \u00ebsht\u00eb ACE-2 me baz\u00eb membranore (enzima konvertuese e angiotenzin\u00ebs 2) (5<\/a>, 6<\/a>). Frenuesit e ACE dhe bllokuesit e receptor\u00ebve t\u00eb angiotenzin\u00ebs (Sartane, ARB) kan\u00eb treguar nj\u00eb rritje n\u00eb shprehjen ACE-2 (n\u00eb indet kardiake<\/em>) n\u00eb modelin e kafsh\u00ebve (7<\/a>). Prandaj, ka lindur shqet\u00ebsim se shprehja m\u00eb e lart\u00eb pulmonare (gjithashtu e pa konfirmuar ende<\/em>) e ACE-2 e lidhur me membran\u00eb me ila\u00e7e, q\u00eb pengojn\u00eb RAS mund t\u00eb \u00e7oj\u00eb n\u00eb nj\u00eb hyrje m\u00eb t\u00eb leht\u00eb t\u00eb virusit n\u00eb qelizat e traktit respirator.<\/p>\n

ACE-2 \u00ebsht\u00eb nj\u00eb homolog i enzim\u00ebs konvertuese t\u00eb njohur angiotenzin\u00ebs (ACE), por nuk pengohet nga frenuesit ACE (8<\/a>). \u00cbsht\u00eb nj\u00eb glikoprotein\u00eb integrale e lidhur me membran\u00eb, q\u00eb shprehet n\u00eb shum\u00eb inde, por m\u00eb fuqish\u00ebm n\u00eb veshka, endoteli, mushk\u00ebri dhe zem\u00ebr (9<\/a>). P\u00ebrve\u00e7 k\u00ebsaj, ekziston nj\u00eb form\u00eb plazmatike qarkulluese e enzim\u00ebs, me sa duket duke derdhur enzim\u00ebn e lidhur me membran\u00ebn n\u00eb qarkullim.<\/p>\n

Sistemi ACE, ACE-2 dhe RAS<\/strong><\/h3>\n

Nd\u00ebrsa ACE katalizon shnd\u00ebrrimin e angiotenzin\u00ebs I n\u00eb angiotenzin\u00eb II dhe n\u00eb k\u00ebt\u00eb m\u00ebnyr\u00eb promovon zhvillimin e efektorit m\u00eb t\u00eb r\u00ebnd\u00ebsish\u00ebm t\u00eb sistemit RAS, ACE-2 i p\u00ebrket t\u00eb ashtuquajturit boshti RAS kund\u00ebr rregullues, i cili zvog\u00eblon efektet RAS ose efektet e angiotenzin\u00ebs II. Angeotenzina II kund\u00ebrvepron angiotenzin\u00ebn 1-7 (Grafiku 1<\/em>).<\/p>\n

\"\"Grafiku 1<\/strong><\/span>
\nAkset RAS vazopressorike dhe vazoprotektive: R\u00ebnd\u00ebsia fiziologjike dhe implikimet terapeutike (mod. sipas [11])<\/em><\/span><\/p>\n

Ky bosht (aks) RAS kund\u00ebr-rregullues p\u00ebrb\u00ebhet nga ACE-2, angiotenzina 1-7 dhe receptori Mas (“Pranuesi proteinik i shoq\u00ebruar me G i angiotenzin\u00ebs 1-7<\/em>“) (10<\/a>). Angiotenzina 1-7 antagonizon drejtp\u00ebrdrejt efektet e angiotenzin\u00ebs II, p\u00ebrmes receptorit Mas (10<\/a>) dhe nd\u00ebrmjet\u00ebson, nd\u00ebr t\u00eb tjera, efekte vazodilatuese dhe antiproliferative. ACE-2 duket se luan nj\u00eb rol t\u00eb dyfisht\u00eb n\u00eb d\u00ebmtimin e mushk\u00ebrive, t\u00eb shkaktuar nga SARS-CoV-2: fillimisht ajo vepron si receptor p\u00ebr hyrjen e virusit, at\u00ebher\u00eb n\u00eb kontekstin e infeksionit SARS-CoV-2 ekziston nj\u00eb rregullim i posht\u00ebm i ACE-2, i cili rrit e d\u00ebmtimin e mushk\u00ebrive (36<\/a>).<\/p>\n

A \u00ebsht\u00eb hipertensioni arterial i shoq\u00ebruar me nj\u00eb prognoz\u00eb m\u00eb t\u00eb dob\u00ebt n\u00eb COVID-19?<\/strong><\/p>\n

Ky v\u00ebzhgim \u00ebsht\u00eb p\u00ebrmbledhur n\u00eb tabel\u00eb dhe bazohet n\u00eb t\u00eb dh\u00ebnat e studimit nga PRC (VR Kina), ve\u00e7an\u00ebrisht nga Wuhan (Provinca Hubei). Sidoqoft\u00eb, nuk mund t\u00eb konkludohet q\u00eb hipertensioni arterial (dhe madje edhe m\u00eb pak t\u00eb nj\u00eb terapie t\u00eb mundshme t\u00eb hipertensionit arterial, p.sh. me frenuesit RAS<\/em>) luan nj\u00eb rol t\u00eb madh n\u00eb nj\u00eb rezultat m\u00eb t\u00eb dob\u00ebt (kurs m\u00eb i r\u00ebnd\u00eb, vdekshm\u00ebri (letalitet<\/em>) m\u00eb e lart\u00eb, domosdoshm\u00ebri m\u00eb e shpesht\u00eb p\u00ebr terapin\u00eb ITS – p\u00ebrfshir\u00eb Respirimin) – kryesisht p\u00ebr faktin se k\u00ebto t\u00eb dh\u00ebna nuk jan\u00eb rregulluar.<\/p>\n

Rregullimi rrall\u00eb<\/strong><\/h3>\n

S\u00eb paku nj\u00eb rregullim p\u00ebr mosh\u00ebn duhet t\u00eb k\u00ebrkohet, n\u00eb m\u00ebnyr\u00eb q\u00eb t\u00eb nxjerrim p\u00ebrfundime t\u00eb vlefshme; M\u00eb kuptimplot\u00eb \u00ebsht\u00eb nj\u00eb rregullim multivariant i shum\u00eb konfrontuesve t\u00eb tjer\u00eb t\u00eb mundsh\u00ebm p\u00ebr rezultatin klinik. Nga studimet e listuara n\u00eb tabel\u00eb, rregullimi \u00ebsht\u00eb b\u00ebr\u00eb vet\u00ebm n\u00eb nj\u00eb studim (12<\/a>).<\/p>\n

N\u00eb analiz\u00ebn univariane, variablat e ndrysh\u00ebm shoq\u00ebroheshin me rritjen e vdekshm\u00ebris\u00eb (p\u00ebrfshir\u00eb hipertensionin arterial, mosh\u00ebn, leukocitoz\u00ebn, rritjen e LDH, ALAT, troponin, CK, kreatinin\u00ebs, PCT etj.). N\u00eb analiz\u00ebn multivariante, vet\u00ebm mosha, rritja e rezultatit SOFA dhe rritja e D-dimers m\u00eb e madhe se 1 \u03bcg\/l, u shoq\u00ebruan me nj\u00eb rritje t\u00eb vdekshm\u00ebris\u00eb kur g\u00eblltiten.<\/p>\n

Si p\u00ebrmbledhje, nj\u00eb lidhje e q\u00ebndrueshme midis hipertensionit arterial dhe rezultatit m\u00eb t\u00eb dob\u00ebt n\u00eb COVID-19 nuk mund t\u00eb vendoset nga t\u00eb dh\u00ebnat e studimit n\u00eb dispozicion.<\/p>\n

SARS-CoV-2 p\u00ebrdor baz\u00ebn e membran\u00ebs ACE-2 dhe proteaz\u00ebn serine transmembrane TMPRSS2 (5<\/a>, 13<\/a>) (Grafiku 2<\/em>) p\u00ebr t\u00eb hyr\u00eb n\u00eb qeliz\u00eb. Si\u00e7 \u00ebsht\u00eb p\u00ebrmendur tashm\u00eb, frenuesit ACE nuk kan\u00eb asnj\u00eb efekt frenues t\u00eb drejtp\u00ebrdrejt\u00eb n\u00eb ACE-2. Sidoqoft\u00eb, n\u00eb rastin e minjve mund t\u00eb tregohet q\u00eb t\u00eb dy frenuesit ACE (Lisinopril<\/em>) dhe Sartane (Lo-sartan<\/em>) mund t\u00eb rregullojn\u00eb ACE-2-mRNA t\u00eb zemr\u00ebs me nj\u00eb faktor 3-4 (7<\/a>). N\u00eb nj\u00eb model tjet\u00ebr t\u00eb kafsh\u00ebve, enalaprili frenues<\/em> i ACE dob\u00ebsoi rregullimin e ul\u00ebt t\u00eb ACE-2 kardiak, pas infarktit t\u00eb miokardit (14<\/a>). Ishte interesante t\u00eb theksohej se ndryshimet n\u00eb ACE-2-mRNA t\u00eb zemr\u00ebs lidhen me ndryshimet n\u00eb nivelet ACE-2 t\u00eb plazm\u00ebs. Losartan<\/em> dhe olmesartan<\/em> rrit\u00ebn nivelin ACE-2 t\u00eb ARN-s\u00eb kardiake 3 her\u00eb n\u00eb nj\u00eb model t\u00eb infarkt post miokard (21<\/a>).<\/p>\n

\"\"Grafiku 2<\/strong><\/span>
\nHyrja e SARS-CoV-2 n\u00eb qeliz\u00eb p\u00ebrmes ACE-2 dhe TMPRSS2 (proteaz\u00eb serine transmembrane e tipit II) (nga 13)<\/em><\/span><\/p>\n

Nj\u00eb aspekt i r\u00ebnd\u00ebsish\u00ebm n\u00eb rregullimin kompleks t\u00eb sistemit lokal RAS \u00ebsht\u00eb bashk\u00ebveprimi i ACE-2 me receptorin AT1; kjo mund t\u00eb tregohet n\u00eb modelin e kafsh\u00ebve, por kuptimi i tij nuk \u00ebsht\u00eb kuptuar plot\u00ebsisht. N\u00eb modelet e kafsh\u00ebve, angiotenzina II \u00e7oi n\u00eb nj\u00eb r\u00ebnie n\u00eb shprehjen ACE-2 p\u00ebrmes brend\u00ebsimit dhe degradimit lizozomik (22<\/a>). Kjo r\u00ebnie n\u00eb ACE-2 u parandalua nga administrimi i antagonist\u00ebve AT1-R (losartan<\/em>) (22<\/a>).<\/p>\n

N\u00eb disa studime te njer\u00ebzit deri m\u00eb sot, nuk \u00ebsht\u00eb demonstruar asnj\u00eb ndikim i ACE-frenuesit ose ARB n\u00eb nivelin ACE-2 t\u00eb plazm\u00ebs (23<\/a>, 24<\/a>).<\/p>\n

Sidoqoft\u00eb, marr\u00ebdh\u00ebnia midis niveleve t\u00eb ACE-2 n\u00eb gjak dhe ind \u00ebsht\u00eb e paqart\u00eb – dhe deri m\u00eb tani \u00ebsht\u00eb studiuar n\u00eb m\u00ebnyr\u00eb t\u00eb pamjaftueshme tek njer\u00ebzit. \u00cbsht\u00eb supozuar q\u00eb nivelet ACE-2 t\u00eb plazm\u00ebs mund t\u00eb paralelizojn\u00eb shprehjen ACE-2 t\u00eb indeve, gj\u00eb q\u00eb do t\u00eb rezultoj\u00eb n\u00eb nj\u00eb norm\u00eb relativisht t\u00eb vazhdueshme t\u00eb derdhjes (25<\/a>).<\/p>\n

Hyrja m\u00eb e leht\u00eb e virusit?<\/strong><\/h3>\n

Bazuar n\u00eb modelet e kafsh\u00ebve t\u00eb p\u00ebrmendura me d\u00ebshmi t\u00eb shprehjes s\u00eb shtuar (kardiake!) t\u00eb ACE-2-mRNA, pati raporte t\u00eb shqet\u00ebsuara (26<\/a>) q\u00eb nj\u00eb shprehje potencialisht e rritur ACE-2 n\u00eb indet e mushk\u00ebrive SARS-CoV mund ta favorizonte q\u00eb t\u00eb hynte n\u00eb indet e frym\u00ebmarrjes. Sidoqoft\u00eb, asnj\u00eb studim nuk ka arritur ende ta mb\u00ebshtes\u00eb k\u00ebt\u00eb supozim. Lidhja midis rritjes s\u00eb shprehjes s\u00eb indeve t\u00eb ACE-2 dhe niveleve t\u00eb ndryshuara t\u00eb plazm\u00ebs \u00ebsht\u00eb ende e paqart\u00eb, por ka lidhje n\u00eb nj\u00eb nga modelet e kafsh\u00ebve t\u00eb p\u00ebrmendura (14<\/a>), por vet\u00ebm p\u00ebr shprehjet kardiake.<\/p>\n

\u00cbsht\u00eb e paqart\u00eb n\u00ebse ndryshime t\u00eb tilla n\u00eb mushk\u00ebri rregullohen n\u00eb m\u00ebnyr\u00eb t\u00eb ngjashme. N\u00ebse ky korrelacion vlen edhe p\u00ebr njer\u00ebzit dhe mushk\u00ebrit\u00eb, t\u00eb dh\u00ebnat e m\u00ebparshme do t\u00eb argumentojn\u00eb kund\u00ebr nj\u00eb ndryshimi n\u00eb shprehjen e indeve ACE-2, pasi nivelet e plazm\u00ebs nuk ishin t\u00eb ndikuara si\u00e7 p\u00ebrshkruhet (23<\/a>, 24<\/a>).<\/p>\n

Ekzistojn\u00eb gjithashtu avantazhe t\u00eb mundshme t\u00eb terapis\u00eb q\u00eb pengojn\u00eb RAS n\u00eb lidhje me COVID-19: Angiotenzina II p\u00ebrmes receptorit AT1 duket se luan nj\u00eb rol thelb\u00ebsor si nj\u00eb nd\u00ebrmjet\u00ebs n\u00eb d\u00ebmtimin pulmonar n\u00eb kontekstin e pneumonis\u00eb virale. N\u00eb p\u00ebrputhje me rrethanat, shprehja e lart\u00eb ACE-2 duket t\u00eb jet\u00eb mbrojt\u00ebse, pasi q\u00eb ACE-2 ul kryesisht nivelet e angiotenzin\u00ebs II n\u00eb vend dhe rrit angiotenzin\u00ebn 1-7 m\u00eb mbrojt\u00ebse, antiproliferues dhe vazodilues. Kjo mund t\u00eb tregohet n\u00eb nj\u00eb model t\u00eb miut me nokaut ACE-2: humbjes s\u00eb shprehjes ACE-2 i paraprin d\u00ebmtimit akut t\u00eb mushk\u00ebrive n\u00eb modele t\u00eb ndryshme. Minjt\u00eb me nokaut ACE-2 kishin d\u00ebmtim m\u00eb t\u00eb r\u00ebnd\u00eb t\u00eb mushk\u00ebrive (27<\/a>). Administrimi i ACE-2 rekombinues mbron mushk\u00ebrit\u00eb nga d\u00ebmtimet e r\u00ebnda. Angiotenzina II prandaj \u00ebsht\u00eb direkt dhe ACE-2 n\u00eb m\u00ebnyr\u00eb t\u00eb kund\u00ebrt shoq\u00ebrohet me d\u00ebmtimin e indeve t\u00eb mushk\u00ebrive. Terapia me frenuesit ACE, si\u00e7 tregohet n\u00eb modelin e kafsh\u00ebve n\u00eb zem\u00ebr, mund t\u00eb rris\u00eb shprehjen ACE-2, e cila duhet t\u00eb ket\u00eb m\u00eb shum\u00eb t\u00eb ngjar\u00eb t\u00eb shoq\u00ebrohet me nj\u00eb p\u00ebrfitim n\u00eb kontekstin e d\u00ebmtimit t\u00eb mushk\u00ebrive. P\u00ebr m\u00eb tep\u00ebr, formimi i angiotenzin\u00ebs II do t\u00eb ngadal\u00ebsohej nga frenimi i ACE.<\/p>\n

Sartan\u00ebt kan\u00eb avantazhin e mundsh\u00ebm q\u00eb, p\u00ebrve\u00e7 rregullimit t\u00eb duksh\u00ebm edhe m\u00eb t\u00eb theksuar t\u00eb ACE-2 (krahasuar me frenuesit ACE), efektet e d\u00ebmshme t\u00eb angiotenzin\u00ebs II pengohen direkt n\u00eb receptorin AT1. P\u00ebr m\u00eb tep\u00ebr, ndarja e bradykinin nuk zvog\u00eblohet si me frenuesit ACE. Kjo zvog\u00eblon efektet an\u00ebsore t\u00eb koll\u00ebs dhe tendenc\u00ebn p\u00ebr angioedem\u00eb.<\/p>\n

P\u00ebrfitimet e antihipertensioneve<\/strong><\/h3>\n

N\u00eb nj\u00eb studim retrospektiv me mbi 30,000 pacient\u00eb t\u00eb pneumonis\u00eb mbi 65 vjet, mund t\u00eb tregohet se marrja e frenuesve ACE ose ARB jo vet\u00ebm q\u00eb \u00e7oi n\u00eb pikat m\u00eb t\u00eb mira t\u00eb shoq\u00ebruara nga pneumonia, por edhe n\u00eb uljen e vdekshm\u00ebris\u00eb (28<\/a>). Nj\u00eb pun\u00eb tjet\u00ebr me pacient\u00eb t\u00eb pneumonis\u00eb virale tregoi vdekshm\u00ebri t\u00eb rritur p\u00ebr pacient\u00ebt me ACE frenues para pranimit n\u00eb spital, por ulur vdekshm\u00ebrin\u00eb me p\u00ebrdorimin e vazhduesh\u00ebm t\u00eb frenuesve ACE (29<\/a>). N\u00eb nj\u00eb model t\u00eb miut me infeksion t\u00eb influenc\u00ebs A H5N1, p\u00ebrdorimi i losartan dob\u00ebsuan n\u00eb m\u00ebnyr\u00eb akute mushk\u00ebrit\u00eb (30<\/a>), i cili u shoq\u00ebrua gjithashtu me nj\u00eb rikuperim t\u00eb shprehjes ACE-2 n\u00ebn terapin\u00eb losartan.<\/p>\n

Nj\u00eb model tjet\u00ebr i miut t\u00eb infeksionit me SARS-CoV duke p\u00ebrdorur ACE-2 rekombinues tregoi parametra t\u00eb p\u00ebrmir\u00ebsuar klinik dhe histopatologjik t\u00eb mushk\u00ebrive (31<\/a>) dhe nj\u00eb ulje t\u00eb konsiderueshme t\u00eb d\u00ebmtimit t\u00eb mushk\u00ebrive p\u00ebr shkak t\u00eb bllokad\u00ebs RAS me losartan (32<\/a>). Nj\u00eb analiz\u00eb e fundit n\u00eb pacient\u00ebt COVID-19 tregoi nivele t\u00eb konsiderueshme t\u00eb rritura t\u00eb angiotenzin\u00ebs II n\u00eb plazm\u00ebn njer\u00ebzore (33<\/a>), e cila n\u00ebnvizon r\u00ebnd\u00ebsin\u00eb e sistemit RAS dhe b\u00ebn p\u00ebrdorimin e mundsh\u00ebm t\u00eb frenuesve t\u00eb RAS p\u00ebr t\u00eb zvog\u00ebluar d\u00ebmtimin e mushk\u00ebrive, q\u00eb vlen t\u00eb merret n\u00eb konsiderat\u00eb.<\/p>\n

P\u00ebrmbledhje<\/strong><\/h3>\n

Sistemi RAS luan nj\u00eb rol t\u00eb r\u00ebnd\u00ebsish\u00ebm n\u00eb zhvillimin dhe nd\u00ebrmjet\u00ebsimin e d\u00ebmtimit t\u00eb mushk\u00ebrive n\u00eb pneumoni virale. Efektet negative t\u00eb angiotenzin\u00ebs II p\u00ebrmes receptorit AT1 dhe efektet mbrojt\u00ebse t\u00eb ACE-2 duket se jan\u00eb n\u00eb plan t\u00eb par\u00eb si tipare t\u00eb zakonshme.
\nEdhe n\u00ebse ACE-2 p\u00ebrdoret p\u00ebr hyrjen e SARS CoV-2 n\u00eb epitelin respirator, rregullimi i shprehjeve ACE-2 pas zgjerimit viral \u00ebsht\u00eb i dokumentuar n\u00eb pothuajse t\u00eb gjitha d\u00ebmtimet virale, e cila shoq\u00ebrohet me d\u00ebmtim m\u00eb t\u00eb madh t\u00eb mushk\u00ebrive.<\/p>\n

N\u00eb koh\u00ebn e tanishme, nuk ka njohuri t\u00eb besueshme q\u00eb lejojn\u00eb nj\u00eb vler\u00ebsim t\u00eb qart\u00eb t\u00eb avantazheve ose disavantazheve t\u00eb mundshme t\u00eb terapis\u00eb q\u00eb pengojn\u00eb sistemin RAS (ACE inhibitor, ARB). Marr\u00ebdh\u00ebnia e p\u00ebrshkruar midis hipertensionit arterial si nj\u00eb nd\u00ebrlikueshm\u00ebri p\u00ebrkat\u00ebse e COVID-19 dhe rezultatit klinik m\u00eb t\u00eb dob\u00ebt fillimisht nuk lejon t\u00eb nxirren p\u00ebrfundime n\u00eb lidhje me terapin\u00eb antihipertensive t\u00eb regjistruar m\u00eb par\u00eb si t\u00eb pamjaftuesh\u00ebm, dhe k\u00ebshtu jo p\u00ebr frenuesit e RAS, por p\u00ebrkundrazi shfaqen p\u00ebr shkak t\u00eb epokave t\u00eb ndryshme t\u00eb E kusht\u00ebzuar p\u00ebr pacient\u00ebt.<\/p>\n

Rekomandimet aktuale<\/strong><\/h3>\n

Rekomandimet e m\u00ebposhtme aktualisht duket se jan\u00eb t\u00eb lejueshme:
\nP\u00ebr pacient\u00ebt me frenuesit aktual t\u00eb RAS t\u00eb p\u00ebrshkruara aktualisht:<\/p>\n

Frenuesit e RAS kan\u00eb efekte dometh\u00ebn\u00ebse, t\u00eb mir\u00eb-dokumentuara, t\u00eb dobishme n\u00eb pikat e ngurta, ve\u00e7an\u00ebrisht te pacient\u00ebt me rrezik kardiovaskular, ve\u00e7an\u00ebrisht n\u00eb pacient\u00ebt me insuficienc\u00eb sistolike t\u00eb zemr\u00ebs, pas infarktit t\u00eb miokardit, dhe n\u00eb pacient\u00ebt me s\u00ebmundje kronike t\u00eb veshkave dhe diabetit. P\u00ebr t\u00eb nd\u00ebrprer\u00eb ose ndryshuar k\u00ebt\u00eb ila\u00e7 bazuar n\u00eb hipoteza ose supozime q\u00eb ende nuk jan\u00eb v\u00ebrtetuar, nuk mund t\u00eb rekomandohet n\u00eb situat\u00ebn aktuale. Mund\u00ebsia e nj\u00eb efekti negativ ose nd\u00ebrlikimi nga nd\u00ebrprerja ka t\u00eb ngjar\u00eb t\u00eb jet\u00eb duksh\u00ebm m\u00eb e madhe sesa nj\u00eb p\u00ebrfitim hipotetik i paprovuar. Mund t\u00eb pritet gjithashtu q\u00eb pacient\u00ebt gjithnj\u00eb e m\u00eb shum\u00eb t\u00eb k\u00ebrkojn\u00eb kontakt me strukturat tashm\u00eb t\u00eb mbingarkuara t\u00eb sistemit sh\u00ebndet\u00ebsor (GP p\u00ebr ndryshimin e ila\u00e7eve dhe farmacive dhe ndoshta dhoma urgjente p\u00ebr p\u00ebrkeq\u00ebsim t\u00eb mundsh\u00ebm t\u00eb s\u00ebmundjeve themelore t\u00eb trajtuara<\/em>).
\nShoq\u00ebria Evropiane e Kardiologjis\u00eb (ESC) koh\u00ebt e fundit ka nxjerr\u00eb nj\u00eb rekomandim (34<\/a>), t\u00eb cilin autor\u00ebt e mb\u00ebshtesin plot\u00ebsisht, duke ditur t\u00eb dh\u00ebnat e paraqitura k\u00ebtu.<\/p>\n

P\u00ebr pacient\u00ebt me infeksion t\u00eb d\u00ebshmuar SARS-CoV-2 ose COVID-19: P\u00ebr momentin nuk ka asnj\u00eb prov\u00eb t\u00eb besueshme p\u00ebr k\u00ebt\u00eb situat\u00eb. N\u00ebse disregulimi i paq\u00ebndruesh\u00ebm i qarkullimit t\u00eb gjakut hipotonik k\u00ebrkon ndalimin e bllokimit t\u00eb ila\u00e7eve RAS, nuk duhet t\u00eb ket\u00eb asnj\u00eb hezitim p\u00ebr ta b\u00ebr\u00eb k\u00ebt\u00eb. Sidoqoft\u00eb, ka prova q\u00eb terapia ARB mund t\u00eb zbus\u00eb potencialisht d\u00ebmtimin e mushk\u00ebrive n\u00eb COVID-19, duke zvog\u00ebluar efektet pulmonare t\u00eb angiotenzin\u00ebs II (35<\/a>). Avantazhi kryesor i ARB ndaj frenuesve ACE \u00ebsht\u00eb nj\u00eb incidenc\u00eb m\u00eb e ul\u00ebt e koll\u00ebs, s\u00eb shkaktuar nga droga (kolla frenuese ACE) p\u00ebr shkak t\u00eb munges\u00ebs s\u00eb nd\u00ebrveprimit me sistemin e bradykinin. Nj\u00eb preferenc\u00eb p\u00ebr nj\u00eb sartan specifik nuk mund t\u00eb p\u00ebrcaktohet, edhe n\u00ebse shumica e t\u00eb dh\u00ebnave paraklinike p\u00ebr losartan jan\u00eb n\u00eb dispozicion. Nj\u00eb studim i rastit, i kontrolluar nga placebo, i etiketuar i hapur, q\u00eb po heton k\u00ebt\u00eb \u00e7\u00ebshtje \u00ebsht\u00eb n\u00eb planifikim dhe pritet t\u00eb filloj\u00eb n\u00eb jav\u00ebt e ardhshme.<\/p>\n

Si ta citoni k\u00ebt\u00eb artikull:
\nDeutsche-Arzteblatt 2020; 117 (13): A 664-7<\/p><\/blockquote>\n

\n

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Koronavirusi SARS-CoV-2 lidhet me receptorin ACE-2 (blu) t\u00eb qeliz\u00ebs njer\u00ebzore me an\u00eb t\u00eb protein\u00ebs spike (t\u00eb kuqe). Foto: selvanegra\/iStock RAPORT MJEK\u00cbSOR – P\u00ebrktheu nga gjermanishtja Arben & Dr. Dashamir \u00c7okaj Deutsche Arzteblatt 2020; 117(13): A-664 \/ B-565 Wendt, Ralph; Beige, Joachim; L\u00fcbbert, Christoph Virusi SARS-CoV-2 p\u00ebrdor receptorin ACE-2 p\u00ebr t\u00eb “infiltruar” trupin. \u00cbsht\u00eb e diskutueshme […]<\/p>\n","protected":false},"author":1,"featured_media":53220,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[2,36],"tags":[],"class_list":["post-53219","post","type-post","status-publish","format-standard","has-post-thumbnail","category-artikuj","category-shkence"],"yoast_head":"\nCOVID-19: Ndikimi nga Antihipertonik\u00ebt - FJALA e LIR\u00cb<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/jehonashqiptare.al\/fjala\/covid-19-ndikimi-nga-antihipertoniket\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"COVID-19: Ndikimi nga Antihipertonik\u00ebt - FJALA e LIR\u00cb\" \/>\n<meta property=\"og:description\" content=\"Koronavirusi SARS-CoV-2 lidhet me receptorin ACE-2 (blu) t\u00eb qeliz\u00ebs njer\u00ebzore me an\u00eb t\u00eb protein\u00ebs spike (t\u00eb kuqe). 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