{"id":10487,"date":"2008-01-14T13:41:05","date_gmt":"2008-01-14T10:41:05","guid":{"rendered":"https:\/\/www.synevo.ro\/afectiuni\/profil-anemie\/"},"modified":"2020-07-10T12:14:02","modified_gmt":"2020-07-10T09:14:02","slug":"profil-anemie","status":"publish","type":"synevo_diseases","link":"https:\/\/old.synevo.md\/ru\/afectiuni\/profil-anemie\/","title":{"rendered":"Profil anemie"},"content":{"rendered":"<p><strong>Anemia<\/strong> este una din situa\u0163iile frecvent \u00eent\u00e2lnite \u00een practica medical\u0103. Din punct de vedere func\u0163ional, se define\u015fte printr-o mas\u0103 eritrocitar\u0103 insuficient\u0103 pentru asigurarea unei cantit\u0103\u0163i adecvate de oxigen \u0163esuturilor periferice. \u00cen practic\u0103, se consider\u0103 anemie atunci c\u00e2nd concentra\u0163ia de hemoglobin\u0103, hematocritul \u015fi\/ sau num\u0103rul de eritrocite sunt sub valorile de referin\u0163\u0103.<sup>1<\/sup><br><strong>Anemia nu reprezint\u0103 o boal\u0103 \u00een sine ci un semn de boal\u0103<\/strong>.<\/p><hr class=\"wp-block-separator\"\/><p><strong>Clasificarea<\/strong> anemiei este important\u0103 \u00een strategia diagnostic\u0103. Dou\u0103 tipuri de clasific\u0103ri sunt larg utilizate: morfologic\u0103 \u015fi func\u0163ional\u0103.<\/p><p><strong>1. Clasificarea morfologic\u0103 <\/strong>a anemiilor are \u00een vedere aprecierea m\u0103rimii, formei \u015fi a gradului de \u00eenc\u0103rcare cu Hb a eritrocitelor. Trei tehnici principale sunt disponibile clinicianului pentru aprecierea acestor aspecte: calcularea indicilor eritrocitari, examinarea frotiului sanguin \u015fi analiza curbei de distribu\u0163ie a volumului eritrocitar.<sup>2<\/sup> \u00cencadrarea morfologic\u0103 a anemiilor poate sugera unele mecanisme de boal\u0103, ceea ce permite dirijarea investiga\u0163iilor ulterioare, c\u0103tre un anumit grup de factori etiologici.<sup>3<\/sup><br>Dup\u0103 acest criteriu, anemiile se \u00eempart \u00een: normocitare (MCV 80-100fl), microcitare (MCV &lt;80fl) \u015fi macrocitare (MCV &gt;100fl).<\/p><p><strong>Anemiile microcitare<\/strong> au drept caracteristic\u0103 patogenic\u0103 comun\u0103 deficien\u0163a \u00een sinteza hemoglobinei, cu apari\u0163ia hipocromiei. Biosinteza normal\u0103 a hemoglobinei are loc \u00een citoplasma eritrobla\u015ftilor din m\u0103duva osoas\u0103 \u015fi necesit\u0103 prezen\u0163a \u00een cantit\u0103\u0163i optime ale celor trei componente: fierul, protoporfirina \u015fi globina.2 \u00cen func\u0163ie de nivelul deficien\u0163ei se deosebesc anemii microcitare din cadrul unor: afec\u0163iuni ale metabolismului fierului (ex. anemia feripriv\u0103, anemia cronic\u0103 simpl\u0103), boli ale sintezei moleculelor de globin\u0103 (ex. hemoglobinopatii, talasemii) \u015fi boli ale sintezei de hem \u015fi porfirin\u0103 (anemii sideroblastice).<br>Cea mai frecvent\u0103 cauz\u0103 este deficitul de fier, anemia feripriv\u0103 fiind \u015fi cea mai \u00eent\u00e2lnit\u0103 form\u0103 de anemie de pe glob.<sup>1 <\/sup>Sc\u0103derea cantit\u0103\u0163ii totale de fier din organism reduce semnificativ aportul de fier la m\u0103duva osoas\u0103 \u015fi are ca urmare anemia microcitar\u0103 hipocrom\u0103 caracteristic\u0103; de asemenea sc\u0103derea fierului tisular este responsabil\u0103 de semne \u015fi simptome revelatoare ca modific\u0103ri de fanere, atrofia mucoaselor, astenia etc., caracteristice acestui tip de anemie. Boala afecteaz\u0103 ambele sexe \u015fi toate v\u00e2rstele, dar predomin\u0103 la femei \u015fi copii.<sup>4<\/sup><\/p><p><strong>Anemia cronic\u0103 simpl\u0103<\/strong>, a doua ca frecven\u0163\u0103, este o anemia u\u015foar\u0103 sau moderat\u0103 la pacien\u0163i cu boli infec\u0163ioase, inflamatorii sau neoplazice, care persist\u0103 mai mult de 1-2 luni \u015fi a c\u0103rei caracteristic\u0103 este hiposideremia \u00een prezen\u0163a unor ample depozite de fier reticuloendotelial.<sup>5<\/sup><br>Afec\u0163iunile ereditare, care au la baz\u0103 o anormalitate \u00een sinteza moleculelor de globin\u0103, pot fi \u00eemp\u0103r\u0163ite \u00een: hemoglobinopatii \u2013 caracterizate prin variante de hemoglobin\u0103 anormal\u0103 structural \u015fi talasemii \u2013 familie de anemii cu mare heterogenicitate clinic\u0103, care au \u00een comun sinteza deficitar\u0103 a uneia sau mai multor lan\u0163uri polipeptidice din hemoglobina normal\u0103. Clinic, aceste afec\u0163iuni se manifest\u0103 de obicei sub forma de anemie hemolitic\u0103, dar unele sunt func\u0163ional normale \u015fi prin urmare f\u0103r\u0103 manifest\u0103ri clinice (\u201cclinically silent\u201d). <sup>6<\/sup> Un rol important \u00een diagnosticul de laborator \u00eel au hemograma, frotiul sanguin, electroforeza Hb.<br>Anemiile sideroblastice<em> <\/em>sunt un grup heterogen de boli, ereditare sau dobandite, caracterizate prin prezen\u0163a de \u201csideroblasti inelari\u201d \u00een maduva osoas\u0103, ca urmare a acumul\u0103rii de fier in mitocondrii.<sup>7<\/sup> Excesul de fier mitocondrial se consider\u0103 consecin\u0163a sintezei insuficiente a hemului, ca rezultat al sc\u0103derii produc\u0163iei de protoporfirin\u0103 sau afect\u0103rii leg\u0103rii fierului de protoporfirin\u0103. Gradul hipocromiei \u015fi microcitozei variaz\u0103 considerabil de la o form\u0103 de anemie sideroblastic\u0103 la alta. Adesea dimorfismul eritrocitar este accentuat, cu o popula\u0163ie microcitar\u0103 hipocrom\u0103 care coexist\u0103 cu o popula\u0163ie de eritrocite normale sau chiar macrocitare.<sup>8<\/sup><\/p><p><strong>Anemiile macrocitare <\/strong>se pot \u00eemp\u0103r\u0163i \u00een dou\u0103 grupuri pe baza criteriilor biochimice \u015fi morfologice: anemii megaloblastice \u015fi non-megaloblastice.<br>\u00cen anemiile megaloblastice marca morfologic\u0103 este reprezentat\u0103 de prezen\u0163a precursorilor eritroizi anormali \u00een m\u0103duva osoas\u0103, caracteriza\u0163i prin dimensiuni crescute \u015fi alter\u0103ri specifice \u00een aspectul cromatinei nucleare. Aceste celule distincte reprezint\u0103 expresia morfologic\u0103 a unei anomalii biochimice, respectiv \u00eent\u00e2rzierea sintezei de ADN. Rata sintezei hemoglobinei, respectiv sinteza ARN, nu este afectat\u0103 \u00een timp ce rata diviziunilor celulare este redus\u0103, \u00een consecin\u0163\u0103 componentele citoplasmatice, \u00een special Hb sunt sintetizate \u00een exces \u00een timpul \u00eent\u00e2rzierii \u00eentre diviziunile celulare, duc\u00e2nd la formarea unor eritrocite de dimensiuni crescute. Cele dou\u0103 modific\u0103ri caracteristice de pe frotiul de s\u00e2nge care permit diferen\u0163ierea anemiilor megaloblastice sunt prezen\u0163a macroovalocitelor \u015fi a neutrofilelor cu nucleu hipersegmentat. \u00cen anemia megaloblastic\u0103 VEM este de obicei &gt;110 fL (110 \u2013 130 fL, chiar p\u00e2n\u0103 la 160 fL). Cele mai frecvente cauze sunt deficitul de vitamina B12 \u015fi deficitul de folat.<sup>9<\/sup><br>Anemiile macrocitare non-megaloblastice nu au un mecanism patogenic comun; ele reprezint\u0103 anemiile macrocitare \u00een care precursorii eritroizi medulari sunt normali; sinteza ADN nu este afectat\u0103; VEM este de obicei u\u015for crescut (100 \u2013 110 fL); ex. anemiile asociate cu eritropoiez\u0103 accentuat\u0103 (anemia hemolitic\u0103 \u015fi posthemoragic\u0103), alcoolism, boli hepatice, hipotiroidism, sindroame mielodisplazice, anemia mieloftizic\u0103, anemia aplastic\u0103, anemia sideroblastic\u0103 dob\u00e2ndit\u0103, etc.1<\/p><p><strong>Anemiile normocitare <\/strong>se \u00eempart \u00een: anemia asociat\u0103 cu r\u0103spuns eritropoietic adecvat (anemia posthemoragic\u0103, anemia hemolitic\u0103 \u2013 poate fi \u015fi u\u015for macrocitar\u0103), anemie asociat\u0103 cu secre\u0163ie sc\u0103zut\u0103 de eritropoietin\u0103 (ex. anemia din insuficien\u0163\u0103 renal\u0103, anemia din bolile hepatice, anemia din insuficien\u0163ele endocrine, anemia din bolile cronice -poate fi \u015fi microcitar\u0103), anemie asociat\u0103 cu r\u0103spuns medular inadecvat (ex. anemia aplastic\u0103, anemia mieloftizic\u0103, anemii mielodisplazice, anemia diseritropoetic\u0103).<sup>1,10<\/sup><\/p><p>2<strong>. Clasificarea func\u0163ional\u0103 <\/strong>a anemiilor se refer\u0103 la aprecierea produc\u0163iei de eritrocite de c\u0103tre m\u0103duva osoas\u0103.<sup>3 <\/sup>Determinarea num\u0103rului relativ sau absolut de Rt reprezint\u0103 un indicator important al activit\u0103\u0163ii eritropoietice medulare, furniz\u00e2nd o apreciere ini\u0163ial\u0103, dac\u0103 anemia se datoreaz\u0103 alter\u0103rii produc\u0163iei eritrocitare sau pierderii de eritrocite \u00een circula\u0163ie (prin s\u00e2ngerare sau hemoliz\u0103). <sup>11,12,13<\/sup> In func\u0163ie de cifra de reticulocite anemiile se \u00eempart \u00een hiporegenerative \u015fi regenerative .<\/p><div class=\"wp-block-columns is-layout-flex wp-container-core-columns-is-layout-1 wp-block-columns-is-layout-flex\"><div class=\"wp-block-column is-vertically-aligned-center is-layout-flow wp-block-column-is-layout-flow\" style=\"flex-basis:33.33%\"><p><strong>Teste disponibile \u00een laboratoarele 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href=\"https:\/\/old.synevo.md\/ru\/shop\/electroforeza-hemoglobinei\/\">Electroforeza hemoglobinei<\/a>\r\n                    <div class=\"sysprod-product-price\">\r\n                        <span>Pre\u021b:<\/span>\r\n                        <span>260.00 lei<\/span>\r\n                    <\/div>\r\n                                            <div class=\"sysprod-product-addcart\">\r\n                            <a\r\n                                href=\"?add-to-cart=9222\"\r\n                                data-quantity=\"1\"\r\n                                class=\"addToCart button product_type_simple add_to_cart_button ajax_add_to_cart \"\r\n                                data-product_id=\"9222\"\r\n                                data-product_sku=\"CH29\"\r\n                                rel=\"nofollow\"\r\n                            ><div><\/div><\/a>\r\n                        <\/div>\r\n                                    <\/div>\r\n                    <\/div>\r\n    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{\r\n    flex-shrink: 0;\r\n    position: relative;\r\n    width: 38px;\r\n    height: 38px;\r\n    margin-left: 24px;\r\n    margin-right: 24px;\r\n}\r\n.synevo-shop-products .sysprod-product-addcart .button {\r\n    top: unset;\r\n    right: unset;\r\n}\r\n<\/style><\/div><\/div><hr class=\"wp-block-separator\"\/><p><small><strong>Bibliografie:<\/strong><\/small><\/p><p><small>1. Glader B. Anemia: General Considerations, \u00een Wintrobe\u2019s Clinical Hematology, Philadelphia. 2004, 948-975<br>2. G. Richard Le, Anemia: A Diagnostic Strategy, \u00een Wintrobe\u2019s Clinical Hematology, 1999, 908-921<br>3. Dan Coli\u0163\u0103, Anemiile. Generalit\u0103\u0163i, Clasificare, \u00een Tratat de Medicin\u0103 Intern\u0103, Hematologie partea I, 1997, 556-567<br>4. N. Munteanu, Anemia feripriv\u0103, \u00een Tratat de Medicin\u0103 Intern\u0103, Hematologie partea I, 1997, 579<br>5. Robert T. Means, Jr, The Anemia of Chronic Disorders, \u00een Wintrobe\u2019s Clinical Hematology, 1999,1011<br>6. John N. Lukens, The Abnormal Hemoglobins: General Principles, \u00een Wintrobe\u2019s Clinical Hematology, 1999, 1329<br>7. N. Munteanu, Anemii sideroblastice, \u00een Tratat de Medicin\u0103 Intern\u0103, Hematologie partea I, 1997, 614<br>8. Sylvia S. Bottomley, Sideroblastic Anemias, \u00een Wintrobe\u2019s Clinical Hematology, 1999, 1022-1024<br>9. Carmel L. Megaloblastic Anemias: Disorders of Impaired DNA Synthesis, \u00een Wintrobe\u2019s Clinical Hematology. Lippincott, Williams, and Wilkins, Philadelphia, 11 ed. 2004, 1367-1413<br>10. Thomas L, Bartl R. Hematology, in Clinical Laboratory Diagnostics. 1998, 463-547<br>11. B Weinberg. Monunuclear Phagocytes, in Wintrobe\u2019s Clinical Hematology. Philadelphia ed. 2004, 349-377<br>12. DeMott W, Tilzer L. Hematology, in Laboratory Test Handbook. Hudson (Cleveland) ed. 1994, 517-617<br>13. Desai S. Complete Blood Count, in Clinicians\u2019s Guide to Laboratory Medicine. 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