{"id":10003,"date":"2020-04-23T03:53:40","date_gmt":"2020-04-23T00:53:40","guid":{"rendered":"https:\/\/www.synevo.ro\/product\/glucozo-6-fosfat-dehidrogenaza-g6-pdh\/"},"modified":"2025-02-04T16:24:50","modified_gmt":"2025-02-04T14:24:50","slug":"glucozo-6-fosfat-dehidrogenaza-g6-pdh","status":"publish","type":"product","link":"https:\/\/old.synevo.md\/ru\/shop\/glucozo-6-fosfat-dehidrogenaza-g6-pdh\/","title":{"rendered":"\u0413\u043b\u044e\u043a\u043e\u0437\u043e-6-\u0444\u043e\u0441\u0444\u0430\u0442\u0434\u0435\u0433\u0438\u0434\u0440\u043e\u0433\u0435\u043d\u0430\u0437\u0430 (G6-PDH)"},"content":{"rendered":"<p><strong><em>\u041e\u0431\u0449\u0430\u044f \u0438\u043d\u0444\u043e\u0440\u043c\u0430\u0446\u0438\u044f<\/em><\/strong><\/p>\n<p>Deficitul eritrocitar de G-6-PD este o afectiune ereditara X-linkata caracterizata prin diminuarea in grad variabil a activitatii acestei enzime care catalizeaza transformarea glucozo-6-fosfatului in 6-fosfo-gluconat (6-PG), prima etapa a ciclului pentozelor. Este cea mai frecventa enzimopatie umana afectand aproximativ 400 milioane de persoane din intreaga lume<sup>1;2;5;7;8<\/sup>.<\/p>\n<p>Circuitul metabolic in care este implicata G-6-PD asigura un potential reducator sub forma NADP care protejeaza structurile functionale ale eritrocitului de procesele de oxidare. Deficitul de G-6-PD este inclus<\/p>\n<p>intr-un grup heterogen de anemii hemolitice ereditare nonsferocitare, alaturi de deficitul de piruvatkinaza, Hb Z\u03cbrich si deficitul de glutation<sup>5<\/sup>.<\/p>\n<p>Gena care codifica sinteza de G-6-PD se gaseste pe cromozomul X, dar exista si o pseudogena (aparuta prin duplicatie genetica) situata pe cromozomul 17<sup>4;8<\/sup>.<\/p>\n<p>Deficitul este determinat de una din anomaliile care pot afecta gena implicata in sinteza acestei enzime (deletii mici sau mutatii punctiforme), cu urmatoarele consecinte:<\/p>\n<p style=\"padding-left: 30px;\">1. sinteza unei cantitati scazute de enzima normala;<\/p>\n<p style=\"padding-left: 30px;\">2. sinteza de molecule enzimatice cu afinitate redusa pentru substratul specific;<\/p>\n<p style=\"padding-left: 30px;\">3. sinteza de molecule enzimatice cu stabilitate redusa;<\/p>\n<p style=\"padding-left: 30px;\">4. sinteza de molecule cu alterari asociate<sup>1;8<\/sup>.<\/p>\n<p>Femeile heterozigote nu prezinta manifestari clinice de anemie hemolitica deoarece cromozomul X normal\u00a0 mentine o activitate suficienta a G-6-PD. La aceste persoane deficitul heterozigot ofera o oarecare protectie impotriva parazitului Plasmodium falciparum<sup>7<\/sup>. Femeile homozigote pentru G-6-PD vor avea manifestari clinice de anemie hemolitica dupa ingestia de substante oxidante.<\/p>\n<p>Barbatii care au mostenit de la mama cromozomul X \u00a0purtator al genei deficitare (hemizigoti) vor prezenta un deficit de G-6-PD exprimat complet<sup>2;4;8<\/sup>.<\/p>\n<p>Prin studii electroforetice s-au obtinut peste 300 de izoenzime ale G-6-PD. Enzima normala este denumita G-6-PD<sup>\u0411<\/sup>. Populatia neagra prezinta enzima deficitara GPD<sup>\u0410<\/sup> cu o incidenta de 20% in populatie si cu o activitate redusa la\u00a0 5 \u2013 15% din valoarea normala. La persoanele de rasa caucaziana cu deficit de G-6-PD eritrocitar se gaseste cel mai adesea izoenzima de tip M sau GD<sup>Med<\/sup> (mediteraneana), cu activitate foarte redusa<sup>4,8<\/sup>.<\/p>\n<p>In tara noastra deficitul de G-6-PD reprezinta 10% din totalul anemiilor hemolitice, frecventa generala fiind de aproximativ 0.01%<sup>1<\/sup>.<\/p>\n<p>Fenomenele hemolitice pe care le poate determina deficitul de G-6-PD sunt declansate de:<\/p>\n<p style=\"padding-left: 30px;\">\u25cf diverse medicamente: antimalarice (clorochin, mepacrin, primachin), antipiretice si analgezice (aspirina in cantitati mari, fenacetin), sulfamide, PAS, acid nalidixic, furazolidon, nitrofurantoin, chinidina, albastru de metilen, vitamina K, acid ascorbic in cantitati mari, cloramfenicol, probenecid;<\/p>\n<p style=\"padding-left: 30px;\">\u25cf alimente: boabe de Vicia fava;<\/p>\n<p style=\"padding-left: 30px;\">\u25cf infectii virale;<\/p>\n<p style=\"padding-left: 30px;\">\u25cf infectii bacteriene;<\/p>\n<p style=\"padding-left: 30px;\">\u25cf modificari ale pH-ului sanguin in cursul unor tulburari metabolice (diabetice sau de alta natura)<sup>1;7<\/sup>.<\/p>\n<p>Incapacitatea suntului pentozelor de a genera in absenta G-6-PD o cantitate suficienta de glutation redus (GSH) faciliteaza oxidarea proteinelor, formarea de glutation oxidat (GSSG) si de methemoglobina (MetHb). Agregatele de hemoglobina denaturata care se fixeaza pe suprafata interna a membranelor eritrocitare determina ridigizarea si deformarea acestora, ceea ce duce la distrugerea eritrocitelor la nivelul splinei. Procese de degradare oxidativa pot surveni si la nivelul proteinelor structurale sau enzimelor continute in membrana eritrocitelor, conducand in cele din urma la liza celulara.<\/p>\n<p>In cazul infectiilor bacteriene sau virale se pare ca unul din factorii implicati ar fi formarea unei cantitati crescute de peroxid de hidrogen de catre leucocitele care fagociteaza agentii infectiosi.<\/p>\n<p>Hemoliza asociata consumului de Vicia fava (favism la populatia mediteraneana) este probabil determinata atat de derivati oxidanti pirimidinici (divicina si izouramil) cat si de factori imunologici<sup>1;8<\/sup>. Toate persoanele cu favism au valori de G-6-PD scazute, dar nu toate persoanele cu deficit enzimatic au favism<sup>5;8<\/sup>.<\/p>\n<p>Marea majoritate a pacientilor cu deficit de G-6-PD prezinta o suferinta hematologica numai dupa expunerea la infectii virale\/bacteriene sau in urma ingestiei de medicamente (mentionate mai sus) care suprasolicita capacitatea reducatoare a celulei<sup>1;5<\/sup>.<\/p>\n<p>Simptomatologia clinica a deficitului eritrocitar de G-6-PD se rezuma la manifestari caracteristice pentru anemia hemolitica de tip intrinsec; este important de mentionat ca acestea sunt intalnite numai la acele persoane cu activitatea enzimatica mai mica de 20% din valoarea normala. Dupa o perioada de 2-3 zile de la expunerea la factorul declansator apar febra, durerile abdominale, diareea iar urina devine rosie pana la maronie (hemoglobinurie), ca urmare a hemolizei intravasculare. Anemia hemolitica este moderata pana la severa; reticulocitele si celulele rosii tinere au activitate enzimatica mai mare decat cele mai batrane si prin urmare sunt mai rezistente la hemoliza. Episodul hemolitic stimuleaza eritropoieza si induce hiperplazia maduvei osoase eritroide<sup>1<\/sup>.<sup>\u00a0 <\/sup>Hemograma efectuata in puseele hemolitice indica o anemie normocroma normocitara cu reticulocitoza marcata si\u00a0 posibila prezenta in hematii a corpilor Heinz, punctatiilor bazofile, corpilor Howell-Jolly; corespunzator cu hemoliza apar crescute bilirubina indirecta si activitatea LDH. Rezistenta osmotica este normala<sup>1;5;8<\/sup>. Evolutia este de obicei autolimitanta.<\/p>\n<p>Mai rar, deficitul de G-6-PD se prezinta ca o anemie hemolitica cronica de intensitate usoara sau medie ce se exacerbeaza cu ocazia infectiilor<sup>8<\/sup>.<\/p>\n<p>Aproximativ 5% din nou-nascutii cu deficit enzimatic pot dezvolta icter neonatal dupa primele 24 ore de la nastere. La copiii asiatici si mediteraneeni icterul neonatal si icterul nuclear sunt mai frecvente.<\/p>\n<p>Diagnosticul este stabilit prin dozarea G-6-PD eritrocitare. Heterozigotii prezinta doua populatii de eritrocite; proportia acestora influenteaza gradul deficitului detectat.<\/p>\n<p>Diagnosticul diferential se face cu deficitul de piruvatkinaza (determinare enzimatica) si hemoglobinopatii (electroforeza hemoglobinei)<sup>3;5<\/sup>.<\/p>\n<p>Pacientii afectati\u00a0 trebuie\u00a0 sa fie avertizati asupra riscului legat de consumul medicamentelor mentionate mai sus. Sfatul genetic are importanta deosebita atunci cand intr-o familie apare un baiat afectat si mama este heterozigota: riscul de transmitere a bolii este de 50% la fiecare sarcina cu fat de sex masculin<sup>8<\/sup>.<\/p>\n<p><strong><em>Pregatire pacient<\/em><\/strong> <em>-<\/em> proba se poate recolta \u00e1 jeun sau postprandial, dar nu in timpul sau imediat dupa un episod de hemoliza, dupa ingestia recenta de antimalarice sau o transfuzie, deoarece exista riscul de a se \u00a0obtine rezultate fals negative<sup>3;6<\/sup>.<\/p>\n<p><strong><em>Specimen recoltat <\/em><\/strong>\u2013 sange venos<sup>6<\/sup>.<\/p>\n<p><strong><em>Recipient de recoltare <\/em><\/strong>\u2013 vacutainer cu EDTA K3<sup>6<\/sup>.<\/p>\n<p><strong><em>Cantitate recoltata<\/em><\/strong> \u2013 cat permite vacuumul<sup>6<\/sup>.<\/p>\n<p><strong><em>Prelucrare necesara dupa recoltare <\/em><\/strong>\u2013 proba de sange integral se refrigereaza imediat<sup>6<\/sup>.<\/p>\n<p><strong><em>Stabilitate proba <\/em><\/strong>\u2013 sangele integral este stabil <em>7 zile<\/em> la 2\u20138\u00b0C<sup>6<\/sup>.<\/p>\n<p><strong><em>Metoda <\/em><\/strong>- <span style=\"text-decoration: underline;\">fotometrica (enzimatica)<\/span><sup>6<\/sup>.<\/p>\n<p><strong><em>Valori de referinta <\/em><\/strong>\u2013 8.0-13.0 U\/gHb<sup>6<\/sup>.<\/p>\n<p><strong><em>Limita de detectie <\/em><\/strong>\u2013 0.8 U\/gHb<sup>6<\/sup>.<\/p>\n<p><strong><em>Interpretarea rezultatelor<\/em><\/strong><\/p>\n<p><strong><span style=\"text-decoration: underline;\">Clasificarea OMS a variantelor genetice de G-6-PD<\/span><\/strong><span style=\"text-decoration: underline;\">:<\/span><\/p>\n<p style=\"padding-left: 30px;\">Clasa I: activitatea G-6-PD este mai mica de 10% din cea normala (deficit sever); aceasta varianta este asociata cu anemie hemolitica cronica nesferocitara.<\/p>\n<p style=\"padding-left: 30px;\">Clasa II: activitatea G-6-PD este mai mica de 10% din cea normala (deficit sever); aceasta varianta este asociata cu hemoliza acuta intermitenta.<\/p>\n<p style=\"padding-left: 30px;\">Clasa\u00a0 III: activitatea G-6-PD reprezinta 10 \u2013 60% din cea normala (deficit moderat); exista un risc de hemoliza acuta dupa expunerea la factori declansatori.<\/p>\n<p style=\"padding-left: 30px;\">Clasa IV: activitatea G-6-PD este aproape de normal; pacientii sunt asimptomatici.<\/p>\n<p style=\"padding-left: 30px;\">Clasa V: activitate G-6-PD crescuta, fara implicatii clinice<sup>5<\/sup>.<\/p>\n<p><strong><span style=\"text-decoration: underline;\">Valori crescute ale activitatii G-6-PD<\/span><\/strong><\/p>\n<p>Pot fi intalnite in:<\/p>\n<p style=\"padding-left: 30px;\">-anemii pernicioase (pana la de 3 ori nivelul normal) si alte anemii macrocitare; nivelul crescut se mentine mai multe luni, chiar dupa administrarea de vitamina B<sub>12<\/sub>;<\/p>\n<p style=\"padding-left: 30px;\">-purpura trombocitopenica imuna (PTI); se normalizeaza la scurt timp dupa splenectomie;<\/p>\n<p style=\"padding-left: 30px;\">-come hepatice;<\/p>\n<p style=\"padding-left: 30px;\">-hipertiroidism;<\/p>\n<p style=\"padding-left: 30px;\">-infarct miocardic;<\/p>\n<p style=\"padding-left: 30px;\">-pierderi cronice de sange<sup>4;5<\/sup>.<\/p>\n<p><strong><em>Limite si interferente<\/em><\/strong><\/p>\n<p>Probele hemolizate pot da rezultate eronate<strong><em>\u00a0<\/em><\/strong><\/p>\n<p>Activitatea enzimatica este crescuta in reticulocite\u00a0 astfel incat un eventual deficit poate fi mascat daca proba s-a recoltat in cursul unui puseu hemolitic. In acest caz se recomanda repetarea recoltarii la un interval de 2 \u2013 3 saptamani<sup>3;6;7<\/sup>.<strong>\u00a0<\/strong><\/p>\n<p><span style=\"font-size: small;\">\u00a0<\/span><\/p>\n<p><span style=\"font-size: small;\">\u0411\u0438\u0431\u043b\u0438\u043e\u0433\u0440\u0430\u0444\u0438\u044f<\/span><\/p>\n<p><span style=\"font-size: small;\">1. Ana Stan. Hematologie Laborator. Citologie. Bucuresti, Editura Medicala 2004, 367-369.<\/span><\/p>\n<p><span style=\"font-size: small;\">2. Delia Mut Popescu \u2013 Hematologie clinica. Note de curs. Editia a II-a, Editura Medicala 2003, 77-78.<\/span><\/p>\n<p><span style=\"font-size: small;\">3. Diagnostic Tests 1991 \u2013 Springhouse Corporation, Springhouse, Pensylvania, 238.<\/span><\/p>\n<p><span style=\"font-size: small;\">4. Frances Fischbach. Blood Studies; Hematology and Coagulation. In A Manual of Laboratory &amp; Diagnostic Tests, Lippincott Williams &amp; Wilkins, USA, 7 Ed., 2004, 96-97.<\/span><\/p>\n<p><span style=\"font-size: small;\">5. Jacques Wallach. Interpretarea testelor de diagnostic. Editia a VII-a, Editura Stiintelor Medicale, 491, 527- 529.<\/span><\/p>\n<p><span style=\"font-size: small;\">6. Laborator Synevo. Referinte specifice tehnologiei de lucru utilizate 2010. Ref Type: Catalog.<\/span><\/p>\n<p><span style=\"font-size: small;\">7. Matthew R. Pincus, Richard A. McPherson. Henry\u2019s Clinical Diagnosis and Management by Laboratory Methods 21st Edition, Saunders, 2007. Erythrocytic Disorders, 533-544.<\/span><\/p>","protected":false},"excerpt":{"rendered":"<p>\u0413\u043b\u044e\u043a\u043e\u0437\u043e-6-\u0444\u043e\u0441\u0444\u0430\u0442\u0434\u0435\u0433\u0438\u0434\u0440\u043e\u0433\u0435\u043d\u0430\u0437\u0430 \u2013 \u043a\u043b\u044e\u0447\u0435\u0432\u043e\u0439 \u0444\u0435\u0440\u043c\u0435\u043d\u0442 \u043f\u0435\u043d\u0442\u043e\u0437\u043e\u0444\u043e\u0441\u0444\u0430\u0442\u043d\u043e\u0433\u043e \u043f\u0443\u0442\u0438, \u0432 \u0445\u043e\u0434\u0435 \u043a\u043e\u0442\u043e\u0440\u043e\u0433\u043e \u043f\u0440\u043e\u0434\u0443\u0446\u0438\u0440\u0443\u0435\u0442\u0441\u044f \u0432\u043e\u0441\u0441\u0442\u0430\u043d\u043e\u0432\u043b\u0435\u043d\u043d\u044b\u0439 \u041d\u0410\u0414\u0424-\u041d, \u0438\u0441\u043f\u043e\u043b\u044c\u0437\u0443\u0435\u043c\u044b\u0439 \u043a\u0430\u043a \u0434\u043e\u043d\u043e\u0440 \u0432\u043e\u0434\u043e\u0440\u043e\u0434\u0430 \u0432 \u0440\u0435\u0430\u043a\u0446\u0438\u044f\u0445 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\u042d\u0440\u0438\u0442\u0440\u043e\u0446\u0438\u0442\u044b, \u043d\u0435 \u0441\u043f\u0440\u0430\u0432\u043b\u044f\u044e\u0449\u0438\u0435\u0441\u044f \u0441 \u043e\u043a\u0441\u0438\u0434\u0430\u0442\u0438\u0432\u043d\u044b\u043c \u0441\u0442\u0440\u0435\u0441\u0441\u043e\u043c, \u043f\u043e\u0434\u0432\u0435\u0440\u0433\u0430\u044e\u0442\u0441\u044f \u0440\u0430\u0437\u0440\u0443\u0448\u0435\u043d\u0438\u044e (\u0433\u0435\u043c\u043e\u043b\u0438\u0437\u0443).<\/p>\n<p>\u0423 \u0447\u0435\u043b\u043e\u0432\u0435\u043a\u0430 \u0433\u0435\u043d, \u043a\u043e\u0434\u0438\u0440\u0443\u044e\u0449\u0438\u0439 \u04136\u0424\u0414, \u0438\u043c\u0435\u0435\u0442 \u0431\u043e\u043b\u044c\u0448\u043e\u0435 \u0447\u0438\u0441\u043b\u043e \u0432\u0430\u0440\u0438\u0430\u0446\u0438\u0439 (\u043f\u043e\u043b\u0438\u043c\u043e\u0440\u0444\u0438\u0437\u043c\u043e\u0432). \u041c\u0443\u0442\u0430\u0446\u0438\u0438 \u043a\u043e\u0434\u0438\u0440\u0443\u044e\u0449\u0435\u0433\u043e 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