Noutati terapeutice in insulino-rezistenta din sindromul ovarului polichistic

1 Septembrie, 2010 - 23:00

In ultimii 60 de ani care au trecut de la descrierea sindromului ovarului polichistic (SOP) s-au facut progrese remarcabile in investigatiile clinice si definirea sindromului, precum si in ceea ce priveste consecintele directe sau indirecte ale acestei afectiuni ce se pot extinde de-a lungul intregii vieti a pacientelor.

Pe langa caracteristicile clinice de hiperandrogenism si anovulatie cronica, multe paciente cu SOP au insulino-rezistenta si risc crescut de diabet zaharat tip II jogos casino online.

In cursul ultimului deceniu a devenit clar ca hiperinsulinismul si rezistenta la insulina sunt caracteristici predominante la majoritatea pacientelor diagnosticate cu SOP, prezente in cel putin 50% din cazuri.

Chiar daca hipersecretia insulinica este evidentiata la circa 70% dintre femeile obeze cu SOP, aceasta caracteristica este prezenta chiar si in 20-40% dintre pacientele non-obeze.

De asemenea, femeile afectate de SOP pot avea risc mare de boala cardiovasculara. Relatia intre aceste efecte metabolice si etiologia SOP nu este inca bine definita Bonus Fara Depunere

In conditiile in care etiopatogenia SOP este neelucidata pe deplin iar manifestarile sale clinico-biologice sunt extrem de heterogene, tratamentul este departe de a fi unic.

Terapia incearca interceptarea uneia sau mai multor verigi ale cercului patogenic; sunt vizate principalele simptome si consecintele lor pe termen lung: hirsutismul si alte elemente de virilizare (acnee, alopecie etc.),
anovulatia si tulburarile de ciclu menstrual, rezistenta la insulina si hiperinsulinismul, alterarile metabolismului lipidic, ca si tulburarile psiho-comportamentale, prezenta hirsutismului si eventual a obezitatii reprezentand o cauza de profund stress psihologic, social si material, o lupta permanenta pentru acceptarea de catre societate in general, de anturaj in special.

Tratamentul se aplica in functie de tabloul clinic (severitatea elementelor de virilizare), de prezenta insulino-rezistentei si de dorinta pacientei de a avea sarcina.

Tratamentul tulburarilor metabolice din SOP urmareste corectarea rezistentei la insulina si a hiperinsulinismului, a perturbarilor metabolismului lipidic si obezitatii, tratamentul dovedindu-se consumator material, de timp si
frustrant atat pentru pacient cat si pentru medic, atat timp cat nu exista un tratament etiologic ideal.

Se stie ca insulino-rezistenta si hiperinsulinemia compensatorie reprezinta trasaturi metabolice caracteristice ale pacientelor cu SOP. Cresterea concentratiei plasmatice a insulinei pare a juca un rol important in fiziopatologia hiperandrogenismului din SOP, deoarece insulina stimuleaza
productia ovariana de androgeni si totodata scade sinteza hepatica de SHBG, inducand cresterea testosteronului liber.

Obezitatea, frecvent asociata cu SOP, constituie un factor de agravare atat al hiperandrogenismului cat si al celorlalte semne clinice din sindromul ovarului polichistic.

Ipoteza ca hiperinsulinemia poate agrava hiperandrogenismul si contribuie la infertilitatea femeilor cu ovare polichistice, mai ales in cazul celor obeze, a generat o preocupare serioasa pentru studiul eficacitatii dietei si tratamentului cu medicamente care scad nivelul insulinei in SOP.

Astfel s-a sugerat ca reducerea greutatii corporale prin dieta amelioreaza actiunea insulinei asupra tesuturilor tinta si reduce hiperinsulinemia din SOP, ducand la modificarea statusului hormonal si metabolic si
cresterea fertilitatii (Pasquali).

In afara scaderii ponderale, exista o serie de agenti terapeutici utili in
ameliorarea hiperinsulinemiei, printre care se numara si medicamentele antidiabetice- thiazolidindionele.

Thiazolidindionele sunt o clasa noua de antidiabetice orale ce cuprinde trei preparate: troglitazona, rosiglitazona si pioglitazona. Efectele terapeutice ale acestei clase includ: cresterea transportului mediat de insulina al glucozei si reducerea insulinorezistentei la nivelul ficatului, tesutului adipos si muschiului scheletic iar in vitro s-a demonstrat cresterea captarii bazale si insulin-stimulate a glucozei precum si accentuarea exprimarii GLUT1 si GLUT4 atat in adipocite cat si in miocite.

Efectele thiazolidindionelor sunt mediate de interactiunea cu PPAR g, receptor nuclear ce regleaza transcriptia a numeroase gene implicate in metabolismul glucidic si lipidic; PPAR g joaca de asemenea un rol central in diferentierea si exprimarea genelor adipocitare.

Acest receptor pare sa fie un reglator important al adipogenezei, avand doua izoforme: PPAR g1 care se exprima ubicvitar si PPAR g2 care este exprimat predominent in tesutul adipos.

Desi receptorul nu este implicat direct in calea de semnalizare a insulinei, medicamentele cu actiune insulin-sensibilizatoare ca thiazolidindione se leaga de acesta cu afinitate crescuta, activand reglarea transcriptiei genice. O mutatie rara a PPAR g (P115Q) in vecinatatea imediata a unui situs de reglare a fosforilarii conduce la un receptor activ constitutional.

Purtatorii acestei mutatii prezinta obezitate extrema si insulino-rezistenta marcata. in vitro, supraexprimarea acestei mutatii in fibroblastii de cultura rezulta in diferentierea rapida a acestora in adipocite.

Deci, aceasta forma rara de obezitate rezulta din forma activa constitutional a PPAR g ce duce la adipogeneza accentuata dar, totodata,
sensibilizeaza corpul la actiunea insulinei.

Troglitazona administrata in doza de 400 mg/zi la pacientele obeze cu SOPV a ameliorat parametrii metabolici si hormonali; un numar semnificativ de paciente au prezentat ovulatie.

Troglitazona, s-a dovedit a imbunatatii metabolismul glucozei si insulino-sensibilitatea la pacientii cu diabet zaharat de tip II. Mai multe studii au aratat ca administrarea a 400 mg de troglitazona zilnic scade nivelul insulinei circulante si amelioreaza statusul metabolic si hormonal la femei obeze cu SOP.

Corectarea nivelelor excesive de testosteron, trigliceride si activator de plasminogen duce la scaderea riscului pe termen lung a complicatiilor cardiovasculare la aceste femei.

In plus, s-a demonstrat ca troglitazona amelioreaza disfunctia ovulatorie si hirsutismul, diminuand hiperandrogenia si insulino-rezistenta la pacientele cu SOP, in directa corelatie cu doza si cu minime reactii adverse.

Desi studiile au mentionat efectele benefice ale troglitazonei asupra disfunctiilor metabolice si ovulatorii, nu s-a demonstrat clar daca acestea sunt secundare cresterii sensibilitatii la insulina sau actiunii directe asupra steroidogenezei; in acest sens, s-a raportat un efect direct, dependent de doza, al troglitazonei asupra productiei de androsteron in culturi de celule tecale de sobolan si asupra secretiei de progesteron in celule granuloase luteinice de cultura umana.

S-a sugerat astfel ca efectele benefice ale acestui medicament in SOP se pot datora nu numai imbunatatirii rezistentei periferice la insulina si hiperinsulinismului, ci si posibilului efect direct al acestuia asupra
steroidogenezei sexoide in general, ovariene in special.

Actiunile benefice ale acestei clase de medicamente se exercita prin actiunea agonista potenta la nivelul PPAR g, existand diferente nesemnificative intre cele trei medicamente din cadrul clasei.

Activarea PPAR g promoveaza cresterea si diferentierea preadipocitelor si poate creste adipozitatea corporala totala. Acest fapt reprezinta un paradox, deoarece grasimea corporala este asociata in general cu rezistenta la insulina, conducand la intrebarea cum un agent adipogen ar
putea imbunatati sensibilitatea la insulina.

Rezistenta la insulina este strans legata de obezitatea centrala mai degraba decat de cea periferica, deoarece o crestere a adipozitatii viscerale conduce la disponibilitate crescuta a lipidelor la nivelul circulatiei portale si sistemice, care la randul ei este asociata cu nivel ridicat de lipide la nivel hepatic (lipotoxicitate) si in muschiul scheletic.

Ficatul adipos este recunoscut ca parte a sindromului de rezistenta la insulina, demonstrandu-se prin rezonanta magnetica nucleara nivel crescut al grasimii intramiocelulare.

Studiile ex vivo au indicat ca efectul adipogenic al rosiglitazonei poate fi depot-specific, stimuland captarea lipidelor in tesutul subcutanat dar nu si in preadipocitele omentale. Acest efect depot- specific al rosiglitazonei in vivo poate conduce la canalizarea lipidelor dinspre aria viscerala si spre
tesutul subcutanat unde pot fi stocate in siguranta, procesul fiind descris ca ”furtul trigliceridelor”.

Rezultatul poate fi reducerea nivelului portal si sistemic de AGL si scaderea lipotoxicitatii. Acest concept este sustinut de studii animale care demonstreaza scaderea acizilor grasi circulanti si a grasimii intrahepatice in tratamentul cu rosiglitazona, precum si cresterea grasimii extramiocelulare dar nu si a celei intramiocelulare, astfel prevenind sau imbunatatind rezistenta la insulina.

Alte studii au completat informatiile asupra efectelor pozitive ale tratamentului cu rosiglitazona la pacientii cu DZ tip II, si anume s-a demonstrat imbunatatirea semnificativa a profilului metabolic
(exprimata prin mentinerea in limite rezonabile a hemoglobinei glicozilate) si sensibilitatii la insulina la nivel hepatic, muscular si in tesutul adipos; totodata, creste distributia glucozei, reducand atat hiperglicemia cat si hiperinsulinismul.

Reducand necesarul de insulina, scade hipersecretia de insulina din celulele beta (evidentiata prin scaderea raportului insulina/proinsulina)
si poate astfel reduce sau preveni expansiunea celulelor beta.

Tinand cont de efectul direct al rosiglitazonei asupra celulelor beta-pancreatice si de scaderea nivelului AGL care duce la scaderea lipotoxicitatii pancreatice, se poate afirma ca acest medicament ar putea avea potentialul de prezervare a functiei celulelor beta si de a intarzia
progresia bolii in DZ tip II.

S-au studiat de asemenea efectele rosiglitazonei asupra riscului cardiovascular prezent la pacientii cu DZ tip II. Astfel, sindromul metabolic sau de insulina-rezistenta se caracterizeaza prin anomalii
in sistemul fibrinolitic, in particular cresterea nivelului inhibitorului activatorului plasminogenului (PAI-1) si o concentratie mare a activatorului plasminogenului tisular (tPA), precum si nivel ridicat de AGL.

La acestea se asociaza dislipidemia, caracterizata prin reducerea HDL-colesterol, cresterea LDL-colesterol si a trigliceridelor. Acest tablou biochimic caracterizeaza atat DZ tip II cat si SOP.

Cercetarile au evidentiat scaderea expresiei PAI-1 in endoteliul vascular, a activitatii PAI-1 antigen si a tPA, indicand o imbunatatire a functiei fibrinolitice in DZ tip II in cursul tratamentului cu rosiglitazona.

De asemenea, s-a raportat o crestere a nivelului de HDL3-colesterol la o doza de 8mg/zi minimum 100 saptamani, cu reducerea raportului colesterol total /HDL-colesterol, alaturi de o scadere a concentratiei serice de trigliceride. Dupa o crestere initiala, in primele saptamani de
tratament, a nivelului de LDL-colesterol, acesta revine la valorile initiale, raportul LDL- colesterol/Apo B ramanand nemodificat.

Toate aceste date, alaturi de constatarea clinica de reducere a microalbuminuriei si de scadere a tensiunii arteriale diastolice, conduc la concluzia ca rosiglitazona are un efect benefic asupra factorilor de risc cardio-vascular la pacientii cu DZ tip II, avand potentialul de a reduce sau preveni boala cardiovasculara in aceasta afectiune. Ramane de demonstrat daca aceste efecte se mentin si in cazul pacientilor cu SOP aflate in tratament cu rosiglitazona.

Alt efect favorabil al troglitazonei, care ramane sa fie cercetat si in cazul rosiglitazonei, consta in diminuarea semnificativa a concentratiilor testosteronului total si liber, precum si a nivelului plasmatic de 17-hidroxiprogesteron si delta4-androstendion bazale si dupa stimulare cu GnRH,
aceasta reducere a nivelului de androgeni aparand independent de orice modificare in nivelul gonadotropilor (delta4-androstendionul fiind cel mai important marker al productiei de androgeni indiferent de sursa).

Aparitia unor cazuri de deces prin insuficienta hepatica la pacientii tratati cu troglitazona a determinat interzicerea utilizarii acesteia din martie 2000.

Sunt insa diferente semnificative intre cei trei reprezentanti ai acestei clase in ceea ce priveste efectele adverse, astfel hepatotoxicitatea este mult redusa in cazul pioglitazonei si rosiglitazonei comparativ cu troglitazona, la aceasta din urma efectul putand fi legat de lantul unic lateral de tocoferol.

Sunt insa diferente semnificative intre cei trei reprezentanti ai acestei clase in ceea ce priveste efectele adverse, astfel hepatotoxicitatea este mult redusa in cazul pioglitazonei si rosiglitazonei comparativ cu troglitazona, la aceasta din urma efectul putand fi legat de lantul unic
lateral de tocoferol.

Totusi, se recomanda monitorizarea functiei hepatice inainte si in timpul
tratamentului cu thiazolidindione si excluderea de la tratament a pacientelor cu afectiuni hepatice pre-existente.

Alte efecte secundare ce pot apare sunt legate de retentia de fluid si cresterea volumului plasmatic, asociate cu reducerea aparenta a hematocritului si hemoglobinei, care pot conduce uneori la edeme dar fara a fi detectate influente asupra tensiunii arteriale sau functiei cardiace. Se recomanda totusi prudenta in utilizarea acestora la pacientii cu insuficienta cardiaca sau anemie.

Terapia cu thiazolidindione in SOP urmeaza sa fie evaluata. Studiile efectuate pana in prezent sugereaza ca rezultatele clinice (ovulatia) si biologice sunt posibile dupa trei luni de tratament.

Se recomanda ca administrarea terapiei sa se efectueze discontinuu sub stricta monitorizare, fiind exclusa administrarea lor la femeile gravide avand in vedere retardul in dezvoltarea fetala care apare in studiile pe animale.

Abordarea pacientelor cu SOP trebuie facuta preventiv si curativ. Tratamentul preventiv trebuie inceput cu diagnosticarea anomaliilor metabolice pentru care se recomanda ca investigatii de rutina minime: TTGO, profilul lipidic, supravegherea tensiunii arteriale. Daca investigarea pacientelor obeze cu SOP pare pe deplin justificata, investigarea pacientelor non-obeze ramane controversata.

S-a dovedit ca femeile cu SOP non-obeze cu anovulatie pot avea toleranta la glucoza alterata semnificativ sau rezistenta la insulina si scaderea HDL-colesterol. Astfel, desi cu risc mai scazut decat pacientele obeze, acestea au totusi risc de dezvoltare a diabetului zaharat tip II sau a bolilor
cardiovasculare, pe termen lung.

Sindromul ovarului polichistic, ca orice sindrom in care etiologia este incerta si mecanismele discutabile, ”beneficiaza” de solutii terapeutice in continua cautare, fiecare pas fiind o speranta, ”noutatile terapeutice”- o normalitate.

(Dr. Lucica Grigorascu, medic specialist endocrinolog-CMDTA ”N. Kretzulescu”
Dr. Alina Sucaliuc, medic specialist endocrinolog, Institutul de Endocrinologie, ”C.I.Parhon”
Prof. Dr. Constantin Dumitrache, Institutul de Endocrinologie ”C.I.Parhon”)

Bibliografie:
1. Nisoli E, Vettor R, et al. Nutrient chaannelling - regulated peroxisome proliferator - activated receptor - alfa - 2 (PPAR - 2) and leptin gene expression in human subcutaneous fat. Diabetologia 42: 495 - 496, 1999.
2. Ehrmann DA, Schneider DJ, et al. Troglitazone improves defects in insulin action, insulin secretion, ovarian steroidogenesis and fibrinolysis in women with polycystic ovary syndrome, J Clin Endocrinol Metab 82: 2108, 1997.
3.Chang Jeffrey R, Heindel Jerrold J, Dunaif Andrea. Polycystic ovary syndrome, 2002

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Sunteti de acord cu modificarea examenului de rezidentiat propusa de ministrul Sanatatii?
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