PMA

Sindrome da iperstimolazione ovarica severa (OHSS): fisiopatologia e diagnosi

La sindrome da iperstimolazione ovarica severa (OHSS) è una sindrome iatrogena, conseguenza della stimolazione ovarica per induzione dell’ovulazione multipla in corso di Procreazione medico-assistita (PMA). Insieme all’aumentata incidenza di gravidanze multiple e di gravidanze extra-uterine, la OHSS costituisce la terza e più grave delle complicanze della tecnica IVF. Il monitoraggio follicolare ecografico (MF) oltre ad essere indispensabile per programmare il timing del pick-up risulta sempre più utile strumento  di valutazione del rischio di insorgenza della OHSS soprattutto dopo la introduzione degli analoghi nei protocolli di induzione di crescita follicolare multipla (CFM) che ha reso inutile il  monitoraggio ormonale dell’estradiolo.

Incidenza:

L’incidenza della sindrome di iperstimolazione ovarica varia tra 1%  e 30% con una media di 3.8%  riportata da vari AA. (1). Questa notevole variabilità è dovuta soprattutto alle diverse valutazioni dei sintomi riferiti dalle pazienti ai singoli operatori (Tab. 1).

CLASSIFICAZIONE OHSS:

Rabau et al. per primi  nel 1967 classificarono la OHSS in tre categorie o classi (lieve, moderata e grave) ognuna suddivisa in due  gradi (2). Tale classificazione è ancora valida con le modifiche apportate da Schenker e Weinstein nel 1978 (3) e da Golan nel 1989 (4).

FISIOPATOLOGIA:

La stimolazione ovarica con gonadotropine causa una crescita follicolare multipla nella fase follicolare precoce (5). L’ovaio iperstimolato somiglia in modo impressionante ad un ovaio PCOS  e contiene un caleidoscopio follicolare di ogni tipo e misura comprese cisti piccole e grandi (6).

L’iperstimolazione ovarica produce: 1) Ingrossamento delle ovaie da  crescita follicolare multipla (CFM), neoformazione vascolare da incrementata sintesi di VEGF (7) con particolare neovascolarizzazione perifollicolare e formazione di cisti luteiniche e 2) successiva luteinizzazione massiva (8). Trounson e Coll. riferendosi ai protocolli senza analoghi ritenevano che gli alti tassi ematici di E2  fossero  il motivo scatenante della sindrome (9,10); valori di E2 > 6.000 pg/ml hanno il 38% di probabilità di sviluppare OHSS. Ma la sindrome si scatena anche in presenza di tassi plasmatici di estrogeni non eccessivamente elevati o addirittura normali. In quest’ultimo caso sarebbe da ipotizzare  un iperestrogenismo locale follicolare. L’ingrossamento delle ovaie produce tutta la  sintomatologia di tipo compressivo: distensione addominale, dolori addominali, nausea e vomito (tab. 2).

La luteinizzazione massiva è responsabile di tutta la grave sintomatologia di tipo vascolare-idroelettrolitico inducendo a livello ovarico iperproduzione di istamina, interleleuchine (IL-1, IL-2, IL-6, VEGF) e prostaglandine che a loro volta determinano un danno capillare ed una aumentata permeabilità vascolare con perdita di fluidi e proteine dal compartimento intravascolare con ipovolemia, oliguria, ascite e idrotorace. Infatti la somministrazione di antagonisti dei recettori H per l’istamina e di inibitori della PG-sintetasi (Indometacina) riducono nettamente l’ascite. Una grave ipovolemia causa anche una ridotta perfusione renale che aumenta il riassorbimento del sodio e dell’acqua nel tubulo prossimale (11), determinando oliguria e bassi livelli di sodio urinario. Lo scambio di H+ e K+ con il Na a livello del tubulo distale si riduce, determinando un accumulo di H+ e K+, ipercalcemia e tendenza all’acidosi (12).  L’ipovolemia, a sua volta, induce attivazione del sistema renina-angiotensina e conseguente emoconcentrazione che facilita l’insorgenza di fenomeni tromboembolici (trombofilia acquisita) e coagulazione intravasale disseminata (CID). La paziente OHSS è una paziente disidradata in un mare di acqua.

La trombofilia ereditaria (predisposizione genetica alla trombosi) è un carattere complesso ed i geni che la determinano sono considerati dei geni di suscettibilità che devono interagire con fattori ambientali esterni per il manifestarsi della malattia  (gravidanza, contraccezione orale, interventi chirurgici, deficit vitaminici, etc). Si può brevemente definire come tendenza a sviluppare trombi intravascolari principalmente a livello delle succlavie e delle giugulari. Clinicamente è caratterizzata da deplezione di fluido intravascolare e aumento della viscosità ematica con deficit di proteina C, proteina S e protrombina; resistenza alla proteina C attivata dovuta alla mutazione genica nel fattore V (Fattore V di Leiden) e al polimorfismo del gene MTHFR 677T  (metiltetraidrofolato). La trombofilia acquisita presenta spesso anche Ac anticardiolipina (34), antilupus, deficit proteina S, deficit antitrombina e resistenza acquisita alla proteina C. Spesso è conseguente a OHSS tipo IV-V  (13-16).

L’alto numero dei follicoli giustifica da solo l’ingrossamento delle ovaie. Tutti gli AA.  concordano sul riscontro di una media di follicoli/ovaio nettamente superiore nelle pazienti OHSS rispetto a quella di pazienti  di controllo (16.75  vs. 8.42).  Blankstein et al. nel 1987 hanno dimostrato una correlazione fra il numero di follicoli medi e piccoli e la percentuale di insorgenza della OHSS (1). Invece Tal e Coll. ritengono che i follicoli di piccole dimensioni (diam. <11 mm) sono in diretta  correlazione con la incidenza di OHSS (20). I follicoli piccoli anche se non giungono a maturazione completa, tuttavia  non vanno incontro ad atresia e continuano a crescere dopo somministrazione di HGC aumentando la produzione di estrogeni mentre i follicoli di grandezza normale sono stati aspirati e quindi non possono nè aumentare di volume nè produrre ulteriori quantità di estrogeni. La somministrazione di HCG  è il principale fattore di rischio con un ovaio che contiene  numerosi  follicoli di piccole dimensioni (tab. 3). La somministrazione di HCG, come il tasso plasmatico di estradiolo, fa aumentare il PR ma anche la percentuale di OHSS (18,19). Un tasso di E2 > 6.000 pg/ml dovrebbe indurre a sospendere il ciclo di stimolazione. L’utilizzo di analoghi del Gn-RH fa aumentare il rischio di insorgenza di OHSS per l’effetto fare-up, per il blocco del surge precoce di LH, per il maggior numero di fiale di gonadotropine utilizzate.

MATERIALI e METODI:

Su un gruppo di 532 pazienti sottoposte a induzione di ovulazione multipla in cicli IVF dal 1° gennaio 1990 al 30 Ottobre 1996 sono state osservati 31 casi di OHSS (5,82 %). Per la  diagnosi di OHSS ci si attiene ai criteri di Rabau e al. (10) modificati da Shenker e Weinstein (11). Tutte le pazienti sono state in cura presso il Fertility Center di Cardito -Napoli-  e il Centro di Sterilità dell’Ospedale San Paolo di Napoli.

Le pazienti erano suddivise in 4 gruppi omogenei per numero e patologia e sottoposti a 4 diversi protocolli di iperstimolazione ovarica controllata (COH) : i primi tre  prevedevano l’utilizzo di Gn-RH-a e Gonadotropine secondo i classici schemi tipo lungo e di tipo corto o flare up; il quarto  protocollo  prevedeva l’uso delle sole gonadotropine senza analogo. In quest’ultimo gruppo si è avuta la maggior parte dei casi di OHSS (17/31) e quelli più gravi (tab. 4).

Il giorno della iniezione di HCG è stato  convenzionalmente chiamato giorno 0. I parametri ecografici valutati erano il diametro medio delle ovaie, il numero totale di follicoli secondari suddivisi in follicoli  piccoli (Æ 5-11 mm), medi (Æ 12-16 mm) e grandi (Æ 17-31 mm), il tipo di endometrio (IUS), lo spessore di quest’ultimo e la presenza di falda liquida nel Douglas (tab.5). Gli ecografi utilizzati sono stati Ansaldo AU 450 e Toshiba entrambi con sonda convex da 3,5 mHz e sonda endovaginale da 6.5 mHz. Quest’ultima preferita per la maggiore precisione e per essere lo strumento utilizzato per il pick-up.

RISULTATI:

A)  Numero totale di follicoli:

Al monitoraggio follicolare (MF) nei primi giorni di stimolazione  non si notano significative differenze fra i gruppi che svilupperanno OHSS e quelli che non la svilupperanno; ma al giorno della iniezione di HCG (giorno 0) vi è un  numero totale di follicoli significativamente maggiore nel gruppo OHSS rispetto al resto delle pazienti non-OHSS (19±9.45 versus 8.55±6.84). Il rischio di insorgenza di OHSS in base al numero totale di follicoli è del 5% per un numero di follicoli < 7 per ciascun ovaio,  raggiunge rapidamente il 60%  con un numero di follicoli di 8 per ciascun ovaio e quindi aumenta proporzionalmente al numero dei follicoli. La prova del nove è nell’aumento dei valori sierici di estradiolo che paradossalmente si osserva 1-4 giorni dopo l’ultima iniezione di gonadotropine (v. grafico 1).

B) Percentuale di follicoli piccoli:

Questi follicoli per la maggior parte sono di piccole dimensioni (diametro < 11 mm).  Già molti AA. hanno confermato l’esistenza di una correlazione fra il numero di follicoli di piccole dimensioni e il rischio OHSS (1, 15, 16). Nella nostra ricerca le pazienti OHSS classe I (I° e II° grado) hanno una popolazione follicolare equamente distribuita fra follicoli piccoli, medi e grandi con modesta predominanza dei follicoli grandi; le paz. OHSS II classe (gradi 3° e 4°) presentano una predominanza dei follicoli medi mentre per i casi più severi di  classe III (gradi 5° e 6°) era netta la predominanza dei follicoli piccoli ed in quest’ultimo caso troviamo una convergenza di dati con altri AA. (1). Aumentando la severità della sindrome aumenta la percentuale di follicoli piccoli e diminuisce il diametro medio dei follicoli (tab. 5).

Alcuni AA. addirittura non hanno trovato correlazione con il numero totale di follicoli nè con i follicoli maturi ma solo con i follicoli di diametro < 11 mm (9). La spiegazione di ciò è data dal fatto che  già i  follicoli piccoli sono formidabili produttori di estrogeni, e dopo il pick-up continuano a crescere spesso non monitorizzati  sotto l’influsso dell’iniezione di HCG  e dell’HMG ancora in circolo fino a diventare follicoli maturi e formidabili produttori di estrogeni. Infatti il tempo di insorgenza della OHSS rispetto al giorno di somministrazione della HCG è relativamente breve per i gradi lievi ed aumenta correlativamente con la gravità della OHSS. I gradi più elevati e severi sono ad insorgenza più tardiva, contemporanei alla crescita dei follicoli più piccoli (graf.  2).

B) Diametro medio ovarico: un incremento del 50% del diametro ovarico iniziale ha prodotto OHSS della Ia classe, un incremento fra il 50 e il 100%  in genere produce una OHSS della IIa classe mentre un incremento > 100% è correlato ad una OHSS della IIIa  classe. Il diametro ovarico medio al giorno 0 nel gruppo di pazienti con gradi I° e II° era 5.4 cm, nei gradi III° e IV° era  8.26 cm e 12.2 cm nei gradi V° e VI°.

C) Falda liquida: quasi sempre assente (22/27) al momento della iniezione di HCG, sempre presente al momento dell’insorgenza di OHSS (tab. 2).

D) tipo IUS

E) Thickness

F) PCOS pattern come risposta al trattamento con Gn-RH prima di iniziare la stimolazione con FSH

 4 pz. Furono ospedalizzate soprattutto a causa della insorgenza di idrotorace e relativi problemi respiratori, tutte erano gravide ed una sola abortì alla 8a settimana.

l’ultimo caso riportato in tabella prevedeva COH con Clomid 150 mg/die dal 2° al 6° giorno del ciclo e rapporti mirati

CORRELAZIONE OHSS/RENINA/E2/P

L’attività della angiotensina-renina presenta un picco in fase middleluteale per poi decrescere alla fine del ciclo. Simile andamento presentano E2 e P. Un persistente alto tasso sierico dell’attività reninica avviene nei cicli seguiti da concepimento (29).

Un più alto tasso sierico di angiotensina si riscontra nella OHSS (tab. 7 ).

La renina è implicata nella neo-angiogenesi (annidamento embrione  e funzionalità corpo luteo) e nell’aumentata permebilità vascolare con formazione di edemi ed essudati.

 

Risultati:

  • L’outcome gravidico delle pazienti OHSS è sorprendentemente elevato: delle 26 pazienti OHSS ben 19 (73%) rimasero gravide; 13 (50%) hanno condotto una gravidanza a termine (bambino in braccio), 6 (23,07%) hanno abortito e solo 7 (26,92%) non hanno avuto nessuna gravidanza (tab. 6).  Tulandi già nel 1984 aveva notato che la percentuale di gravidanze nelle donne iperstimolate era 3 volte superiore a quella delle donne non stimolate anche se nella  sua statistica il grado VIº presentava un’incidenza  di aborti elevata (12).
  • La maggiore incidenza delle forme gravi di OHSS si verifica nelle induzioni con Gonadotropine   senza analoghi mentre per le forme lievi  e medie di OHSS non c’è differenza significativa fra i diversi schemi terapeutici adottati (tab. 4). Esiste invece un miglioramento della qualità degli embrioni dovuta alla riduzione dell’LH preovulatorio da parte del Gn-RH-a (15).
  • Le pazienti ipogonadotrope hanno il rischio più basso di sviluppare la OHSS. Il più  importante fattore di rischio è costituito dalla policistosi ovarica (46,15%);  altri fattori di rischio sono la giovane età delle  pazienti (12), l’amenorrea anovulatoria,  basso indice di massa corporea.
  • Il fattore predittivo più importante si conferma il numero totale di follicoli al momento della iniezione di HCG (graf. 1) seguito dalla concentrazione plasmatica dell’estradiolo > 2000 pg/ml (2).

 

 

References:

1) Forman R.G., Ross B., Frydman R., Barlow D.H. et Egan D.: Severe ovarian hyperstimulation syndrome using agonists of gonadotropin-releasing hormone for in vitro fertilization: a European series and a proposal for prevention. Fertil. Steril. vol 53, No.3, March 1990.

2) Rabau E., David A., Serr DM., Mashiach S., Lunenfeld B.: Human Menopausal Gonadotropins for anovulaztion and sterility: results of 7 years  of treatment. Am. J. Obstet. Gynecol. 98:92,1967.

3) Schenker J.G., Weinstein D.: Ovarian Hyperstimulation Syndrome: a current survey. Fertil. Steril. 30:255,1978.

4) Golan A., Ron-El R., Herman A., Soffer Y., Weinraub Z., Capsi E.: Ovarian hyperstimulation syndrome: an update review. Obstet. Gynecol. Surv., 44, 430-440, 1989

5) Hodgen G.D.: The dominant ovarian follicle. Steril. Fertil. 38:281,1982.

6) Orsini L.F., Venturoli S., Lorusso R., Pluchinotta V., Paradisi R., Bovicelli L.:Ultrasonic findings in polycystic ovarian disease. Fertil. Steril. 43:709,1985.

7) Blackstein J., Shalev J., Saadon T. et al.: Ovarian hyperstimulation syndrome: prediction by numbers and size of preovulatory ovarian follicles. Fertil. Steril. 47,597-602, 1987

8) Forman R.G., Frydman R., Egan D., Ross C., Barlow D.H.: Severe ovarian Hyperstimulation Syndrome using Agonists of gonadotropin-releasing hormone for in vitro fertilization: a European series and a proposal for prevention. Fertil. Steril., 53, 502-9, 1990.

9)  In vitro fertilization and assisted reproduction. Brinsden P.R. et Rainsbury P.A. Parthenon Publishing Group Ltd London 1992

10) Trounson A. et Gardner D. K.: Handbook of in vitro fertilization pagg. 11-12 CRC Press, Boca Raton, Florida, USA.

11) Tulandi T., Micinnes R.A., Arronet GH: Ovarian Hyperstimulation following ovulation induction with human menopausal gonadotropin. Int. J. Fertil. 29:113,1984.

12) Polishuk W.Z., Schenker J. G.: Ovarian overstimulation syndrome. Fertil. Steril. 20:443, 1969.

13) Hengel T., Jewelewicz R., Dyrenfurth I.: Ovarian hyperstimulation Syndrome. Am. J. Obstet. Ginecol. 112: 1050, 1972.

14) Blankstein J., Mashiach S., Lunenfeld B. in: Ovulation induction and in vitro Fertilization, Ediz. Year Book Medical Publisher, Inc. Chicago 1986 pagg. 145-148

15) Shalev J., Mashiach S., Lunenfeld B., Serr D.M., Blankstein J.: Ovarian Hyperstimulation Syndrome: prediction by number and size of preovulatory follicles (Abstr. 24). Presented at Esco  VII Monte Carlo 1984. Published by European Sterility Congress, in induction on ovulation, pag 204.

16) Blankstein J, Shalev J, Saadon T et al: “Ovarian hyperstimulation syndrome : prediction by number and size of preovulatory ovarian follicles“.   Fertil Steril 1987;47:597-602.

17) Kodama H, Fukuda J, Karube H, Matsui T, Shimizu Y, Tanaka T: “Characteristics of blood  hemostatic markers in a patient with ovarian hyperstimulation syndrome who actually developed thromboembolism”. Fertil Steril 1995;64:1207-1209.

18) Tal J, Paz B, Samberg I, Lazarov N, Sharf M: ”Ultrasonographic and clinical correlates of menotropin versus sequential clomiphene citrate: menotropin therapy for induction of ovulation”. Fertil Steril 1985;44:342-349.

19) De Stefano V, Finazzi G, Mannucci PM: “Inherited  thrombophilia : pathogenesis, clinical syndromes, and management”. Blood 1996;87:3531-3544.

20) Bick RL, Arun B, Frenkel EP: “Antiphospholipid-thrombosis syndromes”. Haemostasis 1999;29:100-110.

21) Lainas T, et al: “Administration of methylprednisolone to prevent severe ovarian hyperstimulation syndrome in patients undergoing in vitro fertilization”. Fertil Steril 2002;78,3:529-533.

 22) Smitz J., Camus M., Devroey P., Erard P., Wisanto A., Van Steirteghem A.C.: Incidence of severe ovarian Hyperstimulation syndrome after GnRH agonist/HMG superovulation for in vitro fertilization. Human Reproduction Vol. 5 n. 8 pp 933-937,1990.

 23) Salat-Baroux J., Tibi G., Alvarez S., Cornet D., Antoine J.M., Gomes A.: Ultrasonografic prediction of ovarian hyperstimulation after IVF. In abstract book of the VI World Congress on in vitro fertilization Alternate Assisted Reproduction ,. Jerusalem, Israel, 1989,April 2-7, p. 27.

 24) Golan A., Ron-El R., Herman A., Soffer Y., Weinraub Z., Capsi E.: Ovarian hyperstimulation syndrome following D-Trp-6 luteinizing hormone-releasing hormone microcapsules and menotropins for in vitro fertilization. Fertil. Steril. 50,912-916,1988.

 25) Friedman C.I., Schmidt G.E., Chang F.E., Kim M.H.: Severe ovarian Hyperstimulation syndrome following follicular aspiration. Am. J. Obst. Gynec. 150, 436-437, 1984.

 26) Tal J., Paz B., Samberg I., Lazarov N., Sharf M.: Ultrasonografic and clinical correlates of menotropin versus sequential clomiphene citrate: menotropin terapy for induction of ovulation. Fertil. Steril. 44,342-349,1985.

27) Belaisch-Allart J., Belaisch J., Hazout A., Testart J., Fridman R.: Selective oocyte retrieval: a new approach to ovarian hyperstimulation. Fertil. Steril. 50,654-656, 1988.

28) V.       Volpicelli -  – V. Maisto -   0. Daino Narciso – G. Tomasillo  – A. Torre – R. Zarcone: Pattern Endometriale In Cicli Di Procreazione Medica Assistita. ATTI 13° Corso di Aggiornamento su Fertilità, Sterilità e Contraccezione. Congresso Nazionale Società Italiana di Endoscopia e Laser terapia Ginecologica (SIELG). Firenze, 15-17 Maggio 1995.

29) A “Coasting” Period to Prevent Ovarian Hyperstimulation Syndrome (OHSS) IN At Risk Hyperstimulation Cycles for In Vitro Fertilization (IVF).G.S.Letterie, L.A. Marshall, R.K. Matteri, M.K. Angle. The Fertility and Reproductive Endocrine Center at Virginia Mason Medical Center, Seattle, WA. Abstracts 52° Meeting of the Am. Soc. for Reprod. Medicine; Cincinnati, Ohio, Oct 18-22, 1997.

30) Reduced Incidence of the Ovarian Hyperstimulation Syndrome (OHSS) in IVF Cycles of Women With Polycystic Following Laparoscopic Ovarian Diathermy. O.A. Oyesanya,W. C. Cheng, Thomson Medical Centre, Singapore and King’s College School of Medicine and Dentistry, London.

31) F. Scarpellini, R. Boccadoro, M. Sbracia, J.A. Grasso: Effettivness of hugh dose progesterone in the tretment of ovarian Hyperstimulation Syndrome in women undergoing a superovulation program for infertility. Abstracts 52° ° Meeting of the Am. Soc. for Reprod. Medicine; Cincinnati, Ohio, Oct 18-22, 1997.

32) K.A. Jaroudi, G.L. Roca, A.Atared, J. Hollanders, S. Coskun: In vitro maturation of human oocytes for the patients who are at the risk of hyperstimulation.  Abstracts 52° ° Meeting of the Am. Soc. for Reprod. Medicine; Cincinnati, Ohio, Oct 18-22, 1997.

33) Amso N.N., Ahuja K.K., Morris N., Shaw R.W.: The management of predicted ovarian hyperstimulation involving gonadotropin-releasing hormone analog with elective cryopreservation of aal pre-embryos. Fertil. Steril. 53,6,1990,1087-1990.

34) Alam V. et al.: The abnormally large follicle during controlled ovarian hyperstimulation: management and outcome of the cycle. Fertil. Steril. Vol. 63 n. 2, feb. 1995.

35) Navot D. et al.: Direct correlation between plasma renin activity and severity of the ovarian hyperstimulation syndrome.  Fertil. Steril. Vol. 48, n. 1, July 1987, pagg 57-61.

36) Ludwig M et al: “Significant reduction of the incidence of ovarian hyperstimulation syndrome (OHSS) by using the LHRH antagonist Cetrolix in controlled ovarian stimulation for assisted reproduction”. Arch Gynecol Obstetr 2000;264:29-32.

37) Son WY, Yoon SH, Park SJ, Yoon HJ, Lee WD, Lim JH: “Ongoing twin pregnancy after vitrification of blastocysts produced by in-vitro matured oocytes retrieved from a woman with polycystic ovary syndrome: Case report”. Hum Reprod 2002 Nov;17(11):2963-6

38) D’Angelo A, Amso NN.: “Embryo freezing for preventing ovarian hyperstimulation syndrome: a Cochrane review”. Hum Reprod 2002 Nov;17(11):2787

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Queste pagine fanno parte del sito fertilitycenter.it in internet da marzo 2011. I testi, le tabelle, i disegni e le immagini pubblicati in queste pagine sono coperte da copyright ma a disposizione di tutti per copia e riproduzione purchè venga citata la fonte con link al sito www.fertilitycenter.it.

Ringrazio i lettori per la loro cortese attenzione e li prego di voler comunicare le loro osservazioni e consigli su eventuali errori o esposizioni incomplete.

Grazie. Enzo Volpicelli

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