Download - SINDROAME PARANEOPLAZICE
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SINDROAME PARANEOPLA
ZICE
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Reprezinta un grup de semne si simptome asociate unor neoplazii specifice si care
nu se datoreaza invaziei tumorale locale, adenopatiilor sau metastazelor.
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Sunt rezultatul unei mari varietati de mediatori biologici produsi de
catre celulele neoplazice,
sindromul paraneoplazic putand reprezenta forma de debut a cancerului.
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SP nu sunt cauzate de actiunea directa ,locala , mecanica a tumorii asupra organului sau tesutului in care se dezvolta ;
SP nu se afla nici in raport
direct cu actiunea locala a
metastazelor;
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SP pot preceda sau insoti evolutia neoplaziei, pot dispare dupa tratamentul acesteia si sa reapara in momentul
resutei bolii. Frecventa lor clinica este de 7-10%, dar, in realitate , cand sunt cautate sistematic, ajung pana la 30-50%.
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Localizarile primare cel mai frecvent asociate cu SP :
cc. bronho-pulmonar-in special microcelular
cc. pancreasului neuroblastomul cc. colonului cc . prostatei, cc. mamar
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Mecanismele de aparitie variate si incomplet elucidate :
1.Stimularea-(de origine embrionara )-a unor celule tumorale- rezultand producerea de niveluri atipice de hormoni activi biologic sau precursori
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Hormonii polipeptidici se formeaza dintr-un precursor trecand prin fazele de secretie, stocare, excretie :
pre-prohormon -prohormon-hormon ;
primul precursor este inactiv ;
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din hormonul activ biologic se elibereaza grupul
carboxil- inert si cel amino- activ; in tumori degradarea este foarte variabila si se reflecta in diversitatea produsilor hormonali secretati ectopic ,
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Toate celulele organismului contin un material genetic
codificat ce conduce la aceeasi
informatie , reprimata in
majoritatea celulelor;
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-proliferarea neoplazica inhiba/ distruge aceasta represie ,
restabilind, printre altele , si capacitatea de sinteza
hormonala a celulei maligne.
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ADN -ul anormal al celulei neoplazice duce la o sinteza proteica modificata si ,implicit ,
la un hormon diferit de cel natural Mecanismul de secretie hormonala ectopica explica
sd. paraneoplazice metabolice si endocrine
liferarea neoplazica inhiba sau distruge aceasta represie , restabilind, printre altele , si capacitatea de sinteza
hormonala a celulei maligne.
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2.Secretia peptidica - explicata prin 3 ipoteze: a). ipoteza derepresiunii genetice: codul genetic detine informatia necesara initierii secretiei peptidice, in mod normal reprimata, dar care in cazuri patologice poate fi activata (derepresiune)
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b). conceptul celulelor APUD, celule care au aparatul genetic si enzimatic necesar sustinerii acestor secretii peptidice; aceste celule fac parte din tumorile non-endocrine, secretante de factori peptidici;
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c). Ipoteza hibridizarii celulare-secretia polipeptidica
necesara proliferarii , se constituie intr-un mecanism autocrin, de autostimulare
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Identificarea in grupul acestor peptide biologic active
a unor receptori sau factori de crestere cum ar fi factorii de stimulare
ai coloniilor (CSF) si TGF alfa corelati cu aparitia
SP-hematologice /dermatologice
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3. Stimularea de catre tumora
a unui anticorp ce prezinta reactivitate incrucisata cu antigene tumorale , dar si cu celule normale; aceasta ar fi cauza unor sindroame caracterizate prin existenta
unui conflict imunologic.
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- interactiunile antigen tumoral –anticorp - apar in sindroame paraneoplazice
-neurologice -neurovasculare -dermatologice
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Recunoasterea sd . paraneoplazice are importanta in diagnosticul si tratamentul cancerului ;
-recunoasterea lor poate duce la un diagnostic precoce.
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Evolutia clinica a sindromului paraneoplazic poate fi folosita si ca
element prognostic. -calitatea vietii pacientului poate fi imbunatatita prin terapia paleativa, uneori eficienta, a acestor sindroame.
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PRINCIPALELE SINDROAME PARANEOPLAZICE
-ENDOCRINE -METABOLICE -NEUROLOGICE -NEURO- MUSCULARE -OSTEO-ARTICULARE -CUTANATE - HEMATOLOGICE
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-ENDOCRINE -SINDROMUL SECRETIEI INADECVATE DE HORMON ANTIDIURETIC ( SIADH )
Hormonul ADH sau arginin –vasopresina ( AVP )
- secretat de hipotalamus ; rol in mentinerea constanta a osmolaritatii plasmatice
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Este inmagazinat in hipofiza posterioara si este eliberat in caz de hipovolemie sau hiperosmolaritate plasmatica.
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ADH actioneaza asupra tubulilor renali inhiband excretia apei si astfel se reface volumul plasmatic sau osmolaritatea.
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SIADH se caracterizeaza prin :
-hiponatremie - hipoosmolaritate plasmatica
- hiperosmolaritate urinara datorita unei eliminari continue de sodiu.
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Clinic se produce o intoxicatie cu apa si tulburari neuropsihice diverse ce pot simula metastaze cerebrale : cefalee,
stari confuzionale letargie, modificari psihice, convulsii , coma.
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-cauza cea mai obisnuita a SIADH este cancerul pulmonar microcelular.
-Se mai intalneste in limfoame
cc . din sfera cap-gat sarcom Ewing
cancer pancreatic
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Diagnosticul se poate stabili cu mult inainte de instalarea tabloului clinic prin :
determinarea electrolitilor serici
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-hipoosmolaritate plasmatica -
sub 280 mmol/l -osmolaritate urinara superioara celei plasmatice
-excretie urinara continua de sodiu -
peste 20 mmol/l
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Diagnosticul diferential
se face cu: -hiponatremia asociata cu depletia volemica si
sodiul urinar sub 20mEq/l intalnita in :
varsaturi , diaree , sechestrare de lichide , transpiratii excesive.
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Diagnosticul diferential se mai face cu: hiponatremia cu sodiul urinar peste 20 mEq/l cu depletie volemica -
consecinta a utilizarii diureticelor , pierderii de sare, deficiente de mineralocorticoizi, etc.
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-hiponatremia asociata cu expansiuni volemice cu Na urinar
sub 20 mEq /l din : insuficienta cardiaca ,
ciroza , sindrom nefrotic ;
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-hiponatremia cu expansiuni volemice
cu Na urinar peste20 mEq/l - in insuficienta renala
acuta sau cronica ;
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-stari euvolemice –cu hiponatremie-
se pot intalni in: -hipotiroidism -polidipsia psihogena -stress emotional , fizic
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-
Cisplatinul –poate fi cauza unei nefrite cu pierdere de sare- consecutiva hipovolemiei si eliberarii
de AVP intracelular datorita necrozei tumorale indusa de citostatic.
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TRATAMENTUL SIADH :-refacerea echilibrului electrolitic prin restrictia
aportului de lichide la cca.
500 ml /24 ore in cazurile usoare ;
in cazurile severe -administrarea de solutii saline hipertone cu furosemid.
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-SINDROMUL CUSHING - este determinat de tumorile ce produc ACTH cu alta origine decat hipofiza.
Nivelul constant marit de ACTH
produce: -hiperplazie suprarenala cu secretie crescuta de - mineralocorticoizi ,
glucocorticoizi ,androgeni
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Bolnavul prezinta : HTA, hiperpigmentare cutanata, edem, hiperglicemie, distributie anormala a grasimii alcaloza hipokaliemica
astenie scadere ponderala
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BOALACUSHING
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Sindromul Cushing asociat tumorilor ce produc ACTH non-pituitar dependent a fost descris in toate neoplaziile, mai putin sarcoame .
-Cauzele cele mai frecvente:
cancerul pulmonar microcelular tumorile timice
tumorile carcinoide feocromocitomul, etc.
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Cele mai multe sindroame paraneoplazice in
CBP microcelular sunt caracterizate prin
secretie de ACTH insensibila la nivelul glucocorticoizilor circulanti, acesta atingand niveluri serice foarte inalte in contrast cu boala Cushing de cauza suprarenala .
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DIAGNOSTICUL SD. CUSHING
-determinarea nivelului plasmatic al ACTH ;
-urmarirea variatiei diurne a cortizolului
-valori mari ale raportului cortizol/corticosteron seric
( > 80 )
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Tratamentul –tratamentul afectiunii maligne
si al anomaliilor metabolice.
-ketoconazol 400-800mg/zi
-aminoglutetimida 1000-1500 mg/zi- controleaza excesul de corticoizi
-octreoctidul
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HIPERCALCEMIA –se intalneste in: - CBP epidermoid -carcinomul renal -mielom multiplu -cancerul mamar -cancerele ale regiunii cap- gat
-cancer esofagian -limfom non-Hodgkin
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HIPERCALCEMIA PATOGENEZA Secretia de catre celulele neoplazice de : -hormon-like paratiroidieni
-prostaglandine -factor activator al osteoclastelor
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HIPERCALCEMIA Initial s-a considerat ca ar fi secundara bolii metastatice osoase ce determina resorbtia osoasa si eliberarea de calciu in ser.
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S-a constatat , insa, ca dintre bolnavii cu cc. mamar
care au dezvoltat metastaze osoase, numai 15%
aveau hipercalcemie 85% din bolnavii cu cc.mamar
cu hipercalcemie neavand metastaze osoase.
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Cancerul pulmonar epidermoid este responsabil de aproape toate hipercalcemiile asociate cu CBP, rareori cauza fiind metastazele osoase .
Hipercalcemia in cancer este datorata cel mai frecvent
factorilor umorali eliberati direct sau indirect de catre T.
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Factorii circulanti indusi sau secretati de tumora care influenteaza functia osteoclastica includ: vitamina D3 , parathormon (PTH),
proteina inrudita cu PTH, IL-1, IL-6, Prostaglandina E2,
factor de activare a osteoclastelor
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Celulele tumorale secreta factori de crestere care stimuleaza atat osteoclastele cat si osteoblastele. Atat osteoblastelecat si osteoclasteleelibereaza factori de crestere care stimuleaza cresterea tumorala.
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CLINIC manifestari: -gastro -intestinale : anorexie,greturi,varsaturi
-neurologice:oboseala, astenie , depresie , letargie
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CLINIC -renale : poliurie , polidipsie , insuficienta renala -cardiace: tulburari de ritm stop cardiac
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Tratamentul: perfuzii cu solutii saline hidratare adecvata ; -se poate asocia un diuretic -furosemid
( nu se folosesc diuretice tiazidice deoarece induc absortia renala a calciului la schimb cu sodiul ).
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Tratamentul: -Cand sunt prezente niveluri serice mult crescute ale Ca-
bifosfonati : clodronat ,pamidronat ( Aredia ), acid zoledronic ( Zometa );
-inhiba resorbtia osoasa prin inhibitia osteoclastelor si activarea citokinelor;
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Tratamentul: Corticosteroizi - pot avea efect antitumoral direct ;
Calcitonina - inhiba degradarea osoasa prin legarea directa de receptorii osteoclastelor;
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HIPOCALCEMIA - apare in boala metastatica osoasa din cc.prostatei
cc .mamar , cc .pulmonar . -Cauzele:-malnutritia -infectii -hipomagneziemia -chimioterapia
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HIPOCALCEMIA -Clinic: -aritmii cardiace , HTA , insuficienta cardiaca , -edem papilar, cataracta ,
-iritabilitate ; interval ST prelungit pe EKG.
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-Liza tumorala masiva determina scaderile cele mai mari ale calcemiei ; apare, in general ,
dupa tratamentul leucemiilor si limfoamelor sensibile la chimioterapie.
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-Liza tumorala masiva
-Tratament : –solutii perfuzabile
(ser fiziologic 4 -6 l/zi dextroza )
allopurinol
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OSTEOMALACIA -asociata neoplaziilor este rara ;
recunoscuta ca sd.paraneoplazic in cazul tumorilor mezenchimale
din sfera cap-gat si de la nivel osos.
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OSTEOMALACIA -Se datoreaza factorilor osteolitici tumorali circulanti.
-Se caracterizeaza prin hipofosfatemie,hipocalcemie.
Tratament: -rezectie chirurgicala, fosfati,vit.D p.o.
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HIPOGLICEMIA . ca paraneoplazie -se intalneste in tumorile voluminoase
mezenchimale retroperitoneale, hepatice , intratoracice
( fibrosarcom , rabdomiosarcom ,
liposarcom , mezoteliom leiomiosarcom )
Hepatom - hipoglicemia -complicatie
paraneoplazica frecventa - 21 %
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HIPOGLICEMIA . Tumorile secreta factor de crestere insulin-like II determinand :
scaderea insulinei plasmatice,
proinsulinei, peptidului C plasmatic
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HIPOGLICEMIA . -ca paraneoplazie-
Simptomatologia: -tremuraturi -paloare
-transpiratii -hTA -agitatie psihomotorie -convulsii , coma
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HIPOGLICEMIA . -ca paraneoplazie- DIAGNOSTIC -anamneza -ex . clinic - hipoglicemie -scaderea concentratiei plsmatice a glucozei
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HIPOGLICEMIA TRATAMENT forma acuta : solutie dextroza 50% I.v.
forma medie : cresterea nivelului de nutritie ;
hipoglicemia semnificativa : corticosteroizi , glucagon 1 mg. I.m.
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SINDROAME PARANEOPLAZICE NEUROLOGICE
-mecanism autoimun Apar datorita patrunderii de autoanticorpi
la nivel cerebral, nervi periferici, ganglionii radacinii dorsale.
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SINDROAME PARANEOPLAZICE NEUROLOGICE
CEREBRALE SPINALE NERVI PERIFERICI MUSCULATURA SI JONCTIUNE NEUROMUSCULARA
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SINDROAME PARANEOPLAZICE NEUROLOGICE
-nevrite senzitive si motorii -encefalomielite -degenerarea cerebeloasa (autoanticorpi-anti celule Purkinje)-
in cancerul mamar,endometrial.
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DEGENERESCENTA CEREBELOASA
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SINDROAME PARANEOPLAZICE NEUROLOGICE
neuroencefalopatiile- senzitive, motorii;
-retinopatia asociata cancerului
(autoanticorpi anti-antigen retinian 23 kd- cu distructia fotoreceptorilor) in cc.mamar,endometrial ,s.a..
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SINDROAME PARANEOPLAZICE NEUROLOGICE
-sindromul Lambert-Eaton- 60% din bolnavi au un cancer pulmonar microcelular
cauzat de anticorpi ce interfera cu eliberarea de acetilcolina presinaptica la jonctiunea neuromusculara;
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Sindromul Lambert-Eaton-Clinic:
deficite neurologice degenerari cerebeloase astenie hipotonie musculara diplopie,dizartrie, disfagie
parestezii
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SINAPSA-SD.LAMBERT-EATON
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Sindromul Lambert-Eaton- Tratament: -chimioterapie ,plasmafereza
corticoterapie, imunosupresie,
gamma globulina ; -plexopatiile mienterice gastro-intestinale-in CBPmicrocelular
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SINDROAME PARANEOPLAZICE
NEURO -MUSCULARE Polimiozita/ Dermatomiozita -hipotonie musculara progresiva, disfagie ,rash;
Diagnostic - enzime musculare si VSH crescute; EMG ; biopsie musculara
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DERMTOMIOZITA
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SINDROAME PARANEOPLAZICE NEUROMUSCULARE Polimiozita/Dermatomiozita
cc.mamar CBP cc.ovarian Tratament : corticosteroizi -p.o.
doze mari ( 60-80 mg./zi )
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SINDROAME PARANEOPLAZICE DERMATOLOGICE
-Rezultatul depozitarii anticorpilor policlonali autoimuni
in epiderm, vase sangvine cutanate.
Clinic:-rash, modificari vasculare.
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ERITEM PALMAR
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ERITEM NODULAR
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SINDROAME PARANEOPLAZICE DERMATOLOGICE
-Sindrom pemfigus-like –eroziuni ale mucoaselor -eruptii cutanate
-apare in - limfom, leucemie limfocitara -Tratament: corticosteroizi.
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DERMATITA ATOPICA/ PSORIAZIS
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BOALA BAZEX rash
psoriaziform periferic
cc.scuamoase ale tractului
aero-digestiv superior.
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ACANTOSIS NIGRICANS
-Acantosis nigricans-hiperpigmentare cutanata in zonele de flexie- asociere cu cancerul gastro-intestinal,
rar in cc.pulmonar.
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ACANTOSIS NIGRICANS
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ALTE SD. PARANEOPLAZICE -osteoartopatia hipertrofianta Pierre Marie -cc.pulmonare,
-cc.rinofaringe Clinic : -hipocratism digitalic , periostoza
-hipertrofie pseudoacromegalica -tumefactii articulare dureroase -sd. vasomotor -cianoza ,parestezii
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OSTEOARTROPATIE
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Osteoartopatia hipertrofianta Pierre Marie
Simptomele osteo-artropatiei pot
preceda simptomele pulmonare ,
respiratorii / pot apare concomitent sau pot sa le urmeze ; Tratamentul - chirurgical extirparea T (cand este posibil )
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ALTE SD. PARANEOPLAZICE
HEMATOLOGICE -Anemiile aplastice -substanta secretata de T ce perturba eritropoeza ; -Anemii hemolitice autoimune-
limfoame ,cc.ovarian ,gastric , colon ,pancreas;
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ALTE SD. PN . HEMATOLOGICE
- Reactii leucemoide -Trombocitoze -Tulburari de coagulare-tulburari de hemostaza- sangerari ;
-complicatii tromboembolice ;
mecanismele - incomplet cunoscute
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ALTE SD . PARANEOPLAZICE
-tromboflebita migratorie -hepatopatia - din cc.renal -sd .nefrotic -din limfomul Hodgkin
-febra in cc.hepatice , cc . renale, osteosarcom
-casexia neoplazica
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-IMPORTANTA PRACTICA
A SD. PARANEOPLAZICE
1 .pot reprezenta primul semn al bolii ,
permitand un diagnostic precoce , cu instituirea prompta a tratamentului ;
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-IMPORTANTA PRACTICA A SP.
2. la bolnavii cunoscuti pot fi confundate cu evolutia metastatica a bolii si astfel sa se renunte la tratamentele curative , sau , invers , manifestarile metastatice sa fie considerate paraneoplazii si tratate ca atare ;
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SD . PARANEOPLAZICE
3 . pot fi utilizate ca markeri tumorali pentru monitorizarea evolutiei ;
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4 .SD . PARANEOPLAZICE sunt o problema clinica cu rasunet asupra starii generale
si confortului bolnavului , uneori chiar cu risc vital ; Tratamentul lor poate oferi ameliorari importante ale calitatii vietii .
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MULTUMESC !