Malattia autosomica dominante caratterizzata dalla presenza di migliaia di polipi adenomatosi nel colon, che colpisce individui tra i 15 e i 25 anni (Medline Thesaurus).
Inizialmente i polipi sono asintomatici e molto spesso rimangono tali; se sintomatici, i polipi adenomatosi causano ematochezia, occasionalmente crampi o, raramente diarrea. (Nelson, Textbook of Pediatrics, XVI Edition).
La poliposi familiare si manifesta solitamente nella seconda o terza decade di vita. I pazienti più giovani hanno, nella fase iniziale, un basso numero di polipi; questa patologia è caratterizzata, tuttavia, dallo sviluppo graduale di migliaia di polipi sessili lungo tutto il colon. Il cancro colorettale è un evento inevitabile nella storia naturale della poliposi familiare. La trasformazione maligna si riscontra a carico dei polipi ma si può anche sviluppare nella mucosa circostante, che può apparire normale all'endoscopista.
Se cercate attentamente, manifestazioni extraintestinali, come osteomi mandibolari o polipi del tratto gastrointestinale superiore, possono essere rilevate in molti pazienti con poliposi familiare del colon.
I polipi adenomatosi possono essere rilevati a livello dell' ileo, duodeno, regione periampollare, papilla del Vater e antro gastrico. (Wyllie/Hyams, Pediatric Gastrointestinal Disease, Second Edition).
La poliposi familiare del colon è una patologia autosomica dominante. La mutazione principale è localizzata nel gene APC (adenomatous polyposis coli ), situato nel cromosoma 5. La mutazione inattiva il gene e porta all ' inibizione dell ' apoptosi e alla proliferazione delle cellule epiteliali. La maggior parte delle mutazioni sono localizzate nella regione centrale del gene APC; questa regione è chiamata MCR ("mutation cluster region). Delezioni e mutazioni possono realizzarsi a livello di molti cromosomi, causando l ' attivazione di oncogeni e la disfunzione di oncosoppressori, coinvolti nello sviluppo del cancro del colon. (Wyllie/Hyams, Pediatric Gastrointestinal Disease, Second Edition).
La diagnosi dovrebbe essere sospettata in base alla storia familiare. Le alterazioni del gene APC vengono individuate nell ' 80% dei casi dei soggetti con familiarità positiva per poliposi familiare del colon e ciò indica la possibilità di eseguire dei test in soggetti asintomatici, in associazione con la consulenza genica.
La diagnosi viene fatta mediante visualizzazione diretta con coloscopia. (Nelson, Textbook of Pediatrics, XVI Edition).
Molti autori ritengono che la sorveglianza dei pazienti con poliposi asintomatiche familiari dovrebbe iniziare durante l' adolescenza. Altri autori, invece, chiedono un approccio più aggressivo e raccomandano una valutazione del tratto intestinale fin dalla fine della prima decade di vita. Questa raccomandazione è basata sul fatto che trasformazioni maligne sono state riportate anche in pazienti prima dei 9 anni.
La sigmoidoscopia, annuale, deve essere attuata in tutti gli individui a rischio, iniziando dai 12 anni di età, fino ai 40 anni; a questa età la frequenza degli esami può essere ridotta ad un controllo ogni 3 anni. La diagnosi della poliposi familiare del colon è basata sul riscontro di più di 100 polipi adenomatosi nel colon. I polipi sono piccoli, solitamente con diametro inferiore a 5 mm, e sessili, sebbene si incontrino occasionali lesioni peduncolate. La loro superficie è spesso divisa in lobuli da fessure interconesse all ` apice del polipo. Le ghiandole sono rivestite da cellule epiteliali allungate con nuclei ipercreomatici, e il contenuto di mucina è solitamente diminuito. Si riscontrano comunemente numerose figure mitotiche. (Wyllie/Hyams, Pediatric Gastrointestinal Disease, Second Edition).
I pazienti che manifestano il gene della poliposi richiedono la colectomia totale.
L' inteventochirurgico è generalmente necessario per polipi con diametro maggiore di 5 mm, in quanto il rischio di cancro, per lesioni di quelle dimensioni, è maggiore rispetto a quelle con diametri inferiori. Quando ci sono dai 6 ai 9 polipi per centimetro quadrato, la potenzialità di trasformazione maligna è molto importante. I bambini, appartenenti a questa categoria, dovrebbero essere operati prima dei 15 anni; i tempi esatti per la colectomia sono controversi, e non ci sono marker che possano predire la trasformazione maligna dell'adenoma. Tutti i membri della famiglia devono essere esaminati attentamente.
L' anastomosi con tasca ileoanale è considerata superiore all'anastomosi ileoanale o ileorettale, sebbene alcuni chirurghi ritengano che le ultime 2 procedure siano soddisfacenti nel bambino.
Da un punto di vista teorico un intervento dovrebbe eliminare il bisogno di una ileostomia, assicurare la continuità intestinale e la continenza.
L ` anastomosi ileoanale è preferibile alla anastomosi ileorettale perché elimina il rischio di un futuro cancro e non vi è quindi il bisogno di un regolare controllo sigmoidoscopico. I vantaggi di una procedura ileorettale sono una migliore probabilità di continenza anorettale e un periodo di convalescenza più corto. Alcuni ricercatori sostengono l'utilizzo dell'anastomosi ileorettale, qualora non siano scoperti polipi nel retto. Infine, per la possibilità di insorgenza del carcinoma dell'ampolla del Vater, del duodeno e dell' antro gastrico, nei pazienti con poliposi adenomatosa familiare, è necessario condurre regolare sorveglianza del tratto gastrointestinale, anche nei soggetti colectomizzati. (Wyllie/Hyams, Pediatric Gastrointestinal Disease, Second Edition).
Aspirina, sulindac, e amidi resistenti complessi possono ritardare lo sviluppo dei polipi; la loro efficacia è attualmente sconosciuta. (Nelson, Textbook of Pediatrics, XVI Edition).
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Measurement of low picomolar levels of triamcinolone acetonide in human bronchoalveolar lavage fluid by gas chromatography-electron-capture negative-ion mass spectrometry
ANALYTICAL-BIOCHEMISTRY. MAR 1 2001; 290 (1) : 18-25
Reincke-M; Beuschlein-F; Slawik-M; Borm-K
Molecular adrenocortical tumourigenesis
EUROPEAN-JOURNAL-OF-CLINICAL-INVESTIGATION. DEC 2000; 30 Suppl. 3 : 63-68
Burke-MP; Opeskin-K
Sudden death from hyponatremia and hypokalemia in a woman with Gardner syndrome
AMERICAN-JOURNAL-OF-FORENSIC-MEDICINE-AND-PATHOLOGY. MAR 2001; 22 (1) : 84-87
McKinley-AJ; Keenan-RA
Restorative proctocolectomy
JOURNAL-OF-THE-ROYAL-COLLEGE-OF-SURGEONS-OF-EDINBURGH. FEB 2001; 46 (1) : 20-28
Kokawa-A; Kondo-H; Gotoda-T; Ono-H; Saito-D; Nakadaira-S; Kosuge-T; Yoshida-S
Increased expression of cyclooxygenase-2 in human pancreatic neoplasms and potential for chemoprevention by cyclooxygenase inhibitors
CANCER-. JAN 15 2001; 91 (2) : 333-338
Tomlinson-IPM; Roylance-R; Houlston-RS
Two hits revisited again
JOURNAL-OF-MEDICAL-GENETICS. FEB 2001; 38 (2) : 81-85
Saletti-P; Edwin-ID; Pack-K; Cavalli-F; Atkin-WS
Microsatellite instability: Application in hereditary non-polyposis colorectal cancer
ANNALS-OF-ONCOLOGY. FEB 2001; 12 (2) : 151-160
Dove-Edwin-I; Thomas-HJW
Review article: The prevention of colorectal cancer
ALIMENTARY-PHARMACOLOGY-AND-THERAPEUTICS. MAR 2001; 15 (3) : 323-336
Dihlmann-S; Siermann-A; Doeberitz-MV
The nonsteroidal anti-inflammatory drugs aspirin and indomethacin attenuate beta-catenin/TCF-4 signaling
ONCOGENE-. FEB 1 2001; 20 (5) : 645-653
Yang-WC; Mathew-J; Velcich-A; Edelmann-W; Kucherlapati-R; Lipkin-M; Yang-K; Augenlicht-LH
Targeted inactivation of the p21(WAF1/cip1) gene enhances Apc-initiated tumor formation and the tumor-promoting activity of a western-style high-risk diet by altering cell maturation in the intestinal mucosa
CANCER-RESEARCH. JAN 15 2001; 61 (2) : 565-569
Stern-HS; Viertelhausen-S; Hunter-AGW; O'-Rourke-K; Cappelli-M; Perras-H; Serfas-K; Blumenthall-A; Dewar-D; Baumann-E; Lagarde-AE
APC I1304K increases risk of transition from polyp to colorectal carcinoma in Ashkenazi jews
GASTROENTEROLOGY-. FEB 2001; 120 (2) : 392-400
Richter-M; Weiss-M; Weinberger-I; Furstenberger-G; Marian-B
Growth inhibition and induction of apoptosis in colorectal tumor cells by cyclooxygenase inhibitors
CARCINOGENESIS-. JAN 2001; 22 (1) : 17-25
Sivagnanasundaram-S; Islam-I; Talbot-I; Drummond-F; Walters-JRF; Edwards-YH
The homeobox gene CDX2 in colorectal carcinoma: a genetic analysis
BRITISH-JOURNAL-OF-CANCER. JAN 19 2001; 84 (2) : 218-225
Poon-R; Smits-R; Li-C; Jagmohan-Changur-S; Kong-M; Cheon-S; Yu-CY; Fodde-R; Alman-BA
Cyclooxygenase-two (COX-2) modulates proliferation in aggressive fibromatosis (desmoid tumor)
ONCOGENE-. JAN 25 2001; 20 (4) : 451-460
Sharma-RA; Manson-MM; Gescher-A; Steward-WP
Colorectal cancer chemoprevention: biochemical targets and clinical development of promising agents
EUROPEAN-JOURNAL-OF-CANCER. JAN 2001; 37 (1) : 12-22
Regimbeau-JM; Panis-Y; Pocard-M; Hautefeuille-P; Valleur-P
Handsewn ileal pouch-anal anastomosis on the dentate line after total proctectomy - Technique to avoid incomplete mucosectomy and the need for long-term follow-up of the anal transition zone
DISEASES-OF-THE-COLON-AND-RECTUM. JAN 2001; 44 (1) : 43-50
Maguire-AR; Papot-S; Ford-A; Touhey-S; O'-Connor-R; Clynes-M
Enantioselective synthesis of sulindac
SYNLETT-. JAN 2001; (1) : 41-44
Weyant-MJ; Carothers-AM; Dannenberg-AJ; Bertagnolli-MM
(+)-Catechin inhibits intestinal tumor formation and suppresses focal adhesion kinase activation in the Min/+ mouse
CANCER-RESEARCH. JAN 1 2001; 61 (1) : 118-125
Mills-SJ; Mathers-JC; Chapman-PD; Burn-J; Gunn-A
Colonic crypt cell proliferation state assessed by whole crypt microdissection in sporadic neoplasia and familial adenomatous polyposis
GUT-. JAN 2001; 48 (1) : 41-46
Kamarasheva-J; Dummer-R; Schmidt-MH; Kempf-W; Kurrer-MO; Burg-G
Different mechanisms in the tumorigenesis of proximal and distal colon cancers
CURRENT-OPINION-IN-ONCOLOGY. JAN 2001; 13 (1) : 63-69
Middleton-SB; Phillips-RKS
Nonsteroidal antiinflammatory drugs, cyclooxygenase-2, and colorectal cancer prevention
CURRENT-OPINION-IN-GASTROENTEROLOGY. JAN 2001; 17 (1) : 65-71
Zumbrunn,-J; Kinoshita,-K; Hyman,-A-A; Nathke,-I-S
Binding of the adenomatous polyposis coli protein to microtubules increases microtubule stability and is regulated by GSK3 beta phosphorylation.
Curr-Biol. 2001 Jan 9; 11(1): 44-