www.tlfq.ulaval.ca/.../Suisse-carte-cantons.gif Fig n° 3
Sexe – Age
Cohorte globale cas mixtes exclus
F M Sexe Distribution des sexes
Cas mixtes exclus
F 96.67%n=29 M
3.33%
n=1
Fig. n° 4 Fig n°5
Age
52.5 57.5 47.5
52.5 42.5
47.5 37.5
42.5 32.5
- 37.5 27.5
32.5 22.5
27.5 17.5
22.5
Age
Cas mixtes exclus
Nombre
10
8
6
4
2 0
Std. Dev = 10.47 Mean = 38.7 N = 30.00 3 5 4 3 8
2 2 3
Tableau 2 : Données de bases : sexe – âge – durée de prise et d’arrêt de CO (mois)- type de CO – indications aux CO- antécédents
No Sexe Age CO : DuréeStop Type Indic. Antécédents (En gras : potentiellement lié à une dysrégulation hormonale endogène)
1 F 37 72 N ? CO Cautérisation du col utérin pour ectopie glandulaire, migraineuse, app., sténose tronc cœliaque par ligament arqué 2 F 34 168 O Stédiryl D® CO 0
3 F 26 60 N ? CO 0
4 F 53 216 O ? CO Allergie xylocaïne, diarrhées itératives > 20 ans
5 F 34 120 O ? Dysm.Maladie fibrokystique du sein, dysménorrhée, curetage utérin pour ?, intolérance au glucose 6 F 21 72 N ? CO Cystite et herpès génital probable
7 F 40 156 N ? CO Allergie codéine
8 F 24 72 N ? CO app
9 F 45 72 O ? FIV Myomectomie, hystérectomie pour fibrome, EP post op. (clip, thrombectomie bilatérale vv. Iliaques,) stérilisation tubaire suivie de refertilisation
10 F 55 120 O Prémarin® Subst. HTA, hystérectomie & ovariectomie (kyste hémorragique), tubéroplastie pour stérilité, app. , côlon spastique 11 M 48 ø -- -- -- Cyptorchidie bilatérale opérée, iléus sur bride spontanée
12 F 33 84 O minidosée CO Pyélonéphrite, acné traitée par Roaccutane®, ancienne hépatite B guérie ???
13 F 33 168 O ? CO Cholécystectomie, app.
14 F 42 216 N ? CO 0
15 F 33 168 O ? Dysm.Dysménorrhée, app., syndrome Fosse iliaque G 16 F 46 288 N ? CO Fibrome utérin, hémangiome hépatique 17 F 19 6 O Cyclacur®,RU486 Dysm.Dysménorrhée, ovaires polykystiques 18 F 36 ø -- -- -- St.post op genou D et sinus
19 F 39 72 O ? CO Ulcère gastro-duodénal
20 F 48 144 N ? Subst.Hypertension artérielle, Hystérectomie et annexectomie pour endométriose
21 F 48 ? O ? FIV Nodule rénal, 3x FIV
22 F 32 120 N ? CO Thalassémie α hétérozygote, goitre euthyroïdien, hyperlipidémie 23 F 22 72 N Diane 35® CO Brûlures jambes
24 F 30 ? N ? CO RCUH
25 F 33 204 N ? CO Plastie septum nasale pour sinusites à répétition
26 F 49 42 N ? CO OH chronique, côlon spastique, état anxio-dépressif, maladie de Scheuermann 27 F 47 180 N CO Canal lombaire étroit congénital, Hernies discales opérées, spondylodiscite
28 F 46 324 N Stéridyl30® CO RCUH
29 F 56 ø -- -- -- Kyste amibien ss-cut. ?, paludisme, RAA, occl. intestinale, app, nodule thyroïde bénin, hernie hiatale, 2x BPN 30 F 51 72 O ? CO Diabète type 1, st post amygdalecomie, fracture tibia G, 2 césariennes
54
Tableau 3 : Types de lésion et présentations cliniques et biologiques *= croissance malgré arrêt des CO durant 8 et 12 mois
No Lésion Présentation clinique Aigu
Subaigu
Hb g/dl (Ht %)
Tests
Hép. ∆ Taille (cm.) Complic.°
type Hémorragie^
type 1 AH Dl. abdo. diffuse puis épig., N, V, EF, masse, souffle épig. S 13 oui 9,5 Hém. i.lés.
2 AH Dl. en ceinture, ombilic puis HCD, EF, N, V, diarrhée A (23) oui 10 Hém. péritonéal 3 AH Dl. HCG, resp.-dép., N, V, masse, abdo. aigu A 10,8 --- ?, 1 l. sang Hém. Ss caps
4 AH Dl. épigastrique et dorsale, N, V, EF S 14 oui 6* -- ---
5 AH Dl. HCD, asthénie, N S 10,8 oui 15 Hém. i.lés.
6 AH
Dl. bas abdo. type cystite> menstruel> HCD> LRG,
transfixiante, irr. dans épaule, EF, malaise, hépatomégalie A 10,1
---
18
-- --- 7 AH Crampes puis dl. épig. irr. épaules+2 HC>> abdomen aigu S 7.6 oui ?, 1l sang, 10% AH Hém. péritonéal
8 AH Dl. HCD irr, épaule D A 14,1 --- ? Hém. Ss .caps
9 AH Dl. HCD irr. Dos + épaule, angoissante S (38,6) --- 3,5 Hém. i.lés
10 AH Gène puis dl. HCD, ∆ transit S 13.3 oui 8 -- ---
11 AH --- (Per-op. pour iléus) --- 11,6 --- 15 Tum. ---
12 AH --- (Bilan pyélonéphrite) --- 12,4 oui 2,2 * -- ---
13 AH Dl. HCD, V, arrêt CO 6 mois sans effet sur AH A 13,8 oui 15 -- --- 14 AH Douleur épig. puis HCD irr. épaule, N, V A 11,2 oui ?, nécrose Hém. Ss caps
15 AH --- (Cô santé) --- 12,8 oui 6,5 --- ---
16 AH Dl. HCD irr épaule, resp.-dép. A 8.90 --- ? nécrose Hém. Ss caps
17 AH Dl. épig., HCD, V, diarrhées A 9.40 oui 8.00 Hém. péritonéal
18 AH Dl. épig., HCD, EF > 1er Dg pancréatite A 12.90 oui 7.00 Hém. Hép 19 AH Dl épig. 3x/sem., diarrhées A 13.70 oui 8.00 Tum.+ Hém. i.lés.
20 AH Dl. HCD brutal A 11.60 oui 1.70 Hém. Sous caps.
21 AH --- (suivi nodule rénal) --- 13.70 --- 3.80 --- ---
22 HNFtel --- (hépatomégalie lors cô gynécologique) --- 11.60 oui 18.00 --- ---
23 HNFtel Dl. épig.,N, V, EF A 11.70 oui 11.50 --- ---
24 HNFtel --- (bilan cholestase anictérique) --- 13.20 oui 8.00 --- --- 25 HNFtel Dl. épig., HCD >1er Dg pancréatite A 13.90 oui 13.00 --- ---
26 LA Dl. abdo. chron, suivie de 3x dl. diffuses + aigües, ∆ transit S 14,5 oui 9 (mais aussi <5cm)Tum. + Hém. Ss caps + ilés 27 LA --- (suivi biol. hépatique ss AB) --- 14.60 --- 1.50 Hém. i.lés.
28 LA --- (bilan cholestase anictérique) --- 13.70 oui 6.50 Hém i.lés.
29 LA Prurit, inconfort épig. S 11.00 oui 17.00 Hém. Ss caps
30 LA --- (bilan préop) --- 13.10 --- 5.50 --- ---
55 Tableau 4 : lésion –complications - diagnostic et traitement- Follow up (FU en mois)
No Lésion Complic. Nb exa Rx/PBF Embol. OK dx. Lobe hépatique Nb. Lés Traitement chirurgical Complic. post op. im.//tardive FU
1 AH Hém. 5 G 1 Lobectomie G 0 36
2 AH Hém. 4 ☺ D : s. V, VIII 1 Hépatectomie D EP .
3 AH Hém. 3 ☺ G : s. II, III 1 Lobectomie G 0 // fibromyalgie, spasmophilie 264
4 AH +Léiomyome jéj. -- .00 D : s. IV 1 Segmentectomie IV 0 108
5 AH Hém. 4 / PBF ☺ D : s. IV 1 Segmentectomie IV 0 .
6 AH -- 4 x D: s. VII, VIII, VI 1 Hépatectomie D AIT, IU 132
7 AH Hém. 4 ☺ G 1 Lobectomie G 0 .
8 AH Hém. 3 ☺ D : s. V 1 Segmentectomie V 0 120
9 AH Hém. 3/PBF ☺ D centre, s. VIII 3 Hépatectomie D BPN 96
10 AH -- 5 D : s. VII et VIII 1 Hépatectomie D EP, ép. pl. thrombopénie hép. 48
11 AH Tum. 4/PBF ☺ D : s. V, VI, VII 1 Hépatectomie D Bronchopneumonie 60
12 AH -- 2 ☺ D : s. VII 1 Tumorectomie 0 48
13 AH -- 4 ☺ D : s. V 1 Tumorectomie V 0 36
14 AH Hém. 3 ☺ D : s. V, VI, VIII 1 Hépatectomie D Pneumothorax 36
15 AH -- 3 x ☺ D s. V, VIII 3 Hépatectomie D 0 72
16 AH Hém. 3 x D s. VII 1 Hépatectomie D Nécrose hép., empyème D 12
17 AH Hém. 3 x ☺ D, s. IV, comp. VCI 1 Hépatectomie D + s. IV 0 72
18 AH Hém. 4/PBF ☺ D : s. IV 1 Segmentectomie 0 1
19 AH Hém.+Tum 3/PBF D : s. V, VI, VII, VII 1 Hépatectomie D 0 .
20 AH Hém. 1 ☺ D s. VII 1 Hépatectomie D EP ddc 1
21 2 AH +* -- 4/PBF ddc 2 Tumorectomie LG+IV,III,VI 0 .
22 HNFtel multiples -- 3/PBF ddc 7 Hépatectomie D Atélectasie pulm. ddc .
23 HNFtel -- 3 G 1 Lobectomie G 0 48
24 HNFtel -- 4/2x(PBF) ☺ D : s. IV, V, VIII 1 Hépatectomie D partielle biliome 60
25 HNFtel -- 3 D 1 Segmentectomie VII 0 .
26 LA Tum. 3 ☺ ddc :s. VII,II, III, D p.-l. 6 Hépatectomie D 0 72
27 LA Hém. 4/PBF ☺ ddc 8 Tumorectomie II III IV V VI Plexus MSD,Cholépéritoine + 96
28 LA Hém 4/2x(PBF) x ☺ ddc central sur vx. 7 Tumorectomie 0 1
29 LA Hém. 5/2x(PBF) ☺ ddc central II, IV 13 THO Diabète cortico-induit+° 30
30 LA -- 4/PBF ☺ ddc : II,III,IV,V,VI,VIII 19 Lobectomie G 0 15
* hémangiome, HNF, Angio-myolipome rénal, +atélectasie. Pulmonaire, °Myopéricardite, neuronite vestibulaire, osétporose
Tableau 5
P=sign. si ≤0.05, *=val. manquante
Total
Lésion : type, taille - Age – Durée prise de CO – BMI – Stéatose
95% CI de la taille moyenne des différents types de lésions Cas mixte exclus
95% CI de l'âge moyen selon les types de lésions Cas mixte exclus
95% CI des durées moyennes de prise de CO selon les types de lésions Cas mixtes exclus
95% CI Durée moy. prise C0 en mois
]113.70
95% CI des BMI moyen des différents types de lésions Cas mixtes exclus
95% CI du % moyen de stéatose hépatique selon les types de lésions Cas mixte exclus
95% CI des % moyen de stéatose hépatique
] 3.16
Taille du plus grand nodule (Val. manquante=5)
>=5cm N=20
Types de complications selon taille de lésion Cas mixtes exclus
Taille du plus grand nodule (Val. manquante=5)
>=5cm N=25
Biologie
Taille du plus grand nodule (Val. manquante=5)
>=5cm N=20
Biologie & complications – Localisation
Tableaux 6 : base de calcul des sensibilités, spécificités, VPP et VPN
Histologie
61
IV. Références
1. Ishak, K.G., Hepatic neoplasms associated with contraceptive and anabolic steroids.
Recent Results Cancer Res, 1979. 66: p. 73-128.
2. Stenwig, A.E. and T. Solgaard, Ruptured benigns hepatoma associated with an oral contraceptives. Virchows Arch A Pathol Anat Histol, 1975. 367: p. 337-343.
3. Wheeler, D.A., H.A. Edmonson, and T.B. Reynolds, Spontaneus liver cell adenoma in children. Am. J. Clin. Pathol., 1985. 85(1): p. 6-12.
4. International working party, Terminology of Nodular hepatocellular lesions. Hepatology, 1995. 22(3): p. 983-993.
5. Paradis, V., et al., Evidence for the polyclonal nature of focal nodular hyperplasia of the liver by the study of X-chromosome inactivation. Hepatology, 1997. 26(4): p. 891-895.
6. Bioulac-Sage, P., et al., Clinical, Morphologic, and Molecular Features Defining So-called Telangiectatic Focal Nodular Hyperplasias of the Liver. Gastroenterology, 2005.
128: p. 1211-8.
7. Paradis, V., et al., Telangiectatic Focal Nodular Hyperplasia: A Variant of Hepatocellular Adenoma. Gastroenterology, 2004. 126: p. 1323-9.
8. Wanless, I.R., et al., Multiple focal nodular hyperplasia of the liver associated with vascular malformations of various organs and neoplasia of the brain: a new syndrome.
Mod Pathol, 1989. 2(5): p. 456-62.
9. Nguyen, B.N., J.F. Flejou, and B. Terris, Focal nodular hyperplasia of the liver: a comprehensive pathologic study of 305 lesions and recognition of new histologic forms.
Am J Surg Pathol, 1999. 23: p. 1441-54.
10. Kdosi, K., S. Joffe, and S.A. Okon, Hepatic adenoma. e-medicine, 2002: p. 13.
11. Brophy, C.M., et al., Liver Cell Adenoma, Diagnostic and treatement of a rare Hepatic Neoplastic Process. Am J Gastroenterol, 1989. 84(4).
12. Flejou, J.F., et al., Liver adenomatosis. An entity distinct from liver adenoma?
Gastroenterology, 1985. 89(5): p. 1132-8.
13. Veteläinen, R., et al., Liver adenomatosis: re-evaluation of aetiology and management.
Liver Int, 2008: p. 499-508.
14. Ribeiro, A., et al., Management of Liver Adenomatosis: Results With Conservative Surgical Approach. Liver Transpl Surg, 1998. 4(5): p. 388-398.
15. Chiche, L., et al., Liver Adenomatosis: Reappraisal, Diagnosis, and Surgical
Management Eight New Cases and Review of the Literature. Ann Surg, 2000. 231(1): p.
74-81.
16. Zucman-Rossi, J., et al., Genotype-Phenotype Correlation in Hepatocellular Adenoma:
New Classification and relationship with HCC. Hepatology, 2006. 43: p. 515-24.
17. Bioulac-Sage, P., et al., Genotype phenotype classification of hepatocellular adenoma.
World J Gastroenterol, 2007. 13(19): p. 2649-54.
18. Bioulac-Sage, P., et al., Pathological diagnosis of liver cell adenoma and focal nodular hyperplasia: Bordeaux update. J Hepatol, 2007.
19. Bluteau, O., et al., Bi-allelic inactivation of TCF1 in hepatic adenomas. Nature genetics, 2002. 32(2): p. 312-315.
20. Svrcek, M., et al., Regressive liver adenomatosis following androgenic progestin therapy withdrawals: a case report with a 10-years follow-up and a molecular analysis. Eur J Endoc, 2007. 156: p. 617-21.
21. Henson, S.W., H.K. Gray, and M.B. Dockerty, Adenomas. Surg Gynecol Obstet, 1956: p.
23-30.
62
22. Shortell, C.K. and S.I. Schwartz, Hepatic adenoma and focal nodular hyperplasia. Surg Gynecol Obstet, 1991. 173(5): p. 426-31.
23. Edmonson, H.A., B. Henderson, and B. Benton, Liver-Cell Adenomas associated with use of oral contraceptives. N Engl J Med, 1976. 294(9).
24. Rooks, J.B., et al., Epidemiology of hepatocellular adenoma. The role of oral contraceptive use. Jama, 1979. 242(7): p. 644-8.
25. Fechner, R.E., Benign hepatic lesions and orally administered contraceptives. A report of seven cases and a critical analysis of the literature. Hum Pathol, 1977. 8(3): p. 255-68.
26. Kerling, P., et al., Hepatic Adenoma and Focal Nodular Hyperplasia : Clinical,
Pathologic and Radiologic features. Gastroenterology, 1983. 84(5 part I): p. 994-1002.
27. Christopherson, W.M. and E.T. Mays, Liver tumors and contraceptives steroids :
experience with the first one hundred registry patients. J. Natl. Cancer Inst, 1977. 58(2):
p. 167-171.
28. Sörensen, T.I.A. and H. Baden, Benign hepatocellular tumours. Scand. J. Gastroent., 1975. 10: p. 113-119.
29. Benz, E.J. and A.H. Baggenstoss, Focal cirrhosis of the liver : its relation to the so-called hamartoma (adenoma, benign hepatoma). Cancer, 1953. 6 ou 8(4): p. 743-755.
30. Baum, J.K., et al., Possible association between benign hepatomas and oral contraceptives. Lancet, 1973. 2(7835): p. 926-9.
31. Nagorney, D.M., Benign hepatic tumors: focal nodular hyperplasia and hepatocellular adenoma. World J Surg, 1995. 19(1): p. 13-8.
32. Klatskin, G., Hepatic tumors: possible relationship to use of oral contraceptives.
Gastroenterology, 1977. 73(2): p. 386-94.
33. Foster, J.H., et al., Symposium : Benign Liver Tumors. Contemporary Surgery, 1982. 21.
34. Tao, L.C., Oral contraceptive-associated liver cell adenoma and hepatocellular
carcinoma. Cytomorphology and mechanism of malignant transformation. Cancer, 1991.
68(2): p. 341-7.
35. Mays, E.T. and W. Christopherson, Hepatic tumors induced by sex steroids. Semin Liver Dis, 1984. 4(2): p. 147-57.
36. Nissen, E.D., D.R. Kent, and S.E. Nissen, Role of oral contraceptive agents in the pathogenesis of liver tumors. J Toxicol Environ Health, 1979. 5(2-3): p. 231-54.
37. Ishak, K.G., Hepatic neoplasms associated with contraceptives and anabolic steroids.
Recent results in cancer res, 1979. 66: p. 73-128.
38. Knapp, W.A. and B.H. Ruebner, Hepatomas and oral contraceptives. Lancet, 1974: p.
270-271.
39. Foster, J.H., Primary benign solid tumors of the liver. The American Journal of Surgery, 1977. 133: p. 538-541.
40. O'Sullivan, J.P. and R.P. Wilding, Liver hamartomas in patients on oral contraceptives.
Br Med J, 1974. 3: p. 7-10.
41. Christopherson, W.M., E.T. Mays, and G.H. Barrows, Liver tumors in women on contraceptive steroids. Obstet Gynecol, 1975. 46(2): p. 221-3.
42. Naduka, C.C., Hepatic adenoma following short period of oral contraceptive use. J Am Board Fam Pract, 1999. 12(4): p. 337-9.
43. Kay, C.R., Oral contraceptives and liver tumors. Lancet, 1975: p. 127.
44. Sivula, A. and M. Lempinen, A benign hepatocellular adenoma treated by extended right lobectomy. Annales Chirurgiae et Gynaecologiae, 1976. 65: p. 46-51.
45. Minami, Y., et al., Intrahepatic huge hematoma due to rupture of small hepatocellular adenoma : a case report. Hepatology research, 2002. 23: p. 145-151.
63
46. Grabowski, M., U. Stenram, and A. Bergqvist, Focal nodular hyperplasia of the liver, benign hepatomas, oral contraceptives and other drugs affecting the liver. Acta path.
microbiol. scand., 1975. 83(sect A): p. 615-622.
47. Foster, J.H., T.A. Donohue, and M.M. Berman, Familial liver-cell adenomas and diabetes mellitus. N Engl J Med, 1978. 299(5): p. 239-241.
48. Kent, D.R., et al., Effect of pregnancy on liver tumor associated with oral contraceptives.
Obstet Gynecol, 1978. 51(2): p. 148-51.
49. Kent, D.R., et al., Maternal death resulting from rupture of liver adenoma associated with oral contraceptives. Obstet Gynecol, 1977. 50(1 Suppl): p. 5s-6s.
50. Rosales, J., et al., [Hepatic adenoma rupture as a cause of bleeding in the third trimester of pregnancy: report of a case and review of the literature]. Rev Gastroenterol Peru, 2001. 21(4): p. 312-5.
51. Larry Scott, A.R., katz, James H. Duke, Daniel F. Cowan, Nabil F. Maklad, Oral contraceptives, pregnancy, and focular nodular hyperplasia of the liver. JAMA, 1984.
251(11): p. 1461-1463.
52. Hill, M.A., et al., Successful rresection of multifocal hepatic adenoma during pregnancy.
sma, 2002: p. 1-5.
53. Dorothy Hayes, H.L., I.W.E. Hunter, Hepatic cell adenoma presenting with
intraperitoneal haemorrage in the puerperium. British Medical Journal, 1977: p. 1394.
54. Malt, S. and W. Shieber, Benign hepatic tumors secondary to oral contraceptives. Mo Med, 1976. 73(10): p. 561-4.
55. Grangé, J.-D., et al., Liver adenoma and focal nodular hyperplasia in a man with high endogenous sex steroids. Gastroenterology, 1987. 93: p. 1409-1413.
56. Royd, P.R. and G.J. Mark, Multiple Hepatic Adenomas and a Hepatocellular carcinoma in a man on oral methyl testosterone for 11 years. Cancer, 1977. 40: p. 1965-1970.
57. Westaby, D., B. Portmann, and R. Williams, Androgen related primary hepatic tumors in non- Fanconi patients. Cancer, 1983. 51: p. 19471952.
58. Hernandez-Nieto, L., et al., Benign liver-cell adenoma associated with long-term
administration of an androgenic-anabolic steroid (methandienone). Cancer, 1977. 40: p.
1761-1764.
59. Sale, G.E. and K.G. Lerner, Multiple tumors after androgen therapy. Arch Pathol Lab Med, 1977. 101: p. 600-603.
60. Velazquez, I. and B.P. Alter, Androgens and Liver Tumors: Fanconi's Anemia and Non-Fanconi's Conditions. Am J Hematol, 2004. 77: p. 257-67.
61. Socas, L., et al., Hepatocellular adenomas associated with anabolic androgenic steroid abuse in bodybuilders: a report of two cases and a review of the litterature. Br J Sports Med, 2005. 39(e27): p. 1-4.
62. Hayes, D., H. Lamki, and I.W.E. Hunter, Hepatic cell adenoma presenting with intraperitoneal haemorrage in the puerperium. Br Med J, 1977: p. 1394.
63. Goldfarb, J.-P.B., Adénome du foie et hyperplasie nodulaire focale. Relation avec les contraceptifs oraux. Gastroenterol. Clin. Biol., 1979. 3: p. 465-472.
64. Howell, R.R., et al., Hepatic Adenomata with Glycogen Storage Disease. J Am Med Assoc, 1976. 236(13): p. 1481-1484.
65. Rebouissou, S., et al., HNF1 alpha Inactivation Promotes Lipogenesis in Human Hepatocellular Adenoma Independently of SREBP-1 and Carbonhydrate-response Element-biding Protein (ChREBP) Activation. J Biol Chemistry, 2007. 282(19): p.
14437-46.
64
66. Kim, I., et al., Spontaneous hepatocarcinogenesis in farsenoid X receptor-null mice.
Carcinogenesis, 2007. 28(5): p. 940-6.
67. Yang, F., et al., Spontaneous Development of Liver Tumors in the Absence of the Bile Acid Receptor Farsenoid X receptor. Cancer Res, 2007. 67(3): p. 863-7.
68. Jansen, P.L.M., Endogenous bile acids as carcinogens. J Hepatol, 2007.
69. Parker, P., et al., Regression of hepatic adenomas in type Ia Glycogen Storage Disease with diatary therapy. Gastoenterology, 1981. 81: p. 534-536.
70. Reddy, S.K., et al., Resection of hepatocellular adenoma in patients with glycogen storage disease type Ia. J Hepatol, 2007.
71. Antoniades, K. and C.E. Brooks, Jr., Hemoperitoneum from liver cell adenoma in a patient on oral contraceptives. Surgery, 1975. 77(1): p. 137-9.
72. Bacq, Y., et al., Familial Liver Adenomatosis Associated With Hepatocyte Nuclear Factor 1alpha Inactivation. Gastroenterology, 2003. 125: p. 1470-75.
73. Jeannot, E., et al., Hepatocellular adenoma displaying a HNF1alpha inactivation in a patient with familial adenomatous polyposis coli. J Hepatol, 2006. 45: p. 883-6.
74. Reznik, Y., et al., Hepatocyte Nuclear Factor-1-alpha Gene inactivation: Cosegregation between Liver Adenomatosis and Diabetes Phenotypes in Two Maturity-Onset Diabetes of the Young (MODY)3 Families. J Clin Endocrinol Metab, 2004. 89: p. 1476-80.
75. Jeannot, E., et al., Association of CYP1B1 Germ Line Mutations with Hepatocyte Nuclear Factor 1alpha-Mutated Hepatocellular Adenoma. Cancer Res, 2007. 67(6): p. 2611-6.
76. Chen, Y.W., et al., P53 gene and Wnt signaling in benign neoplasms: beta-catenin mutations in hepatic adenoma but not in focal nodular hyperplasia. Hepatology, 2002.
36(4 Pt 1): p. 927-35.
77. Torbenson, M., et al., Hepatic adenomas: analysis of sex steroid receptor status and the Wnt signaling pathway. Mod Pathol, 2002. 15(3): p. 189-96.
78. Bioulac-Sage, P., et al., Genetic Alterations in Hepatocellular Adenomas. Hepatology, 2003: p. 480.
79. Goldfarb, S., Sex hormones and hepatic neoplasia. Cancer Res, 1976. 36(7 PT 2): p.
2584-8.
80. Gala, K.V. and T.W. Griffin, Hepatomas in young women on oral contraceptives: report of two cases and review of the literature. J Surg Oncol, 1983. 22(1): p. 11-4.
81. Nissen, E.D., D.R. Kent, and S.E. Nissen, Etiologic factors in the pathogenesis of liver tumors associated with oral contraceptives. Am J Obstet Gynecol, 1977. 127(1): p. 61-6.
82. Tannapfel, A., et al., INK4a-ARF alterations in liver cell adenoma. Gut, 2002. 51(2): p.
253-8.
83. Libbrecht, L., et al., Hepatic Progenitor Cells in Hepatocellular Adenomas. Am J Surg Pathol, 2001. 25(11): p. 1388-96.
84. Schleger, C., et al., Establishment and characterization of a nontumorigenic cell line derived from a human hepatocellular adenoma expressing hepatocyte-specific markers.
Exp Cell Res, 1997. 236(2): p. 418-26.
85. Handra-Luca, A., et al., Multiple mixed adenoma-focal nodular hyperplasia of the liver associated with spontaneous intrahepatic porto-systemic shunt: a new type of vascular malformation associated with the multiple focal nodular hyperplasia syndrome ? Histopathology, 2005. 48: p. 309-11.
86. Fox, J.G. and A. Lee, The role of helicobacter species in newly recognized gastrointestinal tract diseases of animals. Lab Anim Sci, 1997. 47(3): p. 222-55.
87. Solnick, J.V., et al., Extragastric manifestations of Helicobacter pylori infection--other Helicobacter species. Helicobacter, 2006. 11(Suppl 1): p. 46-51.
65
88. Alyamani, E.J., et al., Helicobacter hepaticus catalase shares surface-predicted epitopes with mammalian catalases. Microbiology, 2007. 153: p. 1006-16.
89. Rice, J.M., Helicobacter hepaticus, a recently recognized bacterial pathogen, associated with chronic hepatitis and hepatocellular neoplasia in laboratory mice. Emerg Infect Dis, 1995. 1(4): p. 129-31.
90. Cosme, A., et al., Systemic AA amyloidosis induced by oral contraceptive-associated hepatocellular adenoma: a 13-year follow up. Liver, 1995. 15(3): p. 164-7.
91. Shibasaki, T., et al., A case of renal amyloidosis associated with hepatic adenoma : The pathogenic role of tumor necrosis factor-alpha. Nephron, 1997. 75: p. 350-353.
92. Cunha, A.S., et al., Inflammatory syndrome with liver adenomatosis: the beneficial effects of surgical management. Gut, 2006: p. 307-309.
93. Williams, A.O. and A.D. Knapton, Hepatic silicosis, cirrhosis, and liver tumors in mice and hamsters : studies of transformation growth factor Bêta expression. Hepatology, 1996. 23: p. 1268-1275.
94. Resnick, M.B., H.P. Kozakewich, and A.R. Perez-Atayde, Hepatic adenoma in the pediatric age group. Clinicopathological observations and assessment of cell proliferative activity. Am J Surg Pathol, 1995. 19(10): p. 1181-90.
95. Leese, T., O. Farges, and H. Bismuth, Liver cell adenomas. A 12-year surgical experience from a specialist hepato-biliary unit. Ann Surg, 1988. 208(5): p. 558-64.
96. Grazioli, L., et al., Liver Adenomatosis: Clinical, Histopathologic, and Imagin Findings in 15 Patients. Radiology, 2000. 216: p. 395-402.
97. Goldfarb, G. and J.P. Benhamou, [Adenoma of the liver and focal nodular hyperplasia.
Relationship with oral contraceptives (author's transl)]. Gastroenterol Clin Biol, 1979.
3(5): p. 465-72.
98. Vana, J., et al., Primary liver tumors and oral contraceptives. Results of a survey. Jama, 1977. 238(20): p. 2154-8.
99. Akovbiantz, A., et al., [Management of liver cell adenoma and focal nodular hyperplasia]. Helv Chir Acta, 1980. 47(5): p. 607-9.
100. Carrasco, D., et al., Multiple hepatic adenomas after long-term therapy with testosterone enanthate. Journal of hepatology, 1985. 1: p. 573-578.
101. Barthelmes, L. and I.S. Tait, Liver cell adenoma and liver cell adenomatosis. HBP, 2006.
8: p. 71-4.
102. Gonzalez, A., et al., An unusual case of hepatic adenoma in a male. J Clin Gastroenterol, 1994. 19(2): p. 179-81.
103. Adlercreutz, H. and R. Tenhunen, Some aspects of the interaction between natural and synthetic female sex hormone and the liver. Am J Med, 1970. 49: p. 630-648.
104. Schorderet, Pharmacology. 1988: Ed. Slatkine, Frison Roche.
105. Desser-Wiest, L., Promotion of liver tumors by steroid hormones. J Toxicol Environ Health, 1979. 5(2-3): p. 203-6.
106. Barnes, A.C., Liver-cell adenomas and oral contraceptives. New England Journal of Medicine, 1976. 294(19): p. 1061.
107. Eckhauser, F.E., et al., Enucleation combined with hepatic vascular exclusion is a safe and effective alternative to hepatic resection for liver cell adenoma. Am Surg, 1994.
60(7): p. 466-71; discussion 472.
108. Pain, J.A., et al., Focal Nodular Hyperplasia of the liver : results of treatement and options in management. Gut, 1991. 32: p. 524-527.
109. Schardein, J.L., et al., Long-term toxicologic and tumorigenesis studies on an oral contraceptive agent in albino rats. Toxicol Appl Pharmacol, 1970. 16(1): p. 10-23.
66
110. Ameriks, J.A., et al., Hepatic cell adenomas, spontaneous liver rupture, and oral contraceptives. Arch Surg, 1975. 110(5): p. 548-57.
111. Christopherson, W.M., E.T. Mays, and G. Barrows, A clinicopathologic study of steroid-related liver tumors. Am J Surg Pathol, 1977. 1(1): p. 31-41.
112. Kalra, T.M., J.C. Mangla, and E.W. DePapp, Benign hepatic tumors and oral contraceptive pills. Am J Med, 1976. 61(6): p. 871-7.
113. Gyorffy, E.J., J.E. Bredfeldt, and W.C. Black, Transformation of hepatic cell adenoma to hepatocellular carcinoma due to oral contraceptive use. Ann Intern Med, 1989. 110(6):
p. 489-90.
114. Scaife, J.F., Liver homeostasis : an in vitro evaluation of a possible chalone. Experiencia, 1970. 26(10): p. 1071-1072.
115. Saetren, H., A principle of auto-regulation of growth. production of organ specific mitose-inhibitors in kidney and liver. Exp Cell Res, 1956. 11: p. 229-232.
116. Porter, L.E., et al., Hepatic estrogen receptor in human liver disease. Gastroenterology, 1987. 92(3): p. 735-45.
117. Bernard Fischer, N.G., Elisabeth A. Saffer, Shu Zheng, Relation of estrogen ant its receptor to rat liver growth and regeneration. Cancer Research, 1984. 44: p. 2410-2415.
118. Francavilla, A., et al., Regenerating rat liver : correlation between estrogen receptor localisation and deoxyribonucleic acid synthesis. Gastroenterology, 1984. 86: p. 552-557.
119. Heston, W.E., G. Vlahakis, and B. Desmukes, Effects of the antifertility drug enovid in five strains of mice, with particular regard to carcinogenesis. J Natl Cancer Inst, 1973.
51(1): p. 209-24.
120. Fox, K.A. and R.B. Lachen, Liver-cell adenomas and peliosis hepatis in mice associated with oxazepam. Research communications in chemical pathology and pharmacology, 1974. 8(3): p. 481-488.
121. Metzler, M. and J.A. Mc Lachlan, Oxidative metabolites of diethylstilbestrol in the fetal, neonatal and adult mouse. Biochimical Pharmacology, 1978. 27: p. 1087-1094.
122. Mishkin, S.Y., et al., Evidence for the hormone depedency of hyperplastic nodules : inhibition of malignant transformation after exogenous 17 Bêta-Estradiol and Tamoxifen.
Hepatology, 1983. 3(3): p. 308-316.
123. Barrett, J.C., Diethylstillbestrol induces neoplastic transformation without measurable gene mutation at two loci. Sciences, 1981. 212: p. 1402-1404.
124. Kent, D.R., E.D. Nissen, and S.E. Nissen, Liver tumors and oral contraceptives. Int J Gynaecol Obstet, 1977. 15(2): p. 137-42.
125. Vessey, M.P., et al., Oral contraceptives and benign liver tumors. Br Med J, 1977: p.
1062-1063.
126. Rohner, A., [Treatment of benign tumors of the liver]. Schweiz Med Wochenschr, 1986.
116(31-32): p. 1044-50.
127. Knowles, D.M., 2nd, et al., The clinical, radiologic, and pathologic characterization of benign hepatic neoplasms. Alleged association with oral contraceptives. Medicine (Baltimore), 1978. 57(3): p. 223-37.
128. Scott, L.D., et al., Oral contraceptives, pregnancy, and focal nodular hyperplasia of the liver. Jama, 1984. 251(11): p. 1461-3.
129. Goldstein, H.M., et al., Angiographics findings in benign liver cell tumors. Radiology, 1974. 110: p. 339-343.
130. Mays, E.T., Standard nomenclature for primary hepatic tumors. (Letter). J Am Med Assoc, 1977. 237(15): p. 1560-1.
67
131. Mays, E.T., Standard nomenclature for primary hepatic tumors : a critical need. J Am Med Assoc, 1976. 236(13): p. 1469-1470.
132. Metzler, M. and G.H. Degen, Sex hormones and neoplasia: liver tumors in rodents. Arch Toxicol Suppl, 1987. 10: p. 251-63.
133. Lingemann, C.H., Liver-cell neoplasms and oral contraceptives. Lancet, 1974: p. 64.
134. Butler, W.H., A review of the hepatic tumors related to mixed-function oxidase induction in the mouse. Toxicologic pathology, 1996. 24(4): p. 484-492.
135. Marsman, D.S. and J.A. Popp, Biological potential of basophilic hepatocellular foci and
135. Marsman, D.S. and J.A. Popp, Biological potential of basophilic hepatocellular foci and