Raadpleeg ook literatuurlijst niet-toxische middelen en behandelingen specifiek bij mond- en keelkanker en slokdarmkanker van arts-bioloog drs. Engelbert Valstar. 

25 september 2019: Bron: CANCER

Slokdarmkanker aan het zogeheten Barret's (onderste deel van de slokdarm en de verbinding met de maag) blijkt vaker te ontstaan en progressie te vertonen naar daadwerkelijke kanker bij diabetes patienten dan bij niet-diabetes patienten. Patienten met diabetes-2 hebben een 34 procent grotere kans op slokdarmkanker van dit onderste gedeelte en van de verbinding tussen slokdarm en maag.
Patienten met naast diatetes ook een reflux - brandend maagzuur (oprisping van de maag die voedsel terugspoelt als het ware naar de slokdarmdarm) hadden ook grotere kans op ontwikkelen van slokdarmkanker en kanker aan de slokdarm/maag verbinding (34 procent). Maar patienten met alleen een reflux hadden geen verhoogd risico op deze vorm van slokdarmkanker. Conclusie is dan ook dat vooral diabetes-2 het grootste risico geeft. 

Conclusie van de onderzoekers:

Deze studie wees uit dat diabetes geassocieerd is met een verhoogd risico op adenocarcinoom van de slokdarm / slokdarmverbinding en dat een gebrek aan bewijs van een associatie met de slokdarm van Barrett suggereert dat diabetes de progressie van Barrett naar maligniteit kan beïnvloeden.

Het zou wat mij betreft ook kunnen zijn dat een gezonde leefstijl en gevarieerd dieet wellicht ook invloed in positieve zin kan hebben want diabetes-2 is met een gezonde leefstijl en gevarieerde gerichte voeding zelfs te genezen. Zelf had ik altijd veel last van brandend maagzuur maar na mijn kanker en verandering naar een gezonde leefstijl is dat helemaal weggegaan. 

Dit blijkt uit een grote freviewstudie van 13 gerandomiseerde studies.

Het originele studierapport: Diabetes in relation to Barrett's esophagus and adenocarcinomas of the esophagus: A pooled study from the International Barrett's and Esophageal Adenocarcinoma Consortium is tegen betaling in te zien.

Deze studie: Association of Barrett’s Esophagus With Type II Diabetes Mellitus: Results From a Large Population-based Case-Control Study al uit 2013 is wel volledig in te zien

Hier het wat summiere abstract van de recente reviewstudie maar het is niet anders. Ik heb zelf wel het PDF in kunnen zien maar kan dat niet delen met anderen. 

 2019 Sep 6. doi: 10.1002/cncr.32444. [Epub ahead of print]

Diabetes in relation to Barrett's esophagus and adenocarcinomas of the esophagus: A pooled study from the International Barrett's and Esophageal Adenocarcinoma Consortium.

Abstract

BACKGROUND:

Diabetes is positively associated with various cancers, but its relationship with tumors of the esophagus/esophagogastric junction remains unclear.

METHODS:

Data were harmonized across 13 studies in the International Barrett's and Esophageal Adenocarcinoma Consortium, comprising 2309 esophageal adenocarcinoma (EA) cases, 1938 esophagogastric junction adenocarcinoma (EGJA) cases, 1728 Barrett's esophagus (BE) cases, and 16,354 controls. Logistic regression was used to estimate study-specific odds ratios (ORs) and 95% CIs for self-reported diabetes in association with EA, EGJA, and BE. Adjusted ORs were then combined using random-effects meta-analysis.

RESULTS:

Diabetes was associated with a 34% increased risk of EA (OR, 1.34; 95% CI, 1.00-1.80; I2  = 48.8% [where 0% indicates no heterogeneity, and larger values indicate increasing heterogeneity between studies]), 27% for EGJA (OR, 1.27; 95% CI, 1.05-1.55; I2  = 0.0%), and 30% for EA/EGJA combined (OR, 1.30; 95% CI, 1.06-1.58; I2  = 34.9%). Regurgitation symptoms modified the diabetes-EA/EGJA association (P for interaction = .04) with a 63% increased risk among participants with regurgitation (OR, 1.63; 95% CI, 1.19-2.22), but not among those without regurgitation (OR, 1.03; 95% CI, 0.74-1.43). No consistent association was found between diabetes and BE.

CONCLUSIONS:

Diabetes was associated with increased EA and EGJA risk, which was confined to individuals with regurgitation symptoms. Lack of an association between diabetes and BE suggests that diabetes may influence progression of BE to cancer.

1. Sharma P. Clinical practice. Barrett’s esophagus. N Engl J Med. 2009;361:2548–2556. [PubMed] []
2. Whiteman DC, Sadeghi S, Pandeya N, et al. Combined effects of obesity, acid reflux and smoking on the risk of adenocarcinomas of the oesophagus. Gut. 2008;57:173–180. [PubMed] []
3. Chow WH, Blot WJ, Vaughan TL, et al. Body mass index and risk of adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst. 1998;90:150–155. [PubMed] []
4. Cook MB, Greenwood DC, Hardie LJ, et al. A systematic review and meta-analysis of the risk of increasing adiposity on Barrett’s esophagus. Am J Gastroenterol. 2008;103:292–300. [PubMed] []
5. Kamat P, Wen S, Morris J, et al. Exploring the association between elevated body mass index and Barrett’s esophagus: a systematic review and meta-analysis. Ann Thorac Surg. 2009;87:655–662. [PubMed] []
6. Abrams JA, Sharaiha RZ, Gonsalves L, et al. Dating the rise of esophageal adenocarcinoma: analysis of Connecticut tumor registry data, 1940–2007. Cancer Epidemiol Biomarkers Prev. 2011;20:183–186. [PMC free article] [PubMed] []
7. Corley DA, Kubo A, Levin TR, et al. Abdominal obesity and body mass index as risk factors for Barrett’s esophagus. Gastroenterology. 2007;133:34–41. quiz 311. [PubMed] []
8. Edelstein ZR, Farrow DC, Bronner MP, et al. Central adiposity and risk of Barrett’s esophagus. Gastroenterology. 2007;133:403–411. [PubMed] []
9. Das A, Thomas S, Zablotska LB, et al. Association of esophageal adenocarcinoma with other subsequent primary cancers. J Clin Gastroenterol. 2006;40:405–411. [PubMed] []
10. Nelsen EM, Kirihara Y, Takahashi N, et al. Distribution of body fat and its influence on esophageal inflammation and dysplasia in patients with Barrett’s esophagus. Clin Gastroenterol Hepatol. 2012;10:728–734. [PMC free article] [PubMed] []
11. El-Serag HB, Graham DY, Satia JA, et al. Obesity is an independent risk factor for GERD symptoms and erosive esophagitis. Am J Gastroenterol. 2005;100:1243–1250. [PubMed] []
12. Pandolfino JE, El-Serag HB, Zhang Q, et al. Obesity: a challenge to esophagogastric junction integrity. Gastroenterology. 2006;130:639–649. [PubMed] []
13. Tilg H, Moschen AR. Visceral adipose tissue attacks beyond the liver: esophagogastric junction as a new target. Gastroenterology. 2010;139:1823–1826. [PubMed] []
14. Jinjuvadia R, Lohia P, Jinjuvadia C, et al. The association between metabolic syndrome and colorectal neoplasm: systemic review and meta-analysis. J Clin Gastroenterol. 2013;47:33–44. [PMC free article] [PubMed] []
15. Johansen D, Stocks T, Jonsson H, et al. Metabolic factors and the risk of pancreatic cancer: a prospective analysis of almost 580,000 men and women in the Metabolic Syndrome and Cancer Project. Cancer Epidemiol Biomarkers Prev. 2010;19:2307–2317. [PubMed] []
16. Rosato V, Bosetti C, Talamini R, et al. Metabolic syndrome and the risk of breast cancer. Recenti Prog Med. 2011;102:476–478. [PubMed] []
17. Pelucchi C, Serraino D, Negri E, et al. The metabolic syndrome and risk of prostate cancer in Italy. Ann Epidemiol. 2011;21:835–841. [PubMed] []
18. Calle EE, Rodriguez C, Walker-Thurmond K, et al. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003;348:1625–1638. [PubMed] []
19. Greer KB, Thompson CL, Brenner L, et al. Association of insulin and insulin-like growth factors with Barrett’s oesophagus. Gut. 2012;61:665–672. [PMC free article] [PubMed] []
20. Rubenstein JH, Davis J, Marrero JA, et al. Relationship between diabetes mellitus and adenocarcinoma of the oesophagus and gastric cardia. Aliment Pharmacol Ther. 2005;22:267–271. [PubMed] []
21. Neale RE, Doecke JD, Pandeya N, et al. Does type 2 diabetes influence the risk of oesophageal adenocarcinoma? Br J Cancer. 2009;100:795–798. [PMC free article] [PubMed] []
22. Jick H, Jick SS, Derby LE. Validation of information recorded on general practitioner based computerised data resource in the United Kingdom. BMJ. 1991;302:766–768. [PMC free article] [PubMed] []
23. Yang YX, Hennessy S, Lewis JD. Type 2 diabetes mellitus and the risk of colorectal cancer. Clin Gastroenterol Hepatol. 2005;3:587–594. [PubMed] []
24. Prentice RL, Kalbfleisch JD, Peterson AV, Jr, et al. The analysis of failure times in the presence of competing risks. Biometrics. 1978;34:541–554. [PubMed] []
25. Jick SS, Kaye JA, Vasilakis-Scaramozza C, et al. Validity of the general practice research database. Pharmacotherapy. 2003;23:686–689. [PubMed] []
26. Lawrenson R, Williams T, Farmer R. Clinical information for research; the use of general practice databases. J Public Health Med. 1999;21:299–304. [PubMed] []
27. Solaymani-Dodaran M, Logan RF, West J, et al. Mortality associated with Barrett’s esophagus and gastroesophageal reflux disease diagnoses-a population-based cohort study. Am J Gastroenterol. 2005;100:2616–2621. [PubMed] []
28. Solaymani-Dodaran M, Logan RF, West J, et al. Risk of extra-oesophageal malignancies and colorectal cancer in Barrett’s oesophagus and gastro-oesophageal reflux. Scand J Gastroenterol. 2004;39:680–685. [PubMed] []
29. Solaymani-Dodaran M, Logan RF, West J, et al. Risk of oesophageal cancer in Barrett’s oesophagus and gastro-oesophageal reflux. Gut. 2004;53:1070–1074. [PMC free article] [PubMed] []
30. El-Serag H, Hill C, Jones R. Systematic review: the epidemiology of gastro-oesophageal reflux disease in primary care, using the UK general practice research database. Aliment Pharmacol Ther. 2009;29:470–480. [PubMed] []
31. Dupont WD. Power calculations for matched case-control studies. Biometrics. 1988;44:1157–1168. [PubMed] []
32. Ai C, Norton EC. Interaction terms in logit and probit models. Econ Lett. 2003;80:123–129. []
33. Buis ML. Stata tip 87: interpretation of interactions in nonlinear models. Stata J. 2010:305–308. []
34. El-Serag HB, Kvapil P, Hacken-Bitar J, et al. Abdominal obesity and the risk of Barrett’s esophagus. Am J Gastroenterol. 2005;100:2151–2156. [PubMed] []
35. Nam SY, Kim BC, Han KS, et al. Abdominal visceral adipose tissue predicts risk of colorectal adenoma in both sexes. Clin Gastroenterol Hepatol. 2010;8:443–450. e441–442. [PubMed] []
36. Ryan AM, Healy LA, Power DG, et al. Barrett esophagus: prevalence of central adiposity, metabolic syndrome, and a proinflammatory state. Ann Surg Jun. 2008;247:909–915. [PubMed] []
37. Leggett CL, Nelsen E, Tian J, et al. Metabolic syndrome as a risk factor for Barrett’s esophagus: a population based case control study. Mayo Clin Proc. 2013;88:157–165. [PMC free article] [PubMed] []
38. Chen SC, Chou CK, Wong FH, et al. Overexpression of epidermal growth factor and insulin-like growth factor-I receptors and auto-crine stimulation in human esophageal carcinoma cells. Cancer Res. 1991;51:1898–1903. [PubMed] []
39. Liu YC, Leu CM, Wong FH, et al. Autocrine stimulation by insulin-like growth factor I is involved in the growth, tumorigenicity and chemoresistance of human esophageal carcinoma cells. J Biomed Sci. 2002;9:665–674. [PubMed] []
40. Takaoka M, Harada H, Andl CD, et al. Epidermal growth factor receptor regulates aberrant expression of insulin-like growth factor-binding protein 3. Cancer Res. 2004;64:7711–7723. [PMC free article] [PubMed] []
41. Kendall BJ, Macdonald GA, Hayward NK, et al. Leptin and the risk of Barrett’s oesophagus. Gut. 2008;57:448–454. [PubMed] []
42. Thompson OM, Beresford SA, Kirk EA, et al. Serum leptin and adiponectin levels and risk of Barrett’s esophagus and intestinal metaplasia of the gastroesophageal junction. Obesity (Silver Spring) 2010;18:2204–2211. [PMC free article] [PubMed] []
43. Gao Q, Horvath TL. Cross-talk between estrogen and leptin signaling in the hypothalamus. Am J Physiol Endocrinol Metab. 2008;294:E817–E826. [PubMed] []
44. Kelty CJ, Gough MD, Van Wyk Q, et al. Barrett’s oesophagus: intestinal metaplasia is not essential for cancer risk. Scand J Gastroenterol. 2007;42:1271–1274. [PubMed] []
45. Hahn HP, Blount PL, Ayub K, et al. Intestinal differentiation in metaplastic, nongoblet columnar epithelium in the esophagus. Am J Surg Pathol. 2009;33:1006–1015. [PMC free article] [PubMed] []
46. Liu W, Hahn H, Odze RD, et al. Metaplastic esophageal columnar epithelium without goblet cells shows DNA content abnormalities similar to goblet cell-containing epithelium. Am J Gastroenterol. 2009;104:816–824. [PMC free article] [PubMed] []
47. Edelstein ZR, Bronner MP, Rosen SN, et al. Risk factors for Barrett’s esophagus among patients with gastroesophageal reflux disease: a community clinic-based case-control study. Am J Gastroenterol. 2009;104:834–842. [PMC free article] [PubMed] []
48. El-Serag H. Role of obesity in GORD-related disorders. Gut. 2008;57:281–284. [PubMed] []
49. Calle EE, Kaaks R. Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nat Rev Cancer. 2004;4:579–591. [PubMed] []
50. Omer ZB, Ananthakrishnan AN, Nattinger KJ, et al. Aspirin protects against Barrett’s esophagus in a multivariate logistic regression analysis. Clin Gastroenterol Hepatol. 2012;10:722–727. [PMC free article] [PubMed] []

Plaats een reactie ...

Reageer op "Diabetes vergroot risico op aan Barrett's gerelateerde slokdarmkanker en kanker van de slokdarmverbinding met de maag met circa 30 procent blijkt uit grote reviewstudie"


Gerelateerde artikelen
 

Gerelateerde artikelen

Beginnende slokdarmkanker >> Chemo plus bestraling voordat >> Diabetes vergroot risico op >> Diagnose: Slokdarmkanker zou >> Hyperthermie: Chemo en bestraling >> Immuuntherapie met gemoduleerd >> Operatie: Kijkoperatie - endoscopie >> PDT - Photodynamische Therapie: >> RFA - Radio Frequency Ablation: >> Vaccinatieprogramma bij maagkanker >>