Læknablaðið - 15.03.1992, Blaðsíða 33

LÆKNABLAÐIÐ
105
magaslímhúðinni enda er ekki unnt að taka
tvö vefjasýni (par) á nákvæmlega sama stað.
SUMMARY
This pilot study was performed at the National
University Hospital in Reykjavík in late 1987.
Blood samples and biopsies from the gastric
mucosa were taken from 47 patients (27 females
and 20 males aged 14-75 years, median age 51
year), chosen randomly from a group of 224
patients undergoing endoscopy at the time of the
study. Two biopsies were taken from each of
the following sites; pylorus, angulus and minor
curvature, one for bacterial culture and the other
for histopathological examination. Blood was
taken for HLA-typing by microlymphocytotoxicity
test. Patients who had received antibiotics within
two weeks of the endoscopy and patients on
anticoagulation therapy or having bleeding
diathesis were excluded. Culture, HLA-typing and
histological examination were performed without
knowledge of results from the other parts of the
study. H. pylori was found in 29 patients (61.7%),
17 females and 12 males aged 19-74 years. Median
age was 56 years. Bacterial cultures for H. pylori,
and histological examination after Warthin-Starry
staining, gave identical results in 94.3% of the
samples. When the HLA groups of H. pylori
positive and negative patients were compared by
Fisher exact test no statistical significance was
found. The relative risk of patients, with positive
H. pylori cultures, to have HLA antigen Aw-19 or
belonging to the group where HLA-B-typing was
unsuccessful, was statistically significant (P<0.05)
when compared to a control group. When H. pylori
negative patients were compared to the control
group they also had a relative risk of belonging
to the same untyped HLA B group (P<0.05). All
47 patients had gastritis according to histology
even though only 21 were diagnosed as such at
endoscopy. Of 29 patients infected with H. pylori
21 (72.4%) had chronic active gastritis and 8 had
chronic gastritis. Only one patient had chronic
active gastritis and negative culture for H. pylori.
Of 18 patients not infected with H. pylori, 17
had chronic gastritis (94.4%) (Yates’ correction
P<0.001).
HEIMILDIR
1. Marshall BJ, Warren JR. Unidentilied curved bacilli
in the stomach of patients with gastritis and peptic
ulceration. Lancet 1984: i; 1311-5.
2. Marshall BJ, Amstrong JA, McGechie DB, Glancy
RJ. Attempt to fulfill Koch’s postulates for pyloric
campylobacter. Med J Austr 1985; 142: 436-9.
3. Drumm B, Sherman P, Cutz E, Karmali M.
Association of Campylobacter pylori in the gastric
mucosa with antral Gastritis in children. N Engl J
Med 1987; 316: 1557-61.
4. Hazell SL, Hennessy WB, Borody TJ, et al.
Campylobacter pyloridis Gastritis II: Distribution
of bacteria and associated inflammation in the
gastroduodenal environment. Am J Gast Roenterol
1987; 82: 297-301.
5. Dooley CP, Cohen H. The clinical significance of
Campylobacter pylori. Review. Ann Int Med 1988;
108: 70-9.
6. Jóhannsson JH, Harðardóttir H, Sigvaldadóttir E, et
al. Campylobacter pylori í magaslímhúð. Framvirk
rannsókn á algengi C. -pylori í magaslímhúð
sjúklinga með einkenni um bólgu eða sár í maga.
Læknablaðið 1989; 75: 191-5.
7. Rotter JI, Rimoin DL, Gursky JM, Terasaki P,
Slurdevant AL. HLA-B5 associated with duodenal
ulcer. Gastroenterology 1977; 73: 438-40.
8. Ellis A, Woodrow JC. HLA and duodenal ulcer. Gut
1979; 20: 760-2.
9. Gough MJ, Rajah SM, Giles GR. HLA antigens
in relationship to duodenal ulceration, gastric acid
secretion and the clinical result following vagotomy.
Br J Surg 1982; 69: 105-7.
10. Kang JY, Doran T. Crampton R, McClenehan W,
Piper DW. HLA antigens and peptic ulcer disease.
Digestion 1983; 26: 99-104.
11. O'Brien BD, Thomson ABR, Dossetor JB. HLA and
peptic ulcer. Dig Dis Sci 1979; 24: 314-5.
12. Buck GE, Gourley WK, Lee WK, Subramanyam
K, Latimer JM, DiNuzzo AR. Relation of
Campylobacter pyloridis to gastritis and peptic ulcer.
J Infect Dis 1986; 153: 664-9.
13. Van Rood JJ, van Leeuwen A, Keuning JJ, Blussé
van Oud Alblas A. The serological recognition of
the human MLC determinants using a modified
cytotoxity technique. Tissue antigens 1975; 5: 73.
14. Tiwari JL, Terasaki Pl. HLA and disease association.
New York: Springer-Verlag, 1985: 4-25.
15. Haldane JBS. The estimation and significance of the
logarithm of a ratio of frequencies. Ann Hum Genet
1956; 20: 309-11.
16. Lamouliatte H, Megraud F, De Mascarel A, Roux D,
Quinton A. »Campy\obacter pyloridis« and epigastric
pain: endoscopic, histological and bacteriological
correlations. Gastroenterol Clin Biol 1987; 11: 212-6.
17. Rauws EAJ, Langenberg W, Houthoff HJ, Zanen HC,
Tytgat GNJ. Campylobacter pyioridis - associated
chronic active antral gastritis. A prospective study
of its prevalence and the effects of antibacterial and
antiulcer treatment. Gastroenterology 1988; 94: 33-
40.
18. Fenoglio-Preiser CM, Lantz PE, Listrom MB, Davies
M, Rilke FO. Gastrointestinal Pathology. An Atlas
and Text. New York: Raven Press, 1989: 136-90.
19. Langenberg ML, Tylgat GNJ, Schipper MEI, Rietra
PJGM, Zanen HC. Campylobacter-like organisms
in the stomach of patients and healthy individuals.
Lancet 1984. i: 1394.
20. Tytgat GNJ, Rauws EAJ, De Koster E.
Campylohacter pylori (Discussion). Scand J
Gastroenterol 1988; 23: 68-81.
21. Myren J. Serck-Hansen A. The gastroscopic
diagnosis of gastritis with particular reference to
mucosal reddening and mucus coverings. Scand J
Gastroenterol 1974; 9: 457-62.
22. Cronstedt JL, Simpson IW. Correlation between
gastroscopic and direct vision biopsy findings.
Gastrointest Endosc 1973; 19: 174-95.