895

of IgG antibodies.8-12 Our data confirm these fmdings andfurther show, in a group of 121 adult patients, that (1) thefalls in IgG titres persist after eradication of bacteria; (2) thesame is true for IgA and IgM antibodies, whether or notthere is a concurrent IgG response; and (3) when end-pointtitres are used for quantifying antibodies, a 60% or greaterdecrease in either IgG or IgA titres confirms eradication ofHpylori. Even a 50% decrease in titres is a very dependableindicator of healing since only 2 of the 23 patients remaininginfected had this degree of drop 6 months after therapy.Only 3 succesfully treated, initially antibody-positivepatients did not have this big drop in IgG titre. Furthermicrobiological and histological studies of these patients areneeded to determine whether the bacteria have beeneradicated fully or only to undetectable levels.

In most patients who were treated with antimicrobialdrugs, there was an initial fall in antibody titres irrespectiveof the final bacteriological result. In patients who weretherapeutic failures, the antibody titres then remained stableor rose. In the patient who was reinfected after the 6-monthvisit, IgG and IgA titres that had fallen sharply showed asharp rise at 12 months.Our results indicate that changes in IgG and IgA titres

offer an easy means of monitoring the disappearance andreappearance of H pylori in the human stomach. Changes inIgA titres were not as consistent as those of IgG titres; 11initially IgA-positive patients did not show a 50% decreasein this titre despite eradication of H pylori 6 months earlier.However, all but 1 of them had a 50% or greater fall in IgGtitre. The main value of IgA titres is in diagnosis andfollow-up of patients who do not produce an IgG responsebut who have raised IgA titres; in our study group 2% fellinto this group. IgM responses were always accompanied bychanges in IgG titres, which limits their value in follow-upstudies. They may be more useful in acute infection andexacerbations of chronic infection. 12

Since a fall in circulating H pylori antibodies is

accompanied by healing of the inflammatory changes in thestomach wall after eradication of helicobacters,13,17 we have acheap and ethical non-invasive method for use in follow-upstudies. Breath tests3.4 are another means of verifying thesuccess of therapy and may be applied a few weeks earlierthan serological tests, but they require special equipment,time, personnel to collect the breath samples, and the use ofeither radioactive material or tracers that can be measured

only with mass spectrometers.The use of serological tests will be useful in the assessment

of healing in individual patients; in large epidemiologicalstudies aimed at finding out the influence of cure of activechronic gastritis on other diseases associated with it, and onthe development of atrophic gastritis, for example;18 in thefollow-up of patients with duodenal ulcers; and in

monitoring efficacy of triple therapy.We thank Yrjo Jahnsson Foundation, the Finnish Medical Research

Council, and the University of Helsinki, for financial aid; Mrs E. Kelo andMrs P. Kosonen for technical help; and Dr A. P. Moran for reading themanuscnpt.

Results of this study were presented in part at the World Congress ofGastroenterology, August, 1990, Sydney, Australia, and at the VIInternational Workshop on Campylobacter, Helicobacter and Related

Organisms, October, 1991, Sydney, Australia).

REFERENCES

1. Parsonnet J, Friedman GD, Vandersteen DP, et al. Helicobacter pyloriinfection and the risk of gastric carcinoma. N Engl J Med 1991; 325:1127-31.

2. Nomura A, Stemmermann GN, Chyou P-H, Kato I, Perez-Perez GI,

Blaser MJ. Helicobacter pylori infection and gastric carcinoma amongJapanese Americans in Hawaii. N Engl J Med 1991; 321: 1132-36.

3. Bell GD, Weil J, Harrison G, et al. 14C-urea breath analysis, a

non-invasive test for Campylobacter pylori in the stomach. Lancet 1987;i: 1367-68.

4. Graham DY, Klein PD, Evans DR Jr, et al. Campylobacter pyloridetected noninvasively by the 13C-urea breath test. Lancet 1987; i:1174-77.

5. Jones DM, Lessells AM, Eldridge J. Campylobacter-like organisms onthe gastric mucosa: culture, histological, and serological studies. J ClinPathol 1984; 37: 1002-06.

6. Sobala GM, Crabtree JE, Pentith JA, et al. Screening dyspepsia byserology to Helicobacter pylori. Lancet 1991; 338: 94-96.

7. Jones DM, Eldridge J, Fox AJ, Sethi P, Whorwell PJ. Antibody to thegastric campylobacter-like organism ("Campylobacter pyloridis")—clinical correlations and distribution in the normal population. J MedMicrobiol 1986; 22: 57-62.

8. Veenendaal RA, Pena AS, Meijer JL, et al. Long-term surveillance aftertreatment of Helicobacter pylori infection. Gut 1991; 32: 1291-94.

9. Vaira D, Holton J, Cairns SR, Falzon M, Polydorou A, Dowsett JF, et al.Atibody titres to Campylobacter pylori after treatment for gastritis.Br Med J 1988; 297: 397.

10. Oderda G, Vaira D, Holton J, Ainley C, Altare F, Ansaldi N. Amoxycillinplus tinidazole for Campylobacter pylori gastritis in children: assessmentby serum IgG antibody, pepsinogen 1, and gastrin levels. Lancet 1989;i: 690-92.

11. Bohemen van CG, Langenberg ML, Rauws EAJ, Oudbier J, WeteringsE, Zanen HC. Rapidly decreased serum IgG to Campylobacter pylorifollowing elimination of Campylobacter in histological chronic biopsyCampylobacter-positive gastritis. Immunol Lett 1989; 20: 59-62.

12. Morris AJ, Ali MR, Nicholson GI, Perez-Perez GI, Blaser MJ. Longterm follow-up of voluntary ingestion of Helicobacter pylori. Ann InternMed 1991; 114: 662-63.

13. Valle J, Seppälä K, Sipponen P, Kosunen TU. Disappearance of gastritisafter eradication of Helicobacter pylori: a morphometric study. Scand JGastroenterol 1991; 26: 1057-66.

14. Goodwin CS, Blincow ED, Warren JR, Waters TE, Sanderson CR,Easton L. Evaluation of cultural techniques for isolating Campylobacterpyloridis from endoscopic biopsies of gastric mucosa. J Clin Pathol1985; 38: 1127-31.

15. Kosunen TU, Hook J, Rautelin HI, Myllylä G. Age dependent increaseof Campylobacter pylori antibodies in blood donors. Scand JGastroenterol 1989; 24: 110-14.

16. Hirschl AM, Pletschette M, Hirschl MH, Berger J, Stanek G, RotterML. Comparison of different antigen preparations in an evaluation ofthe immune response to Campylobacter pylori. Eur J Clin MicrobiolInfect Dis 1988; 7: 570-75.

17. Borody TJ, Carrick J, Hazell SL. Symptoms improve after theeradication of gastric Campylobacter pyloridis. Med J Aust 1987; 146:450-51.

18. Villako K, Maards H, Tammur R, et al. Helicobacter (Campylobacter)pylori infestation and the development and progression of chronicgastritis: results of long-term follow-up examinations of a randomsample. Endoscopy 1990; 22: 114-17.

From The Lancet

Glass-blowers’ cheeks

In the last number of the Progrés Medical, Dr Regnault describesthe condition of dilatation of the cheeks which occurs in glass-blowers, and which, so far as he has discovered, has not receivedmuch attention as regards the condition actually present and thecause of it. The work of glass-blowing is one requiring considerableskill and delicacy, and the apprenticeship necessary is a long one.Consequently boys commence the work, as a rule, at some timebetween the ages of twelve and fifteen, when the cheeks are not yetformed. The change is a gradual one, and for the most part takesplace imperceptibly. When it is commencing there may be slightand unimportant pain. The pain disappears when the dilatation isachieved. It varies in degree, and frequently is only perceived whenthe cheeks are inflated.... Fortunately, the inconveniences to whichthe condition gives rise are for the most part slight.... Regnaultgives the particulars of three cases which he has observed clinically,and calls attention to the interesting fact that sculptors, in

representing Tritons blowing into shells, have reproduced exactlythe deformity described.

(March 5, 1892)