1295

developed triple therapy for H pylori eradication late in 1984 we had opportunity to review true reinfection rates in duodenal ulcer patients 4-6 years after eradication proved at least 4 weeks post therapy by histology and urease test.3 In 64 patients, 45-73 months after H pylori eradication with triple therapy, we did a 14C-urea breath test that had been validated in 58 patients with a sensitivity of 97% and a specificity of 96%. In 2 patients the breath test was positive, indicating H pylori reinfection. Both patients remain symptom-free, which suggests that reinfection has not yet resulted in ulcer recurrence even though they have a history of ulcer-or they may have been reinfected with a non-ulcerogenic H pylori, if such strains indeed exist.4 2 reinfections in 314 post-eradication patient-years gives a the

Identical sections of five original HPLC chromatogramsfrom five successive microdialysis samples in 46-year-old man with episodic headaches. Peaks of 5-HT and 5-HIAA are shaded. During attack, 5-HT concentration increased strikingly to maximum coinciding with greatest pain (horizontal arrow), and with transient peak of 5-HIAA.

endure the pain for more than a few minutes, so that only one or two samples were taken before the attacks were stopped by oxygen inhalation. In the other 2 patients, 5-HT concentrations progressively increased as the attacks developed, and as pain subsided values fell (figure). In these cases, the maximum 5-HT concentration was used to calculate the mean. The large amounts of 5-HT in the vicinity of the STA that were noted during CH attacks (n 6) are probably due to local release. The origin of this release needs to be identified, but its time-course indicates a fast activation-inactivation cycle of secretory cells. Joseph et al4have reported that the skin of CH patients contains numerous 5-HT-immunopositive nerve fibres during attack periods, unlike the skin of patients with migraine or CH patients without attacks. The 5-HT measured during attacks in our study could originate in such nerve fibres. Whatever the origin, our results indicate that 5-HT is probably involved, at a local level, in the pathogenesis of CH. =

Faculté Lariboisière-St Louis, CNRS UA 641, 75010 Paris, France

P. AUBINEAU

Hôpital Lariboisière,

G. CUNIN

Paris

B. BROCHET C. LOUVET-GIENDAJ P. HENRY

Hôpital Pellegrin, Bordeaux

1. Dimitriadou V, Henry P, Brochet B, Mathiau P, Aubineau P. Cluster headache: ultrastructural evidence for mast cell degranulation and interaction with nerve fibres m the human temporal artery. Cephalalgia 1990; 10: 221-28. 2. Medina JL, Diamond S, Fareed J. The nature of cluster headache. Headache 1979; 19: 309-22. 3. Haimart M, Launay JM, Zurcher G, Cauet N, Dreux C, Da Prada M. Simultaneous determination of histamine and N-&agr;-methylhistamine on biological samples by an improved enzymatic single isotope assay. Agents Actions 1985; 16: 71-75. 4. Joseph R, Dhital K, Adams J, Bumstock G, Appenzeller O, Clifford Rose F. Cluster headache: a new approach using fluorescent histochemistry of nerves in temple skin. In: Rose C, ed. Histochemistry in cluster headache. Basel: Karger, 1985: 162-65.

Helicobacter pylori reinfection 4 years

post-eradication olR,—evidence tor the long-term

cure

01 duodenal ulcer atter

eradication of Helicobacter pylorz’ has prompted considerable efforts to develop an efficient H pylori therapy. Various triple therapies are now in clinical trials but we do not know if, in the long term, "cures" will only be transient due to early reinfection. Having

reinfection rate of 0-64% per year. Previous reinfection studies have been on small patient groups with only short follow-up. A recent serological study suggests a community conversion rate of049% per person year in a white US population,s a result consistent with our finding. As follow-up time increases in trials of H pylori eradication, it will be of interest to examine the role of family members positive for Hpylori, the lack of immune protection due to waning antibody cover, and, perhaps, the genetic background of reinfection. Our figures indicate that post-eradication reinfection with H pylori is rare and that efforts directed at the cure of duodenal ulcer by eradication of H pylori are worthwhile.

Centre for Digestive Disease, 144 Great North Road, Five Dock, NSW 2046, Australia

THOMAS BORODY PETER ANDREWS NOEL MANCUSO

EVA JANKIEWICZ SUE BRANDL

George LL, Borody TJ, Andrews P, et al. Cure of duodenal ulcer after eradication of Helicobacter pylori. Med J Aust 1990; 153: 145-49. 2. Moss S, Calam J. Helicobacter pylori and peptic ulcers the present position. Gut 1992; 1.

33: 289-92. 3. Hazell SL, Borody TJ, Gal A, et al. Campylobacter pyloridis gastritis I: detection of urease as a marker of bacterial colonisation and gastritis. Am J Gastroenterol 1987; 82: 292-96. 4. Figura N, Guglielmetti P, Rossolini A, et al. Cytotoxin production by Campylobacter pylori strains isolated from patients with peptic ulcers and from patients with chronic gastritis only. J Clin Immunol 1989; 27: 226. 5. Parsonnet J, Blaser MJ, Guillermo I, et al. Symptoms and risk factors of Helicobacter pylori infection m a cohort of epidemiologists. Gastroenterology 1992; 10:41-46.

2,8-dihydroxyadenine urolithiasis SIR,-Dr Ceballos-Picot and colleagues (April 25, p 1050) that a complete deficiency of adenine to 2,8phosphoribosyltransferase (APRT), leading dihydroxyadenine (2,8-DHA) lithiasis type I, is an underdiagnosed disease. Statistics gathered for the current update of our chapter on demonstrate

APRT deficiency in The Metabolic Basis of Inherited Diseasé support this. Since 1989 the number of type I homozygotes from eighteen countries worldwide, excluding Japan, has risen to 62. 8 are from Iceland (population 256 000) and 21 from France, so just two countries have contributed nearly half these. The number of homozygotes from Japan is a staggering 128.2 This number includes 35 homozygotes for the type I defect (APRT*QO genotype3), making Japan the largest single national group.3 However, most Japanese cases are homozygous for type II (APRT*J), characterised by substantial APRT activity in haemolysates (10-25% of normal) and found only in Japan so far.z3 The mutant enzyme has a reduced affinity for its cofactor, 5-phosphoribosyl-lpyrophosphate, and while activity is demonstrable in vitro, APRT is not functional in intact cells or in vivo. What is the reason for the higher detection rate in France, Iceland, and Japan? The percentage of symptomless homozygotes for the type I defect seems to be the same for all countries, and is about 15% for both types of defect, so that cannot be the explanation. Single ancestral mutations probably contribute to the higher detection rate in both the Japanese2 and Icelandic populations,4but a genetic bias is considered improbable by Ceballos-Picot et al. Diet and climate could contribute but the more likely suggestion is that patients with suspected uric acid lithiasis will be treated successfully with allopurinol without a correct diagnosis, which is regrettable because families carrying a mutant APRT gene need to be aware of this. Acute renal failure may be the