1599

HHV-6 AND EBV DNA IN LYMPHOCYTES AND

MOUTHWASHINGS

HIV infection. The average number of lymphocytes in the samples from HIV-infected individuals was lower than the number in samples from healthy adults. We therefore cannot conclude that the absolute number of lymphocytes carrying the HHV-6 genome is significantly reduced in HIV patients with symptoms but there is a significant increase in absolute concentration of EBV genomes. Increased replication of EBV in HIV-infected individuals is consistent with reports of increased antibody titres and virus isolation rates from such patients.3,4 We have found that, despite the inability of Levy and colleagues to isolate the virus from peripheral blood, HHV-6 DNA is present in the lymphocytes of a large proportion of healthy adults. We can confirm that HHV-6 is often present in the mouth of healthy and HIV-infected individuals (table). These preliminary results indicate differences in the behaviour of HHV-6 and EBV in HIV-infected individuals. Division of Virology, National Institute for Medical Research, London NW7 1AA, UK; and Virology Section, Department of Medical Microbiology, University College and Middlesex Hospital

Medical School, London

M. R. GOPAL B. J. THOMSON

J. FOX R. S. TEDDER R. W. HONESS

1. Lawrence GL, Chee M, Craxton MA, et al. Human herpesvirus-6 is closely related to human cytomegalovirus. J Virol 1990; 64: 287-99. 2. Baer R, Bankier AT, Biggin MD, et al. DNA sequence and expression of the B95-8 Epstein-Barr virus genome. Nature 1984; 310: 207-11. 3. Birx DL, Redfield RR, Tosato G. Defective regulation of Epstein-Barr virus infection in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related disorders. N Engl J Med 1986; 314: 874-79. 4. Rahman MA, Kingsley MKB, Ho M, et al. Enhanced antibody responses to Epstein-Barr virus in HIV-infected homosexual men. J Infect Dis 1989; 159: 472-79.

In 32 children peptic ulcer was diagnosed before 1987, and the relapse rate was 47% (14 out of 30 children followed up for a year or more; 11 relapses (79%) were symptomless, and a second course of ranitidine and continuous maintenance therapy prevented further relapses. When we looked for factors predictive of relapse we found that where ulcers relapsed the children had had higher pre-treatment levels of serum pepsinogen I.3 Since we had found that children with H pylori positive gastritis had a high serum level of pepsinogen I4 we reviewed the slides of antral mucosa and found H pylori in 20 of the 32 children; and all children who relapsed were H pylori positive. Since the relapse rate was significantly higher in H pylori infected children (65% vs 8% in non-infected children; p < 0.001) we suspected that infection favoured relapse. We tried to eradicate H pylori in the 14 with relapses by discontinuing ranitidine maintenance and giving antibiotics, and we also gave antibiotics to 14 H pylori positive cases identified among 28 new cases of peptic ulcer diagnosed since 1987. We used amoxycillin 50 mg/kg plus

tinidazole 20 mg/kg for 4-6 weeks.s In Icases we treated relatives simultaneously because of the high prevalence of H pylori infection in the families.6 H pylori was eradicated in 88%. So far a total of 48 children have been followed up by repeated endoscopies for one year or more after eradication (mean follow-up 2 years) and only 1 has relapsed. No relapses were seen in H pylori negative children. We obtained a satisfactory healing rate with ranitidine and the relapse rate was lower in these children than it is in adults; even so, only H pylori eradication could be said to have cured the disease. H pylori plays an important part in ulcer relapse even if its role in the development of ulcer is not yet proven. In 5 children in our series gastritis associated with H pylori was diagnosed 3-12 months before a second endoscopy revealed duodenal (4 patients) or antral ulcers. These children had not been treated with antibiotics because the infection was identified only retrospectively. Our data support Rauws and Tytgat’s conclusion that eradication of H pylori explains why the relapse rate after CBS, with or without antibiotics, is lower than that seen with H2-receptor antagonists. Department of Paediatrics, Gastroenterology Service, University of Turin, 10125 Turin, Italy

peptic ulcer associated with eradication of Helicobacter pylori

SIR,—Dr Rauws and Dr Tytgat (May 26, p 1233) report no ulcer relapses in 24 patients twelve months after Helicobacter pylori was eradicated with colloidal bismuth subcitrate (CBS) alone or in combination with amoxycillin and metronidazole. Their results are similar to those obtained by Marshall et al,l but since in these studies CBS was always used it is not yet clear whether this result is due to H pylori eradication or to CBS-induced stimulation of prostaglandin production. Our results support the conclusion that H pylori does have a dominant role in ulcer recurrence. In peptic ulcer in childhood we eradicated H pylori with antibiotics, without CBS; the ulcer relapse rate was very low. Since 1982 we have been conducting long-term follow-up on primary peptic ulcers in children,2 studying the healing rate of endoscopically diagnosed ulcers after an 8 week course of ranitidine. Ulcer relapses after treatment have been monitored by 6-monthly endoscopy. Since 1987 culture media for H pylori and rapid urease tests have been available in our unit. So far 60 children have been enrolled (mean age 10 years, range 1-18; 40 males). In 42 the ulcer was at the duodenal bulb, in 15 at the antrum, and in 3 at both sites. Ranitidine 5-10 mg/kg healed the ulcers in 58 patients in 8 weeks, and did so in 6 months in the remaining 2.

BJ, Goodwin CS, Warren JR, et al. Prospective double-blind trial of duodenal ulcer relapse after eradication of Campylobacter pylori. Lancet 1988; ii: 1437-41. Oderda G, Ansaldi N. Peptic ulcers in children. Lancet 1988; i: 302-03. Oderda G, Altare F, Dell’Olio D, Ansaldi N. Prognostic value of serum pepsinogen I in children with peptic ulcer. J Pediatr Gastroenterol Nutr 1988; 7: 645-50. Oderda G, Vaira D, Holton J, Dowsett JF, Ansaldi N. Serum pepsinogen I and IgG antibody to Campylobacter pylori in non-specific abdominal pain in childhood. Gut 1989; 30: 912-16. Oderda G, Vaira D, Holton J, et al. Amoxycillin plus tinidazole for Campylobacter pylori gastritis in children. assessment by serum IgG antibody, pepsinogen I, and gastrin levels. Lancet 1989; i: 690-92. Oderda G, Ansaldi N, Boero M, Ponzetto A, Bellis D. Campylobacter pylori in families of children with gastroduodenal disease due to C pylori. Am J Gastroenterol 1988; 83: 1437-38.

1. Marshall

2. 3. 4.

Cure of

GIUSEPPINA ODERDA MARCO FORNI DOMENICO DELL’OLIO NICOLETTA ANSALDI

5.

6.

Hypothyroidism SIR,—Your June 2 editorial mentions that non-thyroidal illness and

pituitary/hypothalamic disease can produce a similar pattern of thyroid function test results. To identify patients with hypopituitarism we did a cortisol assay on samples with a low thyroxine result and a thyrotropin level that did not indicate primary hypothyroidism. Thus a raised supplementary cortisol (above 650 nmol/1) identifies those with significant non-thyroidal illness and a diagnosis of hypopituitarism is considered in those with low (under 150 nmol/1) cortisol levels. The table shows the patients with hypopituitarism whom this policy has identified over three years from a population of 160 000. None of these cases was suspected on clinical grounds; all arose from the clinician in general practice or the outpatient clinic wishing to exclude primary thyroid disease, and few patients were elderly.’ These patients show that an undetectable thyrotropin level is not typical of central

Cure of peptic ulcer associated with eradication of Helicobacter pylori.

1599 HHV-6 AND EBV DNA IN LYMPHOCYTES AND MOUTHWASHINGS HIV infection. The average number of lymphocytes in the samples from HIV-infected individua...
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