ANTIBODIES TO H PYLORI IN VARIOUS SUBJECTS
The prevalence of H pylori infection in HIV-positive individuals higher than in healthy controls (chi-squared test p < 10-6; odds ratio =4-3, 95% confidence intervals [CI] 2-3, 7.9; table). In HIV-seropositive subjects, a significant difference was seen between symptom-free individuals and those with symptoms (p=001; odds ratio=2-4; 95% CI 1-2, 5-1). However, the percentage of HIV-infected subjects positive for H pylori antibodies was as high as that of HIV-negative individuals at risk of infection. Our findings suggest that the prevalence of H pylori infection in HIV-seropositive individuals is very high. The lower frequency of positivity in ARC and AIDS might be attributable to the use of chemotherapeutic agents active against H pylori or to impaired immune function. However, the virus does not seem to predispose to H pylori infection; indeed, the raised frequency of this organism in at-risk HIV-negative individuals suggests that contamination with H pylori may be facilitated by their lifestyle. We have previously reported a high frequency of H pylori antibodies in homosexual men.4 Finally, our data do not support Logan and colleagues statement that serology is unreliable for the diagnosis of H pylori infection in HIV-positive patients. It is well known that this bacterium causes a local and systemic immune response;s our findings show that serological tests seem to be useful to define the epidemiological pattern of H pylori infection in HIV-positive individuals. was
Competitive inhibition of binding of antibodies to HLA-DQw8 &bgr;53-62 peptide by various peptides. 3 sera (numbers 12, 92, and 110) were preincubated with peptides bradykinin (B), neurotensin (N) (both from Sigma), serum thymic factor (T), DQw8 53-62 (w8), or DQw7 53-62 (w7). The baseline for these experiments (ie, 0% inhibition) was preincubation of the sera with buffer.
antibody classes. IgA
antibodies were not observed. Antibodies bound equally well to thymic serum factor and 2 homologous peptides from HLA-DQ w7 and w8 (differing only in aminoacid 57) (figure). The unrelated peptides bradykinin and neurotensin were not bound. The observation of autoantibodies to thymic serum factor in type I diabetes supports concepts of thymic dysfunction in disease development. The relevance of the surprising cross-reactivity between thymic serum factor and 2 synthetic MHC class II peptides remains to be determined. This work was supported by the Bundesminister for Jugend, Familie, Frauen und Gesundheit and by the Minister fur Wissenschaft und Forschung des Landes Nordrhein-Westfalen. M. S. received a fellowship from the Fujita Health University, Japan. We thank J. Schneider for technical assistance, and Dr B. Kuglin for help with data analysis. Diabetes Research Institute,
University of Dusseldorf, D-4000 Dusseldorf, West
HUBERT KOLB MANSANORI SHINZATO
ANTONIO ACETI DOMENICO CELESTINO Institute for Tropical and Infectious Diseases, La Sapienza University, 00161 Rome, Italy
ALFREDO PENNICA ORIANA LERI MARTA CAFERRO
C, Kottis V, Bndeau C, Métroz-Dayer M-D, Poussier P. Abnormal thymocyte maturation in spontaneously diabetic BB rats involves the deletion of CD4-8 + cells. J Immunol 1990; 144: 923-28 2 Zipris D, Crow AR, Delovitch TL. Evidence for abnormal thymic T-cell development in non-obese diabetic (NOD) mice. Diabetologia 1989; 32: 560A. 3. Dardenne M, Savino W, Gastinel LN, Nabarra B, Bach JF. Thymic dysfunction in the mutant diabetic (db/db) mouse. J Immunol 1983; 130: 1195-99. 4. Dardenne M, Savino W, Bach JF. Autoimmune mice develop antibodies to thymic hormone: production of anti-thymulin monoclonal autoantibodies from diabetic (db/db) and B/W mice. J Immunol 1984; 133: 740-43. 5. Schwimmbeck PL, Yu DTY, Oldstone MBA. Autoantibodies to HLA B27 in the sera of HLA B27 patients with ankylosing spondylitis and Reiter’s syndrome, J Exp Med 1987; 166: 173-81.
Antibodies to Helicobacter pylori in HIV infection SIR,-Dr Logan and colleagues’ findings (June 16, p 1456) suggest that the prevalence of Helicobacter pylori infection in HIV-positive individuals is lower than that in the general population. We have investigated the prevalence of H pylori in HIV-infected subjects living in Italy by seeking specific antibodies in the serum. We examined sera from 157 HIV-seropositive individuals (31 with AIDS, 34 with AIDS-related complex [ARC], and 92 symptomfree) and from 130 HIV-seronegative individuals at risk of infection (80 homosexual men and 50 intravenous drug abusers), enrolled in previous studies.1,2 Serum samples from 85 age-matched healthy subjects were controls. Antibody to H pylori was tested for by a time-resolved fluoroimmunoassay,3 by the method of Aceti and colleagues.2The specificity of the test was confirmed by absorption of antibodies specific to H pylori from the serum assayed and by the failure of Campylobacter coli and Cjejuni to absorb out these specific antibodies.
A, Pennica A, Ippolito G, et al. Antiamebic antibodies in homosexual men. N Engl J Med 1987; 316: 692. 2. Aceti A, Titti F, Verani P, et al. Time-resolved immunofluorescence: a sensitive and specific assay for anti-HIV antibody detection in human sera. J Virol Methods 1987, 16: 303-15. 3. Aceti A, Pennica
A, Leri O, et al. Time-resolved fluoroimmunoassay for Campylobacter pylori antibodies. Lancet 1989; ii: 505. 4. Aceti A, Attanasio R, Pennica A, et al. Campylobacter pylori infection in homosexuals. Lancet 1987; ii: 154-55. 5. Rathbone BJ, Wyatt JI, Worsley BW, et al. Systemic and local antibody responses to gastric Campylobacter pyloridis in non-ulcer dyspepsia. Gut 1986; 27: 642-47.
Aetiology of eosinophilic enteritis SIR,-Dr Prociv and Dr Croese reported a large series of eosinophilic enteritis from Australia (June 2, p 1299), in which the dog hookworm Ancylostoma caninum was implicated as the leading cause based on the rapid response to mebendazole and identification of the hookworm in two of ninety-three cases. I recently treated a case of eosinophilic enteritis in Aldershot, UK, in which the involvement was predominantly in the muscular and serosal layers of the stomach and small bowel. The diagnosis was suspected clinically and was confirmed at laparotomy with biopsies. The patient responded well to oral steroids. Hookworms were not identified in any tissue section or in the faeces. Before surgery and starting steroids the patient received a five-day course of thiabendazole in a dose of 25 mg/kg twice daily. This did not lead to any symptomatic improvement. I suggest that, although A caninum may be the cause of the epidemic in Townsville, Australia, the cause elsewhere remains open to speculation. Cambridge Military Hospital, Aldershot, Hampshire GU11 2AN, UK
N. C. HEPBURN