- Email: [email protected]
CAMPYLOBACTER PYLORI, GASTRIN, AND DUODENAL ULCER
389
CAMPYLOBACTER PYLORI, GASTRIN, AND DUODENAL ULCER
SiR,—Dr Levi and colleagues (May 27,
p 1167) support the that gastric Campylobacter pylori may be a causative factor in duodenal ulcer disease via increased antral gastrin release. We agree that gastrin may be linked to C pylori in the pathogenesis of duodenal ulceration and have demonstrated a reduction of serum gastrin in children with campylobacter-associated gastritis.! However, 6 of Levi’s 31 duodenal ulcer patients (19%) were C
hypothesis
Fig 2-Life-sized human phantom of patient’s foot with melanoma showing thermal neutron fluence at various depths.
(Further details of dosimetry studies from authors.) and 8 units 4 cm from the lesion margin at five points transverse to the central arch on the patient’s right sole. 21 h after the first injection, we irradiated the foot to yield a neutron dose calculated as 1013fem2. The dose received by the centre of the tumour was measured as 1-04 x 1013cmz. 2 weeks after the single capture therapy the lesion had regressed (fig lb) and 9 weeks later, regression was clinically complete with only a 3 mm diameter bluish pigmented spot remaining, which was confirmed to be accumulated melanophages. Fig lc shows complete regression 8tmonths after single NCT. 18 months after NCT, the patient remains well with no
pylori negative by urease testing alone, a surprisingly high proportion. Although McNulty and Wise’s initial experience with this test gave a sensitivity of 88 % ,2 we feel that the high frequency of C pylori negative patients in Levi’s series should have prompted additional tests for C pylori. In our two series of duodenal ulcer patients only 3 of 65 (5%) were C pylori negative by combined culture, urease testing, and histology3 and none of 45 by culture, histology, urease testing, and IgG antibody titres.4 Levi et al took two gastric antral biopsy samples and both were used for urease testing. Why could not one have been processed for culture or histology, which might have revealed C pylori or antral inflammation in urease-negative duodenal ulcer patients? This lack of histological and/or culture information may explain the high percentage of C pylori negativity in Levi’s patients and casts doubt on the validity of the results.
London W1N 8AA
recurrence.
1. 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. 2. McNulty CAM, Wise R. Rapid diagnosis of Campylobacter pyloridis gastritis. Lancet 1986; i: 387. 3. Smith AC, Price AB, Boriello P, Levi AJ. A comparison of ranitidine and tripotassium dicitratobismuth (TBD) in relapse rates of duodenal ulcer: the role of Campylobacter pylori (CP). Gut 1988; 29: A711. 4. Salmon PR, Vaira D, Holton J, et al. A comparison of treatment regimens for Campylobacter pylori (CP) associated duodenal ulcer (DU); preliminary results. Gastroenterol Inter 1988 (suppl 1): no 553.
We thank Masahiro Shiono, Tetsuya Nozaki, Otohiko Aizawa, and Tadashi Sato. Supported by grant-in-aid 63010045 to Y. M. for cancer research from the Japanese Ministry of Education, Science and Culture.
YUTAKA MISHIMA
Department of Dermatology and Special Institute of Cancer, Neutron Capture Therapy, Kobe University School of Medicine, Kobe 650, Japan
CHIHIRO HONDA MASAMITSU ICHIHASHI HIDEFUMI OBARA JUNICHI HIRATSUKA
National Institute of Radiological Chiba
HIROSHI FUKUDA
Sciences,
Research Reactor Institute, Kyoto University, Osaka Shinshu University, Matsumoto
OMEPRAZOLE, CAMPYLOBACTER PYLORI, AND DUODENAL ULCER
Hyogo Medical Center for Adults, Akashi
TONY SMITH DINO VAIRA COLIN AINLEY JOHN HOLTON
Departments of Gastroenterology and Microbiology, Middlesex Hospital,
HIROSHI KARASHIMA TOORU KOBAYASHI
KEIJI KANDA KAZUO YOSHINO
1. Mishima Y, Shimakage T. Thermal neutron capture treatment of malignant melanoma using 10B-dopa and 10B12-chlorpromazine compound. In: Riley V, ed. Pigment cell: Vol II. Basel: Karger, 1976: 394-406 2. Nakanishi M, Ichihashi M, Mishima Y, Matsuzawa T, Fukuda H. Thermal neutron capture therapy of malignant melanoma: in vitro radiobiological analysis. Int J Radiat Biol 1980; 37: 573-80. 3. Mishima Y, Ichihasi M, Nakanishi T, Tsuji M, Ueda M, Nakagawa T, Suzuki T. Cure of malignant melanoma by single thermal neutron capture treatment using melanoma seeking compounds: 10B/melanogenesis interaction to in vitro/in vivo radiobiological analysis to preclinical studies. In: Fairchild RG, Brownell GL, eds. Proc 1st Int Symp Neutron Capture Therapy. New York: US Government Printing Office, 1984; BNL 51730: 355-64. 4. Mishima Y, Ichihashi M, Tsuji M, Hatta S, Ueda M, Honda C, Suzuki T. Treatment of malignant melanoma by selective thermal neutron capture therapy using melanoma-seeking compound. J Invest Dermatol 1989; 92: 321S-25S. 5. Yoshino K, Okamoto M, Kakihana H, Mori Y, Mishima Y, Ichihashi M, Tsuji M, Nakanishi T. Chemical assay of boron and its distribution in melanoma-bearing subjects. In: Hatanaka H, ed. Neutron capture therapy. Niigata: Nishimura, 1986: 291-302. 6 Taniyama K, Fujiwara H, Kuno T, Saito N, Shuntoh H, Sakaue M, Tanaka C. Acute and subacute toxicity of 10B-paraboronophenylalanine. I Proc 2nd Japan-Australia Workshop on Neutron Capture Therapy for Malignant Melanoma. Pigment Cell Res (in press). 7. Kobayashi T, Kanda K, Mishima Y. In situ measurement on 10B concentrations and absorbed dose estimations in human malignant melanoma treated by BNCT. Strahlenther Onkol 1989; 165: 104-06. 8. Mishima Y, Ichihashi M, Hatta S, Honda C, Yamamura K, Nakagawa T. New thermal neuron capture therapy for malignant melanoma melanogenesis-seeking 10&bgr; molecule-melanoma cell interaction from in vitro to first clinical trial. Proceedings 2nd Japan-Australia Workshop on Neuron Capture Therapy for Malignant Melanoma. Pigment Cell Res 1989; 2: 226-34.
SIR,-Dr Levi and colleagues (May 27, p 1167) suggest that Campylobacter pylori in the gastric antrum stimulates gastrin release in duodenal ulcer disease. Omeprazole lowers basal and stimulated gastric acid secretion and results in high healing rates in duodenal ulcer, even in patients resistant to H2-receptor antagonists. Daily administration of 20, 30, or 60 mg for 7-14 days is associated with an increase in basal and postprandial serum gastrin levels.2,3 To evaluate the possible role of omeprazole on gastric colonisation with C pylori, 9 patients with duodenal ulcer disease in whom symptoms persisted after treatment with ranitidine 300 mg daily for at least 3 weeks, were given omeprazole 20 mg twice daily for 28 days. Endoscopy was done before and at the end of omeprazole therapy and gastric juice was sampled by a sterile methodand two antral biopsy specimens were taken. After 28 days the ulcers
were
healed in 8
out
of 9 cases; in
case
2 erosions
were
RESULTS OF C PYLORI CULTURE
-
+
=negative culture, -++=>10* + 10-10; + < < 10’. =
C
pylarijml
of juice
or
biopsy suspension;
CAMPYLOBACTER PYLORI, GASTRIN, AND DUODENAL ULCER
SiR,—Dr Levi and colleagues (May 27,
p 1167) support the that gastric Campylobacter pylori may be a causative factor in duodenal ulcer disease via increased antral gastrin release. We agree that gastrin may be linked to C pylori in the pathogenesis of duodenal ulceration and have demonstrated a reduction of serum gastrin in children with campylobacter-associated gastritis.! However, 6 of Levi’s 31 duodenal ulcer patients (19%) were C
hypothesis
Fig 2-Life-sized human phantom of patient’s foot with melanoma showing thermal neutron fluence at various depths.
(Further details of dosimetry studies from authors.) and 8 units 4 cm from the lesion margin at five points transverse to the central arch on the patient’s right sole. 21 h after the first injection, we irradiated the foot to yield a neutron dose calculated as 1013fem2. The dose received by the centre of the tumour was measured as 1-04 x 1013cmz. 2 weeks after the single capture therapy the lesion had regressed (fig lb) and 9 weeks later, regression was clinically complete with only a 3 mm diameter bluish pigmented spot remaining, which was confirmed to be accumulated melanophages. Fig lc shows complete regression 8tmonths after single NCT. 18 months after NCT, the patient remains well with no
pylori negative by urease testing alone, a surprisingly high proportion. Although McNulty and Wise’s initial experience with this test gave a sensitivity of 88 % ,2 we feel that the high frequency of C pylori negative patients in Levi’s series should have prompted additional tests for C pylori. In our two series of duodenal ulcer patients only 3 of 65 (5%) were C pylori negative by combined culture, urease testing, and histology3 and none of 45 by culture, histology, urease testing, and IgG antibody titres.4 Levi et al took two gastric antral biopsy samples and both were used for urease testing. Why could not one have been processed for culture or histology, which might have revealed C pylori or antral inflammation in urease-negative duodenal ulcer patients? This lack of histological and/or culture information may explain the high percentage of C pylori negativity in Levi’s patients and casts doubt on the validity of the results.
London W1N 8AA
recurrence.
1. 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. 2. McNulty CAM, Wise R. Rapid diagnosis of Campylobacter pyloridis gastritis. Lancet 1986; i: 387. 3. Smith AC, Price AB, Boriello P, Levi AJ. A comparison of ranitidine and tripotassium dicitratobismuth (TBD) in relapse rates of duodenal ulcer: the role of Campylobacter pylori (CP). Gut 1988; 29: A711. 4. Salmon PR, Vaira D, Holton J, et al. A comparison of treatment regimens for Campylobacter pylori (CP) associated duodenal ulcer (DU); preliminary results. Gastroenterol Inter 1988 (suppl 1): no 553.
We thank Masahiro Shiono, Tetsuya Nozaki, Otohiko Aizawa, and Tadashi Sato. Supported by grant-in-aid 63010045 to Y. M. for cancer research from the Japanese Ministry of Education, Science and Culture.
YUTAKA MISHIMA
Department of Dermatology and Special Institute of Cancer, Neutron Capture Therapy, Kobe University School of Medicine, Kobe 650, Japan
CHIHIRO HONDA MASAMITSU ICHIHASHI HIDEFUMI OBARA JUNICHI HIRATSUKA
National Institute of Radiological Chiba
HIROSHI FUKUDA
Sciences,
Research Reactor Institute, Kyoto University, Osaka Shinshu University, Matsumoto
OMEPRAZOLE, CAMPYLOBACTER PYLORI, AND DUODENAL ULCER
Hyogo Medical Center for Adults, Akashi
TONY SMITH DINO VAIRA COLIN AINLEY JOHN HOLTON
Departments of Gastroenterology and Microbiology, Middlesex Hospital,
HIROSHI KARASHIMA TOORU KOBAYASHI
KEIJI KANDA KAZUO YOSHINO
1. Mishima Y, Shimakage T. Thermal neutron capture treatment of malignant melanoma using 10B-dopa and 10B12-chlorpromazine compound. In: Riley V, ed. Pigment cell: Vol II. Basel: Karger, 1976: 394-406 2. Nakanishi M, Ichihashi M, Mishima Y, Matsuzawa T, Fukuda H. Thermal neutron capture therapy of malignant melanoma: in vitro radiobiological analysis. Int J Radiat Biol 1980; 37: 573-80. 3. Mishima Y, Ichihasi M, Nakanishi T, Tsuji M, Ueda M, Nakagawa T, Suzuki T. Cure of malignant melanoma by single thermal neutron capture treatment using melanoma seeking compounds: 10B/melanogenesis interaction to in vitro/in vivo radiobiological analysis to preclinical studies. In: Fairchild RG, Brownell GL, eds. Proc 1st Int Symp Neutron Capture Therapy. New York: US Government Printing Office, 1984; BNL 51730: 355-64. 4. Mishima Y, Ichihashi M, Tsuji M, Hatta S, Ueda M, Honda C, Suzuki T. Treatment of malignant melanoma by selective thermal neutron capture therapy using melanoma-seeking compound. J Invest Dermatol 1989; 92: 321S-25S. 5. Yoshino K, Okamoto M, Kakihana H, Mori Y, Mishima Y, Ichihashi M, Tsuji M, Nakanishi T. Chemical assay of boron and its distribution in melanoma-bearing subjects. In: Hatanaka H, ed. Neutron capture therapy. Niigata: Nishimura, 1986: 291-302. 6 Taniyama K, Fujiwara H, Kuno T, Saito N, Shuntoh H, Sakaue M, Tanaka C. Acute and subacute toxicity of 10B-paraboronophenylalanine. I Proc 2nd Japan-Australia Workshop on Neutron Capture Therapy for Malignant Melanoma. Pigment Cell Res (in press). 7. Kobayashi T, Kanda K, Mishima Y. In situ measurement on 10B concentrations and absorbed dose estimations in human malignant melanoma treated by BNCT. Strahlenther Onkol 1989; 165: 104-06. 8. Mishima Y, Ichihashi M, Hatta S, Honda C, Yamamura K, Nakagawa T. New thermal neuron capture therapy for malignant melanoma melanogenesis-seeking 10&bgr; molecule-melanoma cell interaction from in vitro to first clinical trial. Proceedings 2nd Japan-Australia Workshop on Neuron Capture Therapy for Malignant Melanoma. Pigment Cell Res 1989; 2: 226-34.
SIR,-Dr Levi and colleagues (May 27, p 1167) suggest that Campylobacter pylori in the gastric antrum stimulates gastrin release in duodenal ulcer disease. Omeprazole lowers basal and stimulated gastric acid secretion and results in high healing rates in duodenal ulcer, even in patients resistant to H2-receptor antagonists. Daily administration of 20, 30, or 60 mg for 7-14 days is associated with an increase in basal and postprandial serum gastrin levels.2,3 To evaluate the possible role of omeprazole on gastric colonisation with C pylori, 9 patients with duodenal ulcer disease in whom symptoms persisted after treatment with ranitidine 300 mg daily for at least 3 weeks, were given omeprazole 20 mg twice daily for 28 days. Endoscopy was done before and at the end of omeprazole therapy and gastric juice was sampled by a sterile methodand two antral biopsy specimens were taken. After 28 days the ulcers
were
healed in 8
out
of 9 cases; in
case
2 erosions
were
RESULTS OF C PYLORI CULTURE
-
+
=negative culture, -++=>10* + 10-10; + < < 10’. =
C
pylarijml
of juice
or
biopsy suspension;