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Published on: December 27, 2024
Hemorrhagic gastric carcinoma in an acromegalic patient
H Hasegawa1, M Onda, N Matsukura
1First Department of Surgery, Nippon Medical School, Tokyo, Japan.
Insights
This study reports a rare case of hemorrhagic gastric cancer in an acromegaly patient. Both growth hormone/insulin-like growth factor I and Helicobacter pylori may drive gastric tumor development.
Area of Science:
- Endocrinology
- Gastroenterology
- Oncology
Background:
- Acromegaly is a disorder caused by excess growth hormone (GH) and insulin-like growth factor I (IGF-I).
- Helicobacter pylori (H. pylori) infection is a known risk factor for gastric cancer.
- Gastric carcinoma is a significant global health concern.
Observation:
- A 79-year-old male with acromegaly presented with upper gastrointestinal hemorrhage and angina.
- The patient had elevated serum GH and IGF-I levels, and high anti-H. pylori IgG titer.
- Distal gastrectomy revealed a Type 2 papillary and well-to-moderately differentiated tubular adenocarcinoma.
Findings:
- Gastric cancer tissue showed 1.6 times higher IGF-I receptor mRNA expression than adjacent atrophic mucosa.
- IGF-I mRNA expression was lower in cancer tissue compared to atrophic mucosa.
- Reverse transcription-polymerase chain reaction analysis quantified mRNA levels.
Implications:
- This case highlights a potential link between acromegaly, H. pylori infection, and gastric tumorigenesis.
- Elevated IGF-I signaling may contribute to gastric cancer development in acromegalic individuals.
- Further research is warranted to elucidate the combined roles of GH/IGF-I and H. pylori in gastric cancer.
Abstract:
A rare case of hemorrhagic gastric carcinoma in an acromegalic patient is reported. A 79-year-old Japanese man was referred to our hospital with diagnoses of upper gastrointestinal hemorrhage and angina pectoris. This patient showed typical clinical features of acromegaly, with increased serum growth hormone (GH) and insulin-like growth factor I (IGF-I) level. A high titer of serum anti-Helicobacter pylori (H. pylori) IgG was also observed. After percutaneous transluminal coronary angioplasty treatment for stenosis of the right coronary artery, the patient underwent distal gastrectomy. Gastric cancer was Type 2 macroscopically and was diagnosed histologically as a papillary and well to moderately differentiated tubular adenocarcinoma. Reverse transcription-polymerase chain reaction analysis estimated that the amount of IGF-I receptor mRNA expression in the gastric cancer tissue was 1.6 times higher than that in the adjacent atrophic mucosa, whereas the amount of IGF-I mRNA expression in the cancer tissue was only half that in the atrophic mucosa. Both the stimulatory effects of GH and/or IGF-I on cell proliferation and H. pylori infection in gastric tumorigenesis may have been responsible for the development and growth of gastric carcinoma in this patient.

