[Pancreatic and duodenal metastases from renal cell carcinoma 13 years after radical nephrectomy: a case report].

A 52-year-old male was admitted to our hospital complaining of orthostatic vertigo, fatigue and weight loss, who underwent right total nephrectomy for renal cell carcinoma(RCC) with curative operation 13 years ago (in 1992). Endoscopic examination revealed a submucosal tumor with erosion in the duodenum. The diagnosis made from the biopsy specimens was metastatic RCC in the duodenum. Abdominal CT scan revealed that his metastasis has spread to the pancreas. Five million units of interferon a was administered intramuscularly three times a week for 1 month. He received blood transfusions and palliative care. He died 5 months later because of disease progression. Metastases of RCC have been often reported in the lungs, the liver, and the bones, but rarely in the gastrointestinal tract. This is a very rare case of metastatic RCC in the duodenum, which was diagnosed 13 years after curative right nephrectomy. Since late recurrence is characteristic of renal cell carcinoma, careful long-term follow-up is needed. To our knowledge, this is the 19th case of duodenal metastasis from RCC reported in the literature.

How closely is Helicobacter pylori infection related to gastroduodenal lesions?

BACKGROUND/AIMS: Various studies have indicated a relationship between Helicobacter pylori infection and upper gastrointestinal lesions, but this relationship needs to be assessed in individuals not seeking medical treatment for complaints. METHODOLOGY: We screened community residents for H. pylori infection and upper gastrointestinal lesions during an annual mass health examination aiming to determine relationships between infection and lesions. In 932 examinees we performed a 13C-urea breath test for H. pylori infection, and assessed degree of gastric atrophy by measuring pepsinogen I and II in serum. In 738 subjects we also performed upper gastrointestinal radiography with or without endoscopy. RESULTS: Prevalence of H. pylori infection increased with age, and the ratio of serum pepsinogen I to II decreased with age. Prevalence of H. pylori infection did not differ significantly between subjects with and without radiographically or endoscopically evident lesions. Of H. pylori-positive subjects with peptic ulcer, 73.2% had no recurrence of ulcer despite absence of medical treatment. CONCLUSIONS: Prolonged H. pylori infection was associated with atrophy of the gastric mucosa, but little relationship was evident between H. pylori infection and development or recurrence of peptic ulcer.

Gastric mucosal cell protection by epidermal growth factor in primary monolayer culture of guinea pig gastric mucous cells.

BACKGROUND: Epidermal growth factor (EGF) has an anti-ulcer effect, but the mechanisms of this gastric mucosal protection are incompletely understood. We have suggested the importance of mucin as a mucosal protectant. We investigated whether increased mucin biosynthesis might be involved in the gastric mucosal protection conferred by EGF. METHODS: EGF and then ethanol were added to primary monolayer cultures of guinea pig gastric mucous cells, in which factors such as gastric acid and gastrointestinal hormones were excluded. Mucin and prostaglandin E(2) (PGE(2)) were assayed. RESULTS: Cytoprotection induced by EGF was demonstrated. Mucin biosynthesis and PGE(2) release were both significantly increased by EGF. When endogenous PGE(2) synthesis was inhibited by pretreatment with 10(-5) M or 10(-4) M indomethacin (IND), mucin biosynthesis was still significantly increased by EGF. Ethanol-induced cell damage was concentration-dependent in cultures with no other additions (normal PGE(2) and mucin biosynthesis). Damage by ethanol was decreased by EGF pretreatment (increased PGE(2) and mucin biosynthesis). Damage by ethanol was increased by 10(-5) M IND pretreatment (decreased PGE(2); normal mucin biosynthesis) and by 10(-4) M IND pretreatment (decreased PGE(2) and mucin biosynthesis). Ethanol-induced damage was decreased by EGF pretreatment even in the presence of 10(-5) M and 10(-4) M IND (decreased PGE(2); increased mucin biosynthesis). CONCLUSIONS: Increased mucin biosynthesis, induced by EGF independently of PGE(2), protects gastric mucous cells.