A case of small bowel ulcer caused by NSAIDs and detected after capsule endoscope retention.

We recently detected an annular ulcer thought to have been caused by non-steroidal anti-inflammatory drugs (NSAIDs) when we performed small bowel capsule endoscopy on a patient with suspected small-bowel bleeding and a history of frequent use of oral NSAIDs. The patient was a 64-year-old woman who complained of bloody stools and abdominal pain. The annular ulcer showed concentric stenosis, which caused retention of the capsule endoscope. NSAIDs are some of the most frequently used anti-inflammatory analgesics, and even more frequent use can be expected with the aging of society. No reports to date appear to have described retention of a capsule endoscope due to annular ulceration caused by NSAIDs. We report herein our experience with a patient showing small-bowel ulcer caused by NSAIDs.

Good response chemotherapy for late-recurring gastric cancer in the gluteals, with peritoneal and retroperitoneal dissemination.

A 64-year-old woman presented with advanced gastric cancer (signet ring cell carcinoma) and underwent total gastrectomy in 1996. Postoperative recovery was good, and she was monitored regularly on an outpatient basis. Abdominal computed tomography in 1999 revealed a soft tissue shadow ventral to the origin of the celiac artery. Careful monitoring was continued on an outpatient basis. The patient began to experience gluteal swelling and pain in April 2008. Symptoms rapidly exacerbated and the patient was hospitalized for further examination. Gluteal muscle biopsy revealed signet ring cell carcinoma and bilateral hydronephrosis. Gluteal recurrence of the original gastric cancer was suggested, and systemic chemotherapy consisting of S-1 at 100 mg/day (3 weeks on, 1 week off) and CDDP (day 8) was started. Following the 6th cycle of chemotherapy, gluteal symptoms disappeared and the patient was judged to have achieved clinical complete response (CR). No adverse events or image findings suggesting new recurrence have since been identified. The patient received a total CDDP dose of 585 mg and clinical CR has been maintained as of 14 years after total gastrectomy and 18 months after recurrence.

Endoscopic examination for duodenal ulcer bleeding during transcatheter arterial embolization: analysis of two cases.

Endoscopy is usually effective in treating duodenal ulcer bleeding, but depending on the lesion site and overall patient condition, hemostasis may be difficult to achieve with endoscopy alone. We described two patients with duodenal ulcer bleeding in whom endoscopic hemostasis was difficult. Immediately after transcatheter arterial embolization, endoscopic examination was used to confirm hemostasis and completing of the angiographic procedures.

Study of energy metabolism of skeletal muscles in alcoholic liver disease--expired gas analysis during exercise.

BACKGROUND: The effects of chronic alcohol intake on skeletal muscle are clinically observed as muscle cramps with decrease in the amount of muscle. It was clarified by expired gas analysis that acute alcohol load affects disturbed energy metabolism of skeletal muscle. We studied abnormal energy metabolism of skeletal muscles in alcoholic liver diseases using expired gas analysis. METHODS: Subjects of the study were five inpatients with alcoholic liver disease (fatty liver: one case, hepatic fibrosis: one case, liver cirrhosis: three case). Expired gas analysis during exercise was performed using AEROMONITOR. Minute ventilation, oxygen consumption and carbon dioxide output were monitored, and anaerobic threshold (AT) and respiratory compensation point (RCP) were calculated. RESULTS: The anaerobic threshold, which is the limit of the aerobic exercise, was significantly reduced in patients with alcoholic disease (p < 0.01). The respiratory compensation point, which is the limit of the metabolic compensation of intracellular lactic acidosis, was decreased (p < 0.01). CONCLUSIONS: The results of expired gas analysis during exercise indicate that the aerobic energy metabolism of skeletal muscle had been disturbed in alcoholic liver disease. The reduced RCP suggests that the lactate metabolism in skeletal muscle is also disturbed in alcoholic liver disease. Expired gas analysis during exercise allows determination of the amount of exercise required to treat liver diseases through analysis of AT.

[Analysis of medical care costs for gastroenterological inpatients with alcohol-related disease].

Current estimates suggest that approximately 2.3-2.5 million people in Japan are alcoholics. Of these patients, less than 1% visit alcohol outpatient clinics; most patients visit general clinics. Alcohol is associated with disorders of the gastrointestinal system, circulatory system, nervous system, and other organs. The costs for medical care impose a heavy burden on healthcare financing. Among all, the costs for alcohol-related gastrointestinal diseases are enormous. Reports show that the percentages of medical care costs for alcohol-related gastrointestinal diseases is as high as about 29% of the costs for all gastrointestinal diseases. Our analysis has found that hospital and treatment costs for alcohol-related liver and pancreatic diseases amounted to 35.2% of the costs for all liver and pancreatic diseases. Furthermore, results indicated that the average daily hospital and treatment costs for patients with alcohol-related liver diseases were significantly higher than the costs for patients with non-alcohol-related liver diseases. To reduce medical care costs for alcohol-related diseases, not only treatment of such diseases but also preventive care for pre-alcoholics is crucial. In this context, close contact between general clinics and alcohol outpatient clinics are important, and a network system of support for patients with alcohol-related diseases should be established.

Platelet activation in patients with alcoholic liver disease.

OBJECTIVE: To elucidate the mechanisms of thrombocytopenia in alcoholic liver diseases, we investigated activation status of platelets in patients with alcoholic fatty liver (Al-FL), alcoholic liver cirrhosis (Al-LC) or hepatitis-C liver cirrhosis C (C-LC). METHODS: Platelet activation was evaluated by flow cytometry using monoclonal antibodies against P-selectin (CD62P) and the fibrinogen receptor (PAC-1), both specific for platelet activation, and anti-CD61 antibody for the presence of microparticles (PMP) in seven patients with Al-FL, thirteen patients with Al-LC and, as a non-alcoholic liver disease control, nine patients with C-LC. As a normal control, seventeen healthy subjects without liver dysfunction were also evaluated. RESULTS: Compared with the healthy controls, the platelet count was significantly decreased in patients with alcoholic liver diseases or C-LC. Ten days after discontinuation of alcohol intake, the platelet count was significantly higher in both the Al-FL and Al-LC groups than that measured on admission. There was an inverse correlation between the platelet count and PMP, a marker of platelet activation. The Al-FL, Al-LC and C-LC groups showed significantly higher percentages of platelets positive for CD62P than the healthy controls. The PAC-1 positivity was increased only in the C-LC group. PMP were significantly increased in the Al-FL, Al-LC and C-LC groups compared to that in the healthy group. In the Al-LC group, PMP were significantly decreased 10 days after discontinuation of alcohol intake from that measured on admission. CONCLUSION: Patients with alcoholic liver diseases have increased platelet activation, which may contribute to the occurrence of thrombocytopenia. The formation of PMP might be one of the important factors of thrombocytopenia in alcoholic liver diseases.

Platelet activation in patients with chronic hepatitis C.

OBJECTIVE: To elucidate the mechanisms of thrombocytopenia in chronic hepatitis C (CHC), we investigated platelet activation in patients with chronic viral liver diseases. METHODS: Platelet activation was evaluated with flow cytometry in twenty-five patients with chronic viral hepatitis and 11 patients with liver cirrhosis of viral etiology. Liver biopsies were carried out in all patients. RESULTS: The platelet counts decreased significantly in patients with CHC and in patients with liver cirrhosis compared to controls, but not in patients with chronic hepatitis B (CHB). Patients with CHC had a significantly higher percentage of platelets positive for activation-dependent monoclonal antibodies (MoAbs), and also had a higher percentage of platelet microparticles (PMP), a marker of platelet activation, than patients with CHB. There was a significant correlation between the percentage of PMP and the levels of liver fibrosis markers, such as serum hyaluronate and N-terminal propeptide of type III procollagen (P-III-P), in CHC, suggesting the relationship between platelet activation and liver fibrosis. Platelet activation was markedly enhanced in CHC patients with high histological scores of liver fibrosis. CONCLUSION: Patients with CHC have increased platelet activation, which may contribute to the occurrence of thrombocytopenia in CHC. Liver fibrosis may play a role in activation of platelets in CHC.