[A Case of Primary Gastric Amyloidosis with Fulminant Heart Failure].

A 53-year-old woman was admitted with epigastric discomfort and weakness. Laboratory examination at admission showed mild anemia and proteinuria. Esophagogastroduodenoscopy revealed marked mucosal atrophy, diffuse nodularity and granular appearance with mucosal friability. Biopsy was performed on the antrum and body of the stomach. On the next day, the patient began to complain of severe dyspnea, and hypoxia was present on pulse oximetry. Therefore, emergency echocardiography was conducted and it showed restrictive cardiomyopathy along with thrombus in the left atrium. With time, heart failure was aggravated despite intensive management. The result of gastric biopsy revealed amyloid deposits which stained positively with Congo red. On immunohistochemistry study, kappa and lambda chain were present. In addition, kappa chain was significantly elevated in urine and serum on electrophoresis. Although the patient was finally diagnosed as having primary gastric amyloidosis with restrictive cardiomyopathy, her general condition rapidly deteriorated and died at 12th hospital day. When obscure gastric lesion is encountered, performing gastric biopsy is strongly recommended since it be primary gastric amyloidosis. Herein, we present an unusual case of primary gastric amyloidosis.

A case of endoscopic full-thickness resection in a patient with gastric high-grade dysplasia unsuitable for endoscopic submucosal dissection.

Gastric high-grade dysplasia is an important premalignant lesion in gastric epithelial cells and has a high possibility of transforming to adenocarcinoma. Therefore, biopsy-proven high-grade dysplasia should be treated with en bloc resection methods such as endoscopic mucosal resection or endoscopic submucosal dissection (ESD). We report the case of a 63-year-old male patient, diagnosed with gastric high-grade dysplasia at the angle and lesser curvature side of the lower body. The patient was initially treated with ESD, although histopathology subsequently showed horizontal margin involvement. Since the lesion was diffusely edematous and margins were uncertain because of the previous ESD treatment, we chose to treat the patient with laparoscopy-assisted endoscopic full-thickness resection (EFTR). EFTR is a recently developed procedure, which uses both endoscopic and laparoscopic techniques to resect the full-thickness of the tissue. The final pathologic report revealed high-grade dysplasia and a focal intramucosal carcinoma of 0.8×0.7 cm. We conclude that EFTR can be an effective alternative treatment in gastric high-grade dysplasia unsuitable for ESD.

Changes in Serum Osteocalcin are Not Associated with Changes in Glucose or Insulin for Osteoporotic Patients Treated with Bisphosphonate.

BACKGROUND: Bisphosphonate is used in osteoporosis treatment to repress osteoclast activity, which then decreases levels of osteocalcin (OC). OC, a protein secreted by osteoblasts and released from the bone matrix during osteoclastic bone resorption, has been found to control blood glucose levels by increasing insulin production and sensitivity. The question addressed in this study is whether decreasing OC through bisphosphonate treatment will provoke a change in glucose homeostasis. METHODS: Eighty-four patients with osteoporosis were treated with once-weekly risedronate 35 mg and cholecalciferol 5,600 IU. We measured fasting plasma glucose (FPG), insulin, and undercarboxylated (Glu) and carboxylated (Gla) OC levels at baseline and after 16 weeks. To estimate insulin resistance (IR) and ß-cell function (B)%, homeostasis model assessment (HOMA)-IR and HOMA-B% were also calculated, respectively. RESULTS: The mean FPG level in total subjects increased significantly from 5.3 to 5.5 mmol/L, but no changes in blood glucose were noted in the 24 subjects with impaired fasting glucose. Glu and Gla OC levels declined significantly after treatment. No correlations were observed between changes in OC and changes in glucose, however. CONCLUSIONS: Bisphosphonate treatment for osteoporosis reduced OC, but this change was not associated with changes in glucose metabolism.