Clinical Utility of the Meal Tolerance Test in the Care of Patients with Type 2 Diabetes Mellitus.

Objective The measurement of C-peptide immunoreactivity (CPR) is essential for evaluating the pancreatic ß-cell function and selecting appropriate therapeutic agents in patients with diabetes mellitus. The meal tolerance test (MTT) is simple to administer physiological insulin-stimulating test. Previous studies have reported that several CPR-related indices are useful markers for predicting insulin requirement in type 2 diabetes. In the present study, we investigated the serum CPR response during the MTT in hospitalized patients with type 2 diabetes mellitus in order to clarify the clinical utility of the MTT. Methods We performed the MTT using a test meal with timed measurements of the serum CPR level based on the oral glucose tolerance test over 180 minutes and tested the correlation of various CPR-related indices and clinical factors in patients with type 2 diabetes mellitus. Patients The subjects were patients with type 2 diabetes mellitus who had been admitted to our hospital for diabetes management and education. The final study population consisted of 68 patients. Results The fasting CPR level was correlated with the 24-hour urinary CPR excretion and body mass index. The serum CPR level at 120 minutes in the MTT was strongly correlated with the area under the curve of CPR during the MTT. The patients who needed insulin therapy at 6 months after hospitalization showed a significant lower incremental CPR value from 0 to 120 minutes in the MTT than those who did not need insulin therapy. Conclusion The plasma C-peptide levels at 0 and 120 minutes in the MTT provide essential information for the clinical management of patients with type 2 diabetes mellitus.

Duodenal cancer in a young patient with Peuts-Jeghers syndrome harboring an entire deletion of the STK11 gene.

A 21-year-old woman with Peuts-Jeghers syndrome (PJS) was referred to our hospital for gastrointestinal surveillance. She had been diagnosed as having PJS from a young age based on her family history and the presence of mucocutaneous pigmentation on her lips and oral mucosa. Her mother and brother had PJS harboring an entire deletion of the STK11 gene. She had tetralogy of Fallot, atrial tachycardia, sick sinus syndrome, and mental retardation in her past history. Esophagogastroduodenoscopy identified a protruded lesion with a depressed area that occupied the lumen half-circumferentially in the duodenal second portion and also showed a 10-mm protruded lesion on the anterior wall of the lower gastric body. Colonoscopy revealed a 3-mm protruded lesion on the rectum. No polyp was found in a barium small bowel series. Biopsies were taken from the duodenal tumor and gastric and colon polyps. Histopathologically, the duodenal tumor revealed a well-differentiated tubular adenocarcinoma, whereas gastric and colon polyps showed hamartomatous polyp. Therefore, subtotal stomach-preserving pancreatoduodenectomy was performed, and subsequent histopathological examination revealed that the duodenal tumor consisted of hamartomatous polyp and a well-differentiated tubular adenocarcinoma with invasion to the muscularis propria. Immunohistochemistry revealed accumulation of nuclear p53 protein, but no accumulation of nuclear ß-catenin protein. No RAS mutation was detected. Furthermore, direct sequencing of the STK11 gene in genomic DNA from peripheral blood mononuclear cells did not detect any mutation initially. However, multiplex ligation-dependent probe amplification (MLPA) analysis revealed entire deletion of STK11. These findings suggest that entire deletion of the STK11 gene caused hamartomatous polyps in the entire gastrointestinal tract and, subsequently, duodenal polyps likely gave rise to cancer through p53 mutation.