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Background Postprandial syndrome is characterized by hunger, weakness and anxiety neurosis occurring after meals. Although abnormal glucagon response has been suggested, inaccuracies of the conventional glucagon measurement method have prevented from precise analysis. Recently, a more reliable dual-antibody sandwich enzyme-linked immunosorbent assay for glucagon has been developed. Methods We conducted a 75 g oral glucose tolerance test (OGTT) extending to 4 hours in 14 patients with idiopathic postprandial syndrome. In addition to blood glucose and insulin, we have measured glucagon concentrations using the novel method and analyzed retrospectively. Results Median (lower quartile, upper quartile) of age and BMI were 40 years old (30, 49) and 24.9 (23.1, 26.2), respectively. The OGTT revealed that one patient had a diabetic pattern, and two were glucose intolerant. Fasting insulin was 7.6 μU/mL (6.8, 8.8) and reached 73.7 (54.3, 82.6) at 30 min. Insulin remained elevated until 180 min. The fasting glucagon was 21.1 pg/mL (16.1, 33.8), falling at 60 min to a nadir of 6.9 (3.5, 10.3), one-third of the baseline, then remaining suppressed until 180 min. Furthermore, we have found that two types of glucagon dynamics: one is lower fasting glucagon with further suppression and the other is normal or higher fasting glucagon with subsequent big drop. Conclusions These data suggest that glucagon suppression is stronger in patients with idiopathic postprandial syndrome than in normal subjects previously reported. The present data will contribute to further understanding and future research of this syndrome.

Cancer stem-like cells (CSCs) with high expression of CD44 splice variant (CD44v) have an enhanced capacity for intracellular reduced glutathione synthesis and defense against reactive oxygen species, resulting in resistance to various therapeutic stresses. Sulfasalazine (SSZ), a drug used in the treatment of rheumatoid arthritis (RA), inhibits glutamate–cystine transport, and suppressed CD44v-dependent tumor growth and increased sensitivity to cytotoxic drugs in an in vivo study. Here, we present two cases of CD44v9-positive urogenital cancer with concomitant treatment with SSZ for RA. Patient 1 was a 62-year-old man who had received SSZ for RA beginning 2 months before the diagnosis of urinary bladder cancer. Although he had multiple metastases to the bladder, abdominal, left cervical and left axillary lymph nodes, and brain, complete response with multidisciplinary therapy was maintained for more than 2 years. Patient 2 was a 74-year-old man with castration-resistant prostate cancer who was diagnosed with RA during chemotherapy and a gradual increase in prostate-specific antigen (PSA) level. When SSZ was added, his PSA value (ng/mL) decreased from 12.93 to 5.58 in only 2 weeks and then quickly rebounded, whereas levels of neuron-specific enolase, a neuroendocrine differentiator and CSC marker, remained almost unchanged. We therefore speculate that SSZ treatment may represent a new adjuvant treatment option for patients with CD44v9-positive urogenital cancer.