A Case of Extramedullary Progression Despite of Serologic Improvement in a Patient Treated with Thalidomide for Multiple Myeloma

Thalidomide is an anti-angiogenic agent widely used in patients with multiple myeloma. The response to therapy is commonly monitored using serum and/or urine M protein, as these are known to reflect the tumor burden. Although extramedullary plasmacytomas are tissues with high neovascularization, it has been suggested in some reports that the response to thalidomide in these patients may be inferior, despite changes in the serum M protein level. Herein, we report the case of a patient who newly developed hepatosplenic extramedullary plasmacytoma, despite reduction in the serum M protein level following thalidomide treatment.

Gastric pH and Helicobacter pylori Infection in Patients with Liver Cirrhosis / 대한간학회지

BACKGROUND/AIMS: Data from previous studies on gastric acid secretion and the prevalence of H. pylori in liver cirrhosis patients remain poorly defined. H. pylori is a potential source of NH3, but the possible role of H. pylori in hepatic encephalopathy is not clear. The purpose of this study was to compare gastric acid secretion, the impact of H. pylori infection, and the production of NH3 between cirrhotic patients and healthy, matched controls. METHODS: Twenty-nine patients with liver cirrhosis (HBV, n=12; Alcohol, n=12; HCV, n=5) were matched with 33 healthy persons for age and sex. None of the patients or controls were being treated with antacids, H2-receptor blockers or proton pump inhibitors. The pH and NH3 concentration was measured in gastric juice obtained by endoscopy. H. pylori infection was diagnosed using the rapid urease test. The level of NH3 in venous blood was also measured. RESULTS: The average gastric pH was significantly higher in cirrhosis patients compared to controls (3.91 vs. 2.99, P4) was significantly greater in cirrhosis patients (45 vs. 21%, P<0.05). In contrast, the prevalence of H. pylori infection (62% vs. 58%) and gastric NH3 concentrations (3.4 vs. 3.3 mM/L) were similar between both groups. However, venous NH3 levels were significantly higher in cirrhotics than in controls (63.1 vs. 25.2 micro M/L, P<0.05). The patients with H. pylori infection had significantly higher gastric NH3 concentration (3.8 vs. 1.6 mM/L) and gastric pH (3.87 vs. 2.76, P<0.05) than those without infection, but no significant difference in venous NH3 levels were detected (39.6 vs. 48.1 micro M/L). In patients with cirrhosis, the presence of H. pylori infection was not correlated with either gastric or blood NH3 levels. CONCLUSIONS: The gastric pH of liver cirrhosis patients is higher than that of controls and a larger proportion of cirrhotic patients have hypochlorhydria. The prevalence of H. pylori in liver cirrhosis patients was similar to that in controls and no correlation was found between gastric and blood NH3 levels. Thus, H. pylori infection does not seem to play a major role in generation of elevated NH3 associated with hepatic encephalopathy.