A Case of Psoas Muscle Abscess in Crohn's Disease / 대한소화기내시경학회지

Psoas abscess, complicating Crohn's disease, is a rare condition. Typical symptoms and signs are fever, abdominal tenderness and limb pain. Our patient had fever and abdominal tenderness. The diagnosis is made by abdominopelvic CT scan. Medical therapy with antibiotics, surgical resection of the affected bowel segment with end to end anastomosis and surgical drainage of focus are treatment of choice. We have experienced one case of psoas abscess with Crohn's disease in 28-year-old male patient. He visited our hospital due to diarrhea and lower abdominal pain. The colonoscopy revealed active stage of Crohn's disease. Then he has taken methyl prednisolone and mesalazine. During the hospitalization, we detected anal fistula and psoas abscess on abdominal CT. He was managed with antibiotics and surgical drainage after colectomy. We present the case with brief review of the articles.

Expression of Mucosal Cyto-Chemokine mRNAs in Patients with Helicobacter pylori Infection

BACKGROUND: Helicobacter pylori-induced destruction of the gastroduodenal mucosal barrier is initiated with mucosal infiltration of inflammatory cells. Cytokines and chemokines have been suggested to play important roles in the migration and activation of these inflammatory cells into the mucosa. The present study aimed to investigate expression rates of cyto-chemokine mRNAs using gastric mucosal biopsy specimens. METHODS: In 98 patients infected with Helicobacter pylori, mucosal mRNA expression rates of cytokines (IL-1beta, IL-6, and IL-10), C-C chemokines (macrophage inflammatory protein 1alpha [MIP-1alpha], and macrophage inflammatory protein 1beta [MIP-1beta], monocyte chemotactic and activating factor [MCAF], regulated on activation, normal T cell expressed and presumably secreted [RANTES]) and C-X-C chemokines (IL-8 and growth regulated alpha [GRO-alpha]) were examined using reverse transcription polymerase chain reaction (RT-PCR). RESULTS: The expression rates of mRNA for IL-8, GRO-alpha, MIP-1alpha and RANTES were significantly more increased in H. pylori-positive patients than in H. pylori- negative patients. However, the expressions of IL-1beta, IL-6 and IL-10 mRNA were statistically not different between two groups. After eradication of H. pylori, expressions of mRNA for three cytokines (IL-1beta, IL-6 and IL-10), four C-C chemokines (MIP-1alpha, MIP-1beta, MCAF and RANTES) and two C-X-C chemokines (IL-8 and GRO-alpha) were significantly decreased. CONCLUSION: These results suggest that C-X-C chemokines and some C-C chemokines play important roles in H. pylori-associated peptic ulcer diseases.

Antimicrobial resistance rate of Helicobacter pylori isolates and detection of mechanism of clarithromycin resistance / 대한내과학회지

BACKGROUND: Antimicrobial resistance is considered as the primary reason for eradication failure of Helicobacter pylori. Resistance to clarithromycin is mostly due to the point mutation in H. pylori 23S rRNA gene. The aims of this study were to determine the primary resistance rate to clarithromycin and metronidazole and to examine the mechanism of clarithromycin resistance in H. pylori isolates. METHODS: Seventy-nine strains were isolated from 73 patients within about five years. The susceptibility of H. pylori isolates to clarithromycin and metronidazole were tested by E-test and broth dilution test. To detect point mutations in the 23S rRNA gene, PCR-RFLP (restriction fragment length polymorphism) was performed. Mutations in clarithromycin-resistant strains also were analyzed by direct sequencing. RESULTS: The resistance rate to clarithromycin (>1 mg/L) and metronidazole (>8 mg/L) were 5.1% and 54.4%, respectively. Annual metronidazole-resistant rates were 43.7% (7/16) in 1996-1997, 61.1% (11/18) in 1998, 55.6% (5/9) in 1999, and 55.6% (20/36) in 2000. Annual clarithromycin- resistant rates were 6.3% (1/16) in 1996-1997, 0% (0/18) in 1998, 11.1% (1/9) in 1999, and 5.6% (2/36) in 2000. Two of 4 clarithromycin-resistant isolates contained the A2144G mutation. One isolate contained A2143G mutation. One isolate possibly contained T2183C mutation. Different strains, isolated separately from antrum and body in 6 patients, showed same susceptibility to clarithromycin. However, different strains in two patients showed different susceptibility to metronidazole. CONCLUSION: No significant increase of resistantce rate to both clarithromycin and metronidazole were found within recent five years. Resistance of H. pylori to clarithromycin was caused by A2144G and A2143G mutation mainly and by T2183C mutation possibly.