[Analysis of Hepatitis B Virus Reactivation in Fukuoka University Hospital].

Immunosuppressive therapy or chemotherapy-induced hepatitis B virus (HBV) reactivation can cause se- vere hepatitis in inactive HBV carriers or patients with resolved infection. We surveyed patients with measured HBV DNA levels from 2009 to 2014, and analyzed the clinical profile, treatment regimen and the period leading up to HBV reactivation from therapy start date. Between 2009 and 2014, the total number of HBV viral load measurements taken in our hospital increased 2.3-fold. HBV DNA measurements requested by the Department of Gastroenterology and Hepatology ac- counted for 82.8% of the total in 2009; however, this was reduced to 38.0% in 2014, as the number of re- quests from other departments increased. We referred all patients with reactivated HBV infection to a hepatology specialist. The total number of reactivation patients in 2014 was increased to about 8.2 times that observed in 2009. Nineteen males and 24 females were included in our cohort, and the average age was 69±10.1 years old. Thirty-two patients had previously received chemotherapy, and seven had undergone immunosuppressive treatment. A delay of more than 12 months from commencement of therapy to HBV reactivation was observed in 49% of patients. These results indicate that it is very important to monitor HBV DNA and properly enforce pre-treatment examinations according to the guidelines for prevention and treatment of HBV during immunosuppressive therapy. [Original].

A Hospital-Based Analysis in the Department of Clinical Chemistry for the Patients with HBV Reactivation after Anti-Cancer or Immunosuppressive Therapy.

OBJECTIVES: Anti-cancer and immunosuppressive drugs often induce hepatitis B virus (HBV) reactivation, resulting in lethal hepatitis in the worst cases. It is to elucidate the clinical characteristics of the patients in our hospital, who underwent HBV-related examinations to help prevent HBV-associated hepatitis by reactivation during the two-year period after the announcement of new guidelines by the Ministry of Health, Labour and Welfare of Japan in January 2009. STUDY DESIGN: We enrolled 811 patients who were examined for HBs antigen, anti-HBc antibody, anti-HBs antibody and HBV DNA regarding HBV reactivation. RESULTS: The underlying diseases were hematological malignancies, followed by various other cancers, rheumatoid arthritis, Crohn's disease, and so on. The patients in their 60s showed the peak in the age distribution. The positive ratio of anti-HBc antibody was higher over the age of 40. The rate of reactivation was 7.7% in HBV carriers and 2.0% in the HBV-resolved patients. HBV reactivation occurred in two HBV carriers and four HBV-resolved patients. The three patients, showing hepatitis were two HBV carriers and one HBV-resolved patient without monitoring of HBV DNA, because their therapies started before announcement of the guidelines. In other three patients with reactivation from HBV-resolved infections, HBV DNA returned under detection by immediate administration of entecavir without following hepatitis. CONCLUSION: The patients at high risk of HBV reactivation were prevented from HBV-related hepatitis only by following the guideline. The screening for such patients and monitoring HBV DNA in the guideline are requisite to prevent HBV-related hepatitis.

A novel mutation of CLCNKB in a Japanese patient of Gitelman-like phenotype with diuretic insensitivity to thiazide administration.

The clinical phenotypes of patients with Bartter syndrome type III sometimes closely resemble those of Gitelman syndrome. We report a patient with mild, adult-onset symptoms, such as muscular weakness and fatigue, who showed hypokalemic metabolic alkalosis, elevated renin-aldosterone levels with normal blood pressure, hypocalciuria and hypomagnesemia. She was also suffering from chondrocalcinosis. A diuretic test with furosemide and thiazide showed a good response to furosemide, but little response to thiazide. Although the clinical findings and diuretic tests predicted that the patient had Gitelman syndrome, genetic analysis found no mutation in SLC12A3. However, a novel missense mutation, p.L647F in CLCNKB, which is located in the CBS domain at the C-terminus of ClC-Kb, was discovered. Therefore, gene analyses of CLCNKB and SLC12A3 might be necessary to elucidate the precise etiology of the salt-losing tubulopathies regardless of the results of diuretic tests.

[Antimicrobial susceptibility patterns of Pseudomonas aeruginosa isolated from 2006 to 2008 in Fukuoka University Hospital].

Pseudomonas aeruginosa has been reported to be a leading cause of nosocomial infections. We evaluated the characteristics using 903 P. aeruginosa strains that were isolated in Fukuoka University Hospital from 2006 to 2008. Clinical specimens of P. aeruginosa were detected 47.8% from respiratory tract, 24.4% from urine, and were detected from the pus by 18.9%. Age distribution of the patients was 70 years old or older. Antimicrobial susceptibility ratio of isolates of P. aeruginosa from the outpatients against all agents tested except amikacin had more susceptible than it of isolates from the inpatients. In P. aeruginosa isolates detected from the inpatients, susceptibilities to other antibiotics were about 60% though 93.3% and 83.2% were susceptible to amikacin and piperacillin/tazobactam respectively. Isolation rate of multidrug-resistant P. aeruginosa (MDRP) in all clinical isolates was 3.3%. The report of carbapenem use was obligated in our hospital from the experience of the outbreak by MDRP in 2007, and the infection control team came to regulate the administering of antimicrobial agents more than before. Afterwards, the amounts of the antimicrobial agent use except piperacillin/tazobactam have decreased to 69% compared with the previous year. The susceptibility rates of various antimicrobial agents except amikacin have recovered by 10-17%. These results suggest that there is a necessity for attending to the drug susceptibility and the amount of the antimicrobial agent use.