Actinobacillus actinomycetemcomitans isolated from young Chinese adults with aggressive periodontitis

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Characterization of Actinobacillus actinomycetemcomitans isolated from young Chinese aggressive periodontitis patients

Objective: This study characterized Actinobacillus actinomycetemcomitans isolates from young Chinese aggressive periodontitis patients. Methods: Subgingival plaque samples (two/subject) were collected from diseased subjects < 25 years old (n = 9, mean age 21.1 ± 1.6 years) and age-matched periodontitis-free controls (n = 47, mean age 22.0 ± 1.1 years). Selective and anaerobic culture were used. The serotype, leukotoxin gene (ltx) operon promoter and the cytolethal distending toxin (cdt) genes complex of the A. actinomycetemcomitans isolates were investigated. Effects of the isolates on non-keratinizing periodontal ligament epithelial cells monolayer were studied. Results: Diseased subjects had significantly higher full-mouth bleeding score (p = 0.002) and total viable counts from plaque samples (7.2 × 10 6 vs. 2.1 × 105 CFU/paperpoint, p < 0.005). A. actinomycetemcomitans was isolated from 67%/56% or 6%/4% of diseased or controls subject/sites, respectively (p < 0.001). The proportion of A. actinomycetemcomitans isolatable from aggressive periodontitis or periodontitis-free associated subgingival plaque was low (0.7% vs. 0.1%, p < 0.02). The serotype of the isolates was characterized. All isolates possessed 652-like ltx gene promoter and all but one serotype c isolate from a diseased patient had intact cdtABC genes. That particular strain appeared to confer the least cellular damages on periodontal ligament epithelial monolayer compared to others. Conclusion: This preliminary study confirmed the notion of increased prevalence and quantity of A. actinomycetemcomitans associated with aggressive periodontitis in young patients. The overall ltx promoter and cdt characteristics of the A. actinomycetemcomitans isolates, however, were similar among the diseased and control groups. A strain lacking the cdtABC gene appeared to be less damaging to a periodontal ligament epithelial cell model. Further studies therefore are warranted to clarify the pathogenic role and potentials of A. actinomycetemcomitans in aggressive periodontitis. © Blackwell Munksgaard 2005.published_or_final_versio

Use of biologics for inflammatory bowel disease in Hong Kong: consensus statement

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Dysphagia as a manifestation of esophageal tuberculosis: a report of two cases

<p>Abstract</p> <p>Introduction</p> <p>Esophageal involvement by <it>Mycobacterium tuberculosis </it>is rare and the diagnosis is frequently made by means of an esophageal biopsy during the evaluation of dysphagia. There are few cases reported in the literature.</p> <p>Case presentation</p> <p>We present two cases of esophageal tuberculosis in 85- and 65-year-old male Caucasian patients with initial complaints of dysphagia and epigastric pain. Upper gastrointestinal endoscopy resulted in the diagnosis of esophageal tuberculosis following the biopsy of lesions of irregular mucosa in one case and a sessile polyp in the other. Pulmonary tuberculosis was detected in one patient. In one patient esophageal stricture developed as a complication. Antituberculous therapy was curative in both patients.</p> <p>Conclusion</p> <p>Although rare, esophageal tuberculosis has to be kept in mind in the differential diagnosis of dysphagia. Pulmonary involvement has important implications for contact screening.</p

Successful treatment of hepatitis C after kidney transplantation with combined interferon alpha-2b and ribavirin

The management of acute hepatitis C virus (HCV) infection after renal transplantation (RT) remains controversial, due to the potential risk of interferon-induced graft dysfunction. There is little experience with combined interferon and ribavirin therapy in this group of patients. We treated four consenting RT recipients who developed acute de novo HCV infection with a combination of interferon-alpha 2b and ribavirin. After 48 weeks' treatment, sustained virologic and biochemical remission were achieved in three patients infected with HCV genotypes 1a, 2, and 6a, respectively. The median time from treatment onset to ALT normalization was 8 weeks. The fourth patient was a non-responder infected with genotype 1b. Dose-dependent hemolysis was the most frequent side-effect. No patient developed allograft dysfunction. Our experience indicates that the judicious use of combined interferon and ribavirin can be considered in selected RT recipients with severe acute hepatitis C infection. © 2003 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.link_to_subscribed_fulltex

Successful treatment of hepatitis C after kidney transplantation with combined interferon alpha-2b and ribavirin

The management of acute hepatitis C virus (HCV) infection after renal transplantation (RT) remains controversial, due to the potential risk of interferon-induced graft dysfunction. There is little experience with combined interferon and ribavirin therapy in this group of patients. We treated four consenting RT recipients who developed acute de novo HCV infection with a combination of interferon-alpha 2b and ribavirin. After 48 weeks' treatment, sustained virologic and biochemical remission were achieved in three patients infected with HCV genotypes 1a, 2, and 6a, respectively. The median time from treatment onset to ALT normalization was 8 weeks. The fourth patient was a non-responder infected with genotype 1b. Dose-dependent hemolysis was the most frequent side-effect. No patient developed allograft dysfunction. Our experience indicates that the judicious use of combined interferon and ribavirin can be considered in selected RT recipients with severe acute hepatitis C infection. © 2003 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.link_to_subscribed_fulltex

One-week antibiotics versus maintenance acid suppression therapy for Helicobacter pylori-associated peptic ulcer bleeding

Bleeding peptic ulcer is the most important cause of upper gastrointestinal bleeding. Our aim was to compare the effect of anti- Helicobacter therapy with maintenance treatment of H 2-receptor antagonist in the prevention of relapses of ulcer and bleeding. Patients with bleeding duodenal or gastric ulcers and H. pylori infection were randomized to receive either a one-week course of triple therapy with bismuth subcitrate, metronidazole, and tetracycline plus ranitidine or a six-week course of ranitidine 300 mg/day. After the ulcers healed, the antibiotic-treated patients were not given any medication, whereas the ranitidine-treated patients continued to receive a maintenance dose of 150 mg/day. One hundred twenty-six patients were randomized to receive anti-Helicobacter therapy and 124 patients to receive long-term ranitidine. H. pylori eradication was achieved in 98.2% in those who received triple therapy and 6.1% in those who received ranitidine (P < 0.0001). At the six-week follow-up, ulcer healing was documented in 88.2% in those who received triple therapy and 86.1% in those who received ranitidine (P = 0.639). Recurrent ulcer developed in nine of the ranitidine-treated patients and three of them presented with recurrent upper gastrointestinal bleeding. One patient in the antibiotic group developed recurrent ulcer without rebleeding (P = 0.01). It is concluded that eradication of H. pylori is sufficient for the prevention of recurrent bleeding ulcers.link_to_subscribed_fulltex

Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen

Background: Many patients who have had upper gastrointestinal bleeding continue to take low-dose aspirin for cardiovascular prophylaxis or other non-steroidal antiinflammatory drugs (NSAIDs) for musculoskeletal pain. It is uncertain whether infection with Helicobacter pylori is a risk factor for bleeding in such patients. Methods: We studied patients with a history of upper gastrointestinal bleeding who were infected with H. pylori and who were taking low-dose aspirin or other NSAIDs. We evaluated whether eradication of the infection or omeprazole treatment was more effective in preventing recurrent bleeding. We recruited patients who presented with upper gastrointestinal bleeding that was confirmed by endoscopy. Their ulcers were healed by daily treatment with 20 mg of omeprazole for eight weeks or longer. Then, those who had been taking aspirin were given 80 mg of aspirin daily, and those who had been taking other NSAIDs were given 500 mg of naproxen twice daily for six months. The patients in each group were then randomly assigned separately to receive 20 mg of omeprazole daily for six months or one week of eradication therapy, consisting of 120 mg of bismuth subcitrate, 500 mg of tetracycline, and 400 mg of metronidazole, all given four times daily, followed by placebo for six months. Results: We enrolled 400 patients (250 of whom were taking aspirin and 150 of whom were taking other NSAIDs). Among those taking aspirin, the probability of recurrent bleeding during the six-month period was 1.9 percent for patients who received eradication therapy and 0.9 percent for patients who received omeprazole (absolute difference, 1.0 percent; 95 percent confidence interval for the difference, -1.9 to 3.9 percent). Among users of other NSAIDs, the probability of recurrent bleeding was 18.8 percent for patients receiving eradication therapy and 4.4 percent for those treated with omeprazole (absolute difference, 14.4 percent; 95 percent confidence interval for the difference, 4.4 to 24.4 percent; P=0.005). Conclusions: Among patients with H. pylori infection and a history of upper gastrointestinal bleeding who are taking low-dose aspirin, the eradication of H. pylori is equivalent to treatment with omeprazole in preventing recurrent bleeding. Omeprazole is superior to the eradication of H. pylori in preventing recurrent bleeding in patients who are taking other NSAIDs, such as naproxen. Copyright © 2001 Massachusetts Medical Society.link_to_subscribed_fulltex

Treatment of hepatitis C in kidney transplant recipients with interferon alpha-2b plus ribavirin

Session B. Clinical Nephrology - B7. Hepatitis in glomerular disease, dialysis and transplant patientsLimited data is available for the treatment of hepatitis C virus (HCV) infection in renal allograft recipients, in whom interferon therapy is generally regarded as contraindicated due to potential risks of acute rejection or graft dysfunction. We treated 4 patients who acquired acute hepatitis C in the perioperative period of kidney transplantation. All four patients, who were not HCV carriers before renal transplantation, developed acute transaminitis with negative anti-HCV serology, but positive circulating HCV RNA detectable by PCR. All patients were on cyclosporin-based immunosuppressive protocol. They received interferon alpha-2b (3 MU s.c. thrice weekly) and ribavirin (800-1200 mg p.o. daily according to body weight and hemoglobin levels) treatment. As shown in Table 1, three patients had complete remission with normalization of serum alanine aminotransferase (ALT) level within 4-12 weeks of therapy, and disappearance of serum HCV RNA at 24 and 48 weeks of starting therapy. Two of them had persistently undetectable HCV RNA at 24 weeks after cessation of therapy, while one had just completed the 48-week treatment at the time of writing. The non-responder, in whom treatment was stopped after 24 weeks due to persistent HCV-viremia, was infected with HCV gentotype 1b, which is known to be associated with a less favorable treatment response. All patients had stable renal allograft function throughout the course of treatment. Ribavirin-induced hemolysis, which was dose-dependent, was the most common side-effect. We conclude that combination interferon/ribavirin therapy can be a valid therapeutic option in renal transplant recipients with hepatitis C, but the decision on treatment should take into consideration the severity, progression, and prognosis of the hepatitis, the potential efficacy based on the HCV genotype, and the risk of inducing allograft dysfunction.Link_to_subscribed_fulltex