United Rapid Urease Test Is Superior than Separate Test in Detecting Helicobacter pylori at the Gastric Antrum and Body Specimens.

BACKGROUND/AIMS: The rapid urease test (RUT) is an invasive method to diagnose Helicobacter pylori infection, which relies on the acquisition and examination of gastric antrum and body tissues. We determined and compared the efficacy of RUT when the tissues were examined separately or after being combined. METHODS: Two hundred and fourteen patients were included and underwent esophagogastroduodenoscopy from July 2008 to June 2010. The separate test was defined as evaluating the status of infectivity of H. pylori from the antrum and body separately; whereas the united test was carried out putting both tissues from the antrum and body in the same RUT kit. All RUTs were read by a single observer 1, 3, 6, 12, and up to 24 hours later. We also got two biopsy specimens stained with hematoxylin and eosin and quantified H. pylori density was calculated on a scale of 0 to 3. RESULTS: Overall positivity for H. pylori was 137 (64%) for the separate test and 148 (69.2%) for the united test (p<0.01). The mean time to a positive test was 3.58 hours for the separate test and 1.69 hours for the united test (p<0.01). The correlation between the time to positive RUT and the severity of histology showed r=+0.556 for the antrum (p<0.01) and r=+0.622 for the body (p<0.01). CONCLUSIONS: Combining tissues prior to RUT enhances the detection of H. pylori, as compared with the examination of separate tissues, and shortens the time to develop a positive reaction by approximately 50%. These diagnostic advantages are also accompanied by increased cost-savings.

[A case of perforated xanthogranulomatous cholecystitis presenting as biloma].

Xanthogranulomatous cholecystitis is an unusual inflammatory disease of the gallbladder characterized by severe proliferative fibrosis and the accumulation of lipid-laden macrophages in areas of destructive inflammation. Its macroscopic appearance may occasionally be confused with gallbladder carcinoma. We present a case of perforated xanthogranulomatous cholecystitis presenting as biloma. An 80-year-old woman was referred to our hospital with a 1-week history of abdominal pain and febrile sensation. Abdominal CT showed a biloma in the subhepatic area. The follow-up CT showed that the biloma increased in size. Therefore, ultrasonography-guided aspiration was performed. The aspirated fluid/serum bilirubin ratio was greater than 5, which was strongly suggestive of bile leakage complicated by perforated cholecystitis. She underwent a laparoscopic cholecystectomy with cyst aspiration and adhesiolysis. A histological diagnosis of perforated xanthogranulomatous cholecystitis was made.

The impact of generic clopidogrel bisulfate on platelet inhibition in patients with coronary artery stents: results of the ACCEL-GENERIC study.

BACKGROUND/AIMS: In patients with coronary artery stents, the cost of clopidogrel has been cited as a factor in the premature discontinuation of therapy. Thus, the introduction of lower-cost generic clopidogrel may increase patient compliance. However, platelet inhibition by generic clopidogrel has not been compared to the original clopidogrel formulation in patients with coronary artery stents. METHODS: We prospectively enrolled 20 patients receiving chronic therapy with the original clopidogrel bisulfate (Plavix). After assessing patient compliance with Plavix, maintenance therapy was switched to generic clopidogrel bisulfate (Plavitor). Platelet reactivity was assessed at baseline and 30-day after the switch using conventional aggregometry and the VerifyNow P2Y12 assay. RESULTS: All patients completed maintenance therapy with Plavitor. Before and after switching therapy maximal (36.5 +/- 7.9% vs. 39.8 +/- 16.2%, p = 0.280) and late platelet aggregation (23.5 +/- 10.9% vs. 29.1 +/- 18.3%, p = 0.156) with 5 micromol/L adenosine diphosphate (ADP) stimulus did not differ. Likewise, 20 micromol/L ADP-induced platelet aggregation and P2Y12 reaction unit in patients on Plavitor therapy was comparable to that in patients on Plavix therapy. However, Bland-Altman analysis showed wide limits of agreement between measured platelet reactivity on Plavix vs. Plavitor therapies. CONCLUSIONS: Among patients on Plavix maintenance therapy with coronary stents, replacement with Plavitor shows a comparable inhibition of ADP-induced platelet aggregation. However, due to poor inter-therapy agreement, between two regimens, physicians may be cautious when introducing generic clopidogrel bisulfate.

The impact of smoking on post-clopidogrel platelet reactivity in patients with acute myocardial infarction.

BACKGROUND AND OBJECTIVES: Smoking increases inhibition of clopidogrel-induced platelet reactivity in patients undergoing elective coronary stenting. However, an association between pre-admission smoking (PS) and post-clopidogrel platelet reactivity in patients with acute myocardial infarction (AMI) has not been determined. SUBJECTS AND METHODS: Study cohorts were recruited from a pool of patients at our hospital who were undergoing coronary stenting for AMI (n=134). Immediately after arrival at the emergency room (ER), all patients received a 600 mg loading dose of clopidogrel followed by a maintenance dose of 75 mg/day. Platelet aggregation was measured with light transmittance aggregometry (LTA) after addition of 5 or 20 micromol/L adenosine diphosphate (ADP). RESULTS: Maximal platelet aggregation (Agg(max)) was lower in PS patients after 5 micromol/L ADP (43.6+/-15.7% vs. 48.4+/-12.5%, p=0.096) and 20 micromol/L ADP stimuli (56.2+/-15.6% vs. 61.3+/-11.6%, p=0.073) compared with non-smoking (NS) patients. However, there were no differences in 5 micromol/L (42.6+/-16.3% vs. 43.8+/-15.6%, p=0.776) and 20 micromol/L ADP-induced Agg(max) (54.8+/-14.3% vs. 56.5+/-15.9%, p=0.692) between PS patients <0.5 pack/day and >/=0.5 pack/day. Although more PS patients met the criteria for low post-clopidogrel platelet reactivity (LPPR) (

Implantable cardioverter-defibrillator implantation in a patient with atrial standstill.

We report a 55-year-old female patient who presented with no P waves but with a wide QRS complex escape rhythm at 44 beats/min and prolonged QTc of 0.55 seconds on ECG. The patient had recurrence of ventricular fibrillations and loss of consciousness, and underwent defibrillation and cardiopulmonary resuscitation (CPR) several times because of cardiac arrest. The transthoracic echocardiography showed dilated cardiomyopathy and enlargement of both atria. The Doppler echocardiography documented the absence of A wave in the tricuspid and mitral valve flow. An electrophysiologic study demonstrated electrical inactivity in the right and left atria. Atrial pacing with maximum output did not capture the atria. These findings together with her electrocardiographic finding indicated atrial standstill. Sudden cardiac death was her first clinical manifestation of ventricular arrhythmia. The patient remained asymptomatic after receiving a single chamber implantable cardioverter-defibrillator (ICD) with VVI pacemaker function.