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Selected AbstractsFulminant JC virus encephalopathy with productive infection of cortical pyramidal neurons,ANNALS OF NEUROLOGY, Issue 6 2009Christian Wüthrich PhD The polyomavirus JC (JCV) is the causative agent of progressive multifocal leukoencephalopathy and of JCV granule cell neuronopathy. We present a human immunodeficiency virus,negative patient who experienced development of multiple cortical lesions, aphasia, and progressive cognitive decline after chemotherapy for non,small-cell lung cancer. Brain biopsy and cerebrospinal fluid polymerase chain reaction demonstrated JCV, and she had a rapidly fatal outcome. Postmortem analysis showed diffuse cortical lesions and areas of necrosis at the gray,white junction. Immunostaining showed a productive JCV infection of cortical pyramidal neurons, confirmed by electron microscopy, with limited demyelination. This novel gray matter syndrome expands the scope of JCV clinical presentation and pathogenesis. Ann Neurol 2009;65:742,748 [source] Effect of Point-of-care Influenza Testing on Management of Febrile ChildrenACADEMIC EMERGENCY MEDICINE, Issue 12 2006Srikant B. Iyer MD Abstract Objectives To determine the effect of point-of-care testing (POCT) for influenza on the physician management of febrile children who are at risk for serious bacterial illness (SBI) on the basis of age and temperature and who are presenting to a pediatric emergency department (ED) during an influenza outbreak. Methods Patients 2,3 months of age with temperature of ,38°C and patients 3,24 months of age with temperature of ,39°C who were presenting to a pediatric ED during an influenza outbreak were enrolled into a prospective, quasi-randomized, controlled trial. Influenza testing was performed on enrolled patients by either the POCT or the standard-testing (ST) methods. The two groups were compared in terms of laboratory testing, chest radiography, antibiotic use, visit-associated costs, pediatric ED lengths of stay, inpatient admission, and return visits to the pediatric ED. Similar analyses also were performed on the resulting subgroups of patients on the basis of method of testing (POCT or ST) and test result (positive or negative). Results Of 767 eligible patients, 700 (91%) completed the study. No significant differences were demonstrated between the POCT and ST groups with respect to laboratory tests ordered, chest radiographs obtained, antibiotic administration, inpatient admission, return visits to the pediatric ED, lengths of stay, or visit-associated costs. In the subgroup analysis, the adjusted odds ratios (ORs) for blood culture in influenza test,positive to ,negative patients were 0.59 and 0.71 in the POCT and ST groups, respectively (p = 0.088). The adjusted ORs for urine culture in influenza test,positive to ,negative patients were 0.46 and 0.67 in the POCT and ST groups, respectively (p = 0.005). Conclusions When using a strategy of performing influenza testing on all patients at risk for SBI who presented to a pediatric ED during an influenza outbreak, the method of testing (POCT or ST) did not appear to significantly alter physician management, cost, or length of stay in the pediatric ED. However, if the interaction of the method of testing and the test result (positive or negative) were considered, a positive POCT for influenza was associated with a significant reduction in orders for urinalyses and urine cultures. [source] Cr(III) reactivity and foot dermatitis in Cr(VI) positive patientsCONTACT DERMATITIS, Issue 3 2006Malene Barré Hansen Chromium allergy has become synonymous with Cr(VI) allergy. However, real exposure to chromium from leather products may include both Cr(III) and Cr(VI). In this study, we investigate the reactivity to both Cr(VI) and Cr(III) in consecutive patients to analyse the relation between foot eczema/leather exposure and reactivity to Cr(III). From March 2002 to December 2004, 2211 consecutive patients with suspected allergic contact dermatitis were patch tested with 0.5% potassium dichromate (Cr(VI)) and 13% chromium trichloride (Cr(III)). A total of 71 (3.2%) patients had a positive reaction to Cr(VI), of which 31 also had a positive Cr(III) reaction. No Cr(VI) negative patients had a positive reaction to Cr(III). An increased risk of foot dermatitis was found in Cr(VI) positive patients with a concomitant positive or doubtful reaction to Cr(III) compared with Cr(VI) positive patients with no reactions to Cr(III). The increased risk was not due to a higher degree of sensitivity to Cr(VI). Leather was reported most frequently as the suspected cause of chromium dermatitis (54%). However, Cr(VI) allergics having foot eczema and positive or doubtful Cr(III) reactions often had positive reactions to other shoe allergens. Thus, Cr(III) allergy is part of a multiple shoe allergy pattern. [source] ENDOSCOPIC MICROVASCULAR ARCHITECTURE OF THE PORTAL HYPERTENSIVE GASTRIC MUCOSA ON NARROW BAND IMAGINGDIGESTIVE ENDOSCOPY, Issue 3 2007Seishu Hayashi Background:, We evaluated the endoscopic microvascular architecture of the gastric mucosa in portal hypertension patients using the prototype of narrow band imaging (NBI). Material and Methods:, The study included 103 Helicobacter pylori -negative patients with chronic liver disease (22 without portal hypertension (group 1), 81 with portal hypertension (group 2)). Results:, (i) Abnormality of collecting venules, reddening mucosa, red spots, a mosaic-like pattern, and gastric antral vascular ectasia (GAVE) were observed on the gastric mucosa, and an obscure change in collecting venules (73% vs 14%; P < 0.001), reddening mucosa (49% vs 5%; P < 0.001), red spots (36% vs 5%; P < 0.01) and a mosaic-like pattern (40% vs 5%; P < 0.01) were more frequently observed in group 2 than in group 1. (ii) On magnifying endoscopy with NBI, the mucosa with an obscure change in collecting venules was demonstrated as dilation of the capillaries surrounding the gastric pits in various degrees, and reddening mucosa was observed as extended and swollen gastric pits and various degrees of dilated and convoluted capillaries surrounding the gastric pits. Red spots were demonstrated as extended and swollen gastric pits, dilated and convoluted capillaries surrounding the gastric pits, and intramucosal hemorrhage around these capillaries. GAVE was recognized as partial and marked dilatation of the capillaries surrounding the gastric pits. Conclusion:, Abnormality of collecting venules, swelling of gastric pits, dilatation of capillaries surrounding the gastric pits, intramucosal hemorrhage around capillaries, and partial and marked dilatation of the capillaries were observed on the gastric mucosa in portal hypertension patients. [source] Helicobacter Pylori and Precancerous Gastric LesionsDIGESTIVE ENDOSCOPY, Issue 3 2000Pham Quang Cu Background: To determine the relationship between Helicobacter pylori (H. pylori) infection and the precancerous gastric lesions: atrophic gastritis (AG) and intestinal metaplasia (IM) and dysplasia. Methods: A total of 347 dyspeptic patients, including 141 H. pylori -positive patients and 206 H. pylori -negative patients, were studied alongside age- and sex-matched controls. The patients underwent gastroscopy and endoscopic biopsy for detection of H. pylori, and histological examinations. Helicobacter pylori was detected by a urease test (CLO; Delta West; Bentley, Australia), by histology (H&E stain, Giemsa) and by serology (BioSig; BioMeditech, NJ, USA). Atrophic gastritis, IM and dysplasia were detected by histological examination (Giemsa, H&E stain). Results: There is a higher rate of atrophic gastritis in H. pylori -positive than in H. pylori -negative patients (46 vs 13.5%, odds ratio (OR) = 5.4; P < 0.01). Gastritis in H. pylori -positive patients also has a higher rate of activity than in H. pylori -negative patients. The rate of IM is higher in H. pylori -positive patients than in H. pylori -negative patients (35 vs 11%; OR = 4.3; P < 0.01). Metaplasia is more often diffuse in H. pylori -positive than in H. pylori -negative patients. Dysplasia is more common in H. pylori -positive than in H. pylori -negative patients (12 and 3.8%; OR = 3.3; P < 0.01). Conclusions: This study supports the suggestion of a relationship between H. pylori infection and precancerous gastric lesions. Wherever H. pylori is present, the precancerous lesions are more common and more severe. [source] The outcome of a rapid hepatitis B vaccination programme in a methadone treatment clinicADDICTION, Issue 2 2010Parameswaran Ramasamy ABSTRACT Aim Injecting drug users are a high-risk population for hepatitis B (HBV), but are difficult to engage in vaccination programmes. This study examines the completion rates of a HBV vaccination schedule and seroconversion in a group of patients in methadone maintenance treatment. Methods Patients at a public methadone maintenance programme in Sydney, Australia, were screened for viral hepatitis (hepatitis A, B and C) and offered a rapid HBV vaccination schedule (0, 1 and 2 months). Hepatitis B surface antibody (antiHBs) was retested on completion of the vaccination schedule. Results A total of 143 patients [71.3% male, mean age 33.1 (standard deviation ± 8.3)] enrolled in the project. Forty-nine per cent of patients were HAV antibody (Ab) positive, 81.1% hepatitis C virus (HCV) antibody (Ab) positive and 38.9% antiHBs positive. Exposure to multiple hepatitis viruses was common, with 24.5% testing positive for all three viruses. Seventy-three (83%) of the 88 antiHBs negative patients completed the vaccination schedule. Post-vaccination serology indicated a seroconversion rate of 75.4% (55 of 73) of completors, or 62.5% of eligible participants (55 of 88). Conclusion While there was a high rate of completion of the rapid vaccination schedule in this population, a moderate seroconversion rate was achieved. Further work is required to identify an optimal vaccination schedule in opioid substitution patients. [source] Eradication of Helicobacter pylori increases platelet count in patients with idiopathic thrombocytopenic purpura in JapanEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2005T. Inaba Abstract Background, The effect of Helicobacter pylori eradication on the platelet count in patients with thrombocytopenic purpura is controversial. In this multicentre study, we prospectively assessed the effect of H. pylori eradication therapy in idiopathic thrombocytopenic purpura patients. Materials and methods, Thirty-five consecutive patients with chronic idiopathic thrombocytopenic purpura (11 males and 24 females, a median age of 57) were assessed for H. pylori infection by use of a urea breath test. All patients received 1-week triple therapy (amoxicillin, clarithromycin, and lansoprazole) to eradicate H. pylori. At 6 months, idiopathic thrombocytopenic purpura patients with a platelet count recovery of greater than 100 × 109 L,1 were defined as idiopathic thrombocytopenic purpura responders. Results,Helicobacter pylori infection was observed in 25 (71%) of the 35 patients. All infected patients were cured. Eleven patients were identified as idiopathic thrombocytopenic purpura responders; 24 were considered nonresponders. Platelet counts improved by more than 100 × 109 L,1 in 11 (44%) of the 25 patients cured of H. pylori infection, while none of the 10 patients H. pylori -negative patients experienced the same improvement (P = 0·015). Univariate analysis showed that H. pylori infection and its eradication were significant factors associated with platelet recovery (P = 0·015). Conclusions,Helicobacter pylori infection played a role in the pathogenesis of idiopathic thrombocytopenic purpura in approximately 30% of all patients assessed and 45% of the patients with H. pylori infection. Eradication of H. pylori in idiopathic thrombocytopenic purpura patients led to improved disease activity. [source] High risk of hepatitis B-virus reactivation after hematopoietic cell transplantation in hepatitis B core antibody-positive patientsEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 4 2009Kosei Matsue Abstract We investigated the serological changes in hepatitis B virus (HBV)-related markers in 55 and 26 hepatitis B surface antigen (HBsAg)-negative patients undergoing allogeneic and autologous stem cell transplantation, respectively, over the past 4 yr. Five of the 17 allogeneic and one of the five autologous patients with pretransplant anti-hepatitis B core antigen antibodies (anti-HBc) were HBsAg-positive after transplantation, whereas none of the patients negative for anti-HBc were HBsAg-positive in both groups. All patients who became HBsAg-positive received steroid-containing immunosuppressive therapy for chronic graft versus host disease (GVHD) or myeloma. Four of the six patients developed flare of HBV hepatitis, and two patients did not. One patient developed fulminant hepatitis treated with lamivudine and plasma exchange. Other five patients received entecavir from the detection of HBsAg. Although HBV-DNA levels became below the limit of detection in all patients, HBsAg positivity remained in three patients after 6 months of treatment. We concluded that anti-HBc positivity is a risk factor for reactivation of HBV after both autologous and allogeneic transplantation, and HBV-related markers should be monitored regularly in these patients. We also stress the efficacy of pre-emptive use of antiviral agents in controlling HBV replication and limiting hepatic injury due to reactivation of HBV in these patients. [source] Seronegative myasthenia gravis: disease severity and prognosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2005F. Romi Around 10,20% of myasthenia gravis (MG) patients do not have acetylcholine receptor (AChR) antibodies (seronegative), of whom some have antibodies to a membrane-linked muscle specific kinase (MuSK). To examine MG severity and long-term prognosis in seronegative MG compared with seropositive MG, and to look specifically at anti-AChR antibody negative and anti-MuSK antibody negative patients. Seventeen consecutive seronegative non-thymomatous MG patients and 34 age and sex matched contemporary seropositive non-thymomatous MG controls were included in a retrospective follow-up study for a total period of 40 years. Clinical criteria were assessed each year, and muscle antibodies were assayed. There was no difference in MG severity between seronegative and seropositive MG. However, when thymectomized patients were excluded from the study at the year of thymectomy, seropositive MG patients had more severe course than seronegative (P < 0.001). One seropositive patient died from MG related respiratory insufficiency. The need for thymectomy in seronegative MG was lower than in seropositive MG. None of the seronegative patients had MuSK antibodies. This study shows that the presence of AChR antibodies in MG patients correlates with a more severe MG. With proper treatment, especially early thymectomy for seropositive MG, the outcome and long-term prognosis is good in patients with and without AChR antibodies. [source] Comparative analysis of MLL partial tandem duplication and FLT3 internal tandem duplication mutations in 956 adult patients with acute myeloid leukemiaGENES, CHROMOSOMES AND CANCER, Issue 3 2003Christine Steudel Partial tandem duplication (PTD) of the MLL gene and internal tandem duplication (ITD) of the juxtamembrane region of the FLT3 receptor tyrosine kinase gene have been described in acute myeloid leukemia (AML) patients, preferentially in those with normal cytogenetics. These alterations have been associated with a poor prognosis. In our study, we analyzed the prevalence and the potential prognostic impact of these aberrations in a large unselected and well-defined cohort of 956 patients with AML. Results were correlated with cytogenetic data and clinical outcome. MLL PTD was detected by RT-PCR, subsequent nucleotide sequencing, and Southern blotting. The overall incidence was found to be 5.0% (48/956), whereas FLT3 ITD was detected in 19.2% (184/956). Sixteen cases were positive for both alterations. The rate of MLL PTD in FLT3 ITD positive patients was significantly higher than that in FLT3 ITD negative patients [16/184 (8.7%); 32/772 (4.1%); P = 0.025]. However, both aberrations were highly increased in patients with normal karyotype (MLL PTD 35/431, P = 0.004; FLT3 ITD 132/334, P < 0.001). When restricted to this subgroup, the rate of MLL PTD in patients with FLT3 mutations was not significantly increased. No statistically significant differences were detected between patients positive for MLL PTD and patients negative for MLL PTD in the rate of complete remissions or the overall survival, although we did see a significantly shorter disease-free survival in patients age 60 or younger. In conclusion, although there is an overlap in the mutational spectrum in AML with FLT3 ITD and MLL PTD mutations, our data do not support a common mechanistic basis. Although associated with inferior disease-free survival, the results of this study do not unequivocally support the notion that MLL PTD mutations represent an independent prognostic factor. © 2003 Wiley-Liss, Inc. [source] Study of mutations in Jordanian patients with haemophilia A: identification of five novel mutationsHAEMOPHILIA, Issue 1 2010A. AWIDI Summary., Haemophilia A (HA) is an X-linked recessive bleeding disorder caused by mutations in the factor VIII gene (F8), which encodes factor VIII (FVIII) protein, a plasma glycoprotein, that plays an important role in the blood coagulation cascade. In the present study, our aim was to identify F8 gene mutations in HA patients from Jordan. One hundred and seventy-five HA patients from 42 unrelated families were included in this study. Among these patients, 117 (67%) had severe HA, 13 (7%) had moderate HA and 45 (26%) had mild HA. Severe patients were first tested for intron-22 inversion using long range polymerase chain reaction (PCR), then negative patients were tested for intron-1 inversion using PCR. Sequencing for the entire F8 gene was performed for all severe HA patients who were found negative for intron-22 and -1 inversions and it was also performed for moderate and mild HA patients. HA causative mutations were identified in all patients. Intron-22 and -1 inversions were detected in 52% and 2% of families respectively. Beside these two mutations, 19 different mutations were identified, which include 15 missense and four frameshift mutations. Five novel mutations were identified including one frameshift and four missense mutations. No large deletions or nonsense mutations were detected in patients who participated in this study. Only 17 patients with severe HA were found positive for FVIII inhibitors. The data presented will play an important role for genetic counselling and health care of HA patients in Jordan. [source] Oxidative Damage of the Gastric Mucosa in Helicobacter pylori Positive Chronic Atrophic and Nonatrophic Gastritis, Before and After EradicationHELICOBACTER, Issue 5 2003Federico Iacopini ABSTRACT Background.,Helicobacter pylori is the main cause of gastritis and a primary carcinogen. The aim of this study was to assess oxidative damage in mucosal compartments of gastric mucosa in H. pylori positive and negative atrophic and nonatrophic gastritis. Materials and methods., Five groups of 10 patients each were identified according to H. pylori positive or negative chronic atrophic (Hp-CAG and CAG, respectively) and nonatrophic gastritis (Hp-CG and CG, respectively), and H. pylori negative normal mucosa (controls). Oxidative damage was evaluated by nitrotyrosine immunohistochemistry in the whole mucosa and in each compartment at baseline and at 2 and 12 months after eradication. Types of intestinal metaplasia were classified by histochemistry. Results., Total nitrotyrosine levels appeared significantly higher in H. pylori positive than in negative patients, and in Hp-CAG than in Hp-CG (p < .001); no differences were found between H. pylori negative gastritis and normal mucosa. Nitrotyrosine were found in foveolae and intestinal metaplasia only in Hp-CAG. At 12 months after H. pylori eradication, total nitrotyrosine levels showed a trend toward a decrease in Hp-CG and decreased significantly in Hp-CAG (p = .002), disappearing from the foveolae (p = .002), but remaining unchanged in intestinal metaplasia. Type I and II of intestinal metaplasia were present with the same prevalence in Hp-CAG and CAG, and did not change after H. pylori eradication. Conclusions., Oxidative damage of the gastric mucosa increases from Hp-CG to Hp-CAG, involving the foveolae and intestinal metaplasia. H. pylori eradication induces a complete healing of foveolae but not of intestinal metaplasia, reducing the overall oxidative damage in the mucosa. [source] Serological markers of autoimmunity in patients infected with hepatitis C virus: impact of HIV co-infectionHIV MEDICINE, Issue 6 2005OM Adeyemi Objectives: We sought to evaluate the prevalence, predictors and significance of autoantibody expression in patients with chronic hepatitis C (CHC) with or without HIV co-infection. Methods: Retrospective review of laboratory and histologic data for all patients with CHC who had a liver biopsy available. HIV status was documented in all patients. Results analyzed in SPSS10, Chicago, IL, a p value <0.05 was considered significant. Results: 170 patients with hepatitis C viremia, including 107 (63%) HIV co-infection, who had testing for anti-nuclear antibody (ANA) or anti-smooth muscle antibody (ASMA) and anti-mitochondrial antibody (AMA) were included in the study. Overall, 63% (74/117) of patients were ASMA seropositive and 6% (9/153) were positive for ANA. All 117 patients tested for AMA were negative. HIV co-infected patients were significantly more likely to be ASMA positive 71% (53/75) compared to those with hepatitis C alone (50%) [P=0.026]. There were no significant differences in age, gender, race, risk group, alanine aminotransferase (ALT) levels or grade of inflammation on histology between autoantibody positive and negative patients. ASMA positive patients had significantly higher globulin levels (P=0.036) and a trend towards more bridging fibrosis or cirrhosis. Patients with autoantibody expression rarely had histologic features of AIH. Conclusion: We found a high rate of ASMA seropositivity in our cohort of patients with chronic hepatitis C, and HIV co-infection was associated with significantly higher rates of ASMA expression. Autoantibody expression was not associated with demographic or clinical characteristics and does not necessarily preclude antiviral therapy. [source] Herpes viruses in periodontal compromised sites: comparison between HIV-positive and -negative patientsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 10 2008Sabrina Rosa Grande Abstract Aim: The objective of this study was to compare the frequency of herpes simplex virus type 1 (HSV-1), Epstein,Barr virus (EBV) and human cytomegalovirus (HCMV) in subgingival plaque, saliva and peripheral blood of HIV-positive and-negative patients with periodontal disease. Material and Methods: Fifty HIV-positive subjects (23 with gingivitis, 27 with periodontitis) and 50 healthy HIV-negative patients with chronic periodontitis were included in the study. Parameters of probing depth (PD), clinical attachment level (CAL), gingival index and plaque index were recorded. The samples were processed for viral identification by the nested polymerase chain reaction technique. Results: HCMV was the most prevalent virus in HIV-positive (82%) and-negative patients (84%), and the detection in the three samples was similar (p>0.05). HSV-1 was the least prevalent virus in both groups, being detected in similar frequencies in oral sites and in peripheral blood. EBV-1 was found more frequently in saliva and subgingival plaque of HIV-positive patients than in HIV-negative patients (p0.05). Conclusions: EBV-1 was more frequently recovered in oral sites of HIV-positive patients than in HIV-negative patients. [source] Amoxicillin plus metronidazole in the treatment of adult periodontitis patientsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2001A double-blind placebo-controlled study Abstract Background, aims: The aim of this double-blind, parallel study was to evaluate the adjunctive effects of systemically administered amoxicillin and metronidazole in a group of adult periodontitis patients who also received supra- and subgingival debridement. Methods: 49 patients with a diagnosis of generalised severe periodontitis participated in the study. Random assignment resulted in 26 patients in the placebo (P) group with a mean age of 40 years and 23 patients in the test (T) group which had a mean age of 45 years. Clinical measurements and microbiological assessments were taken at baseline and 3 months after completion of initial periodontal therapy with additional placebo or antibiotic treatment. Patients received coded study medication of either 375 mg amoxicillin in combination with 250 mg metronidazole or identical placebo tablets, every 8 hours for the following 7 days. Results: At baseline, no statistically significant differences between groups were found for any of the clinical parameters. Except for the plaque, there was a significantly larger change in the bleeding, probing pocket depth (PPD) and clinical attachment level (CAL) in the T-group as compared to the P-group after therapy. The greatest reduction in PPD was found at sites with initial PPD of 7 mm, 2.5 mm in the P-group and 3.2 mm in the T-group. The improvement in CAL was most pronounced in the PPD category 7 mm and amounted to 1.5 mm and 2.0 mm in the P- and T-groups, respectively. No significant decrease was found in the number of patients positive for any of the test species in the P-group. The number of patients positive for Porphyromonas gingivalis, Bacteroides forsythus and Prevotella intermedia in the T-group showed a significant decrease. After therapy there was a significant difference between the P- and the T- group in the remaining number of patients positive for P. gingivalis, B. forsythus and Peptostreptococcus micros. 4 subgroups were created on the basis of the initial microbiological status for P. gingivalis positive (Pg-pos) and negative patients (Pg-neg) in the P- and the T-groups. The difference in reduction of PPD between Pg-pos and Pg-neg patients was particularly evident with respect to the changes in % of sites with a probing pocket depth 5 mm. This % decreased from 45% at baseline to 23% after treatment in the Pg-pos placebo subgroup and decreased from 46% to 11% in the Pg-pos test subgroup (p0.005). In contrast, the changes in the proportions of sites with a probing pocket depth 5 mm in the Pg-neg placebo and Pg-neg test subgroup were similar, from 43% at baseline to 18% after treatment versus 40% to 12%, respectively. Conclusions: This study has shown that systemic usage of metronidazole and amoxicillin, when used in conjunction with initial periodontal treatment in adult periodontitis patients, achieves significantly better clinical and microbiological results than initial periodontal treatment alone. Moreover, this research suggests that especially patients diagnosed with P. gingivalis benefit from antibiotic treatment. Zusammenfassung Zielsetzung: Das Ziel dieser placebokontrollierten Doppelblindstudie mit parallelen Gruppen war es, die zusätzlichen Effekte der systemischen Gabe von Amoxicillin und Metronidazol bei Patienten mit Erwachsenenparodontitis zu untersuchen, bei denen auch eine supra- und subgingivale Instrumentierung durchgeführt worden war. Material und Methoden: 49 Patienten mit einer generalisierten schweren Erwachsenenparodontitis nahmen an der Studie teil. Zufällige Zuweisung der Therapien führte zu 26 Patienten in der Placebo-Gruppe (P) mit einem mittleren Alter von 40 und 23 Patienten in der Test-Gruppe (T) mit einem mittleren Alter von 45 Jahren. Klinische Messungen und mikrobiologische Untersuchungen wurden zu Beginn der Therapie sowie 3 Monate nach parodontaler Initialbehandlung mit zusätzlicher Placebo- bzw. Antibiotikagabe durchgeführt. Nachdem alle Zähne mit pathologisch vertieften Taschen subgingival instrumentiert worden waren, erhielten die Patienten eine kodierte Studienmedikation, die entweder aus 375 mg Amoxicillin und 250 mg Metronidazol oder identisch aussehenden Placebotabletten bestand, die die Patienten für 7 Tage alle 8 Stunden einnehmen sollten. Ergebnisse: Zu Beginn der Studie bestand kein statistisch signifikanter Unterschied zwischen den Versuchsgruppen hinsichtlich klinischer Parameter. Nicht für den Plaque Index, aber für Sondierungsblutung, Sondierungstiefen (ST) und klinische Attachmentlevel (PAL) kam es in der T-Gruppe zu signifikant stärkeren Veränderungen im Vergleich zur P-Gruppe. Die stärkste ST-Reduktion bzw. die größten Attachmentgewinne wurden bei Stellen gefunden, die initial ST 7 mm aufgewiesen hatten: P-Gruppe: ST=2.5 mm, PAL=1.5 mm; T-Gruppe: ST=3.2 mm, PAL=2.0 mm. Für keines der untersuchten Parodontalpathogene wurde eine signifikante Reduktion in der P-Gruppe beobachtet, während sich in der T-Gruppe eine signifikante Reduktion für Porphyromonas gingivalis, Bacteroides forsythus und Prevotella intermedia ergab. Nach Therapie ergab sich ein statistisch signifikanter Unterschied zwischen T- und P-Gruppe hinsichtlich Persistenz von P. gingivalis, B. forsythus und Peptostreptococcus micros. Entsprechend dem initialen mikrobiologischen Status für P. gingivalis wurden 4 Untergruppen gebildet: P. gingivalis positive (Pg+) oder (Pg,) Patienten in der T-bzw. P-Gruppe. Der Unterschied zwischen Pg+ und Pg, Patienten war besonders groß hinsichtlich der Veränderung des %-Anteils der Stellen mit ST5 mm. Dieser verringerte sich in der Pg+ P-Untergruppe von 45% auf 23% und in der Pg+ T-Untergruppe von 46% auf 11% (p0.005). Im Unterschied dazu war die Reduktion des Anteils der ST 5 mm in der Pg, P- und T-Untergruppen gleich: P-Gruppe: 43% auf 18%; T-Gruppe von 40% auf 12%. Schlußfolgerungen: Die systemische Gabe von Amoxicillin und Metronidazol zusätzlich zu subgingivaler Instrumentierung bei Patienten mit Erwachsenenparodontitis führt zu signifikant günstigeren klinischen und mikrobiologischen Ergebnissen als die konventionelle Therapie allein. Insbesondere Patienten mit P. gingivalis scheinen von dieser unterstützenden antibiotischen Therapie zu profitieren. Résumé Le but de cette étude parallèle en double aveugle était d'évaluer les effets supplémentaires apportés par l'administration d'amoxicilline et de metronidazole dans un groupe de patients atteints de parodontite de l'adulte qui ont reçu également un débridement supra et sous gingival. 49 patients présentant un diagnostic de parodontite généralisée sévère participèrent à l'étude. La composition des groupes sélectionnés au hasard, était de 26 patients dans le groupe placebo (P) avec un âge moyen de 40 ans et 23 patients dans le groupe test (T) avec une moyenne d'âge de 45 ans. Des mesures cliniques et des prélèvements microbiologiques étaient réalisés initialement et 3 mois après la fin de la thérapeutique parodontale initiale complétée par un placebo ou un traitement antibiotique. Les patients recevaient des médicaments codés pour l'étude de 375 mg amoxicilline combiné avec 250 mg de metronidazol ou des comprimés placebo identiques, toutes les 8 heures pendant les 7 jours suivants. Initalement, aucune différence statistiquement significative entre les groupes n'était observée, pour aucun des paramètres cliniques. En dehors de la plaque, il y avait une modification plus élevée significative pour le saignement, la profondeur de poche au sondage (PPD) et le niveau clinique d'attache (CAL) dans le groupe T, par rapport au groupe P, après traitement. La plus grande réduction pour PPD était observée pour les sites ayant une profondeur de poche au sondage intiale>ou égale à 7 mm, 2.5 mm dans le groupe P et 3.2 mm dans le groupe T. L'amélioration du CAL était plus prononcée pour la catégorie >ou égale à 7 mm et allait jusqu'à 1.5 et 2.0 mm dans les groupes P et T, respectivement. Aucune diminution significative n'était trouvée pour le nombre de patients positifs pour n'importe quelle espèce test dans le groupe P. Le nomber de patients positifs pour Porphyromonas gingivalis, Bacteroides forsythus et Prevotella intermedia dans le groupe T présentait une diminution significative. Après thérapeutique, il y avait une différence significative entre les groupe P et T, en ce qui concerne le nombre de patients positifs pour P. gingivalis, B. forsythus et Peptostreptococcus micros. 4-sous groupes furent créés sur la base de l'état microbiologique pour les patients positifs àP. gingivalis (Pg-pos), et négatifs (Pg-neg), dans les groupes P et T. La différence de réduction de PPD entre les patients Pg-pos et Pg-neg était particulièrement évidente en ce qui concernait les changements en % de sites présentant une profondeur de poche au sondage >ou égale à 5 mm. Ce % diminuait de 45% initialement à 23% après traitement dans le sous-groupe Pg-pos placebo et de 46% à 11% dans le sous-groupe Pg-pos test (p<0.005). A l'inverse, les changements observés dans les proportions de sites avec une profondeur de poche au sondage >5 mm dans les sous-groupes Pg-neg placebo et Pg-neg test étaient similaires, de 43% initialement à 18% après traitement contre 40% à 12% respectivement. En conclusion, cette étude a montré que l'utilisation systèmique de metronidazole et d'amoxicilline, lorsqu'elle est utilisée en complément du traitement parodontal initial chez des patients atteints de parodontite de l'adulte, donne, de façon significative, de meilleurs résultats cliniques et microbiologiques qu'un traitement parodontal initial seul. De plus, cette recherche suggère que les patients porteurs du P. gingivalis bénéficient particulièrement d'un traitement antibiotique. [source] Influence of Helicobacter pylori infection and cetraxate on gastric mucosal blood flow during healing of endoscopic mucosal resection-induced ulcersJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2001Kyoichi Adachi Abstract Background and Aim: Helicobacter pylori (H. pylori) infection is known to affect the gastric microcirculation, and cetraxate is reported to accelerate gastric ulcer healing, possibly by augmenting gastric mucosal blood flow (MBF). The aim of this study is to clarify the effect of H. pylori infection and cetraxate on MBF during gastric ulcer healing. Methods: Forty-two patients who had undergone endoscopic mucosal resection (EMR) were studied. Mucosal blood flow was measured by the use of a laser Doppler flowmeter in the surrounding mucosa and at the ulcer margin, before, 1 day, 1 week and 4 weeks after EMR. Helicobacter pylori infection was confirmed by the use of bacterial culture and histology. After EMR, patients were randomly assigned to receive 30 mg lansoprazole (u.i.d; L-regimen) or 30 mg lansoprazole (u.i.d.) with 200 mg cetraxate (q.i.d; LC-regimen) for 4 weeks. Results: The MBF ratio (MBF at ulcer margin/MBF in surrounding mucosa) 1 week after EMR was significantly lower than that before or 4 weeks after EMR only in H. pylori -positive patients treated with the L-regimen. No such decrease in MBF was observed after 1 week in H. pylori -positive patients treated with the LC-regimen or in H. pylori -negative patients. Conclusion: A transient decrease in MBF was detected at the ulcer margin during healing of EMR-induced ulcers in H. pylori -infected patients. Cetraxate seemed to prevent this decrease in MBF. [source] CORRELATION OF GASTRIC INTESTINAL METAPLASIA AND HELICOBACTER PYLORI INFECTION AMONG FUNCTIONAL DYSPEPTIC PATIENTSJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2000Murdani Abdullah Background: It is generally accepted that intestinal metaplasia (IM) is a pre cursor of gastric cancer and is associated with Helicobacter pylori (Hp) infection. But still little data available about association of IM and Hp in different clinical groups of patients, especially in areas with high Hp prevalence. Aim: to evaluate the IM and itís correlation with Hp infection in consecutive patients with functional dyspepsia (FD). Methods: a retrospective review of our endoscopy database and histological data from January 1997 to December 1999 was made. In this period we performed 3083 upper intestinal endoscopy in patients with FD. Endoscopy procedure was done without any specific preparation for Hp evaluation. Biopsy specimen were taken from antrum and corpus and were stained with Giemsa, H&E and Alcian Blue. Histological data was evaluated by pathologist from Department of Pathology, Medical Faculty, University of Indonesia according to the Sydney System. IM was evaluated as present or absent. One hundred and fourteen consecutive data were eligible for statistical analysis. Results: Histological data of 114 patients with FD was analyzed. Average age was 45.47 years (SD 14.32), male 62.3 % (71/114), and female 37.7 % (43/114). Forty-eight (42.11%) patients with FD were Hp positive on histology and were significantly older than Hp negative. (48.74 +12.65/43.25+15.04; p < 0.05). IM was present in 13 ( 11.4%) patients with FD. They were significantly older than the patients without IM (mean age 55.08+11.98/44.23+14.18; p <0.05) Frequency of IM was similar both in Hp positive and Hp negative patients with FD (12.5%/10.6%; p>0.05). Conclusions: IM among patients with FD was 11.4%. IM was significantly more frequent found in older age but our data suggest that IM is not related to Hp status in FD patients. [source] Determination of the optimal cut-off value for the [13C]-urea breath test based on a Helicobacter pylori -specific polymerase chain reaction assayJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2000Haruhiko Yoshida Abstract Background: This study was conducted to determine the optimal cut-off value and breath sample collection time for the [13C]-urea breath test based on the assessment of Helicobacter pylori status with a gastric juice-based polymerase chain reaction (PCR) assay. Methods and Results: A total of 104 patients took 100 mg [13C]-urea orally and breath samples were collected at 5, 10, 20, 30 and 60 min. The increment of 13CO2: 12CO2 ratio from the baseline (,13C) was measured using a laser spectroanalyser. The PCR assay was positive in 63 and negative in 41 patients. The optimal cut-off value of ,13C was calculated for each sample collection time so that the distance from the geometric mean value among Helicobacter pylori -positive patients and that from the arithmetic mean value among negative patients were simultaneously maximized. The cut-off value of 2.7, at 20 min had the longest distance, being separated by 3.16 SD from the two mean values. Using this cut-off value, the urea breath test showed 100% specificity and 98% sensitivity for the diagnosis of Helicobacter pylori infection. [source] Prevalence and impact of occult hepatitis B infection in chronic hepatitis C patients treated with pegylated interferon and ribavirin,JOURNAL OF MEDICAL VIROLOGY, Issue 5 2010Marion Levast Abstract The prevalence of occult hepatitis B, defined by absence of HBsAg and HBV DNA, ranges widely in patients with hepatitis C. This may influence the treatment of hepatitis C and the severity of liver disease. Sensitive and specific real-time PCR techniques are available commercially and can detect more reliably low HBV DNA levels. The aim of this study was to determine the prevalence of occult hepatitis B virus infection using the COBAS Taqman assay (Roche Diagnostics, Meylan, France) in the serum and liver of HBsAg negative patients with chronic hepatitis C and to evaluate its clinical consequences on liver pathology and its impact on the response to treatment with peg-IFN, and Ribavirin. HBV DNA detection was assessed retrospectively on 140 sera and 113 liver biopsies of HCV positive/HBsAg negative patients before treatment. A 4.4% (5/113) prevalence of occult hepatitis B was recorded in liver samples and in none of the sera. Anti-HBc was not detected in one, three of whom were sustained virological responders to treatment, one was relapsed responder and one was non-responder. Furthermore, in this cohort composed of 12% anti-HBs negative/anti-HBc positive and 20% anti-HBs positive/anti-HBc positive patients, anti-HBc was not associated with pre-therapeutic viral load, ALT serum levels, and histological activity or fibrosis. Using a commercial real-time PCR assay, we observed a low prevalence of occult B hepatitis. This, just as anti-HBC status, had no clinical impact in a large cohort of hepatitis C patients. It therefore does not appear useful to screen for occult hepatitis B in these patients with this test before beginning HCV treatment. J. Med. Virol. 82: 000,000, 2010. © 2010 Wiley-Liss, Inc. J. Med. Virol. 82: 747,754, 2010. © 2010 Wiley-Liss, Inc. [source] Molecular characterization of a variant virus that caused de novo hepatitis B without elevation of hepatitis B surface antigen after chemotherapy with rituximabJOURNAL OF MEDICAL VIROLOGY, Issue 12 2008Masami Miyagawa Abstract Hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)-negative patients following treatment with rituximab has been reported increasingly. The aim of this study was to investigate the molecular mechanisms underlying HBV reactivation in an HBsAg-negative patient. HBV was reactivated in a 75-year-old man following chemotherapy with rituximab, without elevation of HBsAg. The patient's full-length HBV genome was cloned and the entire sequence was determined. Transfection studies were performed in vitro using recombinant wild-type HBV (wild-type), the patient's HBV (patient), and two chimeric HBV constructs, in which the preS/S region of the patient and wild-type virus had been exchanged with one another. Secreted HBsAg and intra- and extra-cellular HBV DNA were measured. The number of amino acid substitutions in HBV from this patient was much higher than in previous reports of HBV mutants, such as occult HBV and vaccine escape HBV mutants. Levels of HBsAg and HBV DNA production in vitro were significantly lower in the patient compared to wild-type transfections. From analyses of the chimeric constructs, the altered preS/S region was responsible mainly for this impairment. These results show that highly mutated HBV can reactivate after chemotherapy with rituximab, despite an unusually large number of mutations, resulting in impaired viral replication in vitro. Severe immune suppression, probably caused by rituximab, may permit reactivation of highly mutated HBV. These findings have important clinical implications for the prevention and management of HBV reactivation and may explain partially the mechanism of recent, unusual cases of HBV reactivation. J. Med. Virol. 80:2069,2078, 2008. © 2008 Wiley-Liss, Inc. [source] Hepatitis C virus seropositivity in a South African Cohort of HIV co-infected, ARV naïve patients is associated with renal insufficiency and increased mortality,JOURNAL OF MEDICAL VIROLOGY, Issue 9 2008Raveen Parboosing Abstract HIV is known to affect the epidemiology, transmission, pathogenesis and natural history of HCV infection whilst studies on the effects of HCV on HIV have shown conflicting results and are confounded by the influence of intravenous drug use and antiretroviral therapy. This study was conducted in KwaZulu-Natal Province in South Africa where HIV is predominantly a sexually transmitted infection. Intravenous drug use is rare in this region and the study population was naïve to antiretroviral therapy. For this study, specimens from selected sentinel sites submitted to a central laboratory for routine HIV testing were screened for anti-HCV IgG antibodies. HIV positive HCV-positive patients were compared to HIV-positive HCV-negative patients in a subgroup of patients within this cohort in order to determine if HCV sero-prevalence was associated with clinical outcomes in a linked anonymous retrospective chart survey. The prevalence of HCV was 6.4% and that of HIV, 40.2% (n,=,1,937). There was a significantly higher prevalence of HCV among HIV infected patients as compared to HIV negative patients (13.4% vs. 1.73% respectively) (n,=,1,937, P,<,0.001). HCV-HIV co-infected patients had significantly increased mortality (8.3 vs. 21%) (n,=,162, P,<,0.02). A significant association was found between HCV serostatus and abnormal urea levels (15.4 vs. 7.3 mmol/L, n,=,134, P,<,0.001) and creatinine levels (252.2 vs. 144.4 µmol/L, n,=,134, P,<,0.01). This study has found that hepatitis C co-infection is more common in HIV positive individuals and is associated with an increased mortality and renal morbidity. J. Med. Virol. 80:1530,1536, 2008. © 2008 Wiley-Liss, Inc. [source] Hepatitis B virus X mutations occurring naturally associated with clinical severity of liver disease among Korean patients with chronic genotype C infection,JOURNAL OF MEDICAL VIROLOGY, Issue 8 2008Hyun-Ju Kim Abstract Few reports have detailed mutation frequencies and mutation patterns in the entire X region according to clinical status. The aims of this study were to elucidate the relationships between mutation patterns and their frequencies in the X region and clinical status in a Korean cohort and determine specific X mutation types, related closely with liver disease progression. All X mutations were determined by direct sequencing in 184 patients with different clinical features. Mutation rates in the X region in patients with more severe liver disease, hepatocellular carcinoma (HCC) (3.6%) or liver cirrhosis (4%) were always significantly higher than in patients with corresponding less severe forms, chronic hepatitis (2.9%) or asymptomatic carriers (2.1%), but no significant difference in mutation rates was found in terms of HBeAg serostatus. All five mutation types (V5M/L, P38S, H94Y, I127T/N, and K130M and V131I) affecting the six codons were found to be related significantly to clinical severity. Among these, two mutation types (V5M/L and K130M and V131I) were observed more frequently in HBeAg negative patients than in HBeAg positive patients. In conclusion, the results suggest that an accumulation of mutations in the X region contributes to disease progression in chronic patients, at least Korean patients with genotype C. Specific mutation types appears to be related more to severe liver diseases such as HCC or liver cirrhosis. In particular, a novel mutation type (V5M/L) discovered firstly during the present study was found to be associated significantly with HCC. J. Med. Virol. 80:1337,1343, 2008. © 2008 Wiley-Liss, Inc. [source] Clinical and virological characteristics of lamivudine resistance in chronic hepatitis B patients: A single center experienceJOURNAL OF MEDICAL VIROLOGY, Issue 3 2005Jian Sun Abstract We have investigated the characteristics of lamivudine-resistant strains in patients with chronic hepatitis B in Guangdong, China, where the predominant genotypes are B and C. Two hundred forty-seven patients treated with lamivudine in Nanfang Hospital were followed-up. Patients with hepatitis B e antigen (HBeAg) positive and hepatitis B virus (HBV)-DNA levels over 7.5,×,106 copies/ml at baseline had a shorter time to the selection of YMDD mutant (P,=,0.02 and 0.00, respectively). The detection of YMDD mutant precedes HBV-DNA breakthrough and alanine transaminase (ALT) flare in about 2 and 3 months, respectively. The ALT flare after the appearance of YMDD mutants was more evident in HBeAg positive patients than HBeAg negative patients (P,=,0.02). After emergence of YMDD mutant, the HBV-DNA level was significantly higher in genotype C patients compared with genotype B patients (P,=,0.02). No significant difference of YMDD mutant pattern was found between patients with genotype B and C. Four kinds of new mutants were found in over two patients including rtL80I, rtG172E, rtG174C, and rtG172E/rtG174C. In vitro transfection and real-time analysis showed that rtG172E, rtG174C, and rtG172E/rtG174C mutants had a decreased replication competence compared with wild type (33%, 27%, and 15% of the wild type HBV, respectively). Our result suggest that genotypic monitoring of YMDD mutant is important for the management of patients treated with lamivudine. J. Med. Virol. 75:391,398, 2005. © 2005 Wiley-Liss, Inc. [source] Molecular epidemiology of molluscum contagiosum virus and analysis of the host-serum antibody response in Spanish HIV-negative patientsJOURNAL OF MEDICAL VIROLOGY, Issue 2 2002Monica Agromayor Abstract Molluscum contagiosum virus (MCV) lesions from Spanish human immunodeficiency virus (HIV)-negative patients were clinically examined and analyzed for virus detection and typing. In a study of 147 patients, 97 (66%) were children under 10 years, of whom 49% had atopic dermatitis. MCV lesions were morphologically indistinguishable among the different age groups, but atopic patients presented larger lesions compared with patients without the disorder. In adults, lesions were observed mainly on the genitals. MCVI was the predominant subtype. The deduced MCVI/MCVII ratio (146:1) was much higher than that found in other geographical areas. Protein preparations of the virus-induced lesions were immunoblotted with sera from 25 MCVI patients. The host-serum antibody response was weak and variable, although no significant differences were found between atopic and nonatopic patients. Three immunoreactive proteins of 74/80, 60, and 35 kDa were detected in almost all the analyzed sera. The 35 and 74/80-kDa proteins were virus specific, whereas the 60-kDa protein band was composed of a mix of human keratins. Immunoblotting of MCV lesions and vaccinia virus-infected cell extracts with either MCV patient serum or a rabbit antiserum against vaccinia virus showed no cross-reactivity of these two human poxviruses at the antigenic level. J. Med. Virol. 66:151,158, 2002. © 2002 Wiley-Liss, Inc. [source] Changes of gastric histology in patients with erosive oesophagitis receiving long-term lansoprazole maintenance therapyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010M. M. Haber Aliment Pharmacol Ther 2010; 32: 83,96 Summary Background, Changes in gastric histology associated with long-term maintenance therapy with lansoprazole for erosive oesophagitis have not been well described. Aim, To evaluate the effect on gastric histology of long-term dose-titrated lansoprazole administered as maintenance therapy for up to 82 months in patients with erosive oesophagitis. Methods, Sequential gastric biopsy specimens were obtained for evaluation of histological changes and Helicobacter pylori infection status. Results, Active and chronic inflammation improved from baseline to final visit in a majority of patients receiving long-term therapy with lansoprazole, irrespective of baseline H. pylori infection status. Reductions in active inflammation in the gastric body and antrum were seen in 53% (17/32) and 67% (20/30) of H. pylori -positive patients, respectively, and in 88% (7/8) and 86% (12/14) of H. pylori -negative patients, respectively. Reductions in chronic inflammation in the gastric body and antrum were seen in 38% (12/32) and 47% (15/32) of H. pylori -positive patients, respectively, and in 58% (70/121) and 57% (68/120) of H. pylori -negative patients, respectively. No clinically meaningful increases in hyperplasia, dysplasia, neoplasia, intestinal metaplasia or atrophy were observed during the follow-up period. Conclusions, Lansoprazole administered as maintenance therapy for up to 6 years in patients with erosive oesophagitis demonstrated gastric mucosal safety and was well tolerated. [source] Review article: Helicobacter pylori -negative duodenal ulcer diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2009J. P. GISBERT Aliment Pharmacol Ther,30, 791,815 Summary Background,Helicobacter pylori infection rates in duodenal ulcer (DU) patients may be lower than previously estimated. Aim, To review the real prevalence of H. pylori -negative DUs and its possible causes. Methods, Bibliographical searches in MEDLINE looking for the terms ,H. pylori' and ,duodenal ulcer'. Results, Mean prevalence of H. pylori infection in DU disease, calculated from studies published during the last 10 years including a total of 16 080 patients, was 81%, and this figure was lower (77%) when only the last 5 years were considered. Associations with H. pylori -negative DU were: (1) False negative results of diagnostic methods, (2) NSAID use (21% in studies with <90% infection rate), (3) Complicated DU (bleeding, obstruction, perforation), (4) Smoking, (5) Isolated H. pylori duodenal colonization, (6) Older age, (7) Gastric hypersecretion, (8) Diseases of the duodenal mucosa, (9) Helicobacter,heilmanii' infection and (10) Concomitant diseases. Conclusion, In patients with H. pylori -negative DU disease, one should carefully confirm that the assessment of H. pylori status is reliable. In truly H. pylori -negative patients, the most common single cause of DU is, by far, the use of NSAIDs. Ulcers not associated with H. pylori, NSAIDs or other obvious causes should, for the present, be viewed as ,idiopathic'. True idiopathic DU disease only exceptionally exists. [source] IgG classification of anti-PF4/heparin antibodies to identify patients with heparin-induced thrombocytopenia during mechanical circulatory supportJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2007S. SCHENK Summary., Commercial immunoassays frequently detect anti-PF4/heparin antibodies during mechanical circulatory support (MCS), but only a small minority of patients develops heparin-induced thrombocytopenia (HIT). Whereas platelet functional tests can distinguish between platelet-activating and non-platelet-activating antibodies, commercial PF4-dependent immunoassays do not. Between 2003 and 2004, 113 patients were placed on MCS. Blood samples were obtained on postimplant day 5,7 for analyses by antibody assays and the functional heparin-induced platelet activation (HIPA) assay. Three distinct groups of patient sera were identified: platelet-activating anti-PF4/heparin antibodies (n = 10), non-platelet-activating anti-PF4/heparin antibodies (n = 53), and anti-PF4/heparin antibody negative (n = 50). Patients with platelet-activating antibodies had the highest risk for thromboembolic events (P < 0.005), whereas those with non-platelet-activating antibodies did not differ from antibody negative patients (P = 0.369). The enzyme-immunoassay and column agglutination assays, which cover all immunoglobulin classes, demonstrated adequate sensitivity and negative predictive value; yet, both lacked specificity with respect to the platelet-activating antibodies. If all antibody positive patients were further classified by an IgG-specific anti-PF4/heparin enzyme-immuno assay, specificity for platelet-activating antibodies increased. Whereas IgG-specific optical density (OD) values below 1.0 were likely for non-platelet-activating anti-PF4/heparin antibodies, higher values were progressively predictive for pathogenic platelet activation. The probability of the development of clinical HIT also increased steeply. In conclusion, platelet-activating anti-PF4/heparin antibodies are relatively common (about 9%) in patients on MCS and are associated with significantly higher thrombotic event rates. Low IgG-specific OD values (< 1.0) in the enzyme-immunoassay indicate low likelihood for the presence of platelet-activating antibodies. These results justify further validation so that anticoagulation during MCS becomes safer and adequate. [source] Changes of gastric mucosal architecture during long-term omeprazole therapy: results of a randomized clinical trialALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2006L. LUNDELL Summary Background, The impact of long-term acid suppression on the gastric mucosa remains controversial. Aim, To report further observations on an established cohort of patients with gastro-oesophageal reflux disease, after 7 years of follow-up. Methods, Of the original cohort randomized to either antireflux surgery or omeprazole, 117 and 98 patients remained in the medical and surgical arms, respectively. Gastric biopsies were taken at baseline and throughout the study. Results, Fifty-three antireflux surgery and 39 omeprazole-treated patients had Helicobacter pylori infection at randomization. Eighty-three omeprazole-treated and 60 antireflux surgery patients remained H. pylori negative over the 7 years, and no change was observed in mucosal morphology except for a change in endocrine cell population (linear and diffuse hyperplasia, P = 0.03). During the 7-year study many patients, who were initially H. pylori infected, had the infection eradicated leaving only 13 omeprazole and 12 antireflux surgery patients still infected. In these patients, omeprazole induced a deterioration of the mucosal inflammation scores (P = 0.01) with a numerical increase of glandular atrophy. Conclusions, Long-term omeprazole therapy does not alter the exocrine oxyntic mucosal morphology in H. pylori -negative patients, but mucosal endocrine cells appear to be under proliferative stimulation; in H. pylori -positive patients there are changes in mucosal inflammation and atrophy. [source] Correlation of clinical characteristics with detection of hepatitis B virus X gene in liver tissue in HBsAg-negative, and HCV-negative hepatocellular carcinoma patientsLIVER INTERNATIONAL, Issue 5 2002Yoichiro Higashi Abstract: Purpose: We studied the clinical features and the etiology of hepatitis B virus surface antigen (HBsAg)-negative and antibody to hepatitis C virus (anti-HCV) negative patients with hepatocellular carcinoma. Methods: A total of 550 patients, hospitalized with an initial diagnosis of HCC were retrospectively studied. Eighty-one of these patients were HBsAg-positive (HB group), 404 patients were anti-HCV positive (HC group). The other 65 patients were negative for both HBsAg and for anti-HCV (NBNC group). We purified HBV-X gene from HCC or non-tumorous liver tissue of 23 NBNC patients using PCR. Results: Clinical features of NBNC as compared with HB and HC patients were as follows, respectively: non-cirrhosis rate (%): 57,37,15 (P = 0.02 for HB, P < 0.00001 for HC), the proportion of patients with normal ALT concentrations (%): 59,28,10 (P = 0.0002 for HB, P < 0.00001 for HC). Forty of 59 NBNC patients (68%) had anti-HBs and/or anti-HBc (healthy controls: 29%, P < 0.00001) and two of 56 had serum HBV DNA. Twelve of 23 NBNC patients had HBV-X gene in HCC and/or non-cancerous liver tissues (52%). None of 52 had serum HCV RNA. Conclusions: The NBNC patients with HCC had a higher frequency of non-cirrhotic liver without liver injury. The presence of the HBV-X gene in HCC suggests a possible role of past HBV infection in the development of HCC. About half of NBNC HCC is associated with seronegativity for HBsAg and positivity for the HBV-X gene in liver tissue. [source] Dysfunction of oesophageal motility in Helicobacter pylori -infected patients with reflux oesophagitisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2001J. C. Y. Wu Background: Helicobacter pylori infection has been suggested to be protective against gastro-oesophageal reflux disease. However, a significant proportion of patients with gastro-oesophageal reflux disease are infected by H. pylori. Aim: To study oesophageal motor function in H. pylori -infected patients with reflux oesophagitis. Methods: Patients with erosive reflux oesophagitis were recruited prospectively for stationary oesophageal manometry and 24-h ambulatory oesophageal pH monitoring. H. pylori status was determined by biopsy urease test. Non-reflux volunteers were recruited as controls. Results: Seventy-four patients with erosive oesophagitis (34 H. pylori -positive, 40 H. pylori -negative) and 48 non-reflux patient controls (22 H. pylori -positive, 26 H. pylori -negative) were recruited. There was no difference in severity of oesophagitis (median grade, 1; P=0.53) or oesophageal acid exposure (total percentage time oesophageal pH < 4, 7.6% vs. 6.8%; P=0.57) between H. pylori -positive and H. pylori -negative groups. Compared to H. pylori -negative patients, H. pylori -positive patients had significantly lower basal lower oesophageal sphincter pressure (12.2 mmHg vs. 15.3 mmHg; P=0.03) and amplitude of distal peristalsis (56.9 mmHg vs. 68.4 mmHg; P=0.03). Ineffective oesophageal motility (14% vs. 7%; P=0.02) and failed oesophageal peristalsis were also significantly more prevalent in H. pylori -positive patients. Conclusions: Among patients with a similar degree of reflux oesophagitis, H. pylori -infected patients have more severe oesophageal dysmotility and lower oesophageal sphincter dysfunction. Oesophageal motor dysfunction probably plays a dominant role in the development of gastro-oesophageal reflux disease in patients with H. pylori infection. 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