Hepatitis C virus transmission following invasive medical procedures.
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Biomedical subjects
Publications and source records attributed to J Belaiche.
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BACKGROUND AND STUDY AIMS: The small intestine is a potential origin of bleeding in patients with unexplained gastrointestinal tract hemorrhage or iron-deficiency anemia. Most reports on the investigation of these patients describe the use of upper tract enteroscopy. The diagnostic yield of combined upper and lower enteroscopy has not been widely assessed and remains to be clarified. The aim of this study was to assess the benefit of lower gastrointestinal tract enteroscopy in occult digestive bleeding. PATIENTS AND METHODS: Between 1 December 1995 and 15 January 1998, 54 patients with gastrointestinal bleeding of unknown origin were prospectively studied using upper and lower video push enteroscopy (44 for chronic iron-deficiency anemia and 10 for unexplained gastrointestinal tract hemorrhage with no potential site having been identified by other investigations). Examinations were done using a Olympus video enteroscope (SIF-100) under general anesthesia in a one-day clinic. An upper tract examination was done first, directly followed by the lower tract investigation. RESULTS: The upper tract enteroscopy was successful in 53 patients (98%) and retrograde ileoscopy in 21 patients (39%). In 18 (38%) cases the technical failure resulted from the impossibility of intubating the ileocecal valve. A potential source of upper gastrointestinal bleeding was detected in 35% of patients with chronic iron-deficiency anemia and in 20% of those with unexplained gastrointestinal tract hemorrhage. The most common lesion in the small bowel was angiodysplasia (25%). The lower tract video push enteroscopy disclosed 11 lesions in patients with chronic anemia. However the lesions, including two ileocecal valve cancers, were mainly located in the colon and had been missed by previous colonoscopy. No case of ileal lesion was detected in this group of patients. In patients with unexplained gastrointestinal tract hemorrhage, three lesions were detected but only one of these was in the ileum. Associated colonic and jejunal lesions were observed in three patients (5.5%). Overall, the diagnostic yield of lower video push enteroscopy was less than 2%. CONCLUSION: This prospective study has shown that using an enteroscope as a colonoscope in the management of patients with gastrointestinal bleeding of unknown origin is of little help. It might actually be more appropriate to perform a second colonoscopy. This however remains controversial and a prospective study is needed to answer that question.
OBJECTIVE: Acute lower gastrointestinal bleeding is a rare complication of Crohn's disease, which represents a diagnostic and therapeutic challenge. The aim of this study was to define epidemiological characteristics and therapeutic options of hemorrhagic forms of Crohn's disease. METHODS: Thirty-four cases of hemorrhagic forms of Crohn's disease were studied retrospectively. Acute lower gastrointestinal hemorrhage was defined as acute rectal bleeding originating in diseased bowel and requiring a transfusion of at least 2 units of red blood cells within 24 h. Upper gastrointestinal tract hemorrhage or anal lesions and postoperative bleeding were excluded. RESULTS: Mean age at time of hemorrhage was 34.2 +/- 14 yr. Mean duration of disease before the hemorrhage was 5.6 +/- 6 yr. The hemorrhage occurred during a flare up of the disease in 35% of cases. The hemorrhage revealed Crohn's disease in 23.5% of cases. The hemorrhage was more frequent in colonic disease (85%) than in isolated small bowel disease (15%) (p < 0.0001). The origin of bleeding was identified in 65% of cases, by colonoscopy (60%), by angiography (3 patients), or at surgery (1 patient). The bleeding lesion was an ulcer in 95% of cases, most often in the left colon. The treatment was surgical in 20.5% (colectomy in 36%), endoscopical (7 patients, including 5 successes), or medical. Hemorrhage recurred in 12 patients (35%) within a mean time of 3 yr (4 days-8 yr), requiring surgery in 3 cases. No death was observed. CONCLUSIONS: This study performed in a series characterized by a nonsurgical recruitment, the largest to date, shows that hemorrhagic forms of Crohn's disease may reveal disease in 23.5%, occurs in quiescent Crohn's disease in two-thirds of cases. Given the potential efficacy of endoscopical or medical treatment, as well as the absence of mortality, a conservative approach may be suggested as first-line therapy in the majority of patients.
Resistance to glucocorticoid therapy has been observed in patients with autoimmune/inflammatory diseases and may be related to the inflammatory process itself. The aim of this study was to examine the ability of tumor necrosis factor alpha (TNFalpha, a proinflammatory cytokine) and interleukin (IL)-10 (an anti-inflammatory cytokine) to differentially regulate the sensitivity of human monocytes/macrophages to glucocorticoids. To accomplish this, we first analyzed the pattern of TNFalpha and IL-10 inhibition by dexamethasone in LPS-stimulated whole-blood cell cultures. Second, we studied the modulation of the sensitivity of these cells to dexamethasone by preincubation with TNFalpha or IL-10 and measurement of LPS-stimulated IL-6 secretion. In addition, we evaluated the effect of dexamethasone on phorbolmyristate-acetate-stimulated IL-1 receptor antagonist secretion by the human monocytic cell line U937. Finally, we investigated whether the modulation of corticosensitivity in TNFalpha- and IL-10-pretreated U937 cells was related to a change of the glucocorticoid receptor concentration and affinity. Dexamethasone had different effects on LPS-induced TNFalpha and IL-10 secretion; whereas it suppressed TNFalpha in a dose-dependent fashion, its effect on IL-10 secretion was biphasic, producing stimulation at lower, and inhibition at higher doses. The concentration of LPS employed influenced the effect of dexamethasone on IL-10 secretion (P < 0.001). Pretreatment with TNFalpha diminished, and with IL-10 improved, the ability of dexamethasone to suppress IL-6 secretion in whole-blood cell cultures (P < 0.01 for both) and to enhance IL-1 receptor antagonist secretion by U937 cells (P < 0.05 for both). TNFalpha decreased (P < 0.001), while IL-10 increased (P < 0.001), the concentration of dexamethasone binding sites in these cells, with no discernible effect on their binding affinity. We conclude that glucocorticoids differentially modulate TNFalpha and IL-10 secretion by human monocytes in a LPS dose-dependent fashion and that the sensitivity of these cells to glucocorticoids is altered by TNFalpha or IL-10 pretreatment; TNFalpha blocks their effects, whereas IL-10 acts synergistically with glucocorticoids. This is accompanied by opposite glucocorticoid receptor changes, respectively opposing and favoring glucocorticoid actions. This study suggests that the pattern of pro-/antiinflammatory cytokine secretion may alter the response of patients to glucocorticoid therapy.
Helicobacter pylori is a worldwide infection. In gastro-duodenal ulcer disease no doubt remains about the necessity of H. pylori eradication. Controversies subsisting in other pathologies such gastro-esophageal reflux, dyspepsia, gastritis, gastric adenocarcinoma or MALT lymphoma are reviewed. Multiple drug combinations have been proposed to cure the infection. These are discussed in the clinical setting of Belgian practice.
Gastro-oesophageal reflux (GER) is more frequent in asthmatic patients than in the community at large. A causative association between the two diseases is suspected. Twenty-four hour ambulatory intraoesophageal pH monitoring represents the golden standard for the diagnosis of GER. The medical and/or surgical treatment of reflux in asthmatic patients with GER can improve pulmonary symptoms and to a lesser extent pulmonary function. The selection of the patients who will benefit from a GER treatment is difficult. Some symptoms like intrinsic asthma, nocturnal crises, could predict a good response to GER treatment.
A 66-year-old man was hospitalized for asthenia, weight loss, fever and chills. A polyarteritis nodosa associated with hepatitis B virus infection in a replicative phase was diagnosed. Etiology, physiopathology, and clinical characteristics of hepatitis B virus-related polyarteritis nodosa will be reviewed, as well as the effectiveness of therapy combining corticosteroïds, interferon alpha and plasma exchanges.
EXPERIMENTAL OBJECTIVES: The interaction between the endocrine and immune systems is a very intriguing area. Endogenous glucocorticoids, as end-effectors of the hypothalamo-pituitary-adrenal axis, inhibit the immune and inflammatory responses and are used as immunosuppressive drugs in many inflammatory, autoimmune and allergic diseases. The aims of this study were to investigate the effects of dexamethasone on the profile of cytokine secretion in whole blood cell cultures from healthy subjects and to analyse the gender-related sensitivity to dexamethasone on each cytokine secretion. RESULTS: There was a significant inhibition by dexamethasone (from 1 to 100 nM) on the secretion of monokines (IL-1beta, IL-6, IL-8 and TNF alpha) and lymphokines (IL-2, IL-4, IL-10 and IFN gamma), either after LPS or PHA stimulation (P < 0.01). Interleukin 4 and IL-10 were less inhibited than IFN gamma (P < 0.05 at 1 nM, P < 0.01 at 10 nM and P < 0.001 from 100 nM to 10 microM). No gender difference was observed in the rate of inhibition of the secretion of each cytokine. CONCLUSION: This study shows that the inhibition of cytokine secretion by dexamethasone is more marked on Th1-type cytokines than on Th2-type cytokines. These data support the idea that glucocorticoids may induce a shift from the Th1 to Th2 profile of cytokine secretion.
TNF-alpha is involved in infectious and immuno-inflammatory diseases. Different individuals may have different capacities for TNF-alpha production. This might determine a predisposition to develop some complications or phenotypes of these diseases. The aims of our study were to assess the inter-individual variability of TNF-alpha production and to correlate this variability to a single base pair polymorphism located at position -308 in TNF gene. We studied 62 healthy individuals. TNF-alpha production after LPS stimulation was evaluated using a whole blood cell culture model. The TNF gene polymorphism was studied by an allele-specific polymerase chain reaction. Other cytokines produced in the culture, soluble CD14 concentrations and expression of CD14 on blood cells were also measured. Among the 62 individuals, 57 were successfully genotyped. There were 41 TNF1 homozygotes and 16 TNF1/TNF2 heterozygotes. TNF-alpha production after LPS stimulation of whole blood cell culture was higher among TNF2 carriers than among TNFI homozygotes (929pg/ml (480-1473pg/ml) versus 521 pg/ ml (178-1307 pg/ml); P<0.05). This difference was even more significant after correction of TNF-alpha production for CD14 expression on blood cells. In conclusion, the single base pair polymorphism at position -308 in the TNF gene may influence TNF-alpha production in healthy individuals.
OBJECTIVES: Corticosteroid dependency in Crohn's disease (CD) is characterized by the need for chronic use of corticosteroids to maintain clinical remission. Several definitions have been used. Depending on the definition, 10-30% of the patients are considered as corticosteroid dependent. The aim of the study was to define a clinical pattern of corticosteroid dependent CD patients. PATIENTS AND METHODS: Epidemiological and clinical characteristics were retrospectively compared between 20 corticosteroid dependent CD patients and 248 non-corticosteroid dependent CD patients by using univariate and multivariate analyses. Corticosteroid dependency was defined either by two successive relapses during the 2 months after discontinuing glucocorticoids (n=5) or by two successive relapses at dose tapering, after successful treatment of a flare-up by using glucocorticoids (n=15). RESULTS: Corticosteroid dependent CD patients were younger at diagnosis (P < 0.001), and were characterized by a higher frequency of colonic location (P< 0.05), but lower frequency of ileal location (P < 0.01), and higher ano-perineal location (P < 0.05). They were also more frequently smokers (P< 0.05) and users of contraceptive pills (P< 0.01). The inflammatory type of the disease was increased (P < 0.01), while the fibrostenotic type was decreased (P < 0.001) in corticosteroid dependent CD patients. By multivariate analysis, a smoking habit (P < 0.01), a colonic location (P < 0.05), a non-fibrostenotic type (P< 0.05) and a younger age at diagnosis (P< 0.05) were shown to be independently associated with corticosteroid dependency. CONCLUSIONS: This study suggests a clinical pattern associated with corticosteroid dependency. Whether this clinical pattern is simply associated with the dependency, or whether a primary decrease of corticosensitivity produces this clinical pattern, is not known. Further prospective studies will have to determine whether the presence of these clinical characteristics is predictive of corticosteroid dependency and whether this prediction will be useful for the management of this condition.
Patients suffering from inflammatory or dysimmunitary diseases may develop various clinical responses to corticotherapy. This brief article describes the various cellular and molecular mechanisms which underly the genetic, endocrine and immunitary factors involved in corticosensitivity, corticoresistance and corticodependence.
Amiodarone is an antiarrhythmic drug widely used to treat a variety of supraventricular and ventricular arrhythmias. However its drawback is a very slow elimination and very frequent adverse effects (thyroid, pulmonary, neurologic, ocular, dermatologic, hepatic disorders). We describe a patient who developed a pseudoalcoholic liver disease and a cirrhosis after use of Amiodarone for a long period of time.
We report a case of hepatoportal sclerosis in a renal transplant patient treated with azathioprine. The initial symptom was ascites. On the biochemical level, there were cholestasis without cytolysis or hepatocellular insufficiency. A presinusoidal portal hypertension was found on haemodynamic studies, without portal thrombosis at CT-scan. A diagnosis of hepatoportal sclerosis was evoked on histology and attributed to azathioprine. This case gives an illustration of a classical albeit rare complication of azathioprine. The indolent pattern of the disease and the risk of variceal bleeding point out the need for a hepatic follow-up during the treatment.
We report seven patients with both myelodysplastic syndrome (MDS) and inflammatory bowel disease (IBD): Crohn's disease in six cases, ulcerative colitis in one case. We describe their characteristics, and those of 10 previously published similar cases are presented here. Median age at diagnosis of IBD (61 years) was high, as compared to the usual age at diagnosis of IBD. IBD was diagnosed first in nine cases, MDS first in one patient, and both diseases were diagnosed simultaneously in seven cases. Concerning IBD, there was a strong predominance of Crohn's disease (15/17 cases), with an unusually high frequency of colonic involvement (11/15 cases). MDS, in 12/17 cases, showed no excess of marrow blasts. Cytogenetic analysis was abnormal in five of the 13 evaluable cases. These observations suggest that the association between MDS and IBD may not be fortuitous in some cases, and that, in particular, patients with IBD and anemia of nonobvious origin should be evaluated for MDS. The pathogenesis of those associations, however, remains unclear.
BACKGROUND/AIMS: Relapses of Crohn's disease are difficult to predict. We assessed the value of serum level of interleukin-6, tumour necrosis factor alpha (TNF-alpha) and soluble TNF receptors as predictors of relapse in quiescent Crohn's disease. PATIENTS/METHODS: Thirty-six patients with inactive Crohn's disease, treated or not, were included. Various clinical and biological parameters, including interleukin-6, TNF-alpha and soluble TNF receptors serum levels were measured at inclusion in the study and the patients were followed clinically for 1 year. The relapse was defined as a Crohn's Disease Activity Index (CDAI) greater than 150 with an increase greater than 100 compared to the inclusion value. We analysed the ability of these parameters to predict relapse in parallel to clinical characteristics and other laboratory parameters. RESULTS: Among the 32 variables tested, interleukin-6 serum level had the greatest ability to predict the time-to-relapse, with 17-fold chance of relapse over a 1-year period for patients with an interleukin-6 serum level greater than 20 pg/ml than for patients with a lower level (P < 0.001). A high serum level of the soluble TNF receptors p55 and p75 also had significant predictive value, in contrast to TNF-alpha serum levels. An interleukin-6 serum level greater than 20 pg/ml and either an acid alpha-1-glycoprotein level greater than 1.1 g/l or a soluble interleukin-2 receptor serum level greater than 95 pM/l were risk factors selected by a stepwise multivariate analysis. In both models a good prognosis group was defined by the absence of the two risk factors, a bad prognostic group by the presence of the two risk factors and an intermediate in between. With both models, the good prognosis group included 17 patients who experienced no relapse over the 1-year follow-up, whereas all patients (seven with the first model and six with the second) in the bad prognosis group had a relapse during the follow-up. Looking specifically at two homogeneous subgroups including either naturally/5-aminosalicylic acid (5-ASA) quiescent or corticoid quiescent patients, a very good predictive value for interleukin-6 serum concentration was also found. CONCLUSION: Interleukin-6 serum level alone or in association with other biological parameters such as acid alpha-1-glycoprotein or the soluble interleukin-2 receptor serum level may be useful for predicting the course of the disease in patients with quiescent Crohn's disease.
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Explore the source record for details and available documents.