Catherine Buffet
University of Paris-Sud
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Digestive Diseases and Sciences | 1995
Claude Altman; Pierre Bedossa; Elisabeth Dussaix; Catherine Buffet
CMV infections of the gastrointestinal tract are common in immunocompromised patients (1). In contrast, reports of CMV infections of the gastrointestinal tract in normal hosts are few (2). Esophageal infection has been previously reported in a single immunocompetent host who was a trauma victim who developed acute erosive esophagitis with CMV inclusions after multiple blood transfusion and a splenectomy (3). CMV may also involve the stomach (4, 5) and small ( 6 -8 ) or large intestine (6, 9-11). In this report, we describe a patient with CMV esophageal infection and normal immunity.
Digestive Diseases and Sciences | 1987
Catherine Buffet; A. Corriat; T. Soni; G. Pelletier; A. Lemonnier; Jean-Pierre Etienne
To the Editor: A 36-year-old female college psychology professor was hospitalized for alcohol abuse 10 weeks prior to admission and placed on disulfiram 125 mg daily. After discharge eight weeks later she began to observe jaundice, anorexia, dark urine, and weakness. Disulfiram was discontinued without benefit. When initially examined by one of us (R.H.R.) she was lucid and deeply jaundiced but without stigmata of chronic liver disease. Within 36 hr, hospitalization was required due to precipitous onset of hepatic coma. There was no history of blood transfusions, illicit drug abuse, exposure to jaundiced patients, or recent alcohol use. Laboratory data showed AST, 1095 IU/liter; alkaline phosphatase, 333 IU/liter; total bilirubin, 31 mg/dl; glucose, 62 mg/dl; prothrombin time, 37.4/11.2 sec, fibrinogen, 62 mg/dl. Antibodies to hepatitis B surface antigen and hepatitis B core antigen were found (attributed to known work-related exposure 10 years earlier). Acetoaminophen levels were undetected. The patients subsequent course was rapidly downhill with the occurrence of gastrointestinal bleeding, pneumonia, cerebral edema, status epilepticus, and renal failure, terminating fatally at one week after entry. Massive hepatic necrosis without fibrosis was seen at postmortem examination. This case represents the thirteenth reported instance of disulfiram-induced hepatitis; seven cases ended fatally. This is the second instance in which encephalopathy occurred after drug treatment was discontinued (1,2). Only one of the other fatal cases lacked fibrosis histologicaIly--a presumed indication of chronic alcohol toxicity. Physicians must be alerted to the potential for hepatotoxic injury in the alcoholic with this agent. Presumably, close monitoring of function tests after initiating treatment will be mandatory.
Digestive Diseases and Sciences | 1986
Catherine Buffet; J. C. Homberg; Gilles Pelletier; K. Turner; Jean-Pierre Etienne
SummaryWe report the findings in two sisters with active cirrhosis and an anti-liver-kidney microsomal antibody (anti-LKM) of the autoimmune type. This unusual disease is characterized by the presence of high levels of antibodies that react with the smooth and rough endoplasmic reticulum of the liver and other tissues. Our patients had the usual features of chronic hepatitis associated with presence of antibodies: they were young girls, they had anti-LKM antibodies of autoimmune type persisting at a high titer during the whole course of the disease, but with no smooth muscle antibodies; one had a low level of IgA. The occurrence of two cases in the same family has not yet been reported and is probably not coincidental because of the rare occurrence of this disease.
Digestive Diseases and Sciences | 1995
F. Durand; Catherine Buffet; Gilles Pelletier; H. Hagege; O. Ink; Jean-Pierre Etienne
To The Editor: The usefulness of hepatocellular carcinoma screening in cirrhotic patients has been questioned (1-3). From July 1987 to September t989, 193 cirrhotic patients (127 males and 66 females; mean age 56 years; range: 34-71 years) were enrolled for hepatocellular carcinoma detection in our institution. In these patients, clinical evaluation, serum c~-fetoprotein assay, and real-time ultrasonography were performed every six months. The causes of cirrhosis were alcoholism, hepatitis B virus, hepatitis C virus, and miscellaneous in 76%, 5%, 2.6%, and 16.4% of the cases, respectively. The diagnosis of hepatocellular carcinoma was either biopsy proven or based on the association of serum ~-fetoprotein level above 500 /~g/liter and focal lesion on ultrasonography. Among these 193 patients, hepatocellular carcinoma was discovered in seven (at enrollment in three patients, at 12 months in three, and at 18 months in one; overall incidence 1.8% per year in our population). The tumor was unifocal in three patients (with only one less than 3 cm in diameter) and multifocal in the remaining four patients. Only one patient underwent surgical treatment--liver transplantation. The estimated survival rate of the seven patients was calculated by the Kaplan-Meier method. Survival rate for these seven patients at 6 and 12 months was 60% and 30%, respectively. Among the 186 patients who did not develop hepatocellular carcinoma, 16 required further investigations because of focal lesion on ultrasound scanning and/or elevation of serum c~-fetoprotein (AFP) level. During the same period, 54 cirrhotic patients (42 males and 12 females; mean age 62 years) were admitted to our institution for symptomatic hepatocellular carcinoma. The diagnosis of hepatocellular carcinoma was made by liver biopsy in 28 patients and by the association of suggestive ultrasonographic findings and of diagnostic levels of AFP (>500 ng/ml) in 24 patients. In another two patients the diagnosis was based on suggestive findings at ultrasound and angiographic examinations and on elevated levels of AFP, <500 ng/ml. None of these patients had been screened for hepatocellular carcinoma previously. The causes of cirrhosis in this group were: alcoholism, hepatitis B virus, and miscellaneous in 78%, 15%, and
Scandinavian Journal of Gastroenterology | 2016
Thibaut Vaysse; Isabelle Boytchev; Guillemette Antoni; Damien Sainte Croix; André Daniel Choury; Valérie Laurent; Gilles Pelletier; Catherine Buffet; Rita Bou-Farah; Franck Carbonnel
Abstract Introduction: There is still uncertainty regarding the efficacy and optimal modalities of extracorporeal shock wave lithotripsy (ESWL) in the treatment of chronic pancreatitis. The aims of the present study were to assess the safety and the efficacy of ESWL, either alone or followed by therapeutic endoscopic retrograde cholangiopancreatography (adjuvant ERCP) and to determine predictive factors of efficacy, in a real-life setting. Patients and methods: This study included all consecutive patients who underwent an ESWL in a single University Hospital between 2001 and 2012. The indication for ESWL was obstructive stone(s) of the main pancreatic duct resulting in either painful chronic pancreatitis or recurrent acute pancreatitis. Success was defined by resolution of pain, no analgesic treatment, no acute pancreatitis and no surgical treatment for chronic pancreatitis 6 months after the ESWL. Results: One hundred and forty-six patients were studied; 6/146 (4%) had a complication of ESWL. Among the 132 patients in whom follow-up was completed, 91 (69%) had an adjuvant ERCP. After 6 months of follow-up, 100/132 (76%) patients achieved success. In multivariate analysis, the single significant predictive factor of the success of the ESWL treatment was chronic pain (p = 0.03). Patients who had chronic pain and needed opioid treatment had less chance of success than patients without chronic pain (OR 95%CI 0.31 [0.07–1.14]). We found no difference in the success rates between patients who underwent adjuvant ERCP and those who had ESWL only (p = 0.93). Conclusion: This study shows that the ESWL is a safe and effective treatment for patients with chronic pancreatitis and obstructive stones within the main pancreatic duct. Systematic association with therapeutic ERCP appears to provide no additional benefit and is therefore not recommended.
The American Journal of Gastroenterology | 2000
Laurent Castéra; Valérie Boige; Laurence Rocher; Jean-Charles Duclos-Vallée; Monique Fabre; Catherine Buffet
TO THE EDITOR: Since the first successful insertion of a metallic prosthesis in 1990 (1), self-expanding metallic stents (SEMS) are increasingly being used for palliation of dysphagia caused by upper gastrointestinal malignancy. Ease of insertion, low procedure-related mortality, and rapid improvement in dysphagia make metal stents a logical choice over plastic ones. Compared to the semirigid plastic prostheses, their safety profile is excellent (2). Tumor ingrowth/overgrowth and stent migration are common, but perforation and procedure related-mortality are exceedingly rare (2, 3). We report a case of refractory ventricular fibrillation after placement of a SEMS. Investigation of dysphagia and weight loss in a 73-yr-old man revealed a stricturing 5-cm tumor at the gastroesophageal junction. Bougie dilation with Savary-Guilliard dilators was performed and biopsies were taken at the time of the initial endoscopy. Histology revealed the tumor to be an adenocarcinoma. The patient had a past history of ischemic heart disease and had been on treatment with amiodarone for episodes of ventricular tachycardia, which had to be discontinued 3 months earlier because of development of side effects. He had not been prescribed any alternative antiarrhythmic since stopping the amiodarone. Computed tomography (CT) of the chest showed local infiltration from the tumor and spread to the regional lymph nodes. In view of his past medical history and CT scan result, surgical treatment was considered inappropriate and he was referred for palliation with a SEMS. Endoscopy was performed under conscious sedation with a combination of midazolam 5 mg and pethidine 25 mg. During the procedure he received supplemental oxygen, and his oxygen saturation was monitored by pulse oximetry. After dilation to 12.8 mm, a size 18-10, Esophacoil stent (Medtronic Instent; Medtronic, Eden Prairie) with a variable release handle, was placed in the lower esophagus and cardia, under fluoroscopy. The prosthesis is constructed from nitinol (nickel-titanium alloy), which is in the form of a tightly wound, coiled spring that shortens and widens on release. Satisfactory position was confirmed at re-endoscopy after placement of the stent. While the endoscope was being withdrawn, the patient’s oxygen saturation dropped, and he became cyanosed and started fitting. As no pulse was palpable, cardiopulmonary resuscitation was commenced. The patient was found to be in ventricular fibrillation (VF). Attempts at resuscitation, including repeated DC shocks, were unsuccessful, and the VF could not be terminated. We believe that, although our patient had underlying risk factors in the form of ischemic heart disease and previous episodes of ventricular tachycardia, the sudden, forceful expansion of the Instent Esophacoil contributed to the development of the VF. Cardiopulmonary complications of sedation, including respiratory depression and arrythmias, are the most common causes of death associated with upper gastrointestinal endoscopies (4, 5). The satisfactory oxygen saturation during the procedure in our patient makes respiratory complication of sedation an unlikely factor. The timing of the VF, on the other hand, suggests that the expansion of the coil prosthesis initiated the fatal arrhythmia by jolting the diseased myocardium. Experience with nitinol coil prostheses is limited, and there have been very few reports in the literature about its complications. Previously it has been reported that the expansion of the Esophacoil may lead to severe pain, necessitating its removal (6), but our report suggests that, very rarely, it may have more serious and unfortunate consequences.
Digestive Diseases and Sciences | 1988
H. Hagege; Catherine Buffet; Gilles Pelletier; A. Roche; Jean-Pierre Etienne
To The Editor: The treatment of pancreatic cholera with metastasis is only palliative. Dr. Oberg et al (1) described two patients with therapy-resistant pancreatic cholera syndrome who were successfully treated with intramuscular human leukocyte interferon. We report here the case of a patient who did not respond to this treatment. A 29-year-old man was hospitalized on July 1985 for severe watery diarrhea (2500 g/day) and flushing attacks. There were hypokaliema (2.2 mmol/liter), gastric hypochlorhydria, and pancreaticocephalic tumor and diffuse hepatic metastasis on computed tomographic scan. Percutaneous liver biopsy showed an islet-cell carcinoma. Plasma vasoactive intestinal polypeptide (VIP) was 1.27 ng/ml (N < 0.30 ng/ml). Gastrin, serotinin, substance P. human pancreatic polypeptide, somatostatin, and thyroid hormones were normal in the plasma. The 5-hydroxyindolacetic acid daily urine output was also normal. Between July and December 1985, three hepatic arterial chemoembolizations and four courses of intravenous 5-fluorouracil and streptozocin failed to control the severe watery diarrhea. Long-acting somatostatin analog (SMS 201-995, Sandoz Laboratories), metoclopramide, nicotinic acid, trifluoperazine, corticosteroids, lithium carbonate, and indometacin did not reduce plasma VIP nor stool volumes. The patient received a 21-day course of intramuscular human alpha-leukocyte interferon (Institut Pasteur, Paris) and a 17-day course of alpha-2recombinant human leukocyte interferon (Dr. J. Bouchet. Boehringer Laboratories, Ingelheim) (Figure 1). The two courses of interferon had no effect on daily stool output or on plasma vasointestinal poiypeptide levels. The tumoral syndrome worsened, and the patient died in February 1986. Some authors reported the effectiveness of the following treatments in pancreatic cholera: longacting somatostatin analog (2), metoclopramide (3),
Digestive Diseases and Sciences | 1988
Catherine Buffet; Hervé Champsaur; Michèle German-Fattal; Thierry Lambert; Marie-José Briantais; Jean-Pierre Etienne
colonoscopy (without entering the terminal ileum) will be normal, the rectal biopsy, for whatever reason involvement of the rectal mucosa seems favored, should not be neglected. This reasoning also pertains to those cases of gross involvement of the cecum and/or ascending colon not reached by the colonoscope. The findings by Prior et al on cecal biopsies are interesting. I have the conviction that if colonoscopy is to be favored over the barium enema as the primary procedure, and then the examination proves to be macroscopically normal and no earlier sigmoidoscopy with biopsies had been performed, biopsies from the rectum should be included among the minimum requirements. BURTON I. KORELITZ, MD Chief, Section o f Gastroenterology Department o f Medicine Lenox Hill Hospital New York, New York
Presse Medicale | 2013
Philippe Sogni; Catherine Buffet
A hyperferritinemia has to be interpreted in relation with age and sex. The clinical evaluation begins with the interpretation of transferrine saturation which has to be controlled with a second fasting blood test. In case of high transferrine saturation associated with hyperferritinemia, HFE testing has first to be realized since the first diagnosis suspected is a HFE hemochromatosis. In case of normal transferrine saturation associated with a hyperferritinemia, the more frequent diagnosis is a metabolic syndrome, an inflammatory syndrome, a syndrome of cellular lysis or an excessive alcohol consumption. In case of HFE hemochromatosis, phlebotomy prevents complications. The goal is to obtain and to maintain a normal-low ferritin level. In case of metabolic syndrome, phlebotomy could be useful in case of high hepatic iron concentration measured with MRI or in case of on-alcoholic steato-hepatitis.
Hepatology | 1999
Laurent Castéra; Isabelle Negre; Kamran Samii; Catherine Buffet