[Obesity and increase in transaminase, a dangerous and obvious link].
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Biomedical subjects
Publications and source records attributed to Catherine Buffet.
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OBJECTIVE: Viruses might be one of the elements that trigger systemic lupus erythematosus (SLE). Steroid therapy may influence the natural history of virus infections. The most frequent extrahepatic manifestations of hepatitis C virus (HCV) including arthralgia, myalgia, sicca syndrome, and antinuclear antibodies, may mimic a connective tissue disease, particularly SLE. Reports on the association between SLE and HCV infection are scarce. We investigated the association of HCV infection and SLE. METHODS: Retrospective case-control monocentric study of 19 patients with SLE and anti-HCV antibodies versus 42 randomized SLE patients without anti-HCV antibodies, matched for age and sex, coming from our cohort of 700 patients with SLE. SLE and HCV-infection features were reviewed. RESULTS: Mode of infection was blood product transfusion, drug addiction, or unknown. Prevalence of lupus clinical manifestations, antinuclear, anti-dsDNA, anti-extractable nuclear antigen antibodies, and complement levels was not different between HCV positive and negative SLE patients. Prevalence of cryoglobulin was higher in SLE patients with anti-HCV antibodies (p < 0.04), but none had a mixed cryoglobulinemia syndrome. ALT activity was increased in 11 HCV positive patients and 13 had detectable HCV RNA. Liver biopsy showed cirrhosis in 2 and mild fibrosis and activity in 5. One patient treated with interferon-alpha had a sustained virological response without SLE flare. Steroid therapy did not seem to alter HCV course. CONCLUSION: SLE in HCV positive patients shows higher prevalence of cryoglobulin without mixed cryoglobulinemia syndrome. HCV infection has moderate signs of biochemical and liver pathological severity. SLE by itself or treated with steroids does not seem to worsen HCV infection.
Osseous metaplasia is rare in tumors of the gastrointestinal tract. We report the case of a 76-year-old man presenting with an adenocarcinoma of the transverse colon containing osseous tissue. Calcifications were seen on the abdominal CT-scan. Pathogenesis of the osseous metaplasia is still unknown.
Helicobacter pylori (Hp) infection is one of the most common chronic bacterial infections worldwide. The pathogenic properties of Hp are due to its ability to survive in the gastric juice, to escape the gastric acidity and to colonise the crypts of the gastric mucosa. Eradication of Hp is needed for patients with a gastroduodenal ulcer associated with Hp gastritis. Eradication modifies the natural history of the disease and greatly reduces the risk of recidive and the consequences of the discovery of Hp have been spectacular, in particular in duodenal ulcer disease. A tritherapy regimen given for 7 days combining a double-dosed proton pump inhibitor, amoxicillin (2 g/d) and clarithromycin (0.5 g bid) is used. Persistent infection may lead to a progression toward atrophy, intestinal metaplasia, dysplasia and eventually cancer. However, systematic eradication in order to reduce the incidence of gastric adenocarcinoma is not recommended. Acquisition of mucosa-associated lymphoid tissue (malt) lymphoma is related to gastritis induced by Hp infection and is commonly postulated as the initial stage in the development of malt lymphoma. Eradication is also indicated for patients with lymphoma with a low degree of malignancy.
We report a unique, previously unreported pancreatic tumor with hepatoid differentiation associated with serous microcystic adenoma in a 70-year-old man. These two lesions localized, respectively, at the body and the tail of the pancreas, were found incidentally on abdominal ultrasonography. Serum alpha-fetoprotein was not increased and no hepatic lesion was displayed on computed tomography. A subtotal pancreatectomy with splenectomy was performed. The patient is alive and well 12 months after resection. Pathological examination showed a very unusual encapsulated solid tumor with hepatocytic differentiation, bile production and immunoreactivity for hepatocyte paraffin-1 antibody. The tumor cells were negative for endocrine (neuron-specific enolase, chromogranin A, synaptophysin) and acinar (amylase, trypsin) markers. Ultrastructurally, zymogen and neurosecretory granules were absent. The features of the tumor were almost indistinguishable from those of hepatocellular adenoma; therefore, we believe that this solid hepatoid tumor may represent a variant of pancreatic adenoma. Recognition of this entity is important because the only reported pancreatic hepatoid tumors to date have been malignant. The main differential diagnoses include hepatoid ductal adenocarcinoma, hepatoid acinar cell carcinoma, primitive hepatoid endocrine tumor, and metastatic hepatocellular carcinoma.
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BACKGROUND: Pancreatitis is the most common complication of ERCP. Calcium channel inhibitors have been shown to prevent the development of experimental pancreatitis. The aim of this randomized, placebo-controlled trial was to determine whether the calcium channel blocker nifedipine prevents post-ERCP pancreatitis. METHODS: Patients referred for ERCP were enrolled. Those being treated with a calcium channel inhibitor and those with acute or chronic pancreatitis were excluded. Nifedipine or placebo was administered orally less than 3 hours before and within 6 hours after ERCP. The main outcome measure was the number of cases of post-ERCP pancreatitis; a secondary outcome was the rate of post-ERCP pain (without pancreatitis) that persisted for 12 or more hours. RESULTS: One hundred fifty-five patients (70 women, 85 men; mean [SD] age 65.8 [18.2] years; range, 23-97 years) were enrolled and randomized to receive nifedipine (76 patients) or placebo (79 patients). The two groups were comparable. Procedures performed were retrograde diagnostic cholangiopancreatography alone (n = 33), biliary sphincterotomy (n = 31), stone extraction (n = 39), stent placement (n = 37), sphincteroplasty (n = 5), and other (n = 3). ERCP was unsuccessful in 5 patients. A single case of severe pancreatitis was observed (placebo group). The rate of post-ERCP pancreatitis was not different between groups (nifedipine, 10 patients, 13.2%; placebo, 14 patients, 17.7%; p = 0.4). The frequency of post-ERCP pain was not different between the groups. The only independent predictor of post-ERCP pancreatitis was difficult cannulation in both groups (OR = 3.78: 95% CI [1.25, 11.45]). CONCLUSION: This study failed to demonstrate a significant effect of nifedipine in the prevention of post-ERCP pancreatitis. A multicenter trial with greater statistical power would be needed to demonstrate a benefit for this drug.
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BACKGROUND: Local and infiltrative extension make some biliary carcinomas accessible to nonoperative intraductal destruction. This study assessed the clinical feasibility and short-term results of local tumor destruction with an intraductal high-intensity US probe during ERCP. METHODS: The probe is a flexible catheter with an 8 x 2.8 mm US transducer and a lumen for a guidewire. Ten patients (6 women, 4 men; mean age 74.8 years) were treated with this device. Lesions treated included carcinoma of the papilla (3), bile duct cholangiocarcinoma (2), Bismuth grade I and II hilar cholangiocarcinomas (4), and intrahepatic cystadenocarcinoma (1). Two patients underwent US therapy before surgery. Treatment was performed during standard ERCP: the probe was inserted through the malignant stricture and US therapy was applied over 360 degrees under fluoroscopic control. RESULTS: No serious adverse effects were observed; right upper abdominal pain developed in one patient for 12 hours. In one patient, histopathologic assessment of the resected tumor revealed extensive coagulation necrosis with inflammation up to 10 mm in depth surrounding the bile duct lumen. In the other operated patient, biopsy specimens from the treated portion of the bile duct were negative for malignancy. There was complete regression of cholangiocarcinoma of the bile duct in our patient, allowing for permanent stent removal (follow-up 30 months). A partial response was noted in 4 other patients and no response in 3 patients. CONCLUSIONS: This new method of intraductal tumor destruction by high-intensity US during ERCP is feasible and can induce objectively measurable tumor necrosis. Long-term follow-up will determine whether this method is curative in some cases and if it can reduce the need for biliary stent placement.
Patients with cirrhosis and portal hypertension have increased thoracic duct lymph flow. Correction of portal hypertension is associated with decreases in thoracic duct flow. The authors present a case of rapid resolution of refractory chylothorax caused by thoracic duct injury proven by lymphangiography and helical CT scan in a patient with cirrhosis of the liver by using a transjugular intrahepatic portosystemic shunt to decrease portal pressure and thereby reduce thoracic duct lymph flow.
Groove pancreatitis is a rare form of segmental chronic pancreatitis which is localized within the head of the pancreas, the duodenum and the common bile duct. Symptoms are due to common bile duct stenosis or duodenal stenosis. Radiologically, there is a pancreatic mass, which hinders differential diagnosis with pancreatic carcinoma. We report here a case of groove pancreatitis observed in a 41-year-old man treated by pancreatoduodenectomy. Histological features of the groove scar were noted. Our case and cases reported in the literature lead to hypotheses concerning the pathogenesis and clinical, biological, and radiological features suggestive of the diagnosis.