Biomedical subjects
Publications and source records attributed to P Perney.
The authors report a case of near complete regression of a focal nodular hyperplasia of the liver over a course of 10 years in a 39 year old woman. This presentation is atypical because of its imaging features (initially typically hypervascular, to eventually become a fibrous scar after undergoing a pseudo-angiomatous phase) and because of its near complete spontaneous regression.
INTRODUCTION: A major episode of hepatic cytolysis, rapidly regressive and occasionally recurrent, evokes a bilary or toxic pathology. We report an exceptional case in which several episodes of cytolysis were secondary to a paroxystic cardiac rhythm disorder. OBSERVATION: A 44 year-old woman was hospitalized 3 times during 4 months for episodes of asthenia and rapidly regressive cytolysis. Lithiasic, viral, metabolic, autoimmune and toxic causes were eliminated. A cardiac rhythm disorder was revealed during the last two episodes and diagnosis was made of intermittent and asymptomatic ventricular tachycardia, secondary to arryhthmogenic right ventricular dysplasia, and was confirmed on the electrocardiogram, cardiac scan and magnetic resonance imaging. Treatment of the cardiac rhythm led to the absence of further relapse. COMMENTS: In our patient, the clinical and chronological imputability appeared highly probable. The responsibility of perturbed cardiac rhythm in the genesis of an ischemic hepatopathy is classical, but little documented. Our observation confirms that severe unexplained cytolysis requires systematic search for a cardiac rhythm disorder, even in the absence of a known or symptomatic cardiopathy.
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BACKGROUND: Porphyria cutanea tarda (PCT) is associated in most cases with iron overload, which may participate in decreased activity of uroporphyrinogen decarboxylase in the liver. The aetiology of this iron overload remains unknown; however, it has been demonstrated that mutations of HFE, the genetic haemochromatosis gene, might be present in a significant proportion of Anglo-Saxon and Italian patients. Furthermore, transferrin receptor polymorphism may influence the affinity of this receptor to its ligand with a subsequent increase of cellular iron absorption and storage. OBJECTIVES: To evaluate the incidence and spectrum of HFE mutations and the relative frequency of the two main alleles of transferrin receptor in patients with PCT originating from southern France, and to evaluate the relationship of these genetic data with iron status, and with hepatitis B and C and human immunodeficiency virus (HIV) infections. METHODS: Thirty-six consecutive patients with either sporadic or familial PCT were prospectively included between 1997 and 2000. Search for the presence of the three main mutations of the HFE gene and identification of the transferrin receptor alleles were performed using polymerase chain reaction followed by enzymatic digestion. Iron parameters and viral status for hepatitis B and C viruses and HIV were determined. RESULTS: Seven patients (19%) showed heterozygous C282Y mutation, but no C282Y homozygote was present; five patients (14%) carried homozygous H63D mutation, while eight (22%) were heterozygous for this mutation. One patient was heterozygous for the S65C mutation (3%). Iron parameters demonstrated overload in all patients, without a clear difference between patients with and without deleterious mutations of the HFE gene. Infection by hepatitis C virus was documented in 20 patients (56%), and was significantly less frequent in patients with deleterious HFE mutations. The profile of transferrin receptor alleles in PCT patients did not show significant variation compared with the general population. CONCLUSIONS: This study confirms the high frequency of HFE mutations in patients with PCT and supports the hypothesis that HFE gene abnormalities might play a significant part in the PCT pathomechanism, probably through iron overload; by contrast, transferrin receptor polymorphisms do not appear to play a significant part in iron overload in PCT.
OBJECTIVES: To describe the characteristics of in-patients with alcoholic liver disease in Hepatogastroenterology and to evaluate whether geographic location was a risk factor for cirrhosis. METHODS: A French, national, multicenter, prospective investigation was performed in the last quarter of 1997. To be included in the study, patients had to have drunk at least 50 g of alcohol per day for the past year or to have cirrhosis. RESULTS: Seventeen centers included 802 patients, 20% had histologically proven cirrhosis or probable cirrhosis. Thirty-five percent had undergone liver biopsy. Twenty five percent of these patients had cirrhosis without acute alcoholic hepatitis and 37% had cirrhosis with acute alcoholic hepatitis. After dividing France along a Bordeaux-Strasbourg axis, there was more histologically proven or probable cirrhosis in the North (46%) than in the South (36%) (P<0.005) while daily alcohol intake was greater the South (150 +/- 6 g) than in the North (129 +/- 4 g) (P<0.0001). When the six variables (age, sex, daily consumption of alcohol over the past 5 years, presence of hepatitis B surface antigen and antibodies to hepatitis C virus, total duration of alcohol abuse) were considered together in stepwise logistic regression analysis, geographic location changed the prediction of cirrhosis. The odds ratio for cirrhosis in patients living to the North of the Bordeaux-Strasbourg axis was 1.9 (95% confidence interval range 1.1-3.2) (P<0.02), suggesting the role of nutritional factors.
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BACKGROUND: Liver iron deposits are frequent in viral C cirrhotic patients but their role is not well defined. AIMS: To investigate the effect of liver iron excess on the prevalence of hepatocellular carcinoma (HCC) in patients with viral C cirrhosis. METHODS: Hepatic iron was evaluated retrospectively using a semiquantitative method in liver biopsies of 104 viral C cirrhotic patients, 48 with HCC and 56 controls (HCC free). Corrected total iron score (0-60) was defined by the sum of three scores: hepatocytic iron score (0-36), sinusoidal iron score (0-12), and portal iron score (0-12), multiplied by 3/3, 2/3, or 1/3 according to the heterogeneous iron localisation in the nodules. RESULTS: After adjustment for known risk factors for HCC, regression analysis showed that iron deposits (corrected total iron score >0) were more frequent in HCC patients than in controls (odds ratio 4.94; 95% confidence interval 1.59-15. 32; p=0.0056). The median of corrected total iron score was significantly higher in HCC patients than in controls (odds ratio 1. 092; 95% confidence interval 1.01-1.13; p=0.021). This liver iron overload was sinusoidal (odds ratio 5.2; 95% confidence interval 1. 82-15.11; p=0.0022). CONCLUSIONS: Liver iron deposition was more frequent and more important in viral C cirrhotic patients with HCC than in HCC free controls. Liver iron overload seems to contribute to the development of HCC in patients with viral C cirrhosis.
Antiphospholipid antibodies (aPL) have been detected in various liver diseases, particularly cirrhosis. The role of alcoholic consumption per se has been suggested. The aim of our study was to assess the prevalence of aPL in patients with alcoholic liver disease at various states and to correlate the presence of aPL with both liver injury and alcoholic consumption. Three groups were prospectively included. Group A: 74 controls (age- and sex-matched); group B: 46 patients with alcoholic steatosis; group C: 28 patients with alcoholic cirrhosis. For each patient, lupus anticoagulant, anticardiolipin antibodies and anti-beta2-glycoprotein I antibodies were tested. The prevalence of aPL (presence of at least one positive test) was 5% in group A, 20% in group B and 50% in group C (P < 0.04). No correlation appeared between aPL and Child Pugh score in group C. No correlation was found between the presence of aPL and alcohol intake in patients with either steatosis or cirrhosis. Our study confirms that aPL positivity is more frequently encountered in patients with alcoholic liver disease than in controls. Their prevalence increases with the degree of histological damage but not with the level of alcoholic intake.
BACKGROUND/AIMS: Bacterial infections, specially Staphylococcus aureus (S. aureus) septicemia, remain a leading cause of death following liver transplantation. It has been demonstrated that nasal carriage of S. aureus is associated with invasive infections in patients undergoing hemodialysis and could be decreased by use of antibiotic nasal ointment. However, in cirrhotic patients, the frequency of nasal carriage is unknown. The aims of this study were to determine the prevalence of S. aureus nasal carriage in cirrhotic patients and to assess nosocomial contamination. METHODS: One hundred and four patients were included in a prospective study, 52 cirrhotic and 52 control (hospitalized patients without cirrhosis or disease which might increase the rate of nasal carriage of S. aureus). On admission and after a few days of hospitalization, nasal specimens from each anterior naris were obtained for culture. S. aureus was identified by the gram strain, positive catalase and coagulase reactions; antibiotic susceptibility was determined using a disk-diffusion test. RESULTS: Both groups were similar with regard to age and sex. The prevalence of nasal colonization on hospital admission was 56% in cirrhotic patients and 13% in control patients (p = 0.001). After an average of 4 days, 42% of cirrhotics and 8% of control patients were colonized (p = 0.001), without any nosocomial contamination. Three strains out of 29 were oxacillin-resistant in cirrhotic patients, and none in controls (p>0.05). There was no statistical difference in carriage rate according to sex, age, cause of cirrhosis and Child-Pugh score. Previous hospitalization (OR, 6.3; 95% CI, 2.3 to 19.9; p = 0.0006) and cirrhosis (OR, 4.4; 95% CI, 1.5 to 13.4; p = 0.0048) were independent predictors of colonization. CONCLUSION: Cirrhotic patients had a higher S. aureus nasal carriage rate than control subjects. Previous hospitalization and cirrhosis diagnosis were correlated to nasal colonization. Further studies are necessary to determine if nasal decontamination could reduce S. aureus infections after liver transplantation.
BACKGROUND/AIMS: Alcoholic cirrhosis remains a controversial indication for liver transplantation, mainly because of ethical considerations related to the shortage of donor livers. The aim of this study was to review experience to date, focusing on survival rates and complications, and the effect of alcohol relapse on outcome and alterations in marital and socioprofessional status. METHODS: The results for 53 patients transplanted for alcoholic cirrhosis between 1989 and 1994 were compared with those for 48 patients transplanted for non-alcoholic liver disease. The following variables were analysed: survival, rejection, infection, cancer, retransplantation, employment and marital status, alcoholic recurrence. The same variables were compared between alcohol relapsers and non-relapsers. RESULTS: Recovery of employment was the only significantly different variable between alcoholic (30%) and non-alcoholic patients (60%). Two factors influenced survival in the absence of alcohol recidivism: age and abstinence before transplantation. For all other variables, there were no differences between alcoholic and non-alcoholic patients, and, within the alcoholic group, between relapsers and non-relapsers. The recidivism rate was 32%. CONCLUSION: The data indicate that liver transplantation is justified for alcoholic cirrhosis, even in cases of recidivism, which did no affect survival and compliance with the immunosuppressive regimen. These good results should help in educating the general population about alcoholic disease.
OBJECTIVES: To study the frequency of tumor seeding after percutaneous biopsy of hepatocellular carcinoma and to evaluate the impact on long-term survival. METHODS: Records of 150 patients with cirrhosis who underwent ultrasound-guided aspiration biopsy for hepatocellular carcinoma between 1989 and 1996 were reviewed in June 1998. Liver transplantation was performed in 7 patients. One to three needle passes were performed with 18 to 20 gauge needles. Follow-up included regular clinical examinations and ultrasonography or computerized tomography. RESULTS: Four cases (2.66%) of subcutaneous metastasis were noted at the needle insertion site; none in transplanted patients. All patients had viral cirrhosis, Okuda class I. Nodules were detected 4, 12, 22 and 24 months after biopsy. The second patient is alive 24 months after tumor seeding. For other patients, survival time was 4, 24 and 60 months respectively, without local tumor extension after surgical resection or radiotherapy. During a mean 11.8 months of follow-up, 127 patients died without tumor seeding. Eleven patients are still being followed and have no signs of needle tract implantation of hepatocellular carcinoma (mean follow-up 34.7 months). CONCLUSION: The prevalence of tumoral seeding after percutaneous biopsy of hepatocellular carcinoma was 2.66%, which is higher than in previous studies. After liver transplantation, no evidence of needle tract seeding was identified. Survival did not seem to be influenced by local evolution.
BACKGROUND: Ecstasy is a synthetic amphetamine which causes a wide variety of adverse effects. Hepatic toxicity was only recently demonstrated but can be quite severe. CASE REPORT: A 27-year-old male with no past medical or surgical history developed jaundice without fever. He was a regular user of ecstasy and had recently increased the number of doses consumed. No evidence of a viral, alcoholic, metabolic or autoimmune mechanism was found which could explain the hepatitis. Complete cure was obtained by discontinuing ecstasy. DISCUSSION: Few cases of ecstasy hepatic toxicity have been reported. Ecstasy was undoubtedly the causal agent in this case since other known causes of acute hepatitis were excluded, confirming the hepatotoxicity of ecstasy reported in the literature. The liver disease has been reported to range form acute regressive hepatitis to fatal liver failure. Iterative exposure can lead to fibrosis. The pathophysiological mechanism of this toxic effect is not well elucidated. Ischemia alone cannot explain all the clinical forms described, particularly cases without hyperpyrexia. Ecstasy must be added to the list of potential causes of acute hepatitis. Exposure must always be searched for in cases of acute hepatitis in young subjects.
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Increased plasma and CSF concentrations of substances which bind to brain benzodiazepine receptors have previously been reported in cirrhotic patients with hepatic encephalopathy (HE). However, their relationship to previous intake of pharmaceutical benzodiazepines has not been clearly established. In the present study, plasma levels of benzodiazepine receptor ligands (BZRLs) were measured using a sensitive radioreceptor assay in 12 control subjects with no evidence of hepatic, neurological or psychiatric illness, 11 cirrhotic patients without HE, 24 cirrhotic patients with moderate (grade I-II) HE and in 45 cirrhotic patients with severe (grade II-IV) HE. In addition, CSF concentrations of BZRLs were measured in 8 cirrhotic patients with HE and an equal number of age-matched controls. Recent intake (within 10 days) of pharmaceutical benzodiazepines was assessed by detailed review of medical files, and interviews with the patient, at least one family member as well as the pharmacist. Significantly increased plasma concentrations of BZRLs were observed in cirrhotic patients with severe encephalopathy (p < 0.02) compared to controls and to cirrhotic patients without (or with mild) neurological impairment. Increased plasma BZRLs could be accounted for by prior exposure to benzodiazepine medication in all cases. CSF concentrations of BZRLs in cirrhotic patients were not significantly different from control values. These findings do not support a role for "endogenous" benzodiazepines in the pathogenesis of HE in chronic liver disease but suggest that pharmaceutic benzodiazepines administered to cirrhotic patients as sedatives or as part of endoscopic work-up could have contributed to the neurological impairment in some patients.
Although the efficacy of 5-fluorouracil (5-FU) modulated by leucovorin is well established for advanced colorectal cancer, the question of the most effective regimen and optimal dose of leucovorin remains unanswered. This prospective randomized trial compares low-dose (group 1) and high-dose (group 2) leucovorin, combined with the same dose of 5-FU to determine whether high-dose leucovorin was more beneficial than low-dose on overall survival. Inclusion criteria were: unresectable metastatic colorectal carcinoma, with or without evaluable tumor response; a performance status of less than grade 3 (World Health Organization classification); and no previous chemotherapy for metastases. Forty-two patients were randomized in group 1 (leucovorin, 20 mg/m2/day, days 1 through 5) and 41 patients in group 2 (leucovorin, 200 mg/m2/day, days 1-5). All the patients in the two groups received a 1-hour infusion of 400 mg/m2/day 5-FU every 4 weeks. The two groups were matched with no statistically significant differences in gender ratio, site of primary tumor, performance status, and tumor extent. Toxicity in the two regimens was low and not significantly different between the two groups. Overall median survival was 346 days in group 1 and 323 days in group 2 and was not significantly different between the two groups. At 1 year, the test of equivalence was significant (p < 0.01), demonstrating an absence of more than 20% benefit in 1-year survival for the high-dose regimen. The use of high-dose leucovorin combined with 5-FU in the 5-day regimen does not significantly improve overall survival for patients who have metastatic colorectal cancer.
AIMS/BACKGROUND: We report the discovery of associated metastatic subcutaneous and metastatic diaphragmatic nodules on the needle track after fine-needle biopsy aspiration under echography, which has not yet been reported in the literature. METHODS: A 35-year-old man with non-replicating hepatitis B virus presented with a tumor that suggested hepatocarcinoma with cirrhosis. A diagnostic needle biopsy was carried out before surgery. Twelve months later, he presented with a series of four continuous metastatic diaphragmatic nodules on the inner wall lining the needle track. Surgery was performed, followed by external radiation (40 Gy). CONCLUSIONS: The risk of seeding following fine-needle biopsy aspiration of hepatocellular carcinoma can no longer be considered negligable. The real risk is probably underestimated. Even for biopsy of lesions localized to the inferior part of the liver, diaphragmatic seeding is possible. This seeding necessitates surgical resection, increasing the therapeutic morbidity of hepatocellular carcinomas. We believe that in cases where investigation of a small hepatic tumor suggests a hepatocellular carcinoma that could be resected, or for candidate patients for liver transplantation. one should not puncture the tumor. If this diagnostic biopsy is essential, then the needle track could be resected upon surgery, after cutaneous external tattooing.
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