30 results on '"Hautekeete ML"'
Search Results
2. Liver-injury Related To Amoxicillin-clavulanic Acid - Interlobular Bile-duct Lesions and Extrahepatic Manifestations
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UCL - Cliniques universitaires Saint-Luc, UCL - MD/MINT - Département de médecine interne, UCL - MD/MNOP - Département de morphologie normale et pathologique, Hautekeete, ML., Horsmans, Yves, Rahier, Jacques, Brenard, R., Henrion, J., Verbist, L., Derue, G., Druez, P., Omar, M., Kockx, M., Hubens, H., Haber, I., Geubel, André, UCL - Cliniques universitaires Saint-Luc, UCL - MD/MINT - Département de médecine interne, UCL - MD/MNOP - Département de morphologie normale et pathologique, Hautekeete, ML., Horsmans, Yves, Rahier, Jacques, Brenard, R., Henrion, J., Verbist, L., Derue, G., Druez, P., Omar, M., Kockx, M., Hubens, H., Haber, I., and Geubel, André
- Abstract
We report eight cases of liver injury related to amoxycillin-clavulanate, Liver biopsy performed in seven patients revealed varying degrees of injury to interlobular bile ducts in all cases. Lesions included irregularity of the nuclei, vacuolization of the cytoplasm, lymphocytic infiltration, destruction and endothelialization of the bile duct epithelium. Ductopenia was not observed. In two patients liver injury was accompanied by prominent extrahepatic manifestations (acute interstitial nephritis in one and acute lacrimal gland inflammation and sialadenitis with prolonged xerostomia in the other). We conclude that interlobular bile-duct lesions of varying severity are a common feature in liver injury related to amoxycillin-clavulanate, Side effects of the drug include acute interstitial nephritis and sialadenitis.
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- 1995
3. HLA association of amoxicillin-clavulanate--induced hepatitis.
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Hautekeete ML, Horsmans Y, Van Waeyenberge C, Demanet C, Henrion J, Verbist L, Brenard R, Sempoux C, Michielsen PP, Yap PS, Rahier J, and Geubel AP
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- Adult, Aged, Aged, 80 and over, Female, HLA-DQ Antigens genetics, HLA-DQ beta-Chains, HLA-DR Antigens genetics, HLA-DRB1 Chains, HLA-DRB5 Chains, Haplotypes, Humans, Male, Middle Aged, Amoxicillin adverse effects, Chemical and Drug Induced Liver Injury immunology, Clavulanic Acid adverse effects, Histocompatibility Antigens Class II analysis
- Abstract
Background & Aims: Drug-induced immunoallergic hepatitis typically affects a minority of patients exposed to a particular drug. Its rarity is believed to be due to metabolic or immunologic idiosyncrasy. The presence of an immunologic idiosyncrasy might imply an HLA association. Previous studies reporting an HLA association of drug-induced hepatitis included only small numbers of patients and used serological HLA typing., Methods: We studied 35 patients with biopsy-documented amoxicillin-clavulanate-induced hepatitis. HLA-A and -B were typed using alloantisera and compared with those of 300 controls (volunteer bone marrow donors). HLA-DRB and -DWB were typed by polymerase chain reaction-line probe assay, with 60 volunteer bone marrow donors serving as controls., Results: The study group was characterized by a higher frequency of DRB1*1501-DRB5*0101-DQB1*0602 haplotype (57.1% vs. 11.7% in controls, P < 0.000005; after correction for the large number of comparisons, P < 0.0002). Patients with DRB1*1501-DRB5*0101-DQB1*0602 haplotype were more likely than patients without it to have a cholestatic (70% vs. 60%) or mixed (30% vs. 13%) than a hepatocellular pattern of hepatitis (0% vs. 27%) (P < 0.05)., Conclusions: Amoxicillin-clavulanate-induced hepatitis is associated with the DRB1*1501-DRB5*0101-DQB1*0602 haplotype. The data support the view that an immunologic idiosyncrasy, mediated through HLA class II antigens, plays a role in the pathogenesis of drug-induced immunoallergic hepatitis. HLA association has a limited impact on the expression of hepatitis.
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- 1999
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4. Efficacy of interferon dose and prediction of response in chronic hepatitis C: Benelux study in 336 patients.
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Brouwer JT, Nevens F, Kleter B, Elewaut A, Adler M, Brenard R, Chamuleau RA, Michielsen PP, Pirotte J, Hautekeete ML, Weber J, Bourgeois N, Hansen BE, Bronkhorst CM, ten Kate FJ, Heijtink RA, Fevery J, and Schalm SW
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- Adult, Aged, Alanine Transaminase blood, Antiviral Agents administration & dosage, Aspartate Aminotransferases blood, Dose-Response Relationship, Drug, Drug Administration Schedule, Female, Follow-Up Studies, Genotype, Hepacivirus genetics, Hepacivirus isolation & purification, Hepatitis C, Chronic blood, Hepatitis C, Chronic pathology, Humans, Injections, Subcutaneous, Interferon alpha-2, Interferon-alpha administration & dosage, Liver Cirrhosis pathology, Male, Middle Aged, Probability, RNA, Viral blood, Recombinant Proteins, Time Factors, Antiviral Agents therapeutic use, Hepatitis C, Chronic therapy, Interferon-alpha therapeutic use
- Abstract
Background/aims: In an attempt to improve the limited efficacy of treatment of chronic hepatitis C with interferon-alpha 3 MU tiw, we studied the effects of double-dose therapy followed by downward titration, and analyzed the pre- and pertreatment factors associated with response or non-response., Methods: Three hundred and fifty-four consecutive patients in 19 centers were randomized to interferon-alpha 3 MU tiw for 6 months or 6 MU tiw for 8 weeks followed by down-titration (3,1 MU tiw) till alanine aminotransferase remained normal and plasma HCV RNA was repeatedly undetectable. The primary outcome measure was sustained alanine aminotransferase and HCV RNA response 6 months after treatment., Results: Three hundred and thirty-six patients received treatment. The sustained response rate for patients receiving 3 MU tiw for 6 months was 14% (9-21%,) and for patients receiving double dose tiw for 8 weeks and thereafter titrated therapy 15% (10-21%) (p=0.8). Pretreatment factors associated with a sustained alanine aminotransferase plus HCV RNA response were the absence of cirrhosis, presence of genotype 2 or 3, a low viral load and, in addition, a low alanine aminotransferase/aspartate aminotransferase ratio; a model was developed to allow estimation of the chance of response for the individual patient. The most powerful predictor of sustained response, however, was plasma HCV RNA at week 4; a positive test virtually precluded a sustained response (1.7%, 0.4-5.0%). If week 4 HCV RNA was not detectable, the chance of a sustained response was 21% (12-34%) for genotype 1 versus 40% (28-54%) for the others (p=0.02). Six MU tiw led to a significantly higher week 4 HCV RNA response (47% not detectable) than 3 MU (37%) (p=0.02). During down-titration this difference in viral on-treatment response was lost., Conclusions: In the treatment of hepatitis C, an early HCV RNA response is a prerequisite for long-term efficacy. Doubling the initial interferon dose increases this early response, but subsequent downward titration negates this effect, especially in genotype 1.
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- 1998
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5. Hepatic stellate cells and liver retinoid content in alcoholic liver disease in humans.
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Hautekeete ML, Dodeman I, Azais-Braesco V, Van den Berg K, Seynaeve C, and Geerts A
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- Biopsy, Cell Differentiation drug effects, Cell Differentiation physiology, Ethanol poisoning, Humans, Lipid Metabolism, Liver Cirrhosis, Alcoholic pathology, Microscopy, Electron, Reference Values, Liver pathology, Liver Diseases, Alcoholic pathology, Retinoids metabolism
- Abstract
Body retinoids are stored in the lipid droplets of hepatic stellate (Ito) cells. In chronic liver disease, the stellate cells differentiate into myofibroblast-like cells, a process whereby they lose their retinoid-containing lipid droplets. We studied the relation between liver retinoid content, the number of lipid droplets per stellate cell, and the number of stellate cells per mm2 in human alcoholic liver disease. Semithin sections of liver biopsies from normal subjects and patients with early (steatosis, inflammation, and mild fibrosis) and late (cirrhosis and cirrhosis with acute alcoholic hepatitis) alcoholic liver disease were morphometrically evaluated. Liver retinoid content was determined by HPLC. In normal patients, liver retinoid content was 901 +/- 213 IU/g of liver (mean +/- SEM). There was a decrease in liver retinoid content in early alcoholic liver disease (409 +/- 50 IU/g) and a further reduction in cirrhosis (153 +/- 50 IU/g). In patients with acute alcoholic hepatitis, retinoid content was strikingly low (5.2 +/- 1.8 IU/g). There was a progressive decrease in the number of stellate cells per mm2 associated with progressive liver damage. We found a fair correlation between the number of stellate cells per mm2 and liver retinoid content in all patient groups (overall correlation: 0.71). In normal subjects, the mean number of lipid droplets per stellate cell was 7.4 +/- 0.7. In patients with early alcoholic liver disease and in patients with alcoholic cirrhosis, this value was increased to 13.6 +/- 0.8 and 10.4 +/- 2.0, respectively. In patients with acute alcoholic hepatitis, only a few lipid droplets were present (4.2 +/- 0.5). There was a good correlation between liver retinoid content and mean number of lipid droplets in normal patients (r = 0.58). In alcoholic cirrhosis, however, correlation was poor (r = 0.34). In early alcoholic liver disease, the correlation was absent (r = 0.004). In conclusion, the major finding of our study is that the correlation between the mean number of lipid droplets per stellate cell and liver retinoid content varies according to the hepatic pathology considered. Marked lipid droplet accumulation occurs in stellate cells in early alcoholic liver disease and, to a lesser extent, in alcoholic cirrhosis, but there is no correlation between the mean number of lipid droplets per stellate cell and liver retinoid content. Therefore, not retinoids but probably lipids are responsible for the accumulation of lipid droplets. We also find that there is a fair correlation between the number of stellate cells per mm2 and liver retinoid content in all patient groups. Finally, we confirm the decrease in hepatic retinoid content that occurs in alcoholic liver disease in humans, even at the early stages of the disease.
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- 1998
6. Symptomatic liver injury probably related to sertraline.
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Hautekeete ML, Colle I, van Vlierberghe H, and Elewaut A
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- Adult, Contraceptives, Oral, Female, Humans, Liver pathology, Liver Function Tests, Antidepressive Agents adverse effects, Chemical and Drug Induced Liver Injury pathology, Liver drug effects, Sertraline adverse effects
- Published
- 1998
7. Hepatitis C virus genotypes: epidemiological and clinical associations. Benelux Study Group on Treatment of Chronic Hepatitis C.
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Kleter B, Brouwer JT, Nevens F, van Doorn LJ, Elewaut A, Versieck J, Michielsen PP, Hautekeete ML, Chamuleau RA, Brénard R, Bourgeois N, Adler M, Quint WG, Bronkhorst CM, Heijtink RA, Hop WJ, Fevery J, and Schalm SW
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- Adult, Africa epidemiology, Aged, Alanine Transaminase blood, Asia epidemiology, Cohort Studies, Europe epidemiology, Female, Genes, Viral genetics, Genotype, Hepatitis C, Chronic genetics, Hepatitis C, Chronic virology, Humans, Male, Middle Aged, Polymerase Chain Reaction, RNA, Viral analysis, South America epidemiology, Hepacivirus genetics, Hepatitis C, Chronic epidemiology
- Abstract
In a cohort of 292 chronic hepatitis C patients living in the Benelux countries the relationship between viral genotype and geographical origin, route of transmission, clinical characteristics and severity of liver disease was analyzed. HCV-RNA isolates could be classified by the Line Probe Assay (LiPA) as 1a, 1b, 2, 3, 4 or 5 in 286 (98%) cases. Patients of European origin were predominantly infected with HCV subtype 1b (164/254, 65%, CI 58-70%), as were patients of Asian origin (7/13, 54%). Patients originating from Surinam (South America) had predominantly type 2 (9/10, 90%), whereas Africans were mainly infected with type 4 (7/9, 77%). Blood transfusion was the mode of transmission in 142 (50%) patients, intravenous drug abuse (IVDA) in 40 (14%), occupational needle accident or tattoo in 11 (4%); no obvious source of infection was found in 93 (33%). In patients infected by blood transfusion, subtype 1b was predominant (70%, CI 61-77%), whereas subtypes la and 3 were predominant in those infected by IVDA (25% and 45%, respectively, p<0.001). Cirrhosis was observed in 68 (24%) patients; in multivariate analysis, factors independently related to cirrhosis were: the duration of infection, age and prior hepatitis B. No significant relationship was found between the severity of fibrosis or liver inflammation and the HCV (sub)types. In summary, in this large cohort of patients in the Benelux countries the hepatitis C virus (sub)type present was clearly related to the country of origin and the route of transmission, but not to the severity of liver disease.
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- 1998
8. Morphology of liver stellate cells and liver vitamin A content in 3,4,3',4'-tetrachlorobiphenyl-treated rats.
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Azaïs-Braesco V, Hautekeete ML, Dodeman I, and Geerts A
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- Animals, Liver cytology, Liver metabolism, Male, Rats, Rats, Wistar, Liver drug effects, Polychlorinated Biphenyls pharmacology, Vitamin A metabolism, Xenobiotics pharmacology
- Abstract
Background/aims: Because xenobiotics decrease the vitamin A stores localized in the liver stellate cells, we investigated morphological alterations in the liver of rats exposed to 3,4,3',4'-tetrachlorobiphenyl. Special attention was given to the morphology of the liver stellate cells and to their relationship to the liver vitamin A content., Methods: Six rats received an intraperitoneal injection of 3,4,3',4'-tetrachlorobiphenyl (300 mumol/kg) in soyabean oil. A further six rats received the vehicle alone. After 7 days, all rats were killed and their livers assayed for vitamin A. Liver stellate cells were examined and counted on liver sections, stained with toluidine blue or immunocytochemically for desmin and, for some animals, for alpha-smooth muscle actin., Results: In the livers of 3,4,3',4'-tetrachlorobiphenyl-treated rats, we found spotty and bridging necrosis, with inflammation and accumulation of desmin-positive liver stellate cells. Steatosis and mild portal inflammation were also observed. 3,4,3',4'-Tetrachlorobiphenyl decreased the liver vitamin A content by 38%, whereas morphometric analyses showed a 40% decrease of the number of toluidine blue-detected liver stellate cells and an 11% increase of desmin-detected liver stellate cells, indicating a likely differentiation of liver stellate cells into myofibroblast-like cells. 3,4,3',4'-Tetrachlorobiphenyl treatment did not modify the expression of alpha-smooth muscle actin. Morphological alterations were more pronounced in periportal than in pericentral areas. The liver vitamin A content was positively correlated (r = 0.56, p < 0.005) with the number of toluidine-blue detected liver stellate cells., Conclusions: 3,4,3',4'-tetrachlorobiphenyl administration results in an accumulation of liver stellate cells that start differentiating into myofibroblast-like cells. The 3,4,3',4'-tetrachlorobiphenyl-induced decrease in liver vitamin A probably results from this differentiation, although other mechanisms cannot be excluded.
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- 1997
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9. The hepatic stellate (Ito) cell: its role in human liver disease.
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Hautekeete ML and Geerts A
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- Acute Disease, Chronic Disease, Humans, Hypervitaminosis A pathology, Hypervitaminosis A physiopathology, Liver physiopathology, Liver Neoplasms pathology, Liver Neoplasms physiopathology, Liver pathology, Liver Diseases pathology, Liver Diseases physiopathology
- Abstract
The hepatic stellate (Ito) cell lies within the space of Disse and has a variety of functions. Stellate cells store vitamin A in characteristic lipid droplets. In the normal human liver, the cells can be identified by the presence of these lipid droplets; in addition, many stellate cells in the normal liver express alpha-smooth muscle actin. In acute liver injury, there is an expansion of the stellate cell population with increased alpha-smooth muscle actin expression; stellate cells appear to play a role in extracellular matrix remodelling after recovery from injury. In chronic liver injury, the stellate cell differentiates into a myofibroblast-like cell with marked expression of alpha-smooth muscle actin and occasional expression of desmin. Myofibroblast-like cells have a high fibrogenic capacity in the chronically diseased liver and are also involved in matrix degradation. In vitamin A intoxication, hypertrophy and proliferation of the stellate and myofibroblast-like cells may lead to non-cirrhotic portal hypertension, fibrosis and cirrhosis. In liver tumours, myofibroblast-like cells are involved in the capsule formation around the tumour and in the production of extracellular matrix within it. The transition of stellate cells into myofibroblast-like cells is regulated by an intricate network of intercellular communication between stellate cells and activated Kupffer cells, damaged hepatocytes, platelets, endothelial and inflammatory cells, involving cytokines and nonpeptide mediators such as reactive oxygen species, eicosanoids and acetaldehyde. The findings suggest that the stellate cell plays an active role in a number of human liver diseases, with a particular reactivity pattern in fibrotic liver disorders.
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- 1997
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10. Cholestatic hepatitis related to quinolones: a report of two cases.
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Hautekeete ML, Kockx MM, Naegels S, Holvoet JK, Hubens H, and Kloppel G
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- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Anti-Infective Agents adverse effects, Chemical and Drug Induced Liver Injury etiology, Cholestasis chemically induced, Ciprofloxacin adverse effects, Ofloxacin adverse effects
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- 1995
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11. Hepatotoxicity of antibiotics.
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Hautekeete ML
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- 4-Quinolones, Adult, Anti-Infective Agents toxicity, Cephalosporins toxicity, Child, Female, Humans, Macrolides, Male, Nitrofurantoin toxicity, Penicillins toxicity, Pregnancy, Tetracyclines toxicity, Trimethoprim, Sulfamethoxazole Drug Combination toxicity, Anti-Bacterial Agents toxicity, Chemical and Drug Induced Liver Injury etiology, Liver drug effects
- Abstract
Several antibiotics can cause severe hepatic injury. It is the purpose of this paper to review the main antibiotics that can cause hepatic injury and discuss the presentation, pattern, and outcome of hepatic injury. In the case of the penicillins, the combination amoxycillin-clavulanate and the penicillinase-resistant penicillins oxacillin, (di-)cloxacillin, and flucloxacillin can cause (mainly cholestatic) hepatitis. Cephalosporins have little hepatotoxicity; ceftriaxone can cause drug-induced gallstones. The potential of erythromycin and several other macrolides to cause (usually cholestatic) hepatitis is well established. Tetracyclines can cause a syndrome mimicking acute fatty liver of pregnancy, but this complication has virtually disappeared. Quinolones seem to be able to cause cholestasis. Sulfamethoxazole/trimethoprim can cause severe hepatotoxicity, especially in patients with acquired immunodeficiency syndrome (AIDS). Finally, nitrofurantoin can cause acute cholestatic and hepatocellular reactions as well as chronic hepatitis mimicking chronic auto-immune hepatitis.
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- 1995
12. Severe hepatotoxicity related to benzarone: a report of three cases with two fatalities.
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Hautekeete ML, Henrion J, Naegels S, DeNeve A, Adler M, Deprez C, Devis G, and Klöppel G
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- Adult, Aged, Benzbromarone administration & dosage, Benzbromarone adverse effects, Biopsy, Chemical and Drug Induced Liver Injury, Chronic, Fatal Outcome, Female, Fibrinolytic Agents administration & dosage, Hepatic Encephalopathy pathology, Hepatitis, Chronic pathology, Humans, Liver drug effects, Liver pathology, Liver Cirrhosis chemically induced, Liver Cirrhosis pathology, Male, Thrombophlebitis drug therapy, Thrombophlebitis pathology, Venous Insufficiency drug therapy, Venous Insufficiency pathology, Benzbromarone analogs & derivatives, Chemical and Drug Induced Liver Injury pathology, Fibrinolytic Agents adverse effects, Hepatic Encephalopathy chemically induced
- Abstract
We report three cases of severe hepatotoxicity related to benzarone, a benzofuran derivative. Our cases include a 35-year-old woman with (sub)fulminant hepatitis, a 67-year-old woman with macronodular cirrhosis, and a 68-year-old man with severe chronic active hepatitis and cirrhosis, with positivity of anti-smooth muscle antibodies. Two patients died. We stress the potential of benzarone to cause hepatotoxicity, which usually resembles severe chronic active hepatitis. Our cases constitute the most severe cases of benzarone hepatotoxicity reported so far, and comprise the first cases of (sub)fulminant hepatitis and cirrhosis related to benzarone.
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- 1995
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13. Liver injury related to amoxycillin-clavulanic acid: interlobular bile-duct lesions and extrahepatic manifestations.
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Hautekeete ML, Brenard R, Horsmans Y, Henrion J, Verbist L, Derue G, Druez P, Omar M, Kockx M, and Hubens H
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- Aged, Amoxicillin adverse effects, Amoxicillin-Potassium Clavulanate Combination, Clavulanic Acids adverse effects, Drug Therapy, Combination, Female, Humans, Inflammation, Lacrimal Apparatus Diseases chemically induced, Male, Middle Aged, Nephritis, Interstitial chemically induced, Sialadenitis chemically induced, Xerostomia chemically induced, Bile Ducts, Intrahepatic pathology, Chemical and Drug Induced Liver Injury
- Abstract
We report eight cases of liver injury related to amoxycillin-clavulanate. Liver biopsy performed in seven patients revealed varying degrees of injury to interlobular bile ducts in all cases. Lesions included irregularity of the nuclei, vacuolization of the cytoplasm, lymphocytic infiltration, destruction and endothelialization of the bile duct epithelium. Ductopenia was not observed. In two patients liver injury was accompanied by prominent extrahepatic manifestations (acute interstitial nephritis in one and acute lacrimal gland inflammation and sialadenitis with prolonged xerostomia in the other). We conclude that interlobular bile-duct lesions of varying severity are a common feature in liver injury related to amoxycillin-clavulanate. Side effects of the drug include acute interstitial nephritis and sialadenitis.
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- 1995
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14. Duodenal diaphragmlike stricture induced by acetylsalicylic acid.
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Blinder GH, Hautekeete ML, Holvoet JP, Kockx MM, and Hubens HK
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- Constriction, Pathologic, Duodenal Obstruction pathology, Duodenal Ulcer chemically induced, Humans, Male, Middle Aged, Aspirin adverse effects, Duodenal Obstruction chemically induced
- Abstract
Many reports have mentioned the role of nonsteroidal antiinflammatory drugs in inducing diaphragm-like strictures in the small and large bowel. These lesions are mostly seen in patients with chronic use of nonsteroidal antiinflammatory drugs. We report the case of a 57-year-old man who developed a diaphragmlike stricture in the second part of the duodenum. The patient had been using a preparation containing acetylsalicylic acid during many years. Although a congenital origin of the diaphragm is not completely excluded, we postulate that this stricture probably occurred as a result of acetylsalicylic acid-induced ulcerations, followed by submucosal fibrosis.
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- 1994
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15. Guillain-Barré syndrome as the presenting manifestation of hepatitis C infection.
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De Klippel N, Hautekeete ML, De Keyser J, and Ebinger G
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- Adult, Biopsy, Female, Hepatitis C pathology, Humans, Liver pathology, Necrosis, Neural Conduction, Polyradiculoneuropathy diagnosis, Hepatitis C complications, Hepatitis C diagnosis, Polyradiculoneuropathy etiology
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- 1993
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16. Contributions of light and transmission electron microscopy to the study of the human fat-storing cell.
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Hautekeete ML, Geerts A, Seynaeve C, Lazou JM, Klöppel G, and Wisse E
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- Adipose Tissue ultrastructure, Biopsy, Cholestasis, Extrahepatic pathology, Fatty Liver pathology, Hepatitis, Chronic pathology, Humans, Lipids analysis, Liver pathology, Liver Cirrhosis pathology, Liver Diseases, Alcoholic pathology, Staining and Labeling, Tolonium Chloride, Adipose Tissue cytology, Liver cytology, Liver Diseases pathology, Microscopy, Microscopy, Electron
- Abstract
We examined the human fat-storing cell (Ito cell, lipocyte) in normal and pathologic liver biopsies using toluidine blue staining and transmission electron microscopy. We studied 5 normal patients, 6 non-alcoholic patients with liver steatosis, 8 patients with early alcoholic liver damage, 4 patients with extrahepatic cholestasis, 10 patients with chronic active hepatitis B (N = 2) or C (N = 8) with mild fibrosis, 5 patients with alcoholic cirrhosis and 4 with posthepatitic cirrhosis. We found that fat-storing cells were increased in patients with alcoholic steatofibrosis and extrahepatic cholestasis and decreased in cirrhotic patients. The mean number of lipid droplets per fat-storing cell was significantly increased in patients with alcoholic steatofibrosis. Transmission electron microscopy confirmed the light microscopic findings, especially the accumulation of lipid droplets in fat storing cells in early alcoholic liver disease. Sometimes lipid droplets with different electron density were noted. In cirrhosis there was a more prominent development of intracellular organelles, and cells often changed into a more elongated, myofibroblast-like shape.
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- 1993
17. Hypersensitivity with hepatotoxicity to mesalazine after hypersensitivity to sulfasalazine.
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Hautekeete ML, Bourgeois N, Potvin P, Duville L, Reynaert H, Devis G, Adler M, and Klöppel G
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- Adult, Female, Humans, Liver pathology, Mesalamine, Aminosalicylic Acids adverse effects, Drug Hypersensitivity etiology, Liver drug effects, Sulfasalazine adverse effects
- Abstract
A 21-year-old woman with Crohn's disease of the colon developed a skin rash after 3 weeks of treatment with sulfasalazine. Administration of sulfasalazine was discontinued. When mesalazine was instituted 1 week later, she developed a severe hypersensitivity reaction characterized by fever, diarrhea, skin rash with subsequent desquamation, marked atypical lymphocytosis, and severe hepatotoxicity. Recovery was complete. The clinical and biological features as well as liver pathology of this case bear a striking resemblance to earlier reports of hypersensitivity reaction with severe hepatotoxicity to sulfasalazine. The authors urge caution when mesalazine is given to a patient with known hypersensitivity to sulfasalazine.
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- 1992
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18. Relation of upper gastrointestinal bleeding to non-steroidal anti-inflammatory drugs and aspirin: a case-control study.
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Holvoet J, Terriere L, Van Hee W, Verbist L, Fierens E, and Hautekeete ML
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- Adolescent, Adult, Age Factors, Aged, Aspirin adverse effects, Case-Control Studies, Duodenal Ulcer complications, Esophagitis, Peptic complications, Female, Humans, Male, Middle Aged, Odds Ratio, Peptic Ulcer Hemorrhage etiology, Risk Factors, Sex Factors, Stomach Ulcer complications, Anti-Inflammatory Agents, Non-Steroidal adverse effects, Gastrointestinal Hemorrhage etiology
- Abstract
We conducted a case-control study in five general hospitals in the region of Antwerp, studying 161 patients (102 men, 59 women) and hospital control subjects matched for age and sex to explore the relation between drug use and upper gastrointestinal bleeding from 'erosive lesions' (peptic oesophagitis, gastric erosions, gastric ulcer(s), or duodenal ulcer(s]. There was a highly significant difference between cases and control subjects in the use of non-steroidal anti-inflammatory drugs (NSAIDs, excluding aspirin) (odds ratio 7.4, p less than 0.001; 95% confidence interval odds ratio 3.7 to 14.7). There also was a significant difference in the use of aspirin (odds ratio 2.2, p = 0.025; 95% CI odds ratio 1.3 to 4.0) and a highly significant difference regarding the presence of antecedents of peptic ulcer disease (odds ratio 5.5, p less than 0.001; 95% CI odds ratio 3.2 to 9.6). There was no significant difference in the use of other drugs, paracetamol and corticosteroids in particular, nor in the use of alcohol or tobacco. The patient group using NSAIDs was older, had more women, and had a higher mortality than the group not using NSAIDs. Among patients with bleeding gastric or duodenal ulcer(s), NSAID users were not more or less likely to have had symptoms of peptic ulcer disease, and had no higher frequency of multiple gastric or duodenal ulcers. The attributable risk for NSAID use was 0.30 (95% CI 0.23 to 0.37) and for aspirin use 0.14 (95% CI 0.08 to 0.20).
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- 1991
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19. Retroperitoneal fibrosis after surgery for aortic aneurysm in a patient with periarteritis nodosa: successful treatment with corticosteroids.
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Hautekeete ML, Babany G, Marcellin P, Gayno S, Palazzo E, Erlinger S, and Benhamou JP
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- Aorta, Abdominal, Blood Vessel Prosthesis, Humans, Male, Middle Aged, Retroperitoneal Fibrosis drug therapy, Time Factors, Aortic Aneurysm surgery, Polyarteritis Nodosa complications, Postoperative Complications drug therapy, Prednisolone therapeutic use, Retroperitoneal Fibrosis etiology
- Abstract
A 54-year-old man with hepatitis B virus-related periarteritis nodosa developed retroperitoneal fibrosis with bilateral hydronephrosis 2.5 months after placement of an aortobifemoral prosthesis for abdominal aortic aneurysm. Retroperitoneal fibrosis disappeared after treatment with corticosteroids. This observation is interesting in the light of the hypothesis that retroperitoneal fibrosis is caused by vasculitis.
- Published
- 1990
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20. Membranous obstruction of the inferior vena cava and hepatocellular carcinoma in a Caribbean patient.
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Hautekeete ML, Brenard R, Hadengue A, Degott C, Babany G, Arrivé L, Lebrec D, Menu Y, Erlinger S, and Benhamou JP
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- Adult, Humans, India ethnology, Male, Thrombocytopenia complications, Vascular Diseases pathology, West Indies epidemiology, Carcinoma, Hepatocellular complications, Liver Neoplasms complications, Vena Cava, Inferior pathology
- Abstract
Membranous obstruction of the inferior vena cava has been reported mainly in South Africa, Japan, and India; in 20-40% of patients the disease is complicated by hepatocellular carcinoma. We report a case of membranous obstruction of the inferior vena cava with hepatocellular carcinoma in a 43-year-old Caribbean man of Indian origin. The Caribbean islands may constitute another geographical area where the population is at risk for the development of membranous obstruction of the inferior vena cava and subsequent hepatocellular carcinoma.
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- 1990
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21. Microvesicular steatosis of the liver.
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Hautekeete ML, Degott C, and Benhamou JP
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- Fatty Liver chemically induced, Fatty Liver pathology, Female, Humans, Liver Diseases complications, Liver Diseases, Alcoholic complications, Metabolism, Inborn Errors complications, Pregnancy, Pregnancy Complications, Reye Syndrome complications, Virus Diseases complications, Fatty Liver etiology
- Abstract
The term "microvesicular steatosis of the liver" refers to a variant form of hepatic fat accumulation whose histologic features contrast with the much more common macrovesicular steatosis. Microvesicular steatosis of the liver was originally described in association with conditions who share a number of biochemical and a limited number of clinical features: acute fatty liver of pregnancy, Reye's syndrome, Jamaican vomiting sickness, sodium valproate toxicity, high-dose tetracycline toxicity and certain congenital defects of urea cycle enzymes; they were thought to constitute an entity of "microvesicular fat diseases". In recent years the disease has been described in a wide variety of conditions: alcoholism, toxicity of several medications, delta hepatitis in South America and Central Africa, sudden childhood death, congenital defects of fatty acid beta oxidation, cholesterol ester storage disease, Wolman disease and Alpers syndrome. Not much is known regarding the pathogenesis of microvesicular steatosis but in many instances the primary defect could be a mitochondrial lesion, and inhibition of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect. The different conditions associated with microvesicular steatosis are heterogenous in many aspects. Maintaining the concept of "microvesicular fat diseases" as a unique entity seems no longer justified.
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- 1990
- Full Text
- View/download PDF
22. Mastitis and toxic shock syndrome.
- Author
-
Demey HE, Hautekeete ML, Buytaert P, and Bossaert LL
- Subjects
- Abscess complications, Abscess microbiology, Adult, Breast Diseases complications, Breast Diseases microbiology, Female, Humans, Mastitis microbiology, Pregnancy, Puerperal Infection microbiology, Staphylococcus aureus isolation & purification, Mastitis complications, Puerperal Infection complications, Shock, Septic etiology
- Abstract
Toxic shock syndrome (TSS) secondary to mastitis or breast abscess is only seldom described. We report a case of definite TSS due to postpartum staphylococcal mastitis which evolved over a period of 3 weeks to a breast abscess, recurring after 2 months. Only the episode of acute mastitis was complicated with TSS, while Staph. aureus could be isolated during the period of mastitis from milk and during drainage of the second breast abscess.
- Published
- 1989
- Full Text
- View/download PDF
23. Purpura fulminans in pneumococcal sepsis.
- Author
-
Hautekeete ML, Berneman ZN, Bieger R, Stevens WJ, Bridts C, Buyssens N, and Peetermans ME
- Subjects
- Acute Kidney Injury complications, Adult, Aged, Chlorambucil therapeutic use, Female, Gangrene complications, Gangrene physiopathology, Hodgkin Disease complications, Hodgkin Disease drug therapy, Humans, Immunoglobulin G isolation & purification, Lymphoma complications, Mechlorethamine therapeutic use, Pneumococcal Infections immunology, Prednisone therapeutic use, Procarbazine therapeutic use, Purpura etiology, Purpura physiopathology, Splenectomy, Vincristine therapeutic use, Antineoplastic Combined Chemotherapy Protocols, Pneumococcal Infections complications, Purpura complications
- Abstract
Two cases of pneumococcal sepsis in splenectomized patients were complicated by purpura fulminans. In addition, acute renal failure developed in both patients, and myolysis in one. Immunological findings in the patient with myolysis suggest a possible role of pneumococcal antigen-containing circulating immune complexes in the pathogenesis of these complications.
- Published
- 1986
24. Necrotizing fasciitis precipitating diabetic ketoacidotic coma.
- Author
-
Hautekeete ML, Nagler JM, Mertens AH, Gerard Y, Mahler C, and Parizel G
- Subjects
- Adult, Combined Modality Therapy, Diabetic Coma diagnosis, Diabetic Coma pathology, Diabetic Ketoacidosis diagnosis, Diabetic Ketoacidosis pathology, Fasciitis diagnosis, Fasciitis pathology, Female, Humans, Necrosis, Time Factors, Diabetic Coma etiology, Diabetic Ketoacidosis etiology, Fasciitis complications
- Abstract
Necrotizing fasciitis is a rapidly spreading infection of the subcutaneous tissue and fascia; diabetes mellitus appears to be the most frequent underlying disease. Early diagnosis and immediate aggressive surgical therapy are paramount to curtail morbidity and mortality, but diagnosis is often difficult and unnecessarily delayed. We describe a case of necrotizing fasciitis precipitating diabetic ketoacidotic coma where correct diagnosis was not made until the 14th hospital day. We stress the fact that physicians caring for critically ill patients should be keenly aware of the possibility of necrotizing fasciitis when tending diabetic patients with unexplained fever; failure to recognize the disease can have devastating results. Finally, we believe this to be the first reported case of diabetic ketoacidotic coma precipitated by necrotizing fasciitis.
- Published
- 1986
- Full Text
- View/download PDF
25. Flow cytometric analysis of T-lymphocyte subpopulations in B-cell chronic lymphocytic leukemia: correlation with clinical stage.
- Author
-
Hautekeete ML, De Bock RF, Van Bockstaele DR, Colpin GC, Berneman ZN, and Peetermans ME
- Subjects
- Adult, Aged, Aged, 80 and over, B-Lymphocytes, Female, Humans, Immunoglobulins analysis, Immunoglobulins classification, Leukemia, Lymphoid blood, Male, Middle Aged, Neoplasm Staging, Flow Cytometry, Leukemia, Lymphoid pathology, T-Lymphocytes classification
- Abstract
Several authors have studied the T-lymphocyte subpopulations in B-cell chronic lymphocytic leukemia (B-CLL), but previous studies were performed after preceding enrichment procedures, which are known to cause selective losses of certain subpopulations. To correct for this deficiency we used flow cytometric analysis, which enabled us to measure subpopulations directly on total blood samples. We studied T-lymphocyte subsets with OKT monoclonal antibodies in 45 patients with B-CLL. Serum levels of IgG, IgA and IgM were assayed simultaneously and findings were correlated with clinical stage (Rai classification). The absolute number of CD4-positive cells decreased in more advanced Rai stages, while the absolute number of CD8-positive cells increased, resulting in a progressive reduction in CD4/8 ratio. Results from patients in stages with equal prognosis (Rai I and II, Rai III and IV) were similar and when these results were grouped the observed differences were highly significant and clearly correlated with all prognostic groups.
- Published
- 1987
- Full Text
- View/download PDF
26. Chronic urticaria associated with coeliac disease.
- Author
-
Hautekeete ML, DeClerck LS, and Stevens WJ
- Subjects
- Celiac Disease diet therapy, Chronic Disease, Humans, Male, Middle Aged, Celiac Disease complications, Urticaria etiology
- Published
- 1987
- Full Text
- View/download PDF
27. Presence of Loa loa microfilariae in ascitic fluid.
- Author
-
Hautekeete ML, Pailoux G, Marcellin P, Girard PM, Degott C, and Benhamou JP
- Subjects
- Adult, Ampicillin therapeutic use, Animals, Cefotaxime therapeutic use, Diethylcarbamazine therapeutic use, Drug Therapy, Combination, Female, Humans, Loiasis drug therapy, Metronidazole therapeutic use, Ascitic Fluid parasitology, Filariasis diagnosis, Loa isolation & purification, Loiasis diagnosis
- Published
- 1989
- Full Text
- View/download PDF
28. Diffuse intravascular coagulation complicating thrombosis of a popliteal aneurysm: a case report.
- Author
-
Mahler C, Parizel G, Hautekeete ML, Nagler JM, Van Goethem JK, and Hermans C
- Subjects
- Aged, Aneurysm diagnostic imaging, Aorta, Abdominal diagnostic imaging, Femoral Artery diagnostic imaging, Humans, Male, Radiography, Thrombosis etiology, Aneurysm complications, Disseminated Intravascular Coagulation etiology, Popliteal Artery diagnostic imaging, Thrombosis complications
- Abstract
Several reports have described the association between diffuse intravascular coagulation (DIC) and arterial aneurysmal disease. We report a patient with extensive arterial aneurysmal disease who developed transient severe DIC during thrombosis of a popliteal aneurysm; following surgical removal of the thrombosed aneurysm, he was found to have chronic subclinical DIC. We believe thrombosis should be added to the complications of aneurysms which can cause DIC, next to dissection and rupture. The chronic DIC occurring after removal of the thrombosed aneurysm was characterized by an abnormal prothrombin time (PTT), low fibrinogen levels and elevated fibrin split products (FDP's); this pattern may be characteristic of the DIC complicating arterial aneurysms.
- Published
- 1986
- Full Text
- View/download PDF
29. Budd-Chiari syndrome.
- Author
-
Hautekeete ML, Brenard R, Hadengue A, and Benhamou JP
- Subjects
- Constriction, Pathologic, Humans, Vena Cava, Inferior pathology, Budd-Chiari Syndrome etiology
- Published
- 1989
- Full Text
- View/download PDF
30. 6-keto-PGF1 alpha levels and prostacyclin therapy in 2 adult patients with hemolytic-uremic syndrome.
- Author
-
Hautekeete ML, Nagler JM, Cuykens JJ, Parizel G, Laekeman GM, and Herman AG
- Subjects
- Adult, Female, Hemolytic-Uremic Syndrome drug therapy, Humans, Male, Radioimmunoassay, 6-Ketoprostaglandin F1 alpha blood, Epoprostenol therapeutic use, Hemolytic-Uremic Syndrome blood
- Abstract
Evidence supports the hypothesis that plasma prostacyclin activity is deficient in hemolytic-uremic syndrome (HUS). We studied 2 adult patients with HUS. Plasma levels of 6-keto-PGF1 alpha, the stable metabolite of prostacyclin, were measured by radioimmunoassay. Both patients were found to have elevated 6-keto-PGF1 alpha levels. These findings are in contradiction with the prostacyclin deficiency hypothesis and with earlier reports of low or undetectable plasma levels of this metabolite. The patients were treated with IV prostacyclin after a single plasma exchange. The first patient, admitted with advanced renal failure, obtained a rapid remission but renal function did not recover; the second patient, admitted with a less pronounced degree of renal failure, reacted slowly to therapy but renal function partially recovered. We believe that, if any benefit is to be expected from prostacyclin therapy in HUS, it should be started early in the course of the disease.
- Published
- 1986
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