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D Henin

Publications and source records attributed to D Henin.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Endolymphatic sac tumor: a rare tumor of internal ear. Report of two cases].

Papillary tumors of the temporal bone are rare and aggressive neoplasms. Recently described, these tumors had initially a presumed middle-ear origin. Only recently, convincing anatomic, morphological and immunohistochemical arguments exist for an endolymphatic sac origin (inner-ear origin). We report two cases of endolymphatic sac tumor. These tumors can be encountered sporadically or in Von Hippel-Lindau disease. They classically grow very slowly, resulting in late clinical manifestations with expansive mass invading temporal bone and extending in posterior fossa. Radiologically, these endolymphatic sac tumors can mimic metastatic carcinoma, paraganglioma, or cerebellar haemangioblastoma specially in von Hippel-Lindau disease. Histology shows a papillary epithelial tumor with hypervascular stroma, without atypia. The treatment for these tumors is surgical and curative when early diagnosed. In apparently sporadic cases, genetic analysis for Von Hippel-Lindau disease should be considered.

Adult↗
PubMed2000

[Adenomatoid tumor of the pleura. Case report].

We report a case of an adenomatoid tumor of particular location within the pleura, incidentally discovered on a pulmonary lobectomy specimen after surgical resection of a pulmonary squamous cell carcinoma. This adenomatoid tumor appeared as a unique pleural mass located away from the primary carcinoma and consisted of a cellular proliferation organised in tubes and sheets. Adenomatoid tumors are considered as benign tumors of mesothelial nature. Their morphological and immunohistochemical features in association with their location to the pleura, warrant a precise analysis to eliminate malignant tumours such as malignant mesothelioma or metastatic adenocarcinoma.

Epithelium↗
PubMed1998

Expression of integrins during liver organogenesis in humans.

Integrins play a pivotal role in organogenesis, by mediating the interactions between differentiating cells and the extracellular matrix. We analyzed the expression of integrins and their ligands during human liver organogenesis. The expression of beta1, beta3, and beta4 integrins and the distribution of several extracellular matrix proteins were studied by immunoperoxidase in fetal liver samples from 5 to 40 weeks' gestation. Hepatoblasts expressed only the beta1, alpha1, alpha5, alpha6, and alpha9 integrin chains. Fetal hepatocytes, emerging at the 8th week of gestation, initially retained the same combination of integrins, but presented a progressive decrease in their expression levels. After 15 weeks' gestation, the expression levels of beta1, alpha1, alpha5, and alpha9 reached levels comparable to those observed in the adult state. Alpha6 expression became undetectable after 30 weeks' gestation. As compared to hepatoblasts, intrahepatic biliary epithelial cells, differentiating at the 8th week of gestation in the ductal plate, were characterized by the progressive loss of alpha1, the marked induction of alpha6, and the de novo acquisition of the beta4, alpha2, and alpha3 integrin chains. The disappearance of integrin receptors for laminin on hepatocytes was associated with the rarefaction of laminin in the perisinusoidal matrix, whereas their induction on biliary epithelial cells was associated with laminin deposition at the point of contact with the ductal plate. In conclusion, integrins likely play an important role in the differentiation of the epithelial and endothelial cell populations of the liver.

Collagen↗
PubMed1998

Changes in liver fibrosis at the end of alpha interferon therapy and 6 to 18 months later in patients with chronic hepatitis C: quantitative assessment by a morphometric method.

BACKGROUND/AIMS: The aims of the study were to determine, in patients with chronic hepatitis C treated with alpha interferon: (i) changes in the morphometric evaluation of liver fibrosis at the end of treatment and 6, 12 and 18 months after treatment; (ii) the predictive value of histologic lesions for the response to treatment, in particular the predictive value of morphometric evaluation of liver fibrosis. METHODS: Seventy patients with chronic hepatitis C who participated in two trials of recombinant interferon alpha 2b treatment were studied. Liver specimens were obtained before and at the end of treatment and 6, 12 or 18 months later. Histologic lesions were assessed according to the Knodell system. Quantitative study of total fibrosis and of Disse space collagen was done by the computerized automated morphometric method. RESULTS: A significant decrease in morphometric Disse space collagen was observed at the end of treatment and 6 months later. This decrease was also observed, although it was not significant, 12 and 18 months after treatment. There was no relationship between this decrease and the biochemical and virological responses or the dose of interferon. The pretreatment Knodell activity score, but not the morphometric evaluation of fibrosis, was a significant predictor of sustained response. CONCLUSION: A decrease in Disse space collagen, as assessed by the sensitive morphometric method, was observed at the end of and 6 months after treatment. This observation is consistent with an anti-fibrogenetic effect of alpha interferon. Mild or moderate histologic activity was associated with a sustained response to therapy.

Antiviral Agents↗
PubMed1998

Detection and localization by in situ molecular biology techniques and immunohistochemistry of hepatitis C virus in livers of chronically infected patients.

Hepatitis C virus (HCV) detection in the livers of chronically infected patients remains a debatable issue. We used immunohistochemistry, in situ hybridization (ISH) alone or after microwave heating with FITC-labeled probes, RT-PCR with unlabeled primers followed by ISH (RT-PCR-ISH), and in situ RT-PCR with FITC-labeled primers (in situ RT-PCRd) to localize the virus in 38 liver biopsy specimens from 21 chronically infected HCV patients treated with interferon-alpha (IFN-alpha). Biopsies were taken at the beginning and end of IFN-alpha treatment and 1 year later. Results were compared with that of HCV-PCR in serum. RT-PCR-ISH and in situ RT-PCRd showed HCV signal in all liver biopsies even in responders with seronegative HCV PCR. This signal was intranuclear, diffuse, or peripheral, in hepatocytes, bile ductule cells, and lymphocytes. Cytoplasmic signals were occasionally observed. Whereas the percentage of labeled hepatocytes remained constant, the number of labeled lymphoid follicles decreased after INF-alpha therapy. Immunohistochemistry resulted in the same pattern of positivity but it was weaker and inconstant. This study indicates the persistency of HCV latency in IFN-alpha responders 1 year after IFN-alpha treatment cessation, a finding that certainly deserves confirmation.

Animals↗
PubMed1997

Apoptosis after ischemia-reperfusion in human liver allografts.

Little is known about the possible contribution of apoptosis to ischemia-reperfusion injury in human liver transplantation. Therefore, we studied postreperfusion surgical biopsy specimens of 16 human liver allografts using the TUNEL assay for in situ demonstration of apoptotic cells. In all patients, a variable proportion of hepatocytes and sinusoidal endothelial cells presented labeled nuclei. The mean +/- standard deviation percentages of positive hepatocytes were 18.7% +/- 12.2% in the whole section, 30.4% +/- 18.7% in the subcapsular region, 14.5% +/- 13.5% in the centrilobular zones, and 10.3% +/- 9.5% in the periportal zones. The percentage of positive hepatocytes were not correlated with the duration of cold ischemia but was higher in grafts harvested from donors with elevated preoperative aspartate aminotransferase (AST) levels. The percentage of positive hepatocytes was correlated with postoperative serum levels of AST (P = .015) and inversely correlated with postoperative serum levels of factor V (P = .019). Apoptotic biliary epithelial cells were detected in only 3 cases. In conclusion, apoptosis is a frequent event in postreperfusion biopsy specimens of liver allografts and probably contributes to preservation injury of hepatocytes.

Adenosine↗
PubMed1995

[Pathologic anatomy of cytomegalovirus encephalomyelitis and varicella-zona virus encephalomyelitis].

Cytomegalovirus (CMV) infection of the nervous system is frequent in acquired immunodeficiency syndrome (AIDS) and can be responsible for encephalitis, encephalomyelitis, meningoradiculitis or polyradiculo-neuropathy. Encephalitis is characterized at microscopy by its periventricular and cerebellar location, and by the presence of cytomegalic cells, containing intranuclear and/or intracytoplasmic inclusions, microglial nodules and necrotic foci. The virus can infect almost all types of cells. Coexistence of CMV and HIV has been observed in giant cells of macrophagic origin. It has been suggested that the two viruses could act in synergy. The nervous system is seldom infected by the varicella-zoster virus (VZV) in AIDS. The infection can be responsible for multifocal leukoencephalitis, ventriculitis, vascular lesions associated or not with cerebral infarction, or with meningomyeloradiculitis. In almost all cell types Cowdry's type A intranuclear inclusions have been found. The virus can be demonstrated by immunohistochemistry or in situ hybridization. VZV antigens have been reported in the walls of vessels damaged by a non inflammatory obliterating vasculopathy or by a granulomatous angiitis. Coexistence of VZV and HIV has been observed in giant cells of macrophagic origin, and synergy between those two viruses has been suspected.

AIDS-Related Opportunistic Infections↗
PubMed1995

[Frontal cerebral abscess, a rare complication of nasosinusal polyposis. Apropos of a case].

Sinusonasal polyposis is frequent but usually benign. A 77-year-old woman with an history of sinusonasal polyps, presented with fever and neurologic impairment. Radiologic imaging showed a polypoïd mass filling the nose and sinuses, eroding the ethmoïd bone, progressing intracranially, and causing brain abscess. The literature is reviewed, according to the relations between brain abscess development and nasal polyposis, with emphasis on intracranial extension of sinusonasal polyps. Treatment of the nasal polyps, usually based on the use of local or general corticosteroïds, can avoid this serious complication.

Aged↗
PubMed1994

Osteosarcoma following radiation treatment for meningioma: report of a case and effective treatment with chemotherapy.

A case of effective chemotherapy in postirradiation sarcoma is reported. A 30-year-old woman underwent a subtotal resection of a benign mixed meningioma followed by a course of radiotherapy. Five years later she developed a skull tumor which was resected. Histological study showed sarcomatous change corresponding most likely to a postirradiation osteosarcoma. Adjuvant chemotherapy (methotrexate, carboplatin, and VP16) was given. A progression occurred 8 months later and the patient was treated unsuccessfully with tamoxifen, LHRH, and later with high dose methotrexate and carboplatin. Six months later a lung metastasis was discovered and she received four cycles of IVP (ifosfamide, vepeside, cisplatin) alternating with IVA (ifosfamide, vepeside, adriamycin). Within 4 months the primary and lung tumours had decreased substantially without evidence of progression at follow-up 5 months later. We conclude that IVP/IVA regimen is a potentially useful therapy when an osteosarcoma of the skull is in progression.

Adult↗
PubMed1994

Adenomatous hyperplasia of the liver in a patient with congenital hepatic fibrosis.

We report the case of a 30-year-old man suffering from congenital hepatic fibrosis, who was treated at age 12 by splenorenal shunt for portal hypertension, and who developed numerous, large hepatic nodules. The patient underwent liver transplantation because of recurrent episodes of acute cholangitis and the presence of foci of dysplasia in the nodules. Histological examination of the surgical specimen showed adenomatous hyperplastic nodules with a few atypical foci in an otherwise fibrous but non-cirrhotic liver. Such lesions have not yet been described in congenital hepatic fibrosis. The respective roles of congenital hepatic fibrosis and splenorenal shunts in the development of these nodules are discussed.

Adult↗
PubMed1994

[Cerebral lymphoma in AIDS: clinical study and clinicopathological correlations].

We report the natural history of 17 brain lymphomas (11 primary, 6 disseminated) from a post-mortem series of 130 patients with AIDS. Primary lymphomas appeared lately in the course of AIDS. They were often associated with a severe T-cell immunodepression and with more frequent opportunistic disorders than disseminated lymphomas. Associated Kaposi's sarcomas were surprisingly frequent. All patients presented with neurological manifestations. Heterogeneous features were seen at CT examination. The CSF was abnormal in 12/13 cases, with an increase of protein contents and secretion of immunoglobulins; it contained activated lymphocytes in 5/6 cases of disseminated lymphomas, and malignant cells in only one case. Cellular density never exceeded 8/mm3 for primary lymphomas, and the lymphocytes were considered normal. The pre-mortem diagnosis of cerebral lymphomas was made in five patients, with a time lapse of 1 to 7 months between the first neurological symptoms and death, and of 5 to 30 days between the diagnosis and death. Cerebral biopsy was diagnostic in 4 cases of primary cerebral lymphomas. In only 1/6 patients with disseminated lymphomas, the diagnosis had been made when the patient was still alive, based on CSF and bone marrow lymphomatous infiltrations. The diagnosis of cerebral lymphoma (7 primary, 5 disseminated) was post-mortem in 12 cases. It was made only at microscopic examination in 2/12 cases of primary lymphomas. The histopathological study frequently showed a multicentric involvement, and always an immunoblastic cell type with plasmablastic differentiation and frequent medium size cells. Marked gliosis and significant necrosis were often observed. Neuropathological lesions associated with HIV-1 infection (toxoplasmosis, CMV and HIV-1 encephalitis) were seen in 8 cases with primary lymphomas.

Adult↗
PubMed1993

Clonidine pretreatment reduces the systemic toxicity of intravenous bupivacaine in rats.

BACKGROUND: Clonidine prolongs the duration of sensory and motor block induced by bupivacaine, and this association, in constant infusion by the epidural route, is used for postoperative analgesia. After a near-fatal intravenous bolus of bupivacaine in dogs, clonidine improves ventricular electrophysiologic parameters, but probably worsens bupivacaine-induced bradycardia and depression of the myocardial contractility. The current study, using a rodent animal model, evaluated the influence of clonidine pretreatment on the systemic toxic effects of bupivacaine overdose induced by a constant intravenous infusion. METHODS: Twenty Wistar male rats were anesthetized with thiopental, and controlled ventilation was started with an equal mixture of O2 and N2O. Electrocardiogram (ECG), electroencephalogram (EEG), and invasive arterial blood pressure were continuously recorded. Clonidine (5 micrograms/kg) or saline was injected intravenously in a randomized fashion. After 15 min, an intravenous infusion of bupivacaine was started at 2 mg.kg-1 x min-1. The time of occurrence of the bupivacaine-induced toxic events was recorded and the doses were calculated. Ten (five in each group) additional rats, pretreated according to the same protocol, were killed at the time of the first dysrhythmia, for blood sampling and plasma bupivacaine concentration measurement. RESULTS: Clonidine reduced heart rate and arterial blood pressure before bupivacaine infusion (P < 0.05). The threshold doses at the first QRS modification (11.3 +/- 5.6 vs. 2.1 +/- 0.9 mg/kg) and the first dysrhythmia (40.6 +/- 15.3 vs. 8.48 +/- 3.7 mg/kg), the increase in EEG total spectral power (33.3 +/- 21.9 vs. 8.2 +/- 5.1 mg/kg), the 25 and 50% reduction in baseline mean arterial pressure and heart rate, the isoelectric EEG (58.6 +/- 14 vs. 22 +/- 6.6 mg/kg), and the final systole (99 +/- 16 vs. 51.8 +/- 14.5 mg/kg) were significantly greater in the clonidine group than in the saline group (P < 0.01). The time between the first dysrhythmia and 50% reduction of baseline mean arterial blood pressure was not different between the groups. In the additional series, the first dysrhythmia occurred later (10.9 +/- 4.5 vs. 3.2 +/- 1.0 min, P < 0.01) and plasma bupivacaine levels were greater (18.7 +/- 8.0 vs. 7.8 +/- 3.2 micrograms/ml, P < 0.01) in the clonidine group than in the saline group. CONCLUSIONS: In this model, clonidine given prophylactically delays the toxic manifestations of bupivacaine overdose and does not accentuate the subsequent hypotension.

Anesthesia, Epidural↗
PubMed1993

Intravenous clonidine does not promote hypoxemia or platelet aggregation in man.

This study was designed to evaluate hypoxemia and platelet aggregation in man following intravenous administration of clonidine. With Institutional approval and following informed consent, 20 patients (ASA I-II) without spontaneous or drug-induced coagulation disorder undergoing elective total hip replacement were studied. They were randomly divided into two groups. Group A (n = 10) received an IV loading dose of 4 micrograms/kg of clonidine in 30 minutes followed by an infusion of 1 microgram/kg/h till the end of the procedure. Group B (n = 10) received saline. Platelet aggregation was assessed before infusion and at the end of both the loading dose and the infusion. PaO2 was measured before anesthesia (FIO2 = 0.21), before femoral cementation (FIO2 = 0.40), 2 min. after prosthesis implantation (FIO2 = 1), before the end of the procedure (FIO2 = 0.40) and in the recovery room (spontaneous breathing with FIO2 = 0.21). Plasma clonidine levels were assessed at the end of both the loading dose and the infusion. At any time considered, no statistical differences were noted between the groups for platelet aggregation and PaO2. We conclude that intravenous clonidine does not clinically promote platelet aggregation nor hypoxemia in man.

Aged↗