PubMed Health⌕ Search

Biomedical subjects

D Hénin

Publications and source records attributed to D Hénin.

At least 55 records · Page 3Linked to original sources
PubMed1994

Expression of c-erbB-2 oncogene product in Barrett's adenocarcinoma: pathological and prognostic correlations.

AIMS: To establish the prevalence of c-erbB-2 protein expression in a surgical series of Barrett's adenocarcinomas; and to correlate this expression with clinicopathological data and prognosis. METHODS: Sixty six surgical specimens of Barrett's adenocarcinomas were included in this retrospective study. Blocks of the tumour and of non-dysplastic Barrett's mucosa were stained with a polyclonal antibody specific for the intracytoplasmic domain of the c-erbB-2 protein. RESULTS: Seven of 66 tumours showed membrane staining for the c-erbB-2 protein. The non-dysplastic Barrett's mucosa was negative in all cases. There was no difference between c-erbB-2 positive and negative tumours with regard to mean age, sex ratio, percentage of alcohol misusers, percentage of smokers, tumour differentiation, depth of invasion, lymph node response, and proliferative activity, assessed by the percentage of tumour cells positive with the MIB-1 antibody directed against the Ki-67 antigen. All c-erb B2 positive tumours were of Lauren's intestinal type compared with negative c-erbB-2 tumours. Patients with c-erbB-2 positive tumours had a significantly poorer prognosis than patients with negative tumours. CONCLUSIONS: The prevalence of Barrett's adenocarcinomas expressing c-erbB-2 found in this study (11%) was similar to that observed in published series of gastric adenocarcinomas. c-erbB-2 protein expression could be an important prognostic indicator in Barrett's adenocarcinoma.

Adenocarcinoma↗
PubMed1993

Overexpression of p53 protein in Barrett's syndrome with malignant transformation.

AIMS: To study the overexpression of p53 protein in Barrett's oesophagus with adenocarcinoma, and to correlate this expression with the pathological features of Barrett's syndrome. METHODS: Immunohistochemical staining was performed on frozen sections with a monoclonal antibody directed against wild type and mutated p53 protein (Pab 1801). Eleven cases of Barrett's adenocarcinoma were studied, seven of which had extensive sampling of benign Barrett's mucosa. RESULTS: Eight of 11 adenocarcinomas overexpressed the p53 protein. Both early and advanced tumours were positive. In Barrett's mucosa around the p53 positive tumours, high grade dysplasia was positive; low grade dysplasia and non-dysplastic mucosa were negative. CONCLUSIONS: P53 gene mutation with ensuing p53 protein overexpression is a common feature of Barrett's adenocarcinoma, both at early and advanced stages. This mutation appears as a relatively late event during the neoplastic transformation of Barrett's oesophagus.

Adenocarcinoma↗
PubMed1993

Cranial pachymeningitis of unknown origin: a study of seven cases.

We report seven patients with cranial pachymeningitis of unknown origin in whom the main clinical features were headaches, ataxia, and cranial nerve palsies. CSF showed inflammatory changes. CT and MRI showed thickening of the falx and of the tentorium. The clinical course was chronic. Four patients improved with prednisolone but became steroid-dependent: in two cases, radiotherapy had no lasting improvement and in one, azathioprine permitted a reduction of the corticosteroids. Five patients had biopsy of the tentorium cerebelli or of the temporal dura mater. In two cases, autopsy revealed extensive pachymeningitis without parenchymal changes. In all instances, microscopic examination of the dura mater showed a cellular infiltrate of polymorphic cells; there were no epithelioid granulomas. Review of the literature discloses seven similar cases. We discuss the relationship of these lesions with inflammatory meningeal masses, the focal pachymeningitis of the Tolosa-Hunt syndrome, and multifocal fibrosis.

Adult↗
PubMed1993

[Is it possible to individualize microvillous large-cell lymphoma among sinusoid lymphomas?].

Microvillous non-hodgkin lymphomas are large cell malignant lymphomas with a sinus growth pattern and the presence of cytoplasmic processes detected by electron microscopy. Microvillous non-hodgkin lymphomas appear to be of B cell lineage. Neoplasms considered in the differential diagnosis include anaplastic large cell Ki-1 lymphomas, malignant histiocytosis and metastatic carcinoma or malignant melanoma. A panel of markers are usually sufficient to recognize all of these neoplasms except microvillous lymphomas. We report a case of microvillous non-hodgkin lymphoma characterized by a histologic pattern mimicking those of anaplastic large cell Ki-1 lymphoma. However, immunohistochemistry study failed to demonstrate presence of activation antigen such as Ki-1, EMA, interleukin 2 receptor. Ultrastructural study showed that neoplastic cells exhibited filliform cytoplasmic processes. This report raise the possibility of an overlap between microvillous non-hodgkin lymphomas and anaplastic large cell Ki-1 lymphomas of B-cell lineage. It must be emphasized that, initially, these two kinds of lymphomas were defined with different morphologic technologies.

Biomarkers, Tumor↗
PubMed1993

The intraportal lymphoid nodule and its environment in chronic active hepatitis C: an immunohistochemical study.

Intraportal lymphoid nodules have been observed in liver biopsy specimens from patients with autoimmune liver disease and chronic active hepatitis C. They are characterized by a nodular lymphocyte aggregate with a germinal center. The purpose of this in situ immunophenotyping study was to determine immunohistochemically the phenotype of immunocompetent cells in and around intraportal lymphoid nodules in patients with chronic hepatitis C. For comparison, we also examined lymphoid nodules in patients with autoimmune liver disease. Liver biopsy specimens from 13 unselected patients with CAH and hepatitis C antibodies and from 7 unselected patients with autoimmune liver disease seen during the same period were studied. Sections of snap-frozen specimens were immunostained with monoclonal antibodies directed against different subsets of T cells, B cells, follicular dendritic cells and macrophages. Intraportal lymphoid nodules were observed in 11 of 13 patients with chronic hepatitis C. They appeared as lymphoid follicles with activated B cells in germinal centers surrounded by a follicular dendritic cell network. A mantle zone of B cells was present around the aggregate of activated B cells. A T-cell zone comprising CD4-positive helper T cells, CD8-positive suppressor/cytotoxic T cells and a few CD25-positive activated T cells expressing interleukin-2 receptor was seen at the periphery of the nodules. Human leukocyte antigen DR was expressed by B cells and by T cells, indicating that T cells were activated. The immunocompetent cells observed in piecemeal necrosis were predominantly CD4 helper T cells, whereas those seen in the lobule were predominantly CD8 suppressor/cytotoxic T cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The prevalence of ulcerated plaques in the aortic arch in patients with stroke.

BACKGROUND AND METHODS: The cause of cerebral infarction is obscure in up to 40 percent of patients with this disorder who are studied prospectively. In this investigation, we determined the frequency of ulcerated plaques in the aortic arch and explored the part they may play in the formation of cerebral emboli. Using an autopsy data bank, we studied the prevalence of ulcerated plaques in the aortic arch in 500 consecutive patients with cerebrovascular and other neurologic diseases who were studied at autopsy. RESULTS: Ulcerated plaques were present in 26 percent of the 239 patients with cerebrovascular disease but in only 5 percent of the 261 patients with other neurologic diseases (P less than 0.001). After we controlled for age and heart weight, the adjusted rates were 16.9 percent and 5.1 percent, respectively (adjusted odds ratio, 4.0; 95 percent confidence interval, 2.1 to 7.8; P less than 0.001). Among the patients with cerebrovascular disease, the prevalence of ulcerated plaques in the aortic arch was 28 percent in the 183 patients with cerebral infarcts and 20 percent in the 56 patients with brain hemorrhage. The prevalence of ulcerated plaques was 61 percent among the 28 patients with no known cause of cerebral infarction, as compared with 22 percent among the 155 patients with a known cause of cerebral infarction (P less than 0.001). After adjustment for covariates, the prevalence was 57.8 percent among patients with no known cause of cerebral infarction and 20.2 percent among those with a known cause (adjusted odds ratio, 5.7; 95 percent confidence interval, 2.4 to 13.6; P less than 0.001). The presence of ulcerated plaques in the aortic arch was not correlated with the presence of extracranial internal-carotid artery stenosis, suggesting that these were two independent risk factors for stroke. CONCLUSIONS: Ulcerated plaques in the aortic arch may play a part in causing cerebral infarction, especially in patients in whom cerebral infarction has no known cause.

Adult↗
PubMed1992

Lymphoma-induced polyradiculopathy in AIDS: two cases.

Progressive polyradiculopathy is a rare, well-documented complication of the acquired immunodeficiency syndrome in man. It has been commonly attributed to a cytomegalovirus (CMV) infection. We report two HIV-infected patients with clinical and electrophysiological features of a unique, subacute, progressive polyradiculopathy. Post-mortem examination in case 1 disclosed an infiltration of the leptomeninges, the lumbar spinal cord, and the anterior and posterior roots by a B-cell immunoblastic lymphoma. Immunochemistry for HIV1 and CMV was negative in the peripheral and the central nervous system. Case 2 showed bone-marrow involvement by a Burkitt type lymphoma. Specific chemotherapy was followed by both clinical improvement of the polyradiculopathy and complete remission on a second bone-marrow biopsy. These findings may indicate that a lymphoma must also be considered a possible cause of polyradiculopathy in AIDS.

Adult↗
PubMed1992

Neuropathology of the spinal cord in the acquired immunodeficiency syndrome.

The neuropathologic findings in the spinal cord were reviewed in 138 consecutive autopsies of patients with the acquired immunodeficiency syndrome. In all cases both the brain and spinal cord were examined by conventional histologic techniques, and in 63 cases immunohistochemistry was used to detect human immunodeficiency virus (HIV), Toxoplasma gondii, cytomegalovirus, and JC papovavirus antigens. The most common observation was a normal spinal cord (60%). Vacuolar myelopathy (VM) was observed in 23 (17%) cases. Human immunodeficiency virus myelitis was evident in 8% of cases. Human immunodeficiency virus myelitis was associated with HIV encephalitis in 65% of the cases. Opportunistic infections of the spinal cord were uncommon, consisting of cryptococcosis (five cases), cytomegalovirus (four cases), toxoplasmosis (one case), and progressive multifocal leukoencephalopathy (one case), and almost always were seen with cerebral and/or systemic infection by these agents. Malignant lymphoma rarely involved the spinal cord (four cases); all were B-cell lymphomas and were associated with cerebral and/or systemic lymphoma. Other abnormalities rarely observed were Wallerian degeneration of the corticospinal tracts or posterior columns (6%) and focal microinfarcts. Most cases of VM (78%) were not associated with HIV myelitis, and in the five patients with both VM and HIV myelitis, HIV-infected cells were not found in the regions affected by VM. In contrast, 65% of cases with VM were associated with HIV encephalitis. The pathogenesis of VM remains unknown; it is probably not due to direct infection by HIV.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Human immunodeficiency virus (HIV) leukoencephalopathy and the microcirculation.

We studied the brains of three patients with acquired immune deficiency syndrome (AIDS), all of whom developed subacutely progressive dementia unassociated with opportunistic infection or neoplasm in the central nervous system. Computed tomographic (CT) scans of the head revealed cortical atrophy, ventricular dilation, and diffuse hypodensity of the centrum semiovale. On microscopic examination, the cerebral and cerebellar white matter in all cases showed diffuse and focal, angiocentric regions of myelin pallor, focal vacuolization, and extensive gliosis. Variable axonal loss and axonal spheroids were evident. The microvasculature showed striking changes, including mural thickening, increased cellularity, and enlargement and pleomorphism of endothelial cells with variable numbers of macrophages and multinucleated giant cells (MNGC), which often contained hemosiderin pigment. Human immunodeficiency virus type 1 (HIV-1) antigens were identified immunocytochemically within perivascular macrophages and MNGC and in some microglial cells. We suggest that the morphologic abnormalities of the microcirculation may be associated with an alteration of the blood-brain barrier. The increased vascular permeability could contribute to damage and loss of the white matter including both myelin and axons, and result in subcortical cerebral atrophy. The HIV-1 infected cells present in relation to the microvasculature may play a role in mediating the vascular injury.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Neuropathology of the acquired immunodeficiency syndrome.

This review attempts to assess critically the literature on the neuropathology of acquired immunodeficiency syndrome in light of our experience with 172 patients with acquired immunodeficiency syndrome who underwent extensive postmortem examinations of the central and peripheral nervous systems. The neuropathologic manifestations of the disease can be divided into three categories: (1) primary or putative/indirect effects of the human immunodeficiency virus, (2) opportunistic infections, and (3) neoplasms. We discuss the known etiologic agents and postulated pathogenetic mechanisms responsible for the broad range of neurologic diseases observed in patients with acquired immunodeficiency syndrome.

AIDS Dementia Complex↗
PubMed1989

The spectrum of changes on 20 nerve biopsies in patients with HIV infection.

Nerve and muscle biopsies were performed on 20 patients with HIV infection and peripheral neuropathy. Nine patients had distal symmetrical peripheral neuropathy (DSPN) (six ARC and three AIDS), six had inflammatory demyelinating polyneuropathy (IDP) (three ARC, one AIDS, and two otherwise asymptomatic patients), one had mononeuropathy multiplex (MM) (AIDS), 1 had mononeuropathy (ARC), one had meningoradiculitis (AIDS), and two had areflexia-associated lymphocytic meningitides (ARC), DSPN exhibited axonal degeneration in four of nine cases and was associated with segmental demyelination in five of nine cases. IDP exhibited segmental demyelination associated with axonal degeneration in four of six cases. Demyelination was more frequent in asymptomatic patients (2 of 2 cases) and in ARC (7 of 12 cases), whereas axonal degeneration was predominant in AIDS (6 of 6 cases). Mononuclear cell infiltration was seen in 1 of 2 asymptomatic patients and in 11 of 12 ARC patients but was exceptionally found in AIDS (1 of 6 cases). Involvement of the walls of small vessels, mostly venules ("subacute microvasculitis"), was found in 1 of 2 asymptomatic patients, in 8 of 12 ARC patients, and never in AIDS. The polyclonal mononuclear cell population was composed mainly of Leu 2 (T8) positive cells in seven cases of ARC. No virions were seen in electron microscopy. HIV was isolated in two cases from the CSF or the nerve biopsy.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases].

We report a neuropathological study of cerebellar infarctions involving the territory of the posterior inferior cerebellar artery (PICA) in 28 cases. Fifteen cases involved the PICA territory only. In 13 cases infarctions in the anterior inferior cerebellar artery (AICA) territory and/or in the superior cerebellar artery (SCA) territory were also present. A thorough post-mortem study of the arterial supply of the brain from the heart up to the cerebellar arteries, including the cervical spine segment of the vertebral arteries was performed in 27 cases. The territory of the cerebellar infarcts has been ascertained. In 15/28 cases (54 percent), infarction involved the PICA territory only (17 infarcts). All of these cases had a benign outcome and death was due to another cause. Six of these were recent infarctions. None had evidence of swelling and tonsillar herniation. Infarcts were generally of small size and involved the entire PICA territory in only 2 cases. Most of these cases were unexpected discovered at autopsy. Cerebellar infarction in the territory of the medial branch of the PICA (9/17 infarcts) drew grossly a set square with a dorsal base and a ventral top headed for the IVth ventricle. Five out of these cases were associated with infarction in the dorsal and lateral medullary territories. Retrospective clinical study showed that they had been unnoticed or overshadowed by other neurological disorders (4 cases), or presented as Wallenberg's syndromes (4 cases), or as a pure vestibular syndrome (due to an infarction involving only the cerebellum) mimicking an acute labyrinthine disorder (1 case). Infarctions in the territory of the lateral branch of the PICA (5/17 infarcts) always occurred without medullary involvement. All of them were unexpectedly discovered at autopsy, and were unnoticed during the life (3 infarcts) or were overshadowed by other neurological disorders (2 infarcts). That was also the case in 2 cases of infarction in the whole PICA territory (3/17 infarcts). Thus infarctions strictly localized to the entire PICA territory only were rare. Thirteen/28 cases (46 p. 100) of infarction in the whole PICA territory were associated with infarction in the AICA and/or the SCA territories. This resulted from an association with other infarctions and not from an abnormally large territory of the PICA. Cerebellar swelling with brain stem compression and tonsillar herniation occurred 8/13 cases (62 p. 100). There were other massive median and paramedian brain stem infarctions involving midbrain, pons or medulla in 55 p. 100 of 13 cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗