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D Hénin

Publications and source records attributed to D Hénin.

66 records · Page 4Linked to original sources
PubMed1989

[Pathologic study of the eye and central nervous system in 25 cases of AIDS].

We have reviewed the clinical and pathologic findings of 25 patients with the acquired immunodeficiency syndrome (AIDS) who had a complete post-mortem examination including a study of the nervous system and of one or both eyes. Cytomegalovirus (CMV) retinitis was the most frequent type of ocular infection observed fundoscopically (9 of 18 cases examined clinically). There were only 3 cases of CMV encephalitis amongst the 8 cases of CMV retinitis documented pathologically. Cerebral toxoplasmosis was found in 12 of the 25 cases and in only one of these could Toxoplasma gondii cysts be demonstrated in the optic nerve. Cotton wool spots were the most frequent lesion observed fundoscopically (10 of 18 cases examined clinically). In the 3 cases where they were observed microscopically they corresponded to cytoid bodies which represented axonal swellings within the nerve fiber layer. The pathogenesis of this lesion in patients with AIDS is not understood. Intraocular lymphoma was present in only one case.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Myelopathy, polymyositis and systemic manifestations associated with the HTLV-I virus].

A case of HTLV-I associated myelopathy in a 51 year-old Haitian woman is reported. MRI showed high signals in the cerebral white matter on T2-weighted images. There also was clinical and electrophysiological evidence of myositis, and a biopsy of the quadriceps muscle showed dense inflammatory infiltrates surrounding several small perimysial blood vessels. The virus was not demonstrated in the muscle. The presence of several systemic abnormalities (polyclonal gammapathy, circulating immune complexes, Sjögren's syndrome) and the vasculitis suggest an immunopathological mechanism for this HTLV-I associated myositis.

Antigen-Antibody Complex↗
PubMed1988

[Neuropathology of human type 1 immunodeficiency virus infection].

The nervous system may be affected at any stage in the course of HIV-1 infection. Acute or subacute inflammatory demyelinating polyradiculoneuropathies occur often early and improve spontaneously. Distal symmetrical axonal, predominantly sensory, painful polyneuropathies occur in the late stages of the disease. Microvasculitis is frequent in the early neuropathies. Spastic and ataxic paraparesis associated with vacuolar myelopathy are rare and probably not related only to HIV-1. Aseptic lymphocytic meningitis may occur as the presenting or sole manifestation of HIV-1 infection. The more frequent subacute encephalitis, probably directly related to HIV-1, is late in the course of the disease. Microscopic changes are suggestive but non-specific (microglial nodules, multinucleated giant cells). According to some authors, HIV-1 infection of the central nervous system macrophages may be early and latent until associated pathologies (opportunistic infections, lymphoma) trigger the replication of HIV-1 by infected macrophages.

Acquired Immunodeficiency Syndrome↗
PubMed1987

[2 cases of Waldenstrom's disease associated with a glioblastoma].

The association of Waldenström disease and glioblastoma was observed in two patients. Both diseases were diagnosed almost simultaneously. In the first patient the diagnosis of glioblastoma was made on cerebral biopsy. In the second case, the diagnosis was confirmed at autopsy. The association of Waldenström's disease and glioblastoma is rare but it does not seem to be coincidental. The physiopathological problems related to this coexistence are discussed.

Aged↗
PubMed1987

[Neuropathological study of 31 cases of acquired immunodeficiency syndrome].

Post-mortem study of every patient who died from AIDS in Pitié-Salpêtrire Hospital from June 1984 to November 1985 was performed without regard to the presence of neurological signs and symptoms. Autopsy were performed in 31/48 cases. Patients had been hospitalized in the Departments of Parasitology-Infectious Disease (24 cases) Internal Medicine (4 cases) and Neurology (3 cases). In every case, formalin-fixed material from the brain and the spinal cord were embedded in paraffin (20 samples), stained with hematoxylin-eosin, PAS, Alcian blue, Giemsa, Grocott and Ziehl techniques and Bodian's silver impregnation along with Luxol fast blue, and, in celloïdin (8 samples), stained with hematoxylin-eosin and Loyez' impregnation. There were 30 men (27 caucasian, 1 egyptian, 1 haïtian, 1 senegalese) and one woman (congolese). Twenty eight (28) patients were homosexuals. AIDS was transfusion-associated in two cases. Neurologic complications revealed the disease in 2 cases. Eighteen (18) patients had neurological signs or symptoms before death. Age range at death was 22-58 (mean 38). Brain weight in AIDS (from 1150 gms to 1750 gms-mean 1428 gms) was not statistically different from the mean weight of 100 male patients in the same age range autopsied in the same laboratory during the identical period (mean 1427 gms, standard deviation: 23). Microscopic abnormalities were present in every brain examined. These included non-Hodgkin lymphoma (3 cases), opportunistic infections (21 cases: 13 toxoplasmosis, 4 cytomegalovirus encephalitis, 3 cryptococcal meningitis, 1 infection by mycobacterium avium-intracellulare), and subacute encephalitis (17 cases, 9 isolated, 8 associated with other disorders). The characteristic changes consisted of lympho-monocytic focal infiltrates (so-called microglial nodules) and mild lympho-monocytic perivascular cuffs in 10 cases. Typical giant cells were seen only in one case. Mild demyelinating changes were also seen in only one case. No spinal cord spongiosis, nor Progressive Multifocal Leukoencephalopathy was found. HIV localization was performed on frozen sections utilizing in situ hybridization techniques (2 cases) and immunohistologic techniques (5 cases). HIV, RNA and proteins, was detected in 2 cases with subacute encephalitis. Infected cells were labeled with macrophage markers, and rarely with T4 lymphocyte markers. Infected astrocytes (identified by anti-GFAP serum) or neurons (identified by anti-NSE serum) were never observed. No giant cells were seen in these two cases.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[Recklinghausen's disease with digestive localizations associated with gastric acid hypersecretion suggesting Zollinger-Ellison syndrome].

We report the case of a 49 year old male patient who had Recklinghausen's disease associated with hyperchlorhydria. The principal features of Recklinghausen's disease were cutaneous localizations and countless digestive tumors, found mainly on the small bowel. The ultrastructural aspect of these tumors was neurinoma or schwannoma. Basal acid gastric hypersecretion and a positive secretin test were highly suggestive of a Zollinger-Ellison syndrome. Gastrinoma was not found at laparotomy even though a gastrin gradient had been demonstrated by pancreatic venous sampling. In a patient with Recklinghausen's disease, neuroendocrine tumors (APUDomas) should be looked for systematically.

Diagnosis, Differential↗
PubMed1983

[Thrombosis of a valve prosthesis: fatal cerebral embolism during thrombolytic treatment].

The authors report the first case of lethal cerebral embolism complicating thrombolytic therapy administered for thrombosis of a mitral valve prosthesis. The incidence of systemic embolism during this form of therapy appears to be at least one in five cases. It may be underestimated and should lead to further discussion as to the indications of thrombolytic therapy and surgery for thrombosis of a left heart valve prosthesis.

Adult↗
PubMed1978

[Amyloid neuropathy associated with a benign monoclonal gammopathy (lambda light chains)].

The authors report a case of non-familial amyloid neuropathy in which there was sensory-motor neuropathy of the 4 limbs, multiple lesions in the cranial nerves, and large subcutaneous amyloid deposits. Biopsy samples showed the presence of amyloid deposits in the interstitial tissues, the vessel walls in the muscle hypodermis, and in the bone marrow. A light monoclonal lambda chain was present in the serum. Immunofluorescent studies of the biopsy specimens showed the presence of elective fluorescence with an anti-lambda immunoserum in the amyloid substance.

Amyloidosis↗
PubMed1977

Cerebromeningeal localizations in acute myeloblastic leukemia of the adult. Clinical and pathological study of 15 cases.

68 consecutive adults were treated for acute myeloblastic leukaemia (A.M.L). Involvement of the central nervous system (CNS) developed in 15 cases. The clinical characteristics of nine of these patients were: symptoms of increased intra-cranial pressure in 5, cranial nerve lesions in 4, peripheral nerve lesions in 5, cord compression in 1, hemispherical symptoms in 7. Lumbar puncture vas performed systematically on seven patients, two of them with evidence of meningeal leukaemia (M.L.). Post-mortem examination was performed on seven patients who died during the first induction treatment: three had evidence of C.N.S. involvement. M.L. developed in three patients during complete hematologic remission (R.C.) In patients younger than 60 years old, the incidence of M.L. was 8/24 (approximately 33%). Medial survival time was reduced:8 months in cases with M.L., compared to 13.5 months. Cerebro-fluid protein levels were increased in six cases without blast cells: in four cases, M.L. occurred within a few months. The frequency of meningeal leukaemia in A.M.I. is under-estimated. Eradication of this frequent complication is difficult. Prophylactic meningeal treatment may be instituted for patients younger than 60, to reduce the incidence of M.L. and to improve the median remission time.

Adolescent↗
PubMedDate not supplied

[Iatrogenic neuropathies].

During the last few years the list of drugs capable of inducing a iatrogenic neuropathy has been considerably lengthened. Drug toxicity to peripheral nerves may be discovered at the experimental stage, but it is usually recognized after the drug has been launched on the market, hence the importance of pharmacovigilance. The responsibility of a drug for the occurrence of neuropathy may be difficult to prove, particularly when the drug is used in the treatment of a disease which, by itself, may be responsible for a lesion of the peripheral nervous system. Iatrogenic neuropathies are usually axonal, but some drugs produce a primary disorder in the myelin-Schwann cell couple. Schwann cell diseases may be induced by drugs, such as perhexiline maleate, amiodarone or chloroquine, which inhibit lysosomal enzyme activity. In such cases inclusions representing fat-loaded lysosomes can be detected in various tissues, and particularly in Schwann cells. In certain patients, notably those treated with gold salts, an immune mechanism might be responsible for neuropathy. Most drug-induced neuropathies are due to a primary lesion of the neuron which is more often an axonopathy than a neuronopathy. It is usually a retrograde distal axonopathy the occurrence of which is attributed to a disorder of the fast retrograde axonal flow. In a few cases, the finding of a biochemical mechanism perturbing the axonal flow may help in preventing the occurrence of a iatrogenic neuropathy.

Amiodarone↗
PubMedDate not supplied

[AIDS dementia].

Human immunodeficiency virus type I (HIV), the etiology of AIDS is also the cause of a primary infection of the central nervous system. The AIDS Dementia Complex is a common and important cause of morbidity in patients in advanced stages of infection. Subacute encephalitis demonstrating, the neuropathogenicity of HIV 1 constitute an human model for slow virus encephalitis.

AIDS Dementia Complex↗