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Biomedical subjects

M Baudrimont

Publications and source records attributed to M Baudrimont.

At least 55 records · Page 3Linked to original sources
PubMed1996

Rabies encephalitis in a patient with AIDS: a clinicopathological study.

A 46-year-old man was bitten by a dog in Mali; anti-rabies vaccination was incomplete. Three months later he was admitted to hospital with fever and diarrhea. Human immunodeficiency virus (HIV) serology was positive and CD4 count was 70/mm3. His status worsened rapidly with confusion hydrophobia and hypersialorrhea. Despite anti-rabies serotherapy and vaccination, he died suddenly 12 days after admission. Immunofluorescence on cerebral tissue samples established rabies encephalitis. Neuropathology showed mild encephalitis with occasional Babès nodules and rare perivascular mononuclear cuffs. Intraneuronal Negri inclusion bodies were remarkably diffuse and abundant. They were clearly demonstrated by immunocytochemistry and electron microscopy. Apoptotic neurons were identified in the brain stem and hippocampus in the vicinity of inflammatory foci. In contrast, apoptosis could not be demonstrated in non-inflammatory areas, even where Negri bodies were numerous. There was no associated HIV encephalitis or opportunistic infection. The occurrence of rabies encephalitis in AIDS represents a random association, but is probably not exceptional as rabies is endemic in many countries and the AIDS epidemic is spreading worldwide. In this case, although the incubation duration and clinical presentation were comparable to those in classical rabies the T-cell-mediated immunosuppression may account for the weak inflammatory reaction and unusually abundant viral multiplication. This observation confirms that all those at risk for rabies, particularly immunocompromised patients, should receive complete anti-rabies treatment including vaccines and specific immunoglobulins, as soon as possible after infection.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Glutamine metabolism and neuropathological disorders in experimental hepatic encephalopathy: effect of transplanted hepatocytes.

BACKGROUND: Physiopathology of hepatic encephalopathy remains unclear. Recent studies have suggested that ammonia would not act by itself but through an increase in glutamine in the brain. We have previously demonstrated that transplantation of syngeneic hepatocytes into the spleen was able to correct both behavioral deficits and plasma amino acid changes observed in portacaval shunted rats. The aim of the present work was to show a correlation between the correction of chronic hepatic encephalopathy by means of intrasplenic hepatocyte transplantation and two parameters, brain glutamine concentration and ultrastructural aspects of astrocytes. METHODS: Inbred male Wistar Furth rats were divided into three groups: sham-operated rats (n = 10), rats subjected to portacaval shunt (n = 10), and rats subjected to portacaval shunt and intrasplenic hepatocellular transplantation of 10(7) hepatocytes isolated from livers of syngeneic rats (n = 10). Chronic hepatic encephalopathy was quantified 30 and 60 days after operation by means of nose-poke exploration and spontaneous activity. Pathologic examination and measurement of glutamine concentrations in the corpus striatus and in the cerebral cortex were performed 60 days after operation. RESULTS: Portacaval shunt rats showed reduced spontaneous activity and nose-poke exploration scores. After portacaval shunt a significant glutamine increase occurred in the corpus striatus and in the cerebral cortex when compared with sham rats (p < 0.05). Ultrastructural examination showed modification of astrocytes named Alzheimer type II after portacaval shunt. Correction of behavioral abnormalities by means of intrasplenic hepatocyte transplantation was associated with partial correction of striatal glutamine increase and with decrease in astrocyte alterations. Cortex glutamine concentration in portacaval shunt-intrasplenic hepatocyte transplantation group and in portacaval shunt rats did not differ significantly. CONCLUSIONS: These data show that intrasplenic hepatocyte transplantation not only prevents neurologic disorders of hepatic encephalopathy but can also decrease glutamine and ultrastructural alterations in the corpus striatus in an experimental model of chronic liver failure. These data are in favor of the involvement of glutamine in chronic hepatic encephalopathy. These results suggest that intrasplenic hepatocyte transplantation might be of therapeutic interest in chronic liver failure.

Animals↗
PubMed1996

Acute retinal necrosis in the course of AIDS: study of 26 cases.

OBJECTIVE: To report 26 cases of acute retinal necrosis (ARN) in HIV-infected patients, to compare these data with the literature and to discuss the clinical spectrum of ARN during HIV infection. DESIGN AND SETTING: Twenty-six HIV-infected patients with ARN, collected from five ophthalmology departments in Paris (France) between 1985 and 1993, were analysed retrospectively. PATIENTS: Twenty-eight patients were enrolled; two were lost of follow-up. Diagnosis of ARN was established on the following criteria: (1) inflammation of the anterior segment and the characteristic triad, and (2) peripheral circular necrosis with centripetal progression toward the posterior pole associated with occlusive periarteritis and inflammation of the vitreous. RESULTS: ARN is a late event in the course of immunosuppression (CD4+ lymphocyte count < 100 x 10(6)/l). The most frequent presenting syndrome is a decrease of visual acuity, but signs related to a retrobulbar optic neuritis may also be present. In 60-90% of cases, vesicular viral eruption, usually shingles, precedes the onset of ARN by several days. Occasionally, neurological impairment is also present. Progression to blindness occurs in 76-85% of cases, bilaterally in 59%, and is usually induced by retinal detachment. This study and literature data suggest that varicella zoster virus (VZV) is directly implicated in the onset of ARN. At present, the most efficient therapeutic schedule is unknown. CONCLUSION: ARN is a rare and serious disease in AIDS patients. It is often associated with VZV infection. There is no preventive or curative efficient treatment. ARN might be considered as another opportunistic infection because of its rapid clinical evolution and severe prognosis.

AIDS-Related Opportunistic Infections↗
PubMed1996

Herpes simplex virus type 1 encephalitis in acquired immunodeficiency syndrome.

Herpes simplex (HSV) infection of the central nervous system is uncommon in AIDS and usually has an atypical topography. This review is centred around the case of a 49-year-old homosexual patient with AIDS who died from diffuse encephalopathy. Neuropathological examination revealed necrotic and haemorrhagic changes involving both temporal lobes, insulae and cingulate gyri. Cowdry type A intranuclear inclusion bodies were abundant but inflammation was minimal. Electron microscopy confirmed characteristic herpes virus particles. Immunocyto-chemistry was positive for HSV type 1 and 2. In situ hybridization and PCR, however, were positive for HSV type 1 but excluded HSV type 2. There was associated cytomegalovirus ventriculitis but clearly separated from HSV encephalitis. There were no histological features of HIV encephalitis and HIV could not be demonstrated by immunocytochemistry or by PCR to demonstrate proviral DNA. Apoptotic neurons were numerous in areas with a severe macrophage reaction. Only two pathological cases with characteristic limbic distribution and necrotic haemorrhagic histologic have been reported previously. The rarity of these reports suggests that in advanced AIDS, the immune reaction causing a typical necrotizing encephalitis cannot be mounted. Distinction between HSV type 1 and 2 infection may be difficult by immunocytochemistry and usually requires in situ hybridization, tissue culture or PCR. In AIDS patients, HSV-1 has been identified as responsible for encephalitis whereas HSV-2 has been more responsible for myelitis. Associated productive HIV infection of the CNS was found in none of the cases. In contrast, cytomegalovirus encephalitis was found in nine of 11 cases of AIDS-associated HSV encephalitis.

Acquired Immunodeficiency Syndrome↗
PubMed1996

[A good model of acute hepatic failure: 95% hepatectomy. Treatment by transplantation of hepatocytes].

The aim of this study was to develop in rats, a model of acute hepatic failure that mimics human fulminant hepatitis and to study the effect on survival of transplantation of isolated hepatocytes. This study showed that the mortality after 90% hepatectomy was reduced by the sole correction of hypoglycemia. On the other hand, 95% hepatectomy appeared as a reliable and reproductable model, associated with a period of hepatic coma, a deep disorder of coagulation, and a high mortality rate (> 80%) despite correction of hypoglycemia. In this model of acute hepatic failure, intraperitoneal transplantation of encapsulated isolated hepatocytes significantly reduced the mortality rate from 80% in the control groups to 31% in the transplanted group. A complete regeneration of the native liver was observed in all rats surviving. All animals survived after explantation of the hollow fibers. Well preserved hepatocytes were observed in hollow fibers two months after transplantation.

Animals↗
PubMed1995

Brain stem encephalitis due to varicella-zoster virus in a patient with AIDS.

We describe a patient infected with human immunodeficiency virus (HIV) who had localized brain stem encephalitis due to varicella-zoster virus (VZV) and no cutaneous eruption. Diagnosis of the infection was based on the presence of Cowdry type A intranuclear inclusions in neurons, astrocytes, and oligodendrocytes positive for VZV (as shown by immunochemical staining). Although this infection is rare, we demonstrate the need for clinicians to include VZV infection in the differential diagnosis of rapidly progressive multiple cranial nerve palsies in HIV-infected patients, particularly because specific treatment for VZV infection is effective and relatively safe.

Acquired Immunodeficiency Syndrome↗
PubMed1995

A prospective evaluation of clinical criteria and polymerase chain reaction assay of cerebrospinal fluid for the diagnosis of cytomegalovirus-related neurological diseases during AIDS.

OBJECTIVE: To study the predictive value of clinical criteria and polymerase chain reaction (PCR) assay of cerebrospinal fluid (CSF) for the diagnosis of cytomegalovirus (CMV)-related neurological disorders during AIDS. SETTING: Four infectious diseases departments in two tertiary referral teaching hospitals in Paris, France. DESIGN AND PARTICIPANTS: One-year prospective study involving 164 consecutive immunosuppressed HIV-seropositive patients undergoing lumbar puncture (LP). METHODS: A tentative diagnostic classification, based on strict operational criteria and PCR assay of CSF, was performed at the time of LP. At the end of the study, tentative diagnoses and PCR results were blindly and independently compared with the firm diagnoses, based on central nervous system histology, clinical outcome and/or viral culture of CSF. RESULTS: The tentative diagnosis showed CMV-related neurological disease in 38 patients, and CMV DNA was detected in 42. Among the 88 patients for whom a firm diagnosis was possible, 26 had a diagnosis of CMV-related neurological disease. The concordance between the tentative and firm diagnoses was 61%, with a kappa index of 0.40. In contrast, the sensitivity and specificity of PCR were respectively 92 and 94%, with positive and negative predictive values of 86 and 97%. The presence of CMV DNA in CSF was associated with an increased risk of death (P < 0.0001). CONCLUSIONS: Unlike clinical criteria, PCR detection of viral DNA in CSF can be used reliably for antemortem diagnosis of CMV-related neurological disease, a frequent complication of AIDS in this study. This rapid method should make a major impact on the management of these patients.

AIDS-Related Opportunistic Infections↗
PubMed1995

Transplantation of allogeneic hepatocytes without immunosuppression: long-term survival.

BACKGROUND: Hepatocyte transplantation could be an alternative to whole liver transplantation. Allogeneic hepatocytes are rejected if transplanted without immunosuppression. The aim of this study was to transplant allogeneic hepatocytes in the peritoneum and to protect them from rejection by encapsulation in a new semipermeable membrane. METHODS: Rat hepatocytes were encapsulated in hydrogel-based hollow fibers, obtained from AN69 copolymer, before being transplanted into the peritoneum of rats. Outcome of allogeneic hepatocytes encapsulated in hollow fibers was compared with that of syngeneic hepatocytes encapsulated in hollow fibers, with that of free allogeneic hepatocytes, and with allogeneic hepatocytes encapsulated in hollow fibers left open. Cell viability was assessed by erythrosin exclusion, structure by electron microscopy, and function by albumin release. RESULTS: Up to 90 days, viability of allogeneic hepatocytes in hollow fibers was greater than 80%. The structure remained normal at electron microscopy. Albumin release was 16.5 +/- 0.3 micrograms/24 hr/10(6) hepatocytes (day 15), 14.2 +/- 2.0 micrograms/24 hr/10(6) hepatocytes (day 30), 8.8 +/- 0.1 micrograms/24 hr/10(6) hepatocytes (day 60), and 11.4 +/- 0.3 micrograms/24 hr/10(6) hepatocytes (day 90). Free hepatocytes and hepatocytes in hollow fibers left open did not survive at day 15. CONCLUSIONS: Viability and function of encapsulated allogeneic hepatocytes were maintained up to 90 days after transplantation, without immunosuppression.

Acrylic Resins↗
PubMed1994

Subacute sensory neuropathy associated with Hodgkin's disease.

We describe 2 patients with Hodgkin's disease (HD) who developed a subacute predominantly sensory neuropathy with areflexia, which improved after tumour removal, and review 6 cases with sensory neuropathies associated with HD from the literature. The neuropathy revealed a relapse of the tumour in patient 1 and was the presenting feature of HD with Castleman's disease-like lesions in patient 2. Nerve conduction velocities were normal, sensory and motor potential amplitudes were reduced, and F waves were increased. Unlike sensory ganglionitis associated with small cell lung cancer, sensory evoked potentials were not abolished. Nerve biopsies showed axonal degeneration and mild perivascular inflammatory infiltrates. We believe that the cases of subacute sensory neuropathies associated with HD that show dramatic improvement after treatment of the underlying tumour correspond to a variant of HD-associated inflammatory demyelinating polyneuropathy rather than to a true paraneoplastic sensory ganglionitis.

Adult↗
PubMed1994

Autosomal dominant arteriopathic leuko-encephalopathy and Alzheimer's disease.

A 49-year-old man suffered from progressive dementia and seizures leading to death after 2 years. CT scans showed severe cortical-subcortical atrophy and hypodensity of the white matter. His father had died at about the same age with similar clinical signs. Two sisters and one brother were also affected. Neuropathological study revealed predominant involvement of the cerebral white matter with myelin loss, gliosis and type I lacunes. The small arteries and arterioles of the white matter and basal ganglia, and, to a lesser extent those of the subarachnoidal space, displayed fibrosis and replacement of the media by an eosinophilic, PAS positive, Congo Red negative, granular substance. Electron microscopy showed swollen myocytes surrounded by collagen, elastin and a compact electron-dense material. Immunofluorescence using antibodies against IgA, IgG, IgM, C1q and C3 stained the abnormal media weakly. In the cortex, there were diffuse senile plaques and neurofibrillary tangles. Immunohistochemistry demonstrated beta/A4 positive material in cortical senile plaques but not in arterial walls. Adventitial macrophages were, however, immunoreactive for gamma-trace. Systemic arterioles were normal. The vascular changes and leukoencephalopathy are comparable to those described in 'Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy' (CADASIL). Similar vascular changes were also observed in nonfamilial cases. An association with Alzheimer changes in the cortex has not been described previously. The relationship between both diseases and the role of each in the causation of the dementia is unclear.

Alzheimer Disease↗
PubMed1994

Immunohistochemical and ultrastructural study of the cornea in Chandler's syndrome. Report of a case.

A corneal specimen obtained by surgery in a 55-year-old woman with Chandler's syndrome was studied by light and transmission electron microscopy as well as by immunocytochemistry. The pathologic features were abnormalities of the endothelially derived cells lining the posterior corneal surface with a fibrous material consisting of collagen fibrils, filaments and banded material similar to that found in the anterior part of Descemet's membrane observed between the endothelial cell layer and Descemet's membrane. The multilayered endothelial cell layer in our case was found to be strongly positive for cytokeratins K7 and KL1 and vimentin and negative for factor-VIII-related antigen, neuron-specific enolase, nerve tissue S-100 protein, epithelial membrane antigen, CD 68, actin and desmin. This immunohistochemical reaction pattern argues in favor of an epithelial origin for cells lining the endothelial cell layer in Chandler's syndrome.

Corneal Diseases↗
PubMed1994

Cytomegalovirus multifocal neuropathy in AIDS: analysis of 15 consecutive cases.

A severe multifocal neuropathy caused by cytomegalovirus (CMV-MN) can occur in the late stage of human immunodeficiency virus (HIV) infection. In a retrospective study, we identified 15 consecutive HIV-positive patients with a diagnosis of CMV-MN based on (1) markedly asymmetric neuropathy, (2) fewer than 100 CD4+ cells per mm3, (3) exclusion of other causes of neuropathy, and (4) characteristic CMV cytopathic changes on neuromuscular biopsy (2 patients), positive CSF culture for CMV (2 patients), or clinical improvement on anti-CMV therapy given for concurrent extraneurologic CMV disease (8 patients) or neuropathy (3 patients). All patients were men and had severe immunosuppression (mean CD4+ cell count, 18 per mm3). The initial symptoms were numbness and painful paresthesias showing a patchy, multifocal distribution. After a mean of 11 weeks (range, 1 to 10 months), the patients developed moderate or severe sensorimotor asymmetric neuropathy. Extraneurologic CMV infection occurred in 10 patients before diagnosis. Electrophysiologic studies showed axonal neuropathy and CMV DNA was present in CSF by the polymerase chain reaction (PCR) technique in 90% of patients tested. Fourteen patients showed a marked improvement 1 to 4 weeks after starting ganciclovir or foscarnet therapy. During follow-up on maintenance therapy (13 patients), the neuropathy relapsed in three patients and probable or confirmed CMV encephalitis occurred in five. Twelve patients died during follow-up, at a mean interval of 9.5 months after their first symptoms. These results extend the clinical spectrum of CMV-MN and show that PCR detection of CMV DNA in CSF may be a useful diagnostic marker.

Acquired Immunodeficiency Syndrome↗
PubMed1994

[Cervico-cerebral atheroma].

Atherosclerosis is the leading cause of death in economically developed countries. The arteries most frequently affected are the aorta, coronary and cerebral arteries. Atherosclerosis only affects large and medium calibre arteries of the general circulation. The lesion involves the arterial intima. The two lesions usually described are lipid striae and atheromatous plaques. The lesions are heterogeneous and it is difficult to correlate them to each other. Atheromatous plaque may be complicated by several types of independent or combined lesions: stenosis of the arterial lumen, haemorrhage into the plaque, ulceration or calcification of the plaque, organisation of a thrombus, aneurysm formation. Lesions predominantly affect the extracranial arteries at the carotid bifurcation and the origin of the vertebral arteries and the cerebral arteries at the origin and termination of the internal carotid artery, the basilar trunk and carotid bulb. The causes of this disease are unknown at the present time. Only the risk factors can be controlled. Pathogenic hypotheses are still highly controversial.

Adult↗