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Biomedical subjects

R Ghérardi

Publications and source records attributed to R Ghérardi.

6 recordsLinked to original sources

Localized neurological necrotizing vasculitides. Three cases with isolated mononeuritis multiplex.

Localized vasculitic neuropathies are increasingly reported. We describe 3 cases of peripheral neuropathy with necrotizing vasculitis confined to nerves and muscles without systemic involvement. These neuropathies were severe and relapsing, in contrast to a usually benign prognosis. Our cases appear to be isolated vasculitic neuropathies, with vasculitis strictly limited to the peripheral neuromuscular system without nonspecific clinical and/or biological systemic involvement.

Aged↗

Human immunodeficiency virus-related vasculitis. Clinical presentation of and therapeutic approach to eight cases.

Vasculitides occurring during the course of human immunodeficiency virus (HIV) infection are heterogeneous in their clinical presentation, time of occurrence, histological findings and etiological factors. Some of them can be directly attributed to HIV infection and their treatment might require new therapeutic approaches, such as plasma exchanges, specific antiviral agents and/or vasodilators. We report 8 cases of vasculitis associated with HIV. Five of them met the classification criteria of polyarteritis nodosa and had symptoms compatible with microscopic polyangiitis. Etiological agents were not identified. Although hepatitis B virus, hepatitis C virus (HCV) and other viruses or opportunistic agents were detected in some patients, HCV was suspected of being the etiological factor in only 1 of them. Focusing on viral and immunological features, the possible mechanisms of vasculitis development in HIV+ patients are discussed. Long-term follow-up indicates a clear benefit of regimens including antiviral agents, vasodilators and plasma exchanges. No deterioration of AIDS status was observed with this treatment and no relapse was recorded.

Adult↗

The spectrum and treatment of virus-associated vasculitides.

It is admitted that viral infections can be responsible for systemic vasculitides. Viruses can be responsible for various types of vasculitis that affect vessels of different sizes. Clinical manifestations are the same as those observed in previously described vasculitides such as polyarteritis nodosa or cryoglobulinemia. When viral infection is diagnosed and considered to be responsible for vasculitis, a specific therapeutic approach must be prescribed. Treatment is based on the combination of antiviral agents and symptomatic or immunomodulating therapies. Antiviral therapy facilitates virus clearance and seroconversion to specific antibodies. In systemic vasculitides, plasma exchanges are a powerful treatment that clears circulating immune complexes. In the case of digital ischemia, vasodilators are also useful. Conversely, steroids and cytotoxic agents stimulate virus replication and favor disease chronicity and deleterious effects due to the presence of the virus. Hepatitis B virus-related polyarteritis nodosa can be cured with the combination of antiviral agents (mainly interferon alpha) and plasma exchanges. Hepatitis C virus-related cryoglobulinemia responds to interferon alpha and sometimes to plasma exchanges, but responses are usually partial and relapses occur in the majority of cases. In HIV-related vasculitides, currently available antiretroviral agents are not able to definitively eradicate the virus but their combination with plasma exchanges can cure the vasculitis. Due to common epidemiologic factors, several viruses can be present in the same patient, and determining their responsibility in the vasculitic process requires careful clinical and virologic analysis and then the selection of a specifically adapted therapeutic regimen. The therapeutic strategy applied in virus-associated vasculitides is therefore based on the etiologic investigations and the choice of a treatment is adapted to the pathogenetic mechanisms.

Humans↗

[Hemato-encephalic barriers. Morphologic data].

Within the cranio-spinal cavity we can consider three compartments: blood, cerebro-spinal fluid and nervous parenchyma and thus, three barriers (Blood-Cerebro-Spinal Fluid, Blood-Brain, Cerebro-Spinal Fluid-Brain). The morphological studies of these barriers were performed with exogenous tracers such as horseradish peroxidase, cytochrome C and ferritin or endogenous tracers such as autologous antiperoxidase immunoglobulins. 1. The blood-brain barrier is exogenous and endogenous tracers proof. It is found on the level of the brain capillary endothelium with tight junctions and rare plasmalemmal vesicles. 2. The blood-cerebro-spinal fluid barrier is found on the level of choroid plexus and of leptomeningeal vessel. In the former, the tracer is stopped by the tight junctions (zonula occludens type) of the choroid plexus epithelium. Besides, there is no morphological evidence of transepithelial passage from blood to cerebro-spinal fluid. In the later, the barrier is, almost always, found on the level of the vascular endothelium. 3. The parenchymatous-cerebro-spinal fluid interface cannot be called a barrier because the diffusion of the tracers is not restricted either by the astrocytic marginal layer or by the ependyma. The circumventricular organs other than choroid plexus are morphologically characterized by the free diffusion of tracers in their perivascular connective space. Subcommissural organs capillaries alone behave like those of the brain. The spinal cord capillaries, in opposition to those of the brain, are characterized by a perivascular connective space, for 40 p. 100 of them. The significance of this fact is still unknown.

Anti-Bacterial Agents↗