1/14. Lesion development in Marburg's type of acute multiple sclerosis: from inflammation to demyelination.We report a patient who suffered from acute inflammatory CNS demyelination and underwent two consecutive diagnostic stereotactic brain biopsies during the early disease course. The first lesion was drawn 33 days after the onset of disseminated neurological symptoms. macrophages and T lymphocytes diffusely infiltrated small vessel walls and the white matter. mRNA for tumor necrosis factor alpha (TNFalpha) and inducible nitric oxide synthase (iNOS) was abundantly expressed. Myelin sheaths were entirely preserved. The second biopsy 76 days later showed confluent demyelinating lesions with a diffuse infiltration of macrophages that were positive for myelin debris, activation markers and TNFalpha and iNOS mRNA. IgG and C9neo deposits were found along myelin sheaths. The patient had received intravenous immunoglobulins (IVIG) prior to biopsy. Findings from this single patient affirm that demyelination follows the migration of inflammatory cells from the circulation into the white matter with subsequent inflammation and demyelination. inflammation alone may be sufficient to cause significant clinical deficits without demyelination. Inflammatory mediators such as TNFalpha and NO are involved at very early stages in the pathogenetic process. IVIG treatment may lead to the deposition of immunoglobulins and to the activation of the complement cascade, but the clinical relevance of this particular finding remains uncertain.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/14. tissue plasminogen activator gene expression in multiple sclerosis brain tissue.Recent studies have implicated tissue-type plasminogen activator (tPA) in neurodegeneration. We studied multiple sclerosis (MS) brain tissue for tPA gene and protein expression in comparison with reference tissue, by in situ hybridisation and immunohistochemistry. MS is characterised by demyelination in the central nervous system. In this study, neuronal cell bodies in MS brain showed high expression of tPA mRNA and protein, while in reference brains, staining for protein and mRNA expression were very low in neurons and mostly restricted to blood vessel walls. In MS, there was an additional staining of mononuclear cells within perivascular cuffs and foamy macrophages within demyelinating plaques. In view of evidence that the final process of demyelination in MS is thought to be enzyme-mediated, our work suggests the involvement of tPA and by inference plasmin, in the demyelinating process. Blocking tPA or plasmin activity may be a potentially beneficial therapeutic approach in MS.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
3/14. Retinal venous sheathing and neovascularization in disseminated sclerosis.A 54-year-old black woman with no significant visual complaint and a diagnosis of disseminated sclerosis of 18 years' duration is presented because of marked bilateral sheathing of the retinal veins, and previously unreported dilated collateral vessels and early neovasularization secondary to peripheral vein occlusion.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/14. Synchronous multifocal osteosarcoma with lymphatic spread in the lung: an autopsy case report.Synchronous multifocal/multicentric osteosarcoma (MOS) is a rare variant of osteosarcoma. We report here an autopsy case of a 15-year-old boy with MOS. Radiological examinations showed multiple sclerotic lesions in the left distal femur and in the ipsilateral proximal tibia without pulmonary metastasis at the first examination. Histological examination showed osteoblastic-type osteosarcoma. Despite high-dose chemotherapy the patient died of multiple bone and lung involvements 6 months after the initial diagnosis. autopsy examination revealed prominent invasion of the tumor cells into lymphatic vessels and pleural dissemination without the formation of bulky, nodular metastasis in the lungs. Metastases in pulmonary hilar lymph nodes were noted without metastasis in other organs. immunohistochemistry revealed that p53 protein was positive in most of the tumor cells. In summary, the present case was characterized by multiple bone involvement and prominent lymphatic spread of sarcoma cells in the lungs.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
5/14. Necrotizing skin lesions and NABs development in a multiple sclerosis patient treated with IFNbeta 1b.A case of a severe necrotizing vasculopathic skin lesions occurred in a 43 year old women affected by multiple sclerosis (MS) submitted to IFNbeta-1b has been described. After two months of therapy the patient presented, in injection sites of the abdomen, arms and legs, numerous ulcers. A biopsy of the lesions was performed and evidenced confluent necrosis of the superficial and deep skin tissue with mild infiltration by inflammatory cells and thrombosis in deep blood vessels. The IFNbeta-1b was immediately discontinued and therapy with corticosteroids was started. After 12 months from the onset of the adverse reaction, the skin vasculopathic lesions cicatrised leaving sclerotic areas on the abdomen. Neutralizing antibodies against IFNbeta-1b (NABs) were strongly positive at the onset of the skin ulcers and slowly decreased until the recovery. A possible role of NABs in the development of the skin lesions has been considered.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
6/14. diagnosis and treatment of multiple sclerosis and amyotrophic lateral sclerosis: neuropathies from bordetella pertussis.Having found positive the research for anti-Bordetella antibodies in the 95.47% of 92 patients affected by defined multiple sclerosis and in the 100% of 55 patients affected by non-patched neuropathies (amyotrophic lateral sclerosis and correlated neuropathies), I reassessed the pathogenesis of the neuropathies from bordetella pertussis. In the two categories of neuropathies (with and without patches), the beginning pathogenetic mechanisms are the same: 1) pertussis re-infection in patients with mucociliary barrier defect; 2) pertussis toxins passage in the blood; and 3) formation of circulating immune complexes. In multiple sclerosis, astrocytes produce class II human leukocyte antigens, the endothelia of the small brain vessels show the "adhesion molecules," and the immune complexes fall in the central nervous system (patches are formed). In amyotrophic lateral sclerosis and in the other non-patched neuropathies, the astrocytes do not produce the class II human leukocyte antigens, the endothelia do not show adhesion molecules, and immune complexes do not fall in the central nervous system; but they increase in blood until they inhibit the ulterior antibodies production. For relative antibodies lack, pertussis toxins fix directly on neuro-epithelia; their pathogenic power and physiopathologic astrocytes role in the central nervous system produce the damage. With a blood sample, we can assess Bordetella etiology. In all these neuropathies, an extended antibiotic therapy to clear mucosae and to prevent reinfections is necessary.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
7/14. Cutaneous ulcerations following subcutaneous interferon beta injection to a patient with multiple sclerosis.We report a case treated with interferon beta-1b for multiple sclerosis (MS), who developed severe cutaneous ulcers after six months of therapy. Interferon beta-1b had been used in a regimen of 8 million IU administered subcutaneously through oblique direction of the needle, twice a week. The cutaneous ulcers developed at inoculation sites, as a result of penetration of interferon beta into dermis. Other underlying diseases of coagulative or bleeding disorders or secondary infection were excluded. Histological features of non-specific inflammatory reactions including hyperplastic changes of blood vessels without any evidence of vasculitis were the prominent features in this case. Corticosteroid and interferon beta-1b therapy was continued on restricted sites on the extremities with care not to repeat injections at the same sites previously used. The administration of interferon beta into subcutaneous fatty tissues vertically reduced the incidence of dermal penetration of drug and occurrence of ulcerations in this patient. We review other case reports of severe cutaneous reactions associated with interferon beta-1b therapy in MS patients and conclude that local cytokine-mediated, adverse, immune reaction or non-specific cutaneous inflammatory reaction to interferon beta-1b initiated the skin ulceration long after institution of therapy at the injection sites, and the reaction might be related to the depth of injection.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
8/14. abdominal wall ulceration and mucinosis secondary to recombinant human interferon-beta-1b.46-year-old woman developed painful ulcers over her lower abdomen in the form of reticulate erythema after injecting interferon beta-1b subcutaneously for multiple sclerosis. skin biopsy revealed multiple superficial thrombosed vessels with focal epidermal necrosis as well as prominent interstitial mucinosis. Treatment with low-molecular-weight heparin followed by a heparinoid resulted in slow healing of the ulcers but also allowed the subcutaneous interferon injections to be continued.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
9/14. Fabry's disease as a differential diagnosis of MS.Fabry's disease is a genetically inherited error of glycosphingolipid metabolism that results from the defective activity of the lysosomal enzyme alpha-galactosidase A (alpha-GalA). The enzymatic defect, caused by an X-linked recessive genes, leads to progressive deposition of neutral glycosphingolipids (predominantly globotriaosylceramide), with terminal alpha-galactosyl moieties, in most visceral tissues and fluids of the body. Cerebrovascular manifestations result from multifocal small-vessel involvement and may include thromboses, basilar arterial ischaemia and aneurysm, seizures, paroxystic hemiplegia or hemianaesthesia, vestibular disorders and frank cerebral haemorrhage. Severe neurological signs may be present without evidence of major thrombosis and are presumably due to multifocal small-vessel occlusive disease. Vascular ischaemia and lipid deposition in peripheral nerves may cause conduction abnormalities (slowed conduction velocities and distal latency). Sensory neurons in spinal ganglia and small myelinated and unmyelinated fibers are affected preferentially.- - - - - - - - - - ranking = 2keywords = vessel (Clic here for more details about this article) |
10/14. Extensive mixed vascular malformation clinically imitating multiple sclerosis--case report.vascular malformations usually develop as a result of influence of teratogenic factor(s) acting in the defined embryonic/fetal period. However, in the case examined by us, various types of vascular malformations formed in different periods of the ontogenic development were found. They were seen in all parts of the central nervous system and clinically mimicked multiple sclerosis. On the background of generalized ischemic lesions of the CNS, certain kinds of vascular malformations were seen: cavernous or fetallike vessels within meninges, superficially located capillary angioma penetrating into the brain and spinal cord white matter, and arterio-venous pathological conglomerates forming meningeal angiomatosis. In pathological vessels, immunocytochemical assessment of vascular endothelium with antibodies against antigens CD31, CD34, von Willebrand factor and lectin ulex europaeus was normal but examination of the vascular basal membrane compounds revealed poor immunoreactivity to laminin and fibronectin. There were no disturbances in expression of angiopoietin, platelet-derived growth factor, transforming growth factor beta and vascular endothelial growth factor receptors Tie-1/2, PDGFR-alpha/beta, endoglin and Flk-1, respectively. The presence of various types of pathological vessels originating from different ontogenic periods indicates remittent or prolonged influence of teratogenic factor(s) in all periods of fetal vessel development.- - - - - - - - - - ranking = 4keywords = vessel (Clic here for more details about this article) |
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