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PubMed1994

Connective tissue disease and sarcoidosis of the central nervous system.

The mechanism for central nervous system (CNS) involvement in connective tissue diseases is variable. Although CNS vasculitis does occur in some connective tissue diseases, it is rare in many others, including systemic lupus erythematosus. Overall, the most common pathogenetic mechanism for CNS dysfunction in patients with connective tissue disease is probably secondary CNS involvement, due either to multiple systemic organ dysfunction (including hypercoagulable or hypofibrinolytic states) or due to CNS and systemic infections. The pathogenetic role of antineuronal antibodies is yet to be defined. Generally, nervous system complications of those collagen diseases that classically produce necrotizing vasculitis should be treated with cytotoxic agents. The less severe vasculitides, particularly temporal arteritis, respond well to steroids, as does sarcoidosis. There are a variety of mechanisms for nervous system disorders in complex multiple system diseases. The etiology is often outside of the nervous system, and results of therapy are highly variable.

Antiphospholipid Syndrome↗
PubMedDate not supplied

Behçet's syndrome/AIDS/cerebral toxoplasmosis: an unusual association.

Few cases of AIDS associated to manifestations suggesting Behçet's syndrome have been reported. This case is of a young married woman who presented, during a period of 7 years, clinical manifestations consistent with the late diagnosis of Behçet's syndrome, when she developed recurrent lymphomonocytic meningoencephalitis. At this time, she was found to be infected by HIV-1. Immunosuppressive doses of glucocorticoid produced an unsatisfactory response and she evolved to death due to CNS toxoplasmosis. The latter diagnosis was presumed on the basis of magnetic resonance imaging findings and proved by necropsy after her third hospital stay. One of the factors hindering the appropriate diagnosis was the low level of CD4 and the CD4/CD8 ratio, sometimes observed in active Behçet's syndrome and higher than those observed in patients with this severe opportunistic infection. No information about the exact period of time she had been infected with HIV-1 is available. So, we do not know whether both diseases were overlooked, if the patient, infected by HIV-1, developed an unusual clinical feature consistent with Behçet's Behçet's syndrome, and subsequently evolved to AIDS.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Topical alpha interferon in the treatment of oral ulcers in Behçet's syndrome: a preliminary report.

The effect of topical recombinant interferon alfa 2c hydrogel (IFN alpha 2C) in the aphthous lesions of the mouth in Behcet's syndrome was assessed in twenty patients in a twelve-week open trial. IFN alpha 2C applied to the mouth for four weeks significantly reduced the number of aphthae in the post-treatment phase compared to the pretreatment and treatment phases. No side effects were recorded. Topical IFN alpha 2C seems to be effective in the treatment of the aphthae in Behcet's syndrome.

Administration, Topical↗
PubMed1989

Defective fibrinolysis in Behçet's syndrome: significance and possible mechanisms.

Reduced fibrinolytic activity has frequently been reported in Behcet's syndrome, but both the underlying mechanism and its relation to the development of thrombosis are unclear. The fibrinolytic activity was studied in seven patients with Behçet's syndrome and 12 patients with idiopathic oral ulceration. The patients with Behçet's disease had significantly reduced resting tissue plasminogen activator(t-PA) both by euglobulin fibrin plate lysis and enzyme linked immunosorbent assay (ELISA), but the tissue plasminogen activator inhibitor(t-PAI) was not significantly different from the control value. After stimulation by venous occlusion the euglobulin fibrin plate lysis results showed three good responders and four poor responders, but neither t-PA antigen nor t-PAI concentrations showed any clear difference between the two groups. Interestingly, three out of the four patients with a history of thrombosis were good responders. The group with oral ulceration showed no significant difference from the controls for any of these measurements. These findings suggest that the reduced resting fibrinolytic activity is usually due to decreased production of t-PA, but that the defective response to stimulation may be multifactorial in origin. The fibrinolytic abnormalities appear unrelated to the development of thrombosis.

Adult↗