21 research outputs found

    Hydatid disease of the ribs: An exceptional location

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    Background. Hydatid disease is a zoonosis caused by larval stages of cestodes belonging to the genus Echinococcus. The rib location is exceptional. It presents a real diagnostic and therapeutic challenge. Objective. To describe the clinical, serological and radiological features and surgical management of rib hydatidosis. Methods. This is a retrospective study conducted over 4 years, on five cases of rib hydatidosis. We analysed the clinical and radiological presentations and the adopted therapeutic procedure. Results. The average age of our patients was 44 years, without gender predominance. The clinical signs were dominated by the presence of an immobile swelling of fluid consistency without inflammatory sign, accompanied by moderate and intermittent localised pain. The laboratory assessment was nonspecific. The radiological assessment, including chest X-ray and thoracic computed tomography, with and without contrast, was essential in order to assess the extent of the lesion. Thoracic magnetic resonance imaging was requested in one case because of suspicions of a spinal extension. All of our patients underwent a rib excision accompanied by medical treatment of albendazole 24 hours after the surgery. The follow-up ranged from 1 year to 4 years and did not show any recurrence. Conclusion. Hydatidosis of the ribs is an exceptional location of hydatid disease. The diagnosis was based on radiology and intraoperative exploration. The treatment remained essentially surgical by rib excision with anthelmintic drugs to prevent recurrence

    Transmembrane TNF protects mutant mice against intracellular bacterial infections, chronic inflammation and autoimmunity

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    Using targeted mutagenesis in mice, we have blocked shedding of endogenous murine TNF by deleting its cleavage site. Mutant mice produce physiologically regulated levels of transmembrane TNF (tmTNF), which suffice to support thymocyte proliferation but cannot substitute for the hepatotoxic activities of wild-type TNF following LPS/D-galactosamine challenge in vivo and are not sufficient to support secondary lymphoid organ structure and function. Notably, however, tmTNF is capable of exerting anti-Listerial host defenses while remaining inadequate to mediate arthritogenic functions, as tested in the tristetraprolin-deficient model of TNF-dependent arthritis. Most interestingly, in the EAE model of autoimmune demyelination, tmTNF suppresses disease onset and progression and retains the autoimmune suppressive properties of wild-type TNF. Together, these results indicate that tmTNF preserves a subset of the beneficial activities of TNF while lacking detrimental effects. These data support the hypothesis that selective targeting of soluble TNF may offer several advantages over complete blockade of TNF in the treatment of chronic inflammation and autoimmunity. © 2006 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim
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