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Your search keyword '"Gross, W.L."' showing total 92 results
Start Over Author "Gross, W.L." Publication Type Academic Journals
92 results on '"Gross, W.L."'

46. Therapiestrategien bei Vaskulitiden.

Author

Holle, J.U., Moosig, F., and Gross, W.L.

Abstract

Copyright of Der Internist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2011
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47. Autoimmunvaskulitiden.

Author

Moosig, F., Holle, J.U., and Gross, W.L.

Abstract

Copyright of Der Internist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2009
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48. Wegener’s granulomatosis: disease course, assessment of activity and extent and treatment.

Author

de Groot, K. and Gross, W.L.

Subjects
*VASCULITIS, *NECROSIS, *EPIDEMIOLOGY, *PATHOLOGY, *THERAPEUTICS
Abstract

Wegener’s granulomatosis (WG) belongs to the group of necrotizing primary systemic vasculitides of unknown etiology, that are associated with anti-neutrophil cytoplasmic antibodies. The pathological hallmark of WG is the coexistence of vasculitis and granuloma. Due to more sensitive diagnostic instruments, especially ANCA testing, the incidence of diagnosis of WG has risen in the past ten years. Although the precise pathophysiology is not understood yet, there is ample evidence that ANCA, which can lead to cytotoxic reactions in the vascular texture, play a major role, possibly promoted by a dysbalance in the anti-idiotypic network. The clinical disease course is typically two-phasic, beginning with a granulomatous inflammation of the upper respiratory tract, that usually is followed by a generalized vasculitic phase, that can range from mild organ dysfuntion to lifethreatening multi-organ failure. Consequently, diagnostic procedures, patients’ assessment and therapeutic regimens need to be individualized, adapted to stage and activity of the disease as well as standardized. [ABSTRACT FROM AUTHOR]

Published
1998
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