Warum gibt es analoge Krankheitsmechanismen bei chronisch entzündlichen Krankheiten?

  title={Warum gibt es analoge Krankheitsmechanismen bei chronisch entz{\"u}ndlichen Krankheiten?},
  author={Rainer H. Straub and Hugo O. Besedovsky and Adriana del Rey},
  journal={Wiener klinische Wochenschrift},
Das ärztliche Ursache-Wirkungsdenken richtet sich in der überwiegenden Zahl der Fälle auf eine einzige Ursache und eine daraus abgeleitete Therapie. Diesen einfachen Zugang scheinen wir unseren Patienten schuldig zu sein, da wir ihnen den Sachverhalt in einfachen Worten erklären wollen. Es sind gerade jene einen einzelnen Baustein betreffenden Defekte besonders überzeugend erklärbar, wenn sie ein gravierendes Problem für den Gesamtorganismus aufwerfen. Das ist zum Beispiel für den plötzlichen… 
2 Citations
Neuroendokrin-immune Interaktionen bei rheumatischen Krankheiten
It is shown that the effects of different hormones and neurotransmitters on the immune system are influenced by: (1) the immune stimulus; (2) preponderance of women versus men with respect to autoimmune diseases; (3) negative effects of ovulation-inducing therapy, oral contraceptives, and hormone replacement therapy; (4) protective effect of hemiplegia; and (5) influence of psychological stress on inflammation.
Neurohormonal activation and inflammation in chronic cardiopulmonary disease: a brief systematic review
Chronic cardiopulmonary disease typically induces and maintains (over)activation of several phylogenetically old adaptational and defensive mechanisms, which contributes to impaired function and worse prognosis in a variety of chronic disease.


Replacement therapy with DHEA plus corticosteroids in patients with chronic inflammatory diseases – substitutes of adrenal and sex hormones
A dysfunction of the hypothalamic – pituitary – adrenal (HPA) axis was found in animal models of chronic inflammatory diseases, and the defect was located in more central portions of the HPA axis.
Cytokine-associated emotional and cognitive disturbances in humans.
In humans, a mild stimulation of the primary host defense has negative effects on emotional and memory functions, which is probably caused by cytokine release, and cytokines represent a novel target for neuropsychopharmacological research.
Integrated evolutionary, immunological, and neuroendocrine framework for the pathogenesis of chronic disabling inflammatory diseases
  • R. Straub, H. Besedovsky
  • Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2003
This integrated systems hypothesis may permit better identification of a patient at risk or in the early stages of developing a CDID such as rheumatoid arthritis and enable more coordinated intervention than is presently attempted.
Involvement of the hypothalamic--pituitary--adrenal/gonadal axis and the peripheral nervous system in rheumatoid arthritis: viewpoint based on a systemic pathogenetic role.
The belief that combined therapeutic approaches on a neuroendocrine immune basis are of crucial importance in a pathogenetically oriented therapy of RA is reinforced.
Changes in dehydroepiandrosterone (DHEA) and DHEA-sulfate plasma levels during experimental endotoxinemia in healthy volunteers.
The present results suggest that similarly to glucocorticoids, the adrenal androgens DHEA and D HEA-S play an important role during early host responses to bacterial infections in humans.
Specific autoantibodies precede the symptoms of rheumatoid arthritis: a study of serial measurements in blood donors.
It is concluded that IgM-RF and anti-CCP testing with appropriately high specificity may assist in the early detection of RA in high-risk populations.
Different roles for androgens and estrogens in the susceptibility to autoimmune rheumatic diseases.
Mutations in TNFRSF13B Encoding TACI Are Associated With Common Variable Immunodeficiency in Humans
These studies represent important descriptions of defined mutations in patients with CVID and IGAD occurring in a significant fraction of these patients in 2 relatively genetically disparate populations.