Adrenal Glands Diagnostic Aspects and Surgical Therapy by Dimitrios A. Linos, Jon A. van Heerden PDF

By Dimitrios A. Linos, Jon A. van Heerden

- Over two hundred beautiful illustrations, starting from intraoperative images, line drawings, diagnostic photographs, pathology slides, tables and graphs can be found to make each one case mentioned understandable and simple to follow.
- conventional and novel healing thoughts are introducedand the newest advancements in minimal-access operative ideas are mentioned and reviewed.
- specializes in a teamwork orientated strategy that identifies the required communications among the numerous scientific disciplines while facing adrenal issues.

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Crofford LJ, Sano H, Karalis K, et al (1993) Corticotropin-releasing hormone in synovial fluids and tissues of patients with rheumatoid arthritis and osteoarthritis. J Immunol 151:1587–1596 30. Cunningham ET Jr,Bohn MC,Sawchenko PE (1990) The organization of adrenergic inputs to the paraventricular and supraoptic nuclei of the rat hypothalamus. J Comp Neurol 292:651–667 31. de Kloet ER, Vreugdenhil E, Oitzl MS, Joels M (1998) Brain corticosteroid receptor balance in health and disease. Endocr Rev 19:269–301 32.

Psychoneuroendocrinology 14:441–449 11. ” Clin Endocrinol 133:779–786 12. Bernardini R, Chiarenza A, Calogero AE, et al (1989) Arachidonic acid metabolites modulate rat hypothalamic corticotropin releasing hormone in vitro. Neuroendocrinology 50:708–715 13. Bernardini R,Kamilaris TC,Calogero AE,et al (1990) Interactions between tumor necrosis factor-alpha, hypothalamic corticotropin-releasing hormone,and adrenocorticotropin secretion in the rat. Endocrinology 126:2876–2881 14. Besedovsky HO, del Rey A (1992) Immune-neuroendocrine circuits: Integrative role of cytokines.

It is believed that an excessive HPA axis response to inflammatory stimuli would mimic the stress or hypercortisolemic state and would lead to increased susceptibility of the individual to a host of infectious agents or tumors as a result of Th-1 suppression, but enhanced resistance to autoimmune/inflammatory disease [39]. In contrast, a defective HPA axis response to such stimuli would reproduce the glucocorticoid- 27 28 Ioannis Kyrou, Constantine Tsigos deficient state and would lead to relative resistance to infections and neoplastic disease,but increased susceptibility to autoimmune/inflammatory disease,such as Hashimoto’s thyroiditis or rheumatoid arthritis [26].

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