Maligne Tumoren der Nebennierenrinde

Allolio, Bruno; Fassnacht, Martin; Arlt, Wiebke

doi:10.1007/s00108-001-0509-1

Cited by 6 publications

(6 citation statements)

References 37 publications

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“…Die pharmakologische Therapie des persistierenden Hypercortisolismus mit Hemmung der Steroidogenese, Osteoporose-und Ulkustherapie und eventueller Antibiotikaprophylaxe wird in diesem Artikel nicht besprochen, ist aber an anderer Stelle erwähnt [1,11].…”

Section: Therapeutische Aspekteunclassified

“…Ein Tumordebulking lohnt bei Hormonexzesssyndromen und verbessert die Ausgangslage für eine eventuelle Chemotherapie [9]. Auch bei R0-Resektion ist die fraktionierte Tumorbettbestrahlung mit einer Gesamtdosis von 40 bis 60 Gy im Stadium II über 8 cm und bei Raumforderungen im Stadium III vernünftig [1,7] …”

Section: Therapeutische Aspekteunclassified

“…Eine Therapie mit Glukokortikoiden ist von der Resttumoraktivität abhängig und sollte großzügig erfolgen. Daten zur ACTH-Suppression analog zur TSH-suppressiven Therapie bei differenzierten Schilddrüsenkarzinomen existieren nicht.Bisher wurden verschiedene Zytostatika bei Tumorprogredienz trotz Mitotane eingesetzt[1,11,23]. Aktuell vergleicht die erste internationale Multicenterstudie zum metastasierten Nebennierenrindenkarzinom (FIRM-ACT, http:///www.firm-act.org) die Effizienz von Etoposid, Doxorubicin und Cisplatin + Mitotane (EDP/M) mit Streptozotocin + Mitotane (Sz/M) als "First-line"-Therapie.…”

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“…Die Prävalenz von Nebennierenrindenkarzinomen bei zufällig nachgewiesenen Nebennierentumoren steigt mit der Tumorgröße und beträgt 2% bei einer Tumorgröße bis 4 cm Durchmesser, 6% bei einem Durchmesser zwischen 4 und 6 cm und 25% bei einem Durchmesser >6 cm. Nebennierenrindenkarzinome haben eine stadienabhängige schlechte Prognose mit einer mittleren Überlebenszeit von 18 Monaten[1].…”

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Bornstein

2007

Internist

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Adrenal masses are one of the most common tumors in humans. They are a very heterogenous group of diseases and include benign and malignant adrenocortical lesions, metastases, pheochromocytomas and other entities. Adrenal masses originating from steroidogenic or chromaffin cells may be silent or the source of subclinical or overt hormone excess, such as primary aldosteronism, hypercortisolism or symptomatic catecholamine excess. On the other hand, adrenal hyperplasia may be the result of excess ACTH secretion in steroid biosynthesis disorders with deficient glucocorticoid secretion, in glucocorticoid resistance, in Cushing's disease, or ectopic ACTH syndrome. Algorithms for endocrine testing, imaging studies and their combination are available for defining the tumor entity and for the characterization of the hormone excess syndromes. Recent developments in molecular biology have provided tools for testing for hereditary tumor syndromes associated with adrenal tumorigenesis and to establish strategies for further treatment and follow-up.

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Section: Therapeutische Aspekteunclassified

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Bornstein

2007

Internist

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“…The examination of patients with adrenal gland tumors, prior to qualification for surgery is aimed at determining the character of the tumor (adenoma, pheochromocytoma, cancer, metastasis, lymphoma, and cyst), its eventual hormonal activity, location, size, and relationship to large blood vessels (1).…”

Section: A S E R E P O R T Smentioning

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Adrenal Tumors - Diagnostics and the Factual Situation

Krajewska

Toutounchi

Fiszer

et al. 2012

Polish Journal of Surgery

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The study presented three cases of patients diagnosed with adrenal tumors subject to surgical intervention during the past 6 months in our Department. The patients presented with radiological diagnostic difficulties, as to the character and location of the primary tumor. the aim of the study was to demonstrate differences between radiological examination results and the factual situation observed during the adrenalectomy. In all the presented cases patients' were subject to laparoscopic intervention. In two cases conversion to open surgery was necessary. The histopathological results of the surgically removed samples were as follows: leiomyoma, myoperycytoma and pheochromocytoma. In selected cases imaging examinations might be of limited value, especially when determining the character and location of the primary lesion of the adrenal gland.

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Wirkungen von Medikamenten auf die Nebennierenrinde und ihre Tumoren

Saeger

Faßnacht²

2006

Pathologe

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The structure of the normal adrenal cortex is changed by stimulating hormones (ACTH) and inhibiting hormonal drugs (especially glucocorticoids). ACTH induces hyperplasia and lipid depletion in the fascicular and reticular zones, whereas glucocorticoids lead to atrophy and lipid accumulation in both zones. In animal experiments, the adrenostatic drug mitotane causes shrinkage of the cells of the fascicular and reticular zones, whereas metyrapone induces a decrease in the steroid producing organelle system and aminoglutethimide leads to an increase in lipids. In the therapy of patients with adrenocortical cancer, mitotane can cause an increase in of necrosis and fibrosis, but also in intracellular lipid. The ultrastructure shows increased liposomes, more pigment-rich lysosomes and laminated bodies.

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Maligne Tumoren der Nebennierenrinde

Cited by 6 publications

References 37 publications

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Adrenal Tumors - Diagnostics and the Factual Situation

Wirkungen von Medikamenten auf die Nebennierenrinde und ihre Tumoren

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