TY  - JOUR
A1  - Nowotny, Hanna
A1  - Ahmed, S. Faisal
A1  - Bensing, Sophie
A1  - Beun, Johan G.
A1  - Brösamle, Manuela
A1  - Chifu, Irina
A1  - Claahsen van der Grinten, Hedi
A1  - Clemente, Maria
A1  - Falhammar, Henrik
A1  - Hahner, Stefanie
A1  - Husebye, Eystein
A1  - Kristensen, Jette
A1  - Loli, Paola
A1  - Lajic, Svetlana
A1  - Reisch, Nicole
T1  - Therapy options for adrenal insufficiency and recommendations for the management of adrenal crisis
JF  - Endocrine
N2  - Adrenal insufficiency (AI) is a life-threatening condition requiring life-long glucocorticoid (GC) substitution therapy, as well as stress adaptation to prevent adrenal crises. The number of individuals with primary and secondary adrenal insufficiency in Europe is estimated to be 20–50/100.000. A growing number of AI cases are due to side effects of GC treatment used in different treatment strategies for cancer and to immunotherapy in cancer treatment. The benefit of hormone replacement therapy is evident but long-term adverse effects may arise due to the non-physiological GC doses and treatment regimens used. Given multiple GC replacement formulations available comprising short-acting, intermediate, long-acting and novel modified-release hydrocortisone as well as subcutaneous formulations, this review offers a concise summary on the latest therapeutic improvements for treatment of AI and prevention of adrenal crises. As availability of various glucocorticoid formulations and access to expert centers across Europe varies widely, European Reference Networks on rare endocrine conditions aim at harmonizing treatment and ensure access to specialized patient care for individual case-by-case treatment decisions. To improve the availability across Europe to cost effective oral and parenteral formulations of hydrocortisone will save lives.
KW  - adrenal insufficiency
KW  - congenital adrenal hyperplasia
KW  - adrenal crisis
KW  - glucocorticoid replacement
KW  - hydrocortisone
KW  - stress instructions
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-308769
SN  - 1355-008X
SN  - 1559-0100
VL  - 71
IS  - 3
ER  - 
TY  - JOUR
A1  - Fuss, Carmina Teresa
A1  - Other, Katharina
A1  - Heinze, Britta
A1  - Landwehr, Laura-Sophie
A1  - Wiegering, Armin
A1  - Kalogirou, Charis
A1  - Hahner, Stefanie
A1  - Fassnacht, Martin
T1  - Expression of the chemokine receptor CCR7 in the normal adrenal gland and adrenal tumors and its correlation with clinical outcome in adrenocortical carcinoma
JF  - Cancers
N2  - Background: The chemokine receptor CCR7 is crucial for an intact immune function, but its expression is also associated with clinical outcome in several malignancies. No data exist on the expression of CCR7 in adrenocortical tumors. Methods: CCR7 expression was investigated by qRT-PCR and immunohistochemistry in 4 normal adrenal glands, 59 adrenocortical adenomas, and 181 adrenocortical carcinoma (ACC) samples. Results: CCR7 is highly expressed in the outer adrenocortical zones and medulla. Aldosterone-producing adenomas showed lower CCR7 protein levels (H-score 1.3 ± 1.0) compared to non-functioning (2.4 ± 0.5) and cortisol-producing adenomas (2.3 ± 0.6), whereas protein expression was variable in ACC (1.8 ± 0.8). In ACC, CCR7 protein expression was significantly higher in lymph node metastases (2.5 ± 0.5) compared to primary tumors (1.8±0.8) or distant metastases (2.0 ± 0.4; p < 0.01). mRNA levels of CCR7 were not significantly different between ACCs, normal adrenals, and adrenocortical adenomas. In contrast to other tumor entities, neither CCR7 protein nor mRNA expression significantly impacted patients' survival. Conclusion: We show that CCR7 is expressed on mRNA and protein level across normal adrenals, benign adrenocortical tumors, as well as ACCs. Given that CCR7 did not influence survival in ACC, it is probably not involved in tumor progression, but it could play a role in adrenocortical homeostasis.
KW  - CCR7
KW  - chemokine receptor
KW  - adrenocortical carcinoma
KW  - adrenal tumors
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-250112
SN  - 2072-6694
VL  - 13
IS  - 22
ER  -