PMID- 8930939
OWN - NLM
STAT- MEDLINE
DCOM- 19970220
LR  - 20181130
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 64
IP  - 5
DP  - 1996 Nov
TI  - Tumor necrosis factor-alpha increases after corticotropin-releasing hormone 
      administration in Cushing's disease. In vivo and in vitro studies.
PG  - 393-7
AB  - The aim of this study was to evaluate the effect of acute human corticotropin 
      (ACTH)-releasing hormone (CRH) administration (100 micrograms, as i.v. bolus) on 
      tumor necrosis factor-alpha (TNF alpha) levels in the inferior petrosal sinuses 
      and in the peripheral blood of 7 patients with Cushing's disease subjected to 
      diagnostic inferior petrosal sinus sampling. Blood samples for ACTH, 
      beta-endorphin (beta-EPH) and TNF alpha were collected from inferior petrosal 
      sinuses and periphery simultaneously. In addition, TNF alpha concentrations were 
      measured after CRH administration (10 nmol/l, 100 nmol/l and 1 mumol/l) in 
      culture medium from primary cultures obtained in 3 of 7 patients. At baseline, 
      plasma ACTH and beta-EPH levels were significantly higher in the inferior 
      petrosal sinus ipsilateral to the ACTH-secreting adenoma than in the 
      contralateral one and in the periphery (p < 0.001) whereas no significant 
      difference was found as far as serum TNF alpha levels were concerned. CRH 
      administration caused a significant increase of ACTH (p < 0.001), beta-EPH (p < 
      0.01) and TNF alpha (p < 0.01) levels greater in the ipsilateral inferior 
      petrosal sinus than in the contralateral one and in the periphery. In addition, 
      CRH increased ACTH, beta-EPH and TNF alpha levels in the culture medium of three 
      ACTH-secreting tumors at the doses of 100 nmol/l and 1 mumol/l (greater than 300, 
      200 and 110% of baseline pretreatment incubation levels, respectively). These 
      data suggest that CRH may increase TNF alpha concentrations in the inferior 
      petrosal sinus ipsilateral to the ACTH-secreting adenoma and in the peripheral 
      blood as well. In addition, it stimulated TNF alpha release both in vivo and in 
      vitro. These findings suggest the possibility that an imbalanced intrapituitary 
      TNF alpha production can be detected in ACTH-secreting adenomas.
FAU - Merola, B
AU  - Merola B
AD  - Department of Molecular and Clinical Endocrinology and Oncology, Federico II 
      University, Naples, Italy.
FAU - Longobardi, S
AU  - Longobardi S
FAU - Colao, A
AU  - Colao A
FAU - Di Somma, C
AU  - Di Somma C
FAU - Ferone, D
AU  - Ferone D
FAU - Di Rella, F
AU  - Di Rella F
FAU - Pivonello, R
AU  - Pivonello R
FAU - Covelli, V
AU  - Covelli V
FAU - Annunziato, L
AU  - Annunziato L
FAU - Lombardi, G
AU  - Lombardi G
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 60617-12-1 (beta-Endorphin)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
SB  - IM
MH  - Adenoma/metabolism
MH  - Adrenocorticotropic Hormone/blood/metabolism
MH  - Adult
MH  - *Corticotropin-Releasing Hormone
MH  - Cushing Syndrome/*blood
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Petrosal Sinus Sampling
MH  - Pituitary Neoplasms/metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism
MH  - beta-Endorphin/blood
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
AID - 10.1159/000127142 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1996 Nov;64(5):393-7. doi: 10.1159/000127142.