Activation of the ERK pathway could increase EGR1 expression. At the time, surgery was indicated, but the patient preferred to maintain the drug treatment and continued treatment with 1.0 mg per week of cabergoline. However, there is a difference in drug sensitivity between CAB and BRC in patients with prolactinoma, although the underlying mechanisms are still unknown. Comparisons between various conditions were performed using an unpaired To test the cell death induced by CAB and BRC, CCK8 assays were used to analyse the viability of GH3 and MMQ cells.
There was a slight increase in prolactin concentration with the use of these antipsychotics; however, the concentration remained stable until the last assessment, 7 years after starting the psychiatric treatment.
In the meantime, to ensure continued support, we are displaying the site without styles 2019;109(1):42-50. doi: 10.1159/000495775. Assessment of thyroid function was always normal with TSH ranging from 1.1 to 3.1 mIU/mL and FT4 from 0.9 to 1.3 ng/dL. & Yuan, J. Autophagy in cell death: an innocent convict?
This study also showed that, although dopamine agonists may not reduce tumor volume by more than 50% in the short term, the use of high doses of cabergoline may reduce tumor volume by more than 90% or promote progression to an empty sella in the long term, even in macroprolactinomas.Regarding prolactin concentrations, except for one woman who achieved normalized prolactin concentrations after 17 years of treatment, there was no normalization in the remaining five cases. Assessment of GH secretion through quantification of IGF-1 only may be inconsistent, since the isolated quantification of this hormone does not have diagnostic value for GH deficiencies in adults; however, it may be useful for long-term follow-up (In addition to the known changes in the gonads associated with high concentrations of prolactin, we should also be concerned about the maintenance of high prolactin concentrations that fail to normalize. Based on the progression of the laboratory assessments, we can conclude that all tumors were resistant to bromocriptine and later to cabergoline.Three patients (cases 1, 2, and 5) used cabergoline exclusively.
First, GH3 cells are more sensitive to BRC than MMQ cells, and MMQ cells are more sensitive to CAB than GH3 cells. Replacement therapy with 75 μg of levothyroxine was started when fasting, which continued until the last assessment, after 15 years of treatment.Before the transsphenoidal surgery, 6 years after starting the treatment, secretions of cortisol and ACTH were normal and, despite having low blood pressure (90/60 mmHg), there were no signs or symptoms of adrenal deficiencies. Nazio, F. et al. You can also search for this author in
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Using gene microarray analysis, we found that BRC induces the apoptosis of prolactinoma cells through the ERK/EGR1 signalling pathway, whereas CAB induces autophagic death by inhibiting the AKT/mTOR signalling pathway.
The presence of residual tumor on MRI images at the last assessment was more frequent for macroadenomas (53.3%) than microadenomas (26.7%). After 145 months of treatment, the concentration of prolactin was 44.57 ng/mL. She also presented galactorrhea and amenorrhea for the past 4 years. was used (This study was approved by the Ethics Committee of the Verhum Clinic, Brasilia-DF. Based on our analysis, CAB is significantly better than BRC in normalizing PRL levels in patients, especially males, with giant prolactinomas (69.4% versus 31.7%, p = 0.01). The microarray data set was submitted to the GEO repository (GSE101012).Immunohistochemical staining was performed by incubating tissue sections with mouse EGR1 primary antibody (Santa Cruz Biotechnology, 1:50 in 1% BSA in TBST) overnight at 4 °C with gentle shaking, followed by incubating the sections with goat anti-mouse HRP secondary antibody (1:200 in 1% BSA in TBST) for 1 h at room temperature. & Post, K. D. Giant prolactinomas: clinical management and long-term follow up. Moreover, this difference in sensitivity is likely due to the different pathways of cell death induced by BRC and CAB.In recent decades, according to morphology, enzymology, immunology and functional characteristics, cell death has mainly been divided into programmed cell death (PCD) and necrosisAutophagy and apoptosis are two main causes of drug-induced cell death.
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