Cargando…
SUN-LB070 Who Killed the Pituitary?
Background: Pituitary apoplexy can be caused by factors like surgery, pregnancy, drugs including anticoagulants and bromocriptine. Chemotherapy as a causal factor, however, has not often been noted in literature. To our knowledge, there are only 2 case reports implicating chemotherapy drugs as a cau...
Autores principales: | , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Endocrine Society
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553397/ http://dx.doi.org/10.1210/js.2019-SUN-LB070 |
Sumario: | Background: Pituitary apoplexy can be caused by factors like surgery, pregnancy, drugs including anticoagulants and bromocriptine. Chemotherapy as a causal factor, however, has not often been noted in literature. To our knowledge, there are only 2 case reports implicating chemotherapy drugs as a cause of pituitary apoplexy. (1) Case: 72 year old male with recently discovered squamous cell lung cancer, presented to clinic for assessment of incidental pituitary mass noted on staging imaging. Initial labs showed hypogonadotropic hypogonadism with normal PRL, TSH and HPA axis. Transphenoidal biopsy of mass showed no metastasis. Subsequently, he was started on carboplatin and paclitaxel for lung cancer. Initial course was complicated by deep venous thrombosis treated with enoxaparin. After his sixth chemotherapy cycle, he presented with sudden onset headache and diplopia consistent with sixth cranial nerve palsy. Initial CT head was negative for hemorrhage and stable, though hypoenhancing sellar mass. Sixth nerve palsy was initially thought to be due to microvascular ischemic event. Labs at this time were notable for undetectable PRL, low TSH (0.03 uIU/ml, N 0.35-4.9 uIU/ml), declining ACTH (14 to 9 pg/ml, N 6-50 pg/ml). He developed significant hyponatremia, concerning for central adrenal insufficiency, requiring urgent treatment with stress dose steroids. Pituitary MRI newly showed enlarging sellar mass, defect in dura and retroclival collection, later thought to be necrotic material from apoplectic pituitary. Surgical intervention was deferred as ophthalmology exam showed no pituitary compromise. After 12 days, he was readmitted with atraumatic bilateral subdural hematomas (SDHs) prompting enoxaparin cessation. Imaging at this time also showed decreased size of the mass. Follow up imaging showed resolution of SDHs with interval reduction of mass size. On final review, his presentation was suspected to be secondary to pituitary apoplexy due to chemotherapy in conjunction with enoxaparin, causing retroclival necrotic tissue and meningeal irritation leading to atraumatic SDHs. Given absence of hemorrhage on initial imaging and known vasculopathic effects of agents like carboplatin (analog of cisplatin), chemotherapy induced apoplexy cannot be excluded. In addition, although rapid regression after pituitary apoplexy has been reported rarely, chemotherapy may have a role in rapid shrinkage post apoplexy. (2) Conclusion: This case highlights potential role of chemotherapy in conjunction with anticoagulation in causing pituitary apoplexy and rapid pituitary tumor shrinkage. Reference: 1. Jang, Je Hun et al. Extensive Pituitary Apoplexy after Chemotherapy in a Patient with Metastatic Breast Cancer Brain tumor research and treatment vol. 6,1: 43-46 2. Jackson, D. L et al. Rapid pituitary apoplexy regression: what is the time course of clot resolution? Case reports in radiology, 2015 Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO. |
---|