bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT589 A Case Of Lymphocytic Hypophysitis In A Young Female With Unilateral Abducens Nerve Palsy
Authors: Yu Jeremy H , Nguyen Michael L , Horani Mohamad Hosam , Shahlapour Mahmood 
Published: October 2023

Abstract
Disclosure: J.H. Yu: None. M.L. Nguyen: None. M.H. Horani: None. M. Shahlapour: None.
Lymphocytic hypophysitis is a neuroendocrine disorder characterized by autoimmune inflammation of the pituitary gland. Lymphocytic hypophysitis is the most common form of hypophysitis with the cause usually unknown. It often occurs in late pregnancy or in the postpartum period with affected individuals presenting with symptoms of headaches of an intensity out of proportion to the size of the lesion and with hypopituitarism. Other manifestations include visual field defects and ocular motility disturbances. We present a case of a 24 year old Female who presents with headache, diplopia, and left-sided CN6 nerve palsy of 4 day duration. She has a known history of amenorrhea for the past year and obesity. She also presents with polydipsia and polyuria. Further workup included MRI of the brain showing a sellar mass with mass effect on optic chiasm and left cavernous sinus lesion. Pituitary hormonal workup showed ACTH 13, LH 0.42, FSH 2.1, TSH 0.442, free T4 1.0, random cortisol 6.3, and prolactin 78. Lumbar puncture with basic CSF studies showed glucose 56, protein 48, nucleated cells 38 (lymph 91%, poly 4%, mono 5%), and RBC 4. ACE, AFP, IgG4, ANA, ANCA, and CEA workup was negative. Biopsy of the mass was performed with results suggesting lymphocytic hypophysitis. Additional immunohistochemistry stains will be performed to evaluate for IgG4 related diseases. The patient would later develop diabetes insipidus and central hypothyroidism weeks later. Discussion: The lymphocytic infiltration causes inflammation, enlargement and fibrosis of the pituitary gland which can produce a mass effect on surrounding tissues. The definitive diagnosis is made via histopathology staining of biopsied sellar or suprasellar tissue. The condition predominantly affects women more than men at a ratio of 8:1.Treatment involves evaluation of pituitary function with management of any hormone deficiencies and alleviating any mass effects due to pituitary inflammation and enlargement. First line treatment usually involves high dose corticosteroids with refractory cases being treated with immunosuppressive medications. Surgery or fractionated radiotherapy can be used if medical therapy fails. In our patient, a biopsy was performed that confirmed lymphocytic hypophysitis with unmasked diabetes insipidus and hypothyroidism presenting weeks after starting on high-dose corticosteroids. Conclusion: This case highlights the unique presentation of lymphocytic hypophysitis including left-sided CN6 nerve palsy, headaches, and hypogonadotropic hypopituitarism. From our knowledge, it is one of the first presentations with unilateral CN6 nerve palsy as a mass effect from lymphocytic hypophysitis.
Presentation: Saturday, June 17, 2023
SAT593 Mechanism Of Kisspeptin Neuron Synchronization In Acute Brain Slices From Female Mice
Authors: Morris Paul G , Herbison Allan Edward 
Published: October 2023

Abstract
Disclosure: P.G. Morris: None. A.E. Herbison: None.
Arcuate kisspeptin (ARNKISS) neurons, which co-express glutamate, neurokinin B and dynorphin, intermittently synchronize their activity to drive pulsatile hormone secretion. However, the mechanisms underlying such network behaviour remains unclear in females. Using an acute Kiss1-Cre GCaMP6 brain slice preparation which maintains spontaneous synchronized ARNKISS neuron burst firing, we were able to both characterise this behaviour and reveal the neurotransmitter receptors contributing to it. Results in diestrous female mice revealed that the order individual neurons took part in synchronizations was only mildly consistent, with a mean Spearman correlation coefficient of 0.43. Spontaneous ARNKISS neuron synchronizations were found to be highly dependent on glutamate transmission via AMPA receptors, as well as Neurokinin B transmission. Inhibition of NMDA receptors did not alter rates of synchronization, and similarly inhibition of kappa opioid receptors had no effect on rate of synchronization or duration of spontaneous events. Combined with previously published data in male mice, these data underscore the importance of AMPA receptors in synchronizing the ARNKISS neuron network, but additionally suggest a sex difference in the relative contribution of neurokinin B to synchronizations.
Presentation: Saturday, June 17, 2023
SAT596 Evidence That Corticotropin-releasing Hormone Receptor 2 Activation Mediates Stress-induced Hyperglycemia
Authors: McCosh Richard B , Kreisman Michael J , Jang Jessica , Jung Jacklyn , Breen Church Kellie M 
Published: October 2023

Abstract
Disclosure: R.B. McCosh: None. M.J. Kreisman: None. J. Jang: None. J. Jung: None. K.M. Breen Church: None.
Stress-induced hyperglycemia refers to the transient increase in blood glucose (BG) levels during stress, which occurs in healthy and diabetic patients. In critically ill patients, stress-induced hyperglycemia is associated with a 2-fold increase in risk of incident diabetes. Thus, stress-induced hyperglycemia is a predictor of or may contribute to glucose dysregulation. In mice, activation of catecholamine neurons in the rostral ventral lateral medulla (rVLM) is necessary for stress-induced hyperglycemia; however, the mechanism by which these cells become activated during stress is not clear. Here, we tested the possibility that corticotropin-releasing hormone receptor 2 (CRHR2) signaling mediates stress-induced hyperglycemia in adult, ovariectomized mice. First, BG levels and rVLM cell activation were examined in two stress models. For psychosocial stress, BG levels were not altered by control treatment. In contrast, placement in a restraint device increased BG levels ∼2-fold, within 30 min, from pretreatment values and BG remained elevated for an additional 90 min. For immune stress, BG was significantly elevated (21% increase) at 30 min post IP injection of lipopolysaccharide (LPS, 10ng/g bw), then returned to baseline levels whereas BG levels were not altered from pretreatment levels in saline injected mice. In tissue collected 2 hr after initiation of restraint stress, the percentage of tyrosine hydroxylase (TH, marker of catecholamine cells) neurons in the rVLM that contained c-Fos (a marker of neural activation) was significantly greater than control mice. Next, we assessed the sufficiency of CRHR2 activation to induce hyperglycemia using the CRHR2 agonist urocortin 2 (UCN2), injected intracerebroventricular (ICV). BG was significantly increased 30 min after injection of both saline and UCN2 (60-80%); however, BG subsequently returned to baseline in saline-treated mice, but remained elevated in mice that received UCN2, similar to restraint stress. To test necessity of CRHR2 activation to induce hyperglycemia, we delivered ICV either the specific CRHR2 antagonist Astressin 2B (A2B) or saline 1 hr before psychosocial or immune stress. In no stress controls, A2B did not alter BG levels compared to saline, yet, BG levels in both groups decreased over time. BG levels were elevated in saline-treated controls 30 min after restraint stress; and, this increase was delayed, although not prevented, by 30 min by A2B pre-treatment. Following LPS injection, BG was increased at 30 min then decreased relative to baseline in saline-treated controls; yet, A2B pre-treatment blocked these changes. Together these data support the hypothesis that CRHR2 signaling is an important mediator of stress-induced hyperglycemia. Assessment of rVLM TH cells is ongoing.
Presentation: Saturday, June 17, 2023
SAT601 The Role Of The Melanocortin System In Ovine Puberty
Authors: Aerts Eliana G , Griesgraber Max J , Thomson Ashleigh , Brown Malori , Seman Andrew , Bowdridge Elizabeth , Hardy Steven L , Goodman Robert L , Nestor Casey , Hileman Stanley M 
Published: October 2023

Abstract
Disclosure: E.G. Aerts: None. M.J. Griesgraber: None. A. Thomson: None. M. Brown: None. A. Seman: None. S.L. Hardy: None. R.L. Goodman: None. C. Nestor: None. S.M. Hileman: None.
The neural mechanisms that regulate the timing of puberty onset are not completely known. In several species, including sheep, puberty onset relies on an increase in gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) secretion as a result of decreased sensitivity to estradiol (E2) inhibition. Additionally, it is unclear how E2 acts in the hypothalamus to inhibit GnRH/LH secretion, as GnRH neurons do not contain estrogen receptor alpha (ERα). Neurons within the arcuate nucleus (ARC) of the hypothalamus that contain kisspeptin, neurokinin B, and dynorphin (KNDy neurons) are critical for the generation of GnRH pulses and contain ERα. Data from our laboratory suggests that KNDy neurons, while critical, may be responding to other inputs that time puberty onset. Proopiomelanocortin (POMC) and Agouti-related peptide (AgRP) neurons in the ARC have been shown to contain ERα and provide input to KNDy neurons, which contain the melanocortin 3 and 4 receptor (MC3R, MC4R). The goal of this work was to assess POMC- and AgRP-positive cell numbers, input onto KNDy neurons, and neuronal activity changes in a puberty-specific manner. Female sheep were ovariectomized and given subcutaneous E2 implants at 5 months (prepubertal, n=4), 8 months (peripubertal, n=5), and 10 months (postpubertal, n=5) of age. Two weeks after surgery, blood samples were collected via jugular venipuncture every 12 minutes for 4 hours and assessed for LH. The sheep were then sacrificed and hypothalamic tissue was perfused, collected, and prepared for staining. The tissue was assessed via immunohistochemistry for POMC, AgRP, kisspeptin, NKB, and c-Fos, a known marker of neuronal activity. Pulsatile LH secretion was, as expected, reduced at 5 months and highest at 10 months. ARC POMC cell numbers did not significantly change over development (p&gt;0.10). The number of ARC POMC close contacts onto ARC kisspeptin neurons increased significantly with development (p&lt;0.05), as well as the percentage of ARC POMC neurons expressing c-Fos (p&lt;0.05). ARC AgRP cell numbers and the percentage of AgRP cells colocalized with c-Fos decreased significantly over time (p&lt;0.05). The number of AgRP close contacts onto ARC NKB cells is currently being analyzed. The percentage of NKB cells colocalizing c-Fos throughout pubertal development also increased significantly (p&lt;0.05). This data supports the hypothesis that the ARC melanocortin system impacts KNDy neurons to regulate GnRH/LH secretion throughout pubertal development.
Presentation: Saturday, June 17, 2023
SAT620 Dopamine Challenge: Treatment Of Pituitary Macroadenoma/Prolactinoma In Patient On Antipsychotic Medication
Authors: Bazhenov Aleksei , Alpertunga Ipek 
Published: October 2023

Abstract
Disclosure: A. Bazhenov: None. I. Alpertunga: None.
Background When hyperprolactinemia is a well-known side effect of antipsychotic medications1, the link between prolonged treatment with dopamine antagonist and the development of lactotroph adenomas is still unclear4. Treating a patient with prolactinoma and psychotic disorder may pose a challenge. Antipsychotic agents can cause increases in prolactin levels. Additionally, treatment of prolactinoma with dopamine agonists may worsen psychotic symptoms. Case presentation We present a case of 56 yo male with a PMH of bipolar disorder with psychotic features who was found to have a macroprolactinoma after 18 years of treatment with antipsychotic medications. At age 30, the patient was diagnosed with Bipolar Disorder with psychotic features. The course of the disease was complicated by numerous hospitalizations and frequent changes to the treatment plan, with different combination of second-generation antipsychotic, haloperidol and antiseizure medications. The patient’s prolactin level was 50 ng/ml at the time. 18 years after the diagnosis, the patient developed severe headaches. An MRI revealed a pituitary macroadenoma measuring 1.3 cm, and a repeat prolactin level resulted in 729 ng/ml. He was started on cabergoline 0.5 mg twice a week. As a result, the prolactin level dropped to 32 ng/ml and the macroprolactinoma size decreased to 1.1 cm. Unfortunately, the patient was lost to follow up. Once he re-established his care, he was started on Olanzapine 15 mg daily, Lamotrigine 200 mg daily and cabergoline 0.5 mg twice a week. After reinitiating cabergoline, the patient developed three maniac episodes, two of which required hospitalization. The dose of the cabergoline was decreased to avoid future maniac episodes. Neurosurgery will be consulted for possible surgery treatment. Discussion The treatment of a patient with prolactinoma and a psychotic disorder poses a particular challenge. We believe that care of these patients requires a multidisciplinary approach, and surgical treatment should be considered for those who cannot tolerate dopamine-agonist therapy. Literature 1. Bostwick JR, et al. Antipsychotic-induced hyperprolactinemia. Pharmacotherapy. 2009;29(1):64-73. 2. Lertxundi U et al. Antipsychotics and pituitary tumors. Int Clin Psychopharmacol. 2019;34(2)89. 3. Andrade EH, et al. Insights in the management of antipsychotics. Case Rep Med. 2010;2010. 4. McCarren M,et al. Follow-up study of a pharmacovigilance signal. J Clin Psychopharmacol. 2012;32(6)743. 5. Bakker IC, et al. Successful treatment of a prolactinoma on antipsychotic drug. Endocrinol Diabetes Metab Case Rep. 2016. 6. The challenges in managing prolactinomas SFEBES2009 Accessed April 11 2023. https://endocrine-abstracts.org 7. Howes OD et al. The role of dopamine in schizophrenia. Biol Psychiatry. 2017;81(1)9. 8.Bamarinejad A, et al. Schizophrenia and Macroprolactinoma: Adv Biomed Res. 2020;9(1)38.
Presentation: Saturday, June 17, 2023
SAT621 Hemorrhage After Treatment: A Case Of Pituitary Apoplexy In Metastatic Prostate Cancer After Leuprolide
Authors: Dillon Martha , Shteyman Sara , Rashid Waleeja , Ramchandani Bhanvi Prakash , Samat Aashish G 
Published: October 2023

Abstract
Disclosure: M. Dillon: None. S. Shteyman: None. W. Rashid: None. B.P. Ramchandani: None. A.G. Samat: None.
Introduction: Hormone-sensitive cancers, including prostate and breast cancer, and some gynecological conditions can be treated with GnRH agonists, including leuprolide. However, pituitary apoplexy is a rare potential complication after administration. Case Description: 71-year-old gentleman with metastatic hormone-sensitive prostate cancer presented with an acute headache after receiving a dose of leuprolide. This was his first GnRH agonist dose after prior Degarelix treatment. After two hours, the patient developed a constant throbbing headache, palpitations, left eye tearing and non-bilious non-bloody vomiting. Vitals were within normal ranges, and initial lab work showed low serum cortisol of 4.6. CT scan of the head showed exophthalmos and a mildly enlarged sella. Subsequent MRI demonstrated pituitary hemorrhage and optic chiasm impingement from resulting swelling. Hormone levels remained normal. Since the patient did not develop visual field defects or other ocular complaints, the decision was to manage the patient medically rather than with surgery. The day after admission, he developed hypotension requiring high dose steroids. After discharge, outpatient repeat MRI showed interval resolution of hemorrhage into a predominantly cystic pituitary macroadenoma. Discussion: With continued stimulation, GnRH agonists desensitize the pituitary and cause a downregulation of hormonal induced cancer growth. However, there is an initial transient burst of stimulation that can induce pituitary apoplexy in patients who already have a large adenoma. The hemorrhage and subsequent swelling cause a sudden severe headache and possible visual loss or hypopituitarism. This is life-threatening due to hypotension from catecholamine insensitive blood vessels in the absence of cortisol. Treatment involves high dose steroids, frequent sodium checks and possible emergency neurosurgery for decompression. It is important with GnRH agonists to watch out for this rare complication, whether the hormonal axis is being suppressed for metastatic cancer treatment or for hormonally driven gynecological conditions. Sources: Briet C, Salenave S, Bonneville JF, Laws ER, Chanson P. Pituitary Apoplexy. Endocr Rev. 2015 Dec;36(6):622-45. doi: 10.1210/er.2015-1042. Epub 2015 Sep 28. PMID: 26414232. Tanios G, Mungo NA, Kapila A, Bajaj K. Pituitary apoplexy: a rare complication of leuprolide therapy in prostate cancer treatment. BMJ Case Rep. 2017 Jul 14; 2017:bcr2016218514. doi: 10.1136/bcr-2016-218514. PMID: 28710301; PMCID: PMC5534692.
Presentation: Saturday, June 17, 2023
SAT623 Everolimus For Treatment-refractory Prolactinomas
Authors: Lin Andrew L , Geer Eliza Brevoort , Page-Wilson Gabrielle , Magge Rajiv S , Young Robert J , Tabar Viviane 
Published: October 2023

Abstract
Disclosure: A.L. Lin: Grant Recipient; Self; Bristol-Myers Squibb. E.B. Geer: None. G. Page-Wilson: None. R.S. Magge: None. R.J. Young: Consulting Fee; Self; Olea Sphere, ICON plc. V. Tabar: None.
Introduction: Treatment-refractory prolactinomas are life-limiting tumors without a standard of care treatment option after the oral alkylator, temozolomide, fails to provide tumor control. Methods: We reviewed an institutional database of pituitary tumors for patients with aggressive prolactinomas who progressed following treatment with a dopamine agonist, radiotherapy and temozolomide. In this cohort of patients with aggressive prolactinomas, we identified 4 patients who were treated with everolimus and we report their response to this therapy. Treatment response was determined by a neuroradiologist, who manually performed volumetric assessment and determined treatment response by Response Assessments in Neuro-Oncology (RANO) criteria. Results: 3 of 4 patients who were treated with everolimus had a biochemical response to therapy and all patients derived a clinically meaningful benefit based upon suppression of tumor growth. While the best overall response as assessed by RANO criteria was stable disease for the 4 patients, a minor regression in tumor size was appreciated in 2 of the 4 patients. Conclusion: Everolimus is an active agent in the treatment of prolactinomas that warrants further investigation.
Presentation: Saturday, June 17, 2023
SAT624 Neurosarcoidosis Presenting With Panhypopituitarism
Authors: Niedzialkowska Ewelina Marta , Blazin Tatjana , Strubchevska Kateryna , Kozyk Marko , Saini Nidhi 
Published: October 2023

Abstract
Disclosure: E.M. Niedzialkowska: None. T. Blazin: None. K. Strubchevska: None. M. Kozyk: None. N. Saini: None.
Introduction: Neurosarcoidosis is estimated to occur in approximately 5-15% patients with sarcoidosis. Pituitary involvement may be present in up to 5% of those cases and can manifest as hypothalamus, adenohypophysis dysfunction or arginine vasopressin deficiency (AVP-D) in isolated fashion or variedly combined. Clinical case: 32 year old male presented with chief complaint of worsening bilateral lower extremity weakness, urinary incontinence, polyuria and polydipsia. 9 months prior to admission the patient was diagnosed with neurosarcoidosis. At that time brain MRI showed diffuse leptomeningeal enhancement, chest CT showed hilar lymphadenopathy, lumbar puncture with CSF analysis showed protein 227 mg/dl (N&lt;38), ACE 6 U/l (N &lt;2.5), WBC 10 (N&lt;5) with 88% lymphocytes. Hilar lymph node biopsy was consistent with non-caseating granuloma. The patient was diagnosed with neurosarcoidosis and started on prednisone and methotrexate. The patient was referred to our institution for further evaluation. On examination gait ataxia and gynecomastia were noted. Laboratory results showed urine specific gravity of 1.001, LH 0.4 mIU/ml (N 0.6-1.2), FSH 1.1 mIU/ml (N 1-12), ACTH &lt;5 pg/ml (N 6-46), cortisol 2.1 ug/dl (N 2.9-19.4), prolactin 10.5 ng/ml (N 2-18), total testosterone 4 ng/dl (N 240-1080), free testosterone 0.1 ng/dl (N 4.8-19), TSH 0.58 uIU/ml (N 0.4-4.5), free ft3 1.5 pg/ml (N 1.7-3.7), free ft4 0.6 ng/dl (N 0.7-1.5), IGF-1 52 ng/ml (N 71-234), Copeptin proAVP of &lt;2.8 pmol/l( N&gt;13.2), urine osmolality of 72 mOsmol/kg, blood osmolality of 297 mOsmol/kg (N &lt;295), vit D 25-OH 9 ng/ml (N 30-100), vit D 1,25-OH 57.3 pg/ml (N 19.9-79.3). MRI of the spine showed extensive nodular enhancement of the leptomeninges of the cervical, thoracic spine and lumbar cauda equina nerve roots. Brain MRI was positive for numerous small nodular enhancement involving leptomeninges and pituitary stalk. The patient was started on desmopressin with significant improvement of symptoms and increase in urine osmolality to 709 mOsmol/kg. Due to risk of hypercalcemia and normal vit D 1,25-OH vitamin D supplementation was not initiated. For neurosarcoidosis the patient was started on pulse dose methylprednisolone and infliximab infusion. Upon discharge he was transitioned to oral hydrocortisone and started on levothyroxine and testosterone replacement therapy. Conclusion: We present a case of pituitary neurosarcoidosis presenting with AVP-D, secondary hypothyroidism, secondary adrenal insufficiency, hypogonadism and growth hormone deficiency. Panhypopituitarism with complete anterior and posterior pituitary dysfunction is extremely rare and might be found in up to 13% cases of pituitary sarcoidosis. The diagnosis should be considered in patients with sarcoidosis and endocrine dysfunctions.
Presentation: Saturday, June 17, 2023
SAT629 Do Antipsychotic Medications Cause Prolactinoma Growth? A Systematic Review Of Imaging And Serum Findings
Authors: Durrani Umar Safwaan 
Published: October 2023

Abstract
Disclosure: U.S. Durrani: None.
Between 2013 and 2018 approximately 4 million adults in the U.S. were reported to be taking antipsychotics. Since increased dopamine levels in the brain are a known etiology for psychosis, antipsychotics function by reducing dopamine levels; dopamine is also a neurotransmitter involved in the regulation of prolactin, a hormone secreted by the pituitary gland which plays a role in lactation and mammary gland development. Prolactinomas are pituitary tumors in which excess prolactin is secreted and their treatment often involves dopamine agonists, which function to decrease prolactin production. Understanding that dopamine agonism decreases prolactin production, our project seeks to examine if dopamine antagonism can cause prolactinoma growth. We aim to answer this question by conducting a PubMed literature review focusing on prolactinoma patients who are concurrently prescribed antipsychotics. Our search yielded 32 studies representing a total of 40 patients. Although imaging data was limited, we used serum prolactin levels as a surrogate marker for prolactinoma growth. Preliminary results uncovered two major themes from our search: the use of certain antipsychotics (risperidone, haloperidol, thioridazine, thiothixene, and amisulpride) was associated with an increase in prolactin levels, and discontinuation led to a decrease in prolactin as well as normalization of the pituitary gland when imaging was provided. However, there were also some exceptions where antipsychotic use had minimal or no effect on prolactinomas. There were 4 patients who took antipsychotics (risperidone, thioridazine) and did not have prolactinoma symptoms until they used other drugs in combination. There were 2 patients taking risperidone without any worsening of their existing prolactinoma when taking the drug in small doses with cabergoline or when using a long acting form. In conclusion, while the relationship between antipsychotic use and prolactinoma growth may not be fully clear, it is known that ceasing medication use can help with treatment of the tumor. We recommend that providers be aware of the potential relationship between these drugs and this tumor and adjust treatment plans accordingly.
Presentation: Saturday, June 17, 2023