bluuebunny/crossref_metadata_2025_split huggingface dataset:
7497 Association between Plasma Prolactin Levels and Menopausal Vasomotor Symptoms
Authors: Galbiati Francesca , Kang Jae Hee , Cote David J , Manson JoAnn E , Kaiser Ursula B 
Published: October 2024

Abstract
Disclosure: F. Galbiati: None. J. Kang: None. D.J. Cote: None. J.E. Manson: None. U.B. Kaiser: None.
Background: High prolactin (PRL) levels inhibit gonadotropin-releasing hormone (GnRH), causing hypogonadism. GnRH release is regulated by neurokinin B (NKB) and kisspeptin. NKB antagonists are used in treatment of menopausal hot flashes and vasomotor symptoms (VMS). In mice and humans with hyperprolactinemic anovulation, kisspeptin restored ovarian cyclicity and LH pulsatility. However, the interplay between kisspeptin and PRL is not fully understood. In two menopausal women with hyperprolactinemia and central hypogonadism, treatment with bromocriptine led to PRL normalization and new-onset VMS, suggesting that hyperprolactinemia inhibited VMS associated with hypogonadism. We aimed to investigate the association between PRL and menopausal VMS in women from the Nurses’ Health Study I and II (NHS, NHSII). We hypothesized that women with higher PRL levels would have a lower frequency/severity of menopausal VMS. Methods: We conducted a cohort study of 2618 females enrolled in NHS (n=1692) and NHSII (n=926) in whom blood samples were collected between 1989-99, were not pregnant or on hormonal therapy, and were either pre or post-menopausal as of blood draw. Subjects were free of breast, ovarian and other cancers, and provided complete data on VMS at menopause as well as in the past 4 weeks (assessed in 2008 in NHS and 2009, 2013, 2017 in NHSII). Plasma PRL was measured as part of 28 case-control studies of various health outcomes. We evaluated the presence and severity of VMS at menopause and 4 weeks prior to the questionnaire, as well as duration (in years) of VMS. We used multiple logistic regression, adjusting for covariates to estimate multivariable-adjusted relative risks (MVRRs) and 95% confidence intervals (CIs). Results: Women were aged 33-65 years at blood draw; range for years from blood draw to menopause was -10 to 10 (median=1.8) years; range for years from blood draw to report of VMS (both at menopause and current VMS) was 9.8 to 22 years. Mean PRL (SD; range) was 14.7ng/mL (10.1; 0.08-246). Women with the highest PRL levels were likely to be younger and less likely to be current smokers or obese. 77.4% of women reported VMS at menopause and 47.6% in recent 4 weeks; 52.3% reported moderate-to-severe VMS at menopause and 32.0% reported VMS in recent 4 weeks. Overall, PRL was not associated with duration of VMS or moderate-to-severe VMS at menopause or in the past 4 weeks; compared to the lowest quintile (≤8.0ng/mL), those in the highest PRL quintile (≥18.2ng/mL) had MVRR of 1.23(95%CI=0.94,1.60) for moderate-to-severe menopausal VMS and 1.03(95%CI=0.67,1.59) for recent VMS. Menopausal status did not affect the association between prolactin levels and VMS. Conclusion: PRL levels were not associated with occurrence, severity, or duration of menopausal VMS in a large cohort of women.
Presentation: 6/1/2024
8427 Association of Circulating Prolactin Levels with Degree of Glycemic Control as Determined by Glycated Hemoglobin
Authors: Hashim Ibrahim A , Abraham Elizabeth 
Published: October 2024

Abstract
Disclosure: I.A. Hashim: None. E. Abraham: None.
Background: Prolactin is suggested to stimulate pancreatic β cells and may thus play a role in glucose metabolism. This retrospective study examined the relationship between circulating prolactin levels and glycated hemoglobin (A1c) levels among diabetics and patients being investigated for glucose intolerance. Methods: A1c values and their corresponding prolactin levels performed over 15 months (July 2021 to October 2022) were retrieved from the electronic medical records and subjected to statistical analysis. Patients’ glycemic status was characterized as normal (A1c ≤5.7%), prediabetic or in control (A1c &gt;5.7 to &lt;6.4 %), diabetic in control (A1c &gt;6.5% to &lt;9.0%), and poorly controlled (A1c &gt;9.0%). Results: A total of 276 patients were included in the study, ages ranged from 12 to 84 (median 37 years) among females (n=229) and from 14 to 75 (median 38 years) among male patients (n=47). In patients with A1c ≤5.7 (n=152, 55.1% of patients) A1c ranged from 4.1 to 5.6 (median 5.3%) and prolactin levels ranged from 14 to 84 (median 36 ng/dL). Patients with A1c levels &gt;5.7 to &lt;6.4 % (n=71, 25.7%) A1c ranged from 5.7 to 6.4 (median 5.9%) and prolactin levels ranged from 1 to 1152 (median 11.9 ng/dL). Patients with A1c levels &gt;6.5 to &lt;9.0 (n=33, 11.9%) A1c ranged from 6.6 to 9.0 (median 7.1%) and prolactin levels from 1.1 to 154.5 (median 11.9 ng/dL). Patients with A1c &gt;9.0% (n=19, 6.9%) A1c ranged from 9.2 to 14.5 (median 10.5%) and prolactin levels ranged from 2.7 to 41.2 (median 14.6 ng/dL). Overall, there was no correlation between A1c and prolactin levels for all study patients (r = -0.03, p= 0.6). There was no significant difference in prolactin levels among patients with normal A1c and those in control (p= 0.57 and 0.33 respectively). However, prolactin levels were lower in patients with poor control (A1c &gt;9%) (p=0.02).Discussion: Markedly elevated but not significantly different prolactin levels were observed in prediabetic patients and those with good control. However, significantly lower prolactin levels were observed in poorly controlled diabetic patients. The study findings suggest a possible role for prolactin in glycemic control and that further studies are required to further investigate pathophysiology and possible mechanism.
Presentation: 6/2/2024
8067 AVP Gene Mutation: A Rare Cause of Diabetes Insipidus
Authors: Navrange Nishika , Williams Maeve , Madhavan Parvathy 
Published: October 2024

Abstract
Disclosure: N. Navrange: None. M. Williams: None. P. Madhavan: None.
Introduction: Arginine vasopressin deficiency (AVP-D), also known as neurohypophyseal or central diabetes insipidus (DI), is marked by a reduced secretion of arginine vasopressin (AVP), resulting in polyuria and polydipsia. AVP-D is a rare disorder, with a prevalence of 1 in 25,000. Typically, the disorder is acquired. However, in less than 5% of cases, it has a genetic etiology. The majority of mutations in the AVP gene are autosomal dominant. Normally, AVP encodes vasopressin, also known as antidiuretic hormone (ADH). It plays a key role in the reabsorption of water in the kidney, the regulation of blood pressure, and controlling the body’s osmotic balance. However, a mutation in this gene leads to a deficient release of ADH, leading to reduced reabsorption of water in the collecting duct and decreased ability to concentrate urine. This results in increased urine output and excessive thirst. The onset and severity of symptoms varies between individuals. Case Report: In this report, we discuss the case of a 40-year-old Caucasian female with familial neurohypophyseal diabetes insipidus. The patient presented to the clinic for follow-up care of DI and hyponatremia. She received her DI diagnosis before the age of 5 and has multiple family members with the condition including her maternal grandfather, mother, and 2 siblings. Additionally, she suspected one of her children was exhibiting excessive urination. Past medical history is also significant for seizure disorder, postpartum cardiomyopathy, Chiari malformation type I and remote history of substance abuse. Vitals were stable with blood pressure of 122/86 mmHg, heart rate of 93 bpm, body mass index of 31.8. Physical exam was unremarkable except for obesity. She is currently managed with DDAVP 0.05 mg twice daily. Previously, imaging was performed to rule out pituitary abnormalities. The patient was referred for genetic testing due to her family history and was found to have a previously described rare autosomal dominant mutation of the AVP protein. The single nucleotide polymorphism in exon 1 results in a missense mutation substituting an alanine nucleotide for threonine (c.55G&gt;A). The patient was counseled to share these results with her children’s pediatrician, as they could benefit from testing for the mutation. Discussion: Our patient has a pathogenic variant in AVP, specifically a missense mutation from Alanine to Threonine at codon 19 of the AVP protein. This mutation is associated with autosomal dominant neurohypophyseal diabetes insipidus. This case provides an example of a rare cause of neurohypophyseal diabetes insipidus and emphasizes the necessity of obtaining detailed family history in patients who have DI and considering genetic testing for patients with suspicion for familial involvement.
Presentation: 6/2/2024
6555 Cabergoline-induced psychiatric symptoms in a patient with a pituitary macroadenoma
Authors: Patel Goonja S , Prater Janna 
Published: October 2024

Abstract
Disclosure: G.S. Patel: None. J. Prater: None.
Cabergoline is a long-acting dopamine agonist that is used for the treatment of hyperprolactinemia, especially in pituitary macroadenomas. It reduces the levels of prolactin (PRL) but is also effective in reducing the tumor size and allows patients to avoid undergoing surgical resection of the mass. It commonly causes side effects such as abdominal pain, bloating, dizziness, and headaches. It rarely can cause new onset psychological side effects or an exacerbation of pre-existing mood and behavioral disorders. We present the case of a male on cabergoline therapy who had new-onset psychiatric symptoms that persisted even after treatment was discontinued. The patient is a 40-year-old male who was found to have a pituitary macroadenoma measuring 2.2 x 1.8 x 1.6 cm on brain MRI after a one-year history of headaches, dizziness, and hearing loss. His vital signs and physical examination were unremarkable. Laboratory investigations revealed a PRL of 1,072 ng/mL. He was started on cabergoline 0.25 mg twice a week which reduced levels of PRL to 465.3 ng/dL. Throughout the next year, his PRL levels remained persistently elevated to &gt;100 ng/dL and the cabergoline dose was steadily increased to 1 mg three times per week. About a year into treatment he began experiencing significant emotional lability, a tendency to cry, and bursts of temper which required the addition of multiple psychiatric medications. After two years of continued psychiatric symptoms, there was an attempt to both reduce cabergoline doses and switch to escalating doses of bromocriptine, both of which resulted in a reduction of psychiatric symptoms but also significant increases in PRL levels. The patient’s mood symptoms returned shortly after switching back to cabergoline, especially with increased doses. He eventually underwent trans-sphenoidal resection for his treatment-resistant pituitary macroadenoma. He was taken off cabergoline before surgery with a significant reduction in his mood symptoms but continues to require psychiatric medications for lasting emotional lability. Although rare, psychiatric side effects of cabergoline have been documented and must be addressed if a patient develops them while receiving treatment. Our patient had a severe presentation of mood symptoms from cabergoline therapy that required multiple psychiatric medications in escalating doses to control. It not only affected his quality of life but also resulted in long-term consequences. It is recommended that patients with similar presentations should be continued on cabergoline with the addition of clozapine as it has less of an effect on PRL levels. Other treatment options also include aripiprazole and quetiapine. However, when patients have treatment resistant macroprolactinomas and are unable to tolerate cabergoline, one would have to consider surgical treatment options for the treatment of hyperprolactinemia from pituitary macroadenomas.
Presentation: 6/1/2024
12343 Cardiac Function Recovery Following Left Adrenalectomy For A Pheochromocytoma With Ectopic ACTH Syndrome
Authors: Williams Tyler D , Lovre Dragana , Galagan Robert C 
Published: October 2024

Abstract
Disclosure: T.D. Williams: None. D. Lovre: None. R.C. Galagan: None.
Background: Pheochromocytoma and Cushing’s Syndrome are implicated in Non-ischemic Cardiomyopathy/Heart Failure with reduced Ejection Fraction (NICM/HfrEF) due to catecholamine induced hypertension and cardiomyocyte toxicity. Subsequent hypoxia and calcium overload in cardiomyocytes results in oxidative stress and cell death. Excess cortisol secretion increases angiotensin II, causing hypertrophy. Subsequent increases in atrogin I lead to myo-fibrinolysis and fibrosis. We present a patient with NICM/HFrEF due to both catecholamine excess and ectopic ACTH syndrome from an adrenal pheochromocytoma. Following adrenalectomy, systolic cardiac function returned to normal. Clinical Case A 42-year-old female was referred to endocrinology after a hypertensive emergency concurrent with NSTEMI, NICM, and HFrEF (EF 45%). Initial work up revealed: Troponin I 0.49 ng/ml; (0 - 0.04 ng/ml), Na+ 140 mmol/L; (136 - 144 mmol/L), K+ 2.3 mmol/L; ​​(3.7 - 5.2 mmol/L), CO2 41 mmol/L; (23 - 29 mmol/L), Glucose 53 mg/dL; (64 - 100 mg/dL), Cortisol 57.2 ug/dL; (5 - 25 ug/dL), ACTH 363.7 pg/mL; (7.2 - 63.3 pg/mL). She failed both 1 mg and 8 mg overnight dexamethasone suppression tests: 0800 cortisol 48.5 ug/dL (&lt; 1.8 ug/dL) & 56.8 ug/dL (&gt; 50% decrease in baseline cortisol level of 57.2 ug/dL) consistent with ectopic ACTH syndrome. Elevated plasma normetanephrine 0.98 nmol/L; (0 - 0.89 nmol/L) and chromogranin A 250 ng/mL; (0 - 103 ng/mL) suggested a neuroendocrine tumor. Pituitary MRI revealed a normal pituitary gland. Abdominal MRI detected a 3.6 x 2.5 cm left adrenal nodule and PET/CT CU-64 showed increased activity (Krenning 4) consistent with a pheochromocytoma. Notwithstanding Ketoconazole (200 mg/day) for 7 months, her EF fell to a low of 15-20%. A left adrenalectomy was performed and post-op 0800 cortisol was 12.3 ug/dL (6.0 - 26.0 ug/dL). Oral hydrocortisone was initiated at 20 mg QAM/10 mg QPM for steroid withdrawal syndrome, tapered over 8 months and withdrawn when a cosyntropin stimulation test 60-min cortisol was 19.3 ug/dL; (&gt;18.0 ug/dL). Eleven months post op, her 0800 cortisol was 8.8 ug/dL and ACTH 27.4 pg/mL. One month post-op, TTE showed EF: 15-20%, six months post-op EF: 25-30%, eight months post-op EF: 35-40% and 15 months post-op EF was normal at 50%. Her heart failure symptoms resolved, and her activity returned to normal. Conclusion This case illustrates a remarkable restoration of cardiac function following resection of a pheochromocytoma. Our patient's case is unique due to the restoration of cardiac function despite the dual impact of excessive catecholamines and cortisol. Our patient’s clinical course contributes to an evolving understanding of cardiomyopathy associated with pheochromocytoma and ectopic ACTH syndrome and highlights the potential for cardiomyopathy reversal with targeted endocrine surgical and medical interventions.
Presentation: 6/1/2024
8081 Case report of sympathetic paraganglioma presenting as chronic catecholamine induced cardiomyopathy
Authors: Tan Zi , Taiwo Adeyinka 
Published: October 2024

Abstract
Disclosure: Z. Tan: None. A. Taiwo: None.
Background: Sympathetic paragangliomas are rare neuroendocrine tumors (&lt;1/100,000) arising from extra-adrenal autonomic paraganglia, generally in the thorax, abdomen, and pelvis. They secrete catecholamines predominantly norepinephrine, which can cause a rare complication of catecholamine-induced cardiomyopathy. Clinical Case: A 33-year-old male, with history of obesity and borderline hypertension not on medication, presented with dyspnea on exertion, worsening paroxysmal nocturia dyspnea of 1 month duration and sudden onset of severe right flank pain. Work up for his chronic shortness of breath revealed: Troponin negative. EKG showed sinus tachycardia. Echocardiogram revealed enlarged left ventricle, severely decreased LV systolic function of 25-30%. Given the absence of angina symptoms, negative troponin, and EKG findings, his new-onset cardiomyopathy was presumed to be non-ischemic. CT chest, abdomen and pelvis was performed for the new onset right flank pain, which revealed a 4.1 cm x 4.0 cm centrally necrotic aortocaval soft tissue mass. This raise a concern about malignancy. A CT-guided Fine-Needle Aspiration of the retroperitoneal mass suggested paraganglioma. Further investigation showed plasma normetanephrine at 5.56 nmol/L (Reference range: 0-0.89 nmol/L), 24 hour urine normetanephrine at 2411 ug/d (Reference range: 114-865 ug/d), and 24 hour urine norepinephrine at 179 ug/d (Reference range: 14-20 ug/d). Plasma metanephrines and plasma dopamine were within the normal range. A gallium DOTATE PET/CT revealed a necrotic aortocaval mass with peripheral uptake, consistent with the known paraganglioma. He was diagnosed with sympathetic paraganglioma complicated with chronic catecholamine-induced cardiomyopathy and had exploratory laparotomy excision of his paraganglioma. Preoperatively, he was treated with phenoxybenzamine and carvedilol. However, his post-surgical course was complicated by acute on chronic heart failure and pneumonia, and he subsequently passed away from a pulseless electrical activity arrest. Conclusion: Although sympathetic paragangliomas rarely presents as catecholamine-induced cardiomyopathy, this case emphasizes the importance of considering hormonal abnormalities in patients who present with non-ischemic cardiomyopathy without high risk factors. Reference: 1. Alessandra Giavarini, Antoine Chedid et al. Acute catecholamine cardiomyopathy in patients with phaechromocytoma or functional paraganglioma. Heart 2013; 99: 1438-1444.
Presentation: 6/2/2024
8252 Central Adrenal Insufficiency Masquerading as Syndrome of Inappropriate Antidiuretic Hormone (SIADH): A Case Report
Authors: Sazon J G , Reyes J L , Chua J V , Kho S A 
Published: October 2024

Abstract
Disclosure: J.G. Sazon: None. J.L. Reyes: None. J.V. Chua: None. S.A. Kho: None.
Hyponatremia, the most common electrolyte imbalance encountered in clinical practice, has various causes and presentation. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) is a frequent hospital-related cause, potentially leading to misdiagnosis with adrenal insufficiency due to shared clinical features which may cause potential deleterious effect. We present a case of a 41-year-old male hyponatremic patient with a two-month history of progressive generalized body weakness and lightheadedness, initially managed as SIADH. Upon admission, the patient persistently showed low serum sodium level (122mmol/L) (NV: 135-145mmol/L), exhibited signs of euvolemic hyponatremia despite fluid restriction, intravenous furosemide, and sodium chloride tablets. Further work-up revealed normocytic normochromic anemia (Hgb 107 g/L) (NV: 120-160g/L), elevated ESR of (31mm/hr) (NV: 0-15mm/hr), low Ft4 (2.97 pmol/L) (NV: 12-22 pmol/L) and normal TSH (2.2 uIU/mL) (NV: 0.27-4.20 uIU/mL). During hospital stay, he experienced an episode of hypotension at 80/50mmHg and hypoglycemia at 65 mg/dL. Investigation revealed adrenal insufficiency secondary to pituitary macroadenoma with apoplexy as showed in magnetic resonance imaging. Patient was started on Prednisone. Pre-operatively, hydrocortisone 100mg IV every 8 hours preoperatively. He underwent transsphenoidal surgery; excising a 2.5cm soft and grayish suprasellar mass. Post-operatively, he was given Prednisone and Levothyroxine resulting in symptom improvement and normal sodium levels.The occurrence of hyponatremia due to adrenal insufficiency is relatively uncommon, emphasizing the need for heightened suspicion when assessing patients with prolonged or recurring hyponatremia. This paper highlight the need to replace glucocorticoid prior supplementation of thyroid hormone in such cases, averting the occurrence of adrenal crisis. This case indicated a mechanism of persistent hyponatremia attributed to secondary adrenal insufficiency, with added therapeutic benefits observed through the use of glucocorticoids and transsphenoidal surgery.
Presentation: 6/1/2024
8147 Central Diabetes Insipidus Following COVID-19 Infection: An Unusual Complication
Authors: Rivera Luisa Bernacet , Inzucchi Silvio E 
Published: October 2024

Abstract
Disclosure: L. Bernacet Rivera: None. S.E. Inzucchi: None.
SARS-CoV 2 infection has been associated with organ-specific complications since the 2020 pandemic, including several endocrinopathies. This has been mostly theorized to be related to high expression of angiotensin-receptor enzyme 2 (ACE-2) receptors in the endocrine system. Since the virus’ main mechanism of entry to host cells is via these receptors, endocrine glands may thus be susceptible for injury. A rarely described complication is isolated central diabetes insipidus (DI). We present a woman who developed spontaneous central DI soon SARS-CoV infection, without other cause. A 41-year-old woman with medical history of gastroesophageal reflux presented to the clinic for evaluation of polydipsia and polyuria. She contracted COVID 19 infection about 3 months prior to presentation. She had mild symptoms and did not require hospitalization or any pharmacological treatment. Approximately 3 weeks following infection she noticed the sudden development of increased urination and thirst. She reported urinating approximately every 2 hours (including 3-4 times overnight) and drinking 1-1.5 gallons of fluid daily, much more than her baseline. Given persistence of symptoms she sought medical attention at a local emergency room (ER) for further evaluation. There was no history of prior pituitary disease, brain masses, head trauma, granulomatous conditions. Workup was significant for serum sodium of 142 mmol/L and urine specific gravity &lt;1.005. She was discharged from the ER to follow with her primary care provider. Patient had a 24-hour urine collection which yielded 6.1 L, with an osmolality of 93 mOsm/kg, while her serum sodium concentration was 141 mmol/L. Pituitary hormonal workup had normal levels of morning cortisol , free T4, TSH, prolactin, LH, FSH, and IGF-1. Due to normal serum osmolality at the time of the urine collection, the patient underwent an overnight water deprivation test of 12 hours to determine etiology of her polyuria. This resulted in a serum sodium of 148 mmol/L, serum osmolality of 300 mOsm/kg, urine osmolality of 159 mOsm/kg, and low serum copeptin level 2 pmol/L confirming the diagnosis of central DI. Patient was initiated on oral DDAVP with improvement in symptoms. A pituitary MRI revealed thickening of the pituitary infundibulum to 4 mm. The presence of central DI and thickening of pituitary stalk were suggestive of infundibuloneurohypophysitis. Other laboratory testing was negative and there was no other explanation for her condition. Follow-up pituitary MRI has shown no change in the pituitary stalk over a one-year period. The relationship between SARS-CoV 2 infection and this patient’s DI remains unclear but the temporal association and lack of other systemic related conditions makes it as strong possibility. They have been case reports with isolated central DI following COVID-19 infection. The pathogenesis remains unclear, but likely involves immune activation.
Presentation: 6/2/2024