bluuebunny/crossref_metadata_2025_split huggingface dataset:
FRI309 Functional Gonadotrophin Secreting Adenoma With Elevated Testosterone—A Rare Entity
Authors: Bulchandani Sheetal , Syal Samriddhi , Sloan Emily A , Sharma Susmeeta Tewari 
Published: October 2023

Abstract
Disclosure: S. Bulchandani: None. S. Syal: None. E. Sloan: None. S.T. Sharma: None.
Introduction: Gonadotroph adenomas are a common type of pituitary neuroendocrine tumor (PitNET). However, most do not lead to elevated sex hormone levels1. Presenting symptoms include headache, visual field deficits, and hypopituitarism.2-3. Gonadotropin-secreting PitNET leading to high circulating testosterone levels are extremely rare. We report a case of a male patient with a gonadotroph PitNET causing hypersecretion of testosterone. Case Report: 53-year-old male with history of hypertension presented for evaluation of dystonia. He also reported fatigue and an episode of diplopia. He had normal libido and sexual function, no mood fluctuations. MRI of the spine performed for evaluation of dystonia revealed a 2.8 cm sellar mass. MRI Pituitary showed a 31 mm in height by 24 mm in width by 19 mm in depth sellar mass suggestive of a pituitary adenoma with compression of the optic chiasm and extension into the left cavernous sinus. Laboratory evaluation revealed an elevated follicle stimulating hormone level (FSH) of 73.6 mIU/ml (1.6-8.0), luteinizing hormone (LH) 13.3mIU/ml (1.5-9.3), elevated total testosterone of 2176 ng/dl (250-1100) and Free testosterone 367.7 pg/mL (35-155), Sex hormone binding globulin of 68 nmol/L, Alpha subunit of 3ng/mL, prolactin 23 ng/ml (4-15.2), no increase with dilution, TSH 2.24 iIU/ml, free thyroxine level 0.9 ng/dL, and AM Cortisol 6.4 mcg/dl. A Cosyntropin stimulation test revealed adrenal insufficiency and treatment with hydrocortisone was initiated. Ophthalmology evaluation revealed left &gt;right asymmetric bitemporal hemianopia. He underwent transsphenoidal resection of the pituitary tumor. Post-operative laboratory evaluation revealed testosterone level of 43.65ng/dL and FSH of 6.6mIU/ml. Pathology showed a gonadotroph PitNet with diffuse nuclear positivity for SF1 and patchy cytoplasmic positivity for FSH with Ki-67 index of 2-3%. Discussion and Conclusion: Most gonadotropinomas are nonfunctional2 and clinically present with hypopituitarism and often low or normal sex hormone levels. We present a rare case of gonadotroph PitNet with elevated testosterone levels not associated with a recognizable clinical syndrome of sex hormone excess. The standard therapy for gonadotropin-secreting macroadenomas is trans-sphenoidal surgery.2-3 Early diagnosis is essential for timely and appropriate management.
Presentation: Friday, June 16, 2023
FRI333 Neurosarcoidosis Induced Panhypopituitarism​
Authors: Alfares Khalid , Han Hye Jeong , Athimulam Shobana 
Published: October 2023

Abstract
Disclosure: K. Alfares: None. H. Jeong Han: None. S. Athimulam: None.
Introduction: We hereby present a rare case of neurosarcoidosis causing panhypopituitarism. According to Martin-Grace et al who conducted a literature search for the timeframe of 2002 to 2014, there were only 8 cases of neurosarcoidosis associated pan hypopituitarism. Case Report: A 35-year-old male with a known diagnosis of sarcoidosis on skin biopsies presented to the hospital for altered mental status, hypernatremia, hypotension and hypothermia. He reported symptoms of polyuria and polydipsia for several weeks prior to admission. MRI of the brain revealed a 3cm mass in the suprasellar region involving the hypothalamus and bilateral optic tracts with mass effect on the anterior third ventricle. No discrete pituitary or stalk lesion was identified. A ventriculostomy tube was placed for developing hydrocephalus. Biopsy of the suprasellar mass revealed non-caseating granuloma, confirming neurosarcoidosis. Laboratory work up revealed elevated serum sodium at 167 mmol/L, high serum osmolality at 381 mOsm/kg and low urine osmolality at 381 mOsm/kg, consistent with diabetes insipidus. Anterior pituitary hormone profile work up revealed low 8am serum cortisol (1.9 mcg/dL) and inappropriately normal ACTH (34 pg/ml), low serum free testosterone (&lt;2.5 ng/dL) and low Luteinizing hormone (0.7 mIU/ml) and low follicular stimulating hormone (&lt; 2.6 mIU/ml), low free T4 at 0.4 ng/dL and inappropriately normal TSH at 2.77 uIU/mL. Serum prolactin was mildly elevated at 86.8ng/mL. Angiotensin converting enzyme level was within normal range at 33 U/L. A diagnosis of panhypopituitarism was made. Treatment was initiated with high dose IV corticosteroids for management of secondary adrenal insufficiency and neurosarcoidosis. He was also started on IV desmopressin and IV levothyroxine for management of his panhypopituitarism. He was transitioned to oral therapy on discharge. Discussion: Panhypopituitarism secondary to neurosarcoidosis is a rare presentation. Panhypopituitarism from sarcoidosis can occur due to infiltration of the pituitary gland or infiltration of the hypothalamus affecting the hypothalamic-pituitary axis. Sarcoidosis should be considered a differential when evaluating patients with symptoms consistent with panhypopituitarism. Prompt diagnosis and initiation of corticosteroids and deficient hormones can be lifesaving.
Presentation: Friday, June 16, 2023
FRI334 A Case Of Delayed Onset Sheehan's Syndrome With Diabetes Insipidus
Authors: Inkollu Sindhura , Estrada Allison 
Published: October 2023

Abstract
Disclosure: S. Inkollu: None. A. Estrada: None.
Introduction: Sheehan's syndrome (SS) is characterized by hypopituitarism that develops due to ischemic pituitary necrosis from severe postpartum hemorrhage. The frequency of SS has declined in developed countries as the result of modern obstetric care. It may present immediately after delivery or many years later with delay up to 32 years after the inciting event.1 SS is characterized by anterior pituitary dysfunction, while diabetes insipidus (DI) is an uncommon complication with an estimated frequency of 5%.2 Here, we present a case of a 58-year-old woman with late onset SS 33 years after delivery, complicated by DI. Clinical Case: A 58-year-old female was referred to endocrine clinic for hypothyroidism with TSH 4.98 mIU/mL (0.27-4.20) and undetectable free T4 (fT4) at &lt;0.1ng/dL (0.8-1.6). Her symptoms included fatigue, dizziness, cold intolerance, dry skin, and hair loss for the past two years. On further questioning, patient reported that she was unable to lactate or menstruate since her last childbirth 33 years ago in Thailand, but never sought evaluation since she had completed her family. She was able to breastfeed her previous 3 children. On examination, she appeared well oriented but lethargic, withdrawn and pale. Axillary and pubic hair was absent. Pituitary hormonal panel demonstrated panhypopituitarism with fT4 &lt;0.1 ng/dL, ACTH 14.2 pg/mL (7.2-63.3), cortisol 0.5 mcg/dL (10-20), prolactin 0.9 ng/mL (4.8-23.3), insulin like growth factor-1 of 10 ng/mL (56-194) and FSH 1.2U/L (25.8-134.8 postmenopausal). MRI of the pituitary showed a partially empty sella turcica. A diagnosis of SS was made and the patient was started on prednisone and levothyroxine. Shortly after starting prednisone, she developed significant polyuria and polydipsia. Given concern for DI unmasked by steroids, she was started on desmopressin 1mcg PO daily. Workup for DI was not done due to financial stressors. She showed marked improvement in general well-being and all her symptoms with hormone replacement. Conclusion: SS is not as rare as assumed in developed countries like USA, likely due to migrant women and unawareness of physicians regarding possibility of late onset SS. DI, though uncommon, still occurs with SS and can be masked by adrenal insufficiency on initial presentation. Clinicians should be aware of this condition as early diagnosis and treatment of SS improves quality of life along with morbidity and mortality to a great extent.
Reference: 1. Otsuka F, Kageyama J, Ogura T, Hattori T, Makino H. Sheehan's syndrome of more than 30 years' duration: an endocrine and MRI study of 6 cases. Endocr J. 1998 Aug;45(4):451-8. doi: 10.1507/endocrj.45.451. PMID: 9881893. 2. Keleştimur F. Sheehan's syndrome. Pituitary. 2003;6(4):181-8. doi: 10.1023/b:pitu.0000023425.20854.8e. PMID: 15237929.
Presentation: Friday, June 16, 2023
FRI345 A Rare Case Of Pituitary Histoplasmosis Presenting With Hypopituitarism
Authors: Jung Andrew , Tan Josenia , Charatz Seth , Azim Salman 
Published: October 2023

Abstract
Disclosure: A. Jung: None. J. Tan: None. S. Charatz: None. S. Azim: None.
A 58-year-old female presented to the endocrine clinic with a history of headache of one year duration. Prior to the visit, she had undergone a right middle lobe lung resection. Histopathology revealed necrotizing granulomas with yeast resembling histoplasmosis on fungal stains. She had no past history to suggest that she was immunocompromised. The patient had completed a three months course of itraconazole. Shortly after, she experienced daily headaches. Pituitary MRI demonstrated an enlarged 1.5cm pituitary gland without compression of the optic chiasm. Laboratory tests showed hypogonadotropic hypogonadism with LH 2.4 mIU/mL (15.9- 54.0), FSH 9.6mIU/mL (23 -116.3), and estradiol 14 pg/mL (&lt;32.2). Free T4 was low 0.7 ng/dL (0.9-1.8) without elevated TSH 1.81 uIU/mL (0.55-4.78). Prolactin was 29.7 ng/mL (2.8-29.2). GH, ACTH, and morning cortisol were normal. Due to the constant headache with hypopituitarism, the decision was made to proceed with transsphenoidal surgery. Pituitary biopsy reported histoplasmosis on Grocott methenamine silver and Periodic acid-Schiff stains. The patient was started on amphotericin B. Repeat MRI confirmed the decrease in size of the pituitary gland after the procedure. Pituitary fungal infections are extremely rare. To our knowledge, this is the first reported case of pituitary histoplasmosis presenting with hypopituitarism. Clinicians should be mindful of the rare etiologies of hypopituitarism when evaluating patients with pituitary enlargement and hypopituitarism.
Presentation: Friday, June 16, 2023
SAT347 Surprising Turn Of Events In A Patient With Weight Gain: Simultaneous Diagnosis Of Macroprolactinoma And Polycystic Ovary Syndrome
Authors: Keskinkilic Ayse Nur , Sistla Divya 
Published: October 2023

Abstract
Disclosure: A.N. Keskinkilic: None. D. Sistla: None.
Background: The differential diagnoses of excess weight gain are broad and endocrinopathies constitute a small proportion of these etiologies. A pattern of associated symptoms, classical exam findings and hormonal testing can signal some endocrine causes. However, diagnosis can still be challenging due to overlapping clinical and biochemical features and concurrent presentations of endocrine disorders. Here, we present a diagnostically challenging rare case of a young female with weight gain who had simultaneous diagnosis of macroprolactinoma and PCOS. Clinical Case: A 34-year-old healthy female presented with one year of weight gain despite lifestyle changes. She also reported headaches, acne, hirsutism, stretch marks, excessive sweating, and had 10 years of amenorrhea while on oral contraceptives (OCs). Labs revealed mildly low free T4 of 0.72 ng/dl (n: 0.70-1.48 ng/dl) and significantly elevated prolactin (PRL) of 259.8 ng/ml (n: 1.2-29.9 ng/ml); normal FSH, LH, GH, IGF, TSH, ACTH, 1 mg dexamethasone suppression test, and 24-hour urinary cortisol. HbA1c, lipid panel, plasma metanephrine and androgen levels were normal. MRI pituitary revealed a 2.1 x 1.9 x 1.5 cm macroadenoma with mild compression to the optic chiasm. A low dose levothyroxine and cabergoline 0.25 mg twice weekly was started with dose increment to 0.5 mg twice weekly. At 6-month follow-up, PRL decreased to 30 ng/ml. Repeat MRI showed a decrease in size of the pituitary adenoma (1.5 x 1.4 x 1.3 cm). However, she could not tolerate cabergoline due to persistent headaches and depression. Hence, she elected to undergo transsphenoidal pituitary resection. Tumor pathology showed sparsely granulated lactotroph adenoma. Post op PRL level normalized, and MRI showed radiological cure of the adenoma. Headaches improved but amenorrhea persisted despite discontinuation of OCs for 6 months. Progesterone challenge tests resulted in withdrawal bleed suggesting anovulation. Repeat work-up ruled out nonclassical CAH, Cushing’s, and androgen-secreting tumors. However, subsequent pelvic ultrasound confirmed polycystic ovarian morphology, suggesting PCOS. The patient preferred to avoid OCs and could not tolerate metformin. She elected progesterone IUD placement for endometrial protection in combination with lifestyle changes with notable improvement in her symptoms. Conclusion: PCOS is a diagnosis of exclusion. Thorough evaluation of symptoms like weight gain, amenorrhea, clinical hyperandrogenism is recommended to rule out serious pathology like prolactinoma. Dual diagnosis of PCOS and macroprolactinoma is rare and should be suspected if menstrual abnormalities persist even after treatment of hyperprolactinemia.
Presentation: Saturday, June 17, 2023
SAT588 Cushing’s Syndrome Due To Ectopic ACTH Secretion From Ovarian Teratomas
Authors: Kang Yu Mi , Gildenberg Melissa S , Quade Bradley J , Blair Rachel A 
Published: October 2023

Abstract
Disclosure: Y. Kang: None. M.S. Gildenberg: None. B.J. Quade: None. R.A. Blair: None.
Background: Approximately 9-18% of Cushing’s syndrome (CS) cases are secondary to ectopic ACTH secretion, most commonly from sources in the lung or mediastinum. However, ACTH-producing tumors are rarely found in distant organs, occasionally making the localization and management challenging. Clinical Case: A 32-year-old woman with class 3 obesity, hidradenitis suppurativa, anxiety, and depression experienced atraumatic pelvic and sacral fractures. DXA scan result showed Z-scores of -3.1 in the lumbar spine, -2.6 in the femur neck, and -0.5 in the total hip. She reported a steady weight-gain of 250 lbs over 7 years despite lifestyle modifications and liraglutide. On examination, she had a round face with plethora, acne, violaceous abdominal striae, and dorsocervical fat pad. Laboratory findings revealed elevated midnight salivary cortisol levels of 453 and 424 ng/dL (n: &lt;100 ng/dL), elevated 24-hour urine cortisol levels of 254 and 741 (n: 3.5-45 mcg), and an abnormal 1 mg dexamethasone suppression test (DST) result at 15.1 ug/dL. AM plasma ACTH and cortisol levels were 190 pg/mL and 18.5 ug/dL, suggesting ACTH-dependent hypercortisolism. The plasma cortisol level after an 8 mg DST was unsuppressed at 13.1 ug/dL with a dexamethasone level of 3,380 ng/dL (n: &gt;800 ng/dL). Abdominal CT and MRI scans showed large bilateral adnexal masses measuring up to 13.7 cm on the left and 9.3 cm on the right, with heterogeneous solid and cystic components, consistent with mature cystic ovarian teratomas. DOTATE-PET scan did not show any areas of increased uptake. The patient underwent a laparoscopic right cystectomy and left oophorectomy, with immediate drop in cortisol (1.6 ug/dL) and signs of adrenal insufficiency post-operatively, requiring hydrocortisone replacement. After holding hydrocortisone for 24 hours prior to laboratory assessment one week post-operatively, her ACTH and cortisol were undetectable, reflecting successful source removal. Pathology report showed neuroendocrine tumor with pituitary differentiation with positive ACTH immunohistochemical staining and Ki-67 proliferative index of 22.6% on the left adnexal mass, and a mature cystic teratoma on the right. Conclusion: Although rare, pituitary differentiation of ovarian teratomas should be considered as a possible source of ectopic ACTH secretion in CS patients without obvious sources identified in commonly involved organs.
Presentation: Saturday, June 17, 2023
SAT600 Absent LH Signaling Rescues The Anxiety Phenotype In Aging Female Mice
Authors: Sims Steven , Barak Orly , Ryu Vitaly , Miyashita Sari , Kannangara Hasni Suhasha , Korkmaz Funda , Macdonald Anne , Gumerova Anisa , Goosens Ki , Zaidi Mone , Yuen Tony , Lizneva Daria , Frolinger Tal 
Published: October 2023

Abstract
Disclosure: S. Sims: None. O. Barak: None. V. Ryu: None. S. Miyashita: None. H.S. Kannangara: None. F. Korkmaz: None. A. Macdonald: None. A. Gumerova: None. K. Goosens: None. M. Zaidi: None. T. Yuen: None. D. Lizneva: None. T. Frolinger: None.
Clinical studies and experimental data together support a role for pituitary gonadotropins, including luteinizing hormone (LH), otherwise considered solely as a fertility hormones, in age-related cognitive decline. Furthermore, rising levels of LH in post-menopausal women have been implicated in the high prevalence of mood disorders. This study was designed to examine the effect of deficient LH signaling, using the global Lhcgr-/- mouse, on both cognitive and emotional behavior in 12-month-old mice. For this, we established and validated a battery of five tests, including Dark-Light Box (DLB), Y-Maze Spontaneous Alternation, Novel Object Recognition (NOR) and contextual and cued Fear Conditioning (FCT) tests. We found that 12-month-old female mice display a prominent anxiety phenotype on DLB and FCT. This phenotype was not seen in female Lhcgr-/- mice, indicating full phenotypic rescue. Furthermore, there was no effect of depleting LHCGRs on recognition memory or working spatial memory on NOR and Y-maze testing, respectively, in 12-month-old mice, notwithstanding the absence of a basal phenotype in wild type littermates. The latter data do not exclude an effect of LH on cognition documented in previous studies. Finally, male mice and 3-month-old male and female mice did not consistently display deficits on any test. The data collectively document, for the first time, that loss of LH signaling reverses age-related emotional disturbances, a prelude to future targeted therapies that block LH action.
Presentation: Saturday, June 17, 2023
SAT602 The Regulation Of Food Intake Via Gastrointestinal Receptors
Authors: Bethea Maigen Michelle , da Silva Teixeira Silvania , Cook Tyler M , Mommandi Marwa , Nault Genna , Sandoval Darleen 
Published: October 2023

Abstract
Disclosure: M.M. Bethea: None. S. da Silva Teixeira: None. T.M. Cook: None. M. Mommandi: None. G. Nault: None. D. Sandoval: None.
Obesity is a global pandemic characterized by excessive fat storage due to an imbalance in energy homeostasis. This metabolic imbalance is driven by increased energy intake relative to energy expenditure. The gut vagal afferent neurons play a critical role in energy homeostasis by sensing the various chemo- and mechano-signals resulting from ingested nutrients and initiating changes in feeding behavior. However, these neurons fail to respond adequately in the context of diet-induced obesity, leading to overeating and ultimately obesity. Bariatric surgeries, which modify the anatomy of the gut, are currently the most effective but also the most invasive treatments for obesity. The mechanism(s) by which bariatric surgery modulates metabolic processes is still not fully understood. The vertical sleeve gastrectomy (VSG) procedure, a bariatric surgery where 80% of the stomach is removed, alters feeding patterns and induces sustained weight loss. Our findings demonstrate that VSG induces alterations in the signals in the gut-brain-axis, resulting in increased activation of the nucleus of the solitary tract (NTS) - a brain region critical for integrating peripheral signals and regulating food intake. Importantly, emerging data demonstrate that neurons that sense intestinal distension play a critical role in the regulation of feeding. We hypothesized that diet induced obesity attenuates intestinal-stretch inhibition of food intake and that VSG restores it. Using non-nutritive substances such as methylcellulose and mannitol to differentiate stomach versus intestinal stretch respectively, we demonstrate that high-fat diet feeding ablates intestinal stretch-induced reductions in food intake while weight loss via dietary intervention, restores this response. More importantly, VSG restores intestinal stretch-induced food intake reduction, suggesting the reactivation of the peripheral neurons that detect intestinal stretch. Taken together, our data provide evidence that VSG alters the signals in the gut-brain-axis by creating an environment where intestinal distension is exaggerated. This effect likely contributes to the sustained weight loss and alterations in feeding patterns observed after VSG. Our findings have important implications for the development of less invasive therapies for obesity that target the gut-brain-axis and feeding behavior.
Presentation: Saturday, June 17, 2023
SAT606 Comparison Of Psychosocial And Immune/Inflammatory Stress On Luteinizing Hormone Pulsatile Secretion
Authors: Jang Jessica , Kreisman Michael J , Breen Church Kellie M 
Published: October 2023

Abstract
Disclosure: J. Jang: None. M.J. Kreisman: None. K.M. Breen Church: None.
Stress induces a physiological response in the body to return to the homeostatic state. It is recognized that many stress types impair reproduction, but the mechanisms conveying inhibition may be distinct and stressor-dependent. Our research aims to understand how stress inhibits the neuroendocrine mechanisms controlling the pulsatile release of luteinizing hormone (LH). This is especially important because pulsatile LH is pivotal to reproductive health in males and females. Immune/inflammatory stressors such as lipopolysaccharides (LPS) cause an inflammatory response, producing peripheral cytokines that can signal to the brain in distinct ways compared to the neural mechanisms employed in response to psychosocial stress. However, how LPS disrupts the neural mechanisms involved in gonadotropin pulsatility is still unknown. Here, we compared the alteration in LH pulses in response to psychosocial restraint stress or immune/inflammatory LPS stress and sought to understand stress-specific regulation of the upstream targets controlling LH synthesis and secretion. Our initial observations demonstrated, in ovariectomized (OVX) female mice, that restraint stress elicited suppression rapidly, within 30 minutes; yet, the response to LPS was delayed, occurring approximately 90 minutes from injection. Therefore, we investigated the prolonged response of the stressors on LH pulses, observing LH pulse profiles 90 minutes to 180 minutes after the initiation of stress. Restraint stress significantly suppressed mean LH, resulting from a suppression of pulse frequency. LPS injected intraperitoneal (IP, 1.5 ug/g) also significantly suppressed mean LH. In contrast to restraint stress, LPS induced a reduction in both frequency as well as LH pulse amplitude. We conducted two follow-up experiments to investigate the lowered LH pulse amplitude during immune/inflammatory stress. The first study assessed hypothalamic kisspeptin gene expression and pituitary LHβ and GnRH receptor expression, in LPS versus restraint animals, to test whether altered gene transcription in LPS animals resulted in lowered LH secretion. The results of this experiment are still pending. The second study tested the LH response to a single bolus of GnRH or kisspeptin. Interestingly, we found equivalent LH increases, to either agonist, in saline versus LPS-treated animals. Collectively, these data indicate that both restraint and immune/inflammatory stress inhibit LH pulse frequency. However, the endogenous LH pulse profiles suggest an additional stressor-specific mechanism that lowers pulsatile LH during immune/inflammatory stress via LPS. Identification of stress pathways that alter endocrine hormones is critical as it allows for the development of therapeutics and medications to treat endocrine disorders.
Presentation: Saturday, June 17, 2023