bluuebunny/crossref_metadata_2025_split huggingface dataset:
8380 Pituitary Stalk Interruption Syndrome, A Rare Cause of Panhypopituitarism
Authors: Abdulkarim Faridat , Alshdifat Esra’a , Feliz Pamela Henriquez , Vargas-Jerez Julia , Zahra Tasneem 
Published: October 2024

Abstract
Disclosure: F. Abdulkarim: None. E. Alshdifat: None. P. Henriquez Feliz: None. J. Vargas-Jerez: None. T. Zahra: None.
Pituitary Stalk Interruption Syndrome, A Rare Cause of Panhypopituitarism Faridat Abdulkarim, MD. Esra’a Alshdifat, MD. Pamela Henriquez Feliz, MD. Julia Vargas- Jerez, MD. and Tasneem Zahra, MD. Introduction: Pituitary stalk interruption syndrome (PSIS) is a rare congenital pituitary anatomical abnormality with reported incidence of 0.5 per 100,000 live births. It is characterized by the triad of thin or interrupted pituitary stalk, absent or ectopic posterior lobe and hypoplastic or aplastic anterior lobe seen on MRI. The anterior pituitary function is usually impaired however the posterior pituitary is usually intact and normal. We report a case of a Now 34-year-old Female who presented to the endocrine clinic with underdeveloped sexual characteristics. MRI done was consistent with PSIS. This is the second case of PSIS we report from our Institution. Case Presentation: A Now 34-year -old Hispanic American Female presented to our endocrine clinic with underdeveloped secondary sexual characteristics. She had panhypopituitarism, including Growth hormone deficiency and was treated with growth hormone from early childhood until age 13-14 years. She re-presented to our clinic at the age of 28 years after being lost to follow up for many years. On physical examination, she was 175cm tall, weighed 89.4kg and BMI 29.1kg/m2Patient has pre-pubertal breast, tanner stage 1, no axillary hair, small external genitalia with scanty pubic hair. Hormonal analysis revealed Estradiol &lt;5 pg/mL (low), FSH 0.4 IU/L (low), LH &lt;0.3 IU/L (low), Progesterone 0.1ng/mL (Low), Testosterone &lt;2.5 ng/dL (8.4- 48.1ng/dl) Prolactin 22.3ng/mL (3.4-24.1 ng/ml), TSH 0.88uIU/mL (0.27-4.20), Free T4 0.5ng/dl (0.9-1.8) , ACTH 7.7pg/mL (7.2-63.3), Baseline AM Cortisol 0.7ug/dL (6.0-18.4) and 5.5 ug/dL after Cosyntropin test, IGF-1 17ng/mL (83-280). Urinalysis revealed normal specific gravity. Chromosome analysis with Normal Karyotype 46XX. Pelvic US revealed Markedly diminutive uterus and ovaries. MRI of the pituitary was highly suggestive of PSIS. She is currently being treated with levothyroxine and hydrocortisone Conclusion: PSIS is a rare congenital abnormality. Fortunately has good prognosis, however if left undiagnosed/untreated has high mortality mainly from Adrenal insufficiency and Myxedema coma. The patient discussed above, has underdeveloped sexual characteristics and primary amenorrheaLaboratory finding consistent with Panhypopituitarism with Normal prolactin which is the case in most patient with PSIS. Imaging revealed atrophic uterus and ovaries, and MRI revealed Findings which are highly suggestive of PSISShe previously had problems with outpatient clinic visits and medication compliance. However, she is currently compliant with hormonal replacement therapy which is the mainstay of treatment.
Presentation: 6/3/2024
7170 Plasticity of the Hypothalamic Tuberoinfundibular Dopaminergic Neuronal Network in Lactating Rats
Authors: Papaioannou P , Georgescu T , Grattan D R , Bunn S , Yip S 
Published: October 2024

Abstract
Disclosure: P. Papaioannou: None. T. Georgescu: None. D.R. Grattan: None. S. Bunn: None. S. Yip: None.
The tuberoinfundibular dopaminergic (TIDA) neurons play a crucial role in regulating prolactin secretion. Their synchronized network activity with slow but highly rhythmic firing pattern is important for dopamine release in rats[1]. While this unique TIDA network activity is vital for prolactin negative feedback in non-lactating conditions, its behaviour during lactation, when prolactin demand is high, remains unknown. Our hypothesis posited that the TIDA neuronal network in lactating rats becomes desynchronized, disrupting the negative feedback loop. To test this, we utilized ex-vivo Ca2+ imaging to simultaneously monitor population-wide TIDA neuron activity in non-lactating (NL; n=13) and lactating (L; n=10) rats injected with a cre-inducible adeno-associated virus (AAV) containing the Ca2+ indicator, GCaMP6s, into their arcuate nucleus. Analysis of neuronal network synchronicity revealed significant desynchronization in the TIDA network during lactation, as indicated by a markedly lower mean correlation coefficient matrix (CM) compared to non-lactating conditions (NL: 0.87±0.02, n= 26 sections vs L: 0.22±0.03, n=29 sections; p&lt;0.001, Student’s t-test). Furthermore, the oscillatory activity patterns of these desynchronized TIDA neurons displayed a significantly lower cell rhythmicity index (RI) in lactating animals compared to non-lactating ones (NL: 0.17±0.01, n=186 cells vs L: 0.70±0.02, n=77 cells; p&lt;0.001, Student’s t-test). Interestingly, within these low rhythmic neurons, some exhibited higher while others showed lower firing frequencies compared to non-lactating TIDA neurons. After 7 days post-weaning (n=4 animals), the TIDA network activity returned to non-lactating behaviour (CM = 0.85 ± 0.04, n=6 sections and RI = 0.17±0.01; n=47 cells). In summary, our findings demonstrate a reversible reconfiguration of the TIDA neuronal networks during lactation, characterized by low rhythmic oscillations and individual unique firing patterns, leading to diminished intercellular synchrony that may impede dopamine release, ultimately facilitating prolactin release to support lactation. Once weaned, the TIDA neuronal network reset to NL state to allow a new reproductive cycle. [1] Lyons, D. J., Horjales-Araujo, E. & Broberger, C. Synchronized network oscillations in rat tuberoinfundibular dopamine neurons: switch to tonic discharge by thyrotropin-releasing hormone. Neuron 65, 217-229, doi:10.1016/j.neuron.2009.12.024 (2010).
Presentation: 6/2/2024
8363 Prevalence and risk factors related to venous thromboembolism events in a large cohort of Cushing disease patients
Authors: Pereira Ana Julia Garcia , Cunha-Neto Malebranche Berardo Carneiro , Batista Rafael Loch , Cescato Valter Angelo Sperling , da Silva Gilberto Ochman , Villares Fragoso Maria Candida Barisson , Glezer Andrea , Machado Marcio Carlos 
Published: October 2024

Abstract
Disclosure: A.J. Pereira: None. M.B. Cunha-Neto: None. V.A. Cescato: None. G.O. Silva: None. M.C. Fragoso: None. A. Glezer: None. M.C. Machado: None.
Background: Cushing’s syndrome (CS) is associated with a hypercoagulation state with an increased risk of venous thromboembolism (VTE) events, regardless of conditions associated with a higher incidence of cardiovascular events. However, the exact risk profile of CS patients who develop VTE events and the prophylactic anticoagulation strategy are heterogeneous in the literature. Objective: To identify the prevalence and risk factors related to VTE events in a large cohort of Cushing’s disease (CD) patients. Patients and Methods: A single-tertiary referral center retrospective study was conducted. Four hundred and eight confirmed CD patients were included, 79% female, median age of 32 years (ranged of 8-71), 73% harbored microadenomas (n=298), evaluated between 1990 to 2022. Most CD patients were submitted to pituitary surgery as the first treatment option. Detailed retrospective data analyses of medical records (physical and electronic) were used to identify and describe the VTE events (VTE group). Numerous clinical, hormonal, radiological and post-surgical parameters were evaluated in VTE group and compared to CD patients without events. Data from both groups were compared using a multivariate logistic regression study aiming to identify the risk profile of VTE events. As a control group, 323 patients with clinically non-functioning pituitary adenomas (NFPA) were evaluated, 51.1% male, median age of 53 years, all with pituitary macroadenomas, submitted to pituitary surgery in the same conditions and Institution. Results: Thirty-five VTE events (8.6%), mainly deep vein thrombosis (60%), were found in CD patients in comparison to only one VTE event in NFPA patient (0.3%). Most events occurred in the preoperative period (54%) and in a hypercortisolism state (71%). After statistical analysis, higher risk factors for VTE events were associated with age &gt;24 years-old, obesity, filling of supraclavicular fossae, purple striae, mood disorders, serum morning cortisol &gt;40 μg/dL, urinary cortisol &gt;3,500 μg/24-h, and in a presence of postoperative complications (cerebrospinal fluid fistula, transient diabetes insipidus, infections). Conclusions: Active Cushing’s disease was associated with a higher rate of VTE events compared to the NFPA control group, especially in those cases with severe hypercortisolism, older patients and with post-surgical complications. In this profile of cases, a prophylactic anticoagulation can be instituted to reduce the morbid mortality.
Presentation: 6/3/2024
8221 Rare and Debilitating Endocrine Complications Post Craniopharyngioma Resection in a 29-year-old Male
Authors: Sargin Pinar , Montoya Jacqueline 
Published: October 2024

Abstract
Disclosure: P. Sargin: None. J. Montoya: None.
Several complications have been reported during the postoperative phase following craniopharyngioma resection, with electrolyte disturbances and hormonal imbalances as two of the most common during the early postoperative period. Central diabetes insipidus (DI) occurs commonly in these patients. In rare cases, patients lose their thirst response to hyperosmolarity, resulting in adipsic diabetes insipidus (ADI). Patients with ADI may develop permanent DI that is often difficult to manage even with proper treatment, leading to multiple hospitalizations, numerous comorbidities including severe hypernatremia and deep vein thrombosis (DVT), high morbidity and mortality. Panhypopituitarism is another common post-operative complication of any suprasellar mass. It is associated with multiple systemic, often life-threatening comorbidities; some are poorly understood. The intricate interplay of hormones in the pituitary gland and their diverse effects on various body systems has hindered our complete comprehension of their synergistic effects and the resulting complications. An otherwise healthy 29-year-old man with craniopharyngioma underwent resection 4 months ago at another facility. His postoperative course was complicated with central DI and panhypopituitarism and he was discharged with desmopressin, levothyroxine, and steroids. He also had a pacemaker placed due to unexplained sick sinus syndrome (SSS) that developed following surgery. He was admitted with lethargy and altered mental status, then was diagnosed with hypovolemic shock in the setting of DI with possible contributing adrenal insufficiency. Laboratory work-up showed hypernatremia (156mEq/L), thrombocytopenia (92k/uL), and macrocytic anemia (7.0g/dL) with normal coagulation factors. Further studies showed extensive occlusive DVT in both legs. A comprehensive work-up was unable to identify the source of cytopenias. After appropriate management, he was discharged home in stable condition. Two weeks later, he presented for the third time with unresponsiveness and worsening severe hypernatremia (170mEq/L). Per the family, he was refusing to drink anything at home. During this admission, the hospital course was prolonged with widely fluctuating Na levels. The diagnosis was concluded as ADI. Eventually, his Na level stabilized, family was educated on adequate water intake. In this complex case with multiple comorbidities, we are highlighting the relationship between panhypopituitarism and its association with SSS and cytopenias with no other identifiable cause. Although it is difficult to prove the causation in our case, some case reports have reported the association between ADI and DVT. The case presented highlights the complex challenges in managing these complications, emphasizing the need for comprehensive care and continuous patient education to mitigate potential adverse outcomes.
Presentation: 6/1/2024
6553 Remission of Cushing’s Disease on Day 6 Post Transsphenoidal Surgery
Authors: Abdou M N , Alhumaidi H 
Published: October 2024

Abstract
Disclosure: M.N. Abdou: None. H. Alhumaidi: None.
Background: Current recommendations for steroids replacement in the immediate post-operative (post op) period after transsphenoidal surgery (TSS) for patients with Cushing’s Disease (CD) are heterogenous and can be misleading. Monitoring daily morning cortisol for 72 hours post TSS with replacing steroids only after detecting low morning cortisol or signs of adrenal insufficiency (AI) has been mentioned in several studies. While some studies recommend either empiric steroids replacement on discharge regardless of status of remission or longer hospital stay for closer cortisol monitoring, others recommended monitoring for 3-4 days and starting steroids on discharge only if morning cortisol was &lt; 415 nmol/L. Case: 60 years old female with a history of type 2 diabetes mellitus, hypertension and dyslipidemia was referred for an evaluation of a pituitary macroadenoma. She had an incidental finding of a pituitary mass measuring 25 mm on a CT brain obtained after a fall 3 months prior to her current visit. MRI pituitary gland revealed a 25x23x22 mm suprasellar mass with cavernous sinus invasion. She reported weight gain and worsening of diabetes control over the 2 years prior to her presentation. On exam, weight was 80 kg, BMI 32.5, BP 110/69, vital signs were otherwise normal. She had central obesity, facial plethora, and frontal hair thinning. Hormonal workup showed elevated 1 mg dexamethasone suppression test: 341 nmol/L (&lt;55). 24h UFC was also high 233 nmol/24 hours (38-208). Morning cortisol 15.5 mcg/dl (6-18) with ACTH 228 pg/ml (7.2-63.3). Prolactin 581 mIU/L (58-418). FSH and LH were at the premenopausal range. TSH, FT4, and IGF-1 were normal. HBA1C 8%. Results were consistent with CD with central hypogonadism and mild elevation of prolactin likely due to stalk effect. Patient was admitted to the hospital for TSS. She had no surgical complications, and no steroids were used to monitor remission. Daily morning cortisol was measured after the surgery, readings were (1631, 668, 469, 224, 318, 110 nmol/l) day 1-6 (D1-D6) post op. She was started on oral Hydrocortisone (HC) 15 mg in the morning and 10 mg in the afternoon on D6 post op after documentation of cortisol level of 110 nmol/l. She was vitally stable and had no signs of AI before starting steroids. 1 day after starting oral HC she developed hypotension and hyponatremia. IV HC 100 mg was given immediately followed by 50 mg every 6 hours. Blood pressure improved with stress dose steroids. She was discharged home on HC 20 mg three times daily, tapered to reach 15, 10 over a period of 2 weeks. Conclusion: We present a case of CD that had a nadir morning cortisol on D6 post op in whom a diagnosis of fatal AI would have been missed if recommendations from some studies were followed. This case highlights the importance of prolonged monitoring for adrenal insufficiency if steroids were not used after surgery for CD.
Presentation: 6/1/2024
8412 Resolution of Central Hypothyroidism shortly after Transsphenoidal Surgery For Cushing’s Disease
Authors: Esper L , Ibrahim A , El Asmar N 
Published: October 2024

Abstract
Disclosure: L. Esper: None. A. Ibrahim: None. N. El Asmar: None.
Background: Cushing's disease is a rare endocrine disorder characterized by excessive cortisol production, resulting in various metabolic disturbances. Hypercortisolism is known to cause central hypothyroidism. The mechanism is complex and involves hypercortisolism mediated decreased TRH and TSH secretion in addition to inhibition of peripheral deiodination. This case details the successful management and recovery of a patient with Cushing's disease and reversal of central hypothyroidism after pituitary surgery.Case:A 43-year-old man was evaluated for central hypogonadism, 20 pound weight gain with central weight distribution, and the development of purple abdominal striae for the past year. He had a normal thyroid exam and appeared euthyroid. He was alsodiagnosed with hypertension and prediabetes in the past yearrequiring medical therapy.A low dose dexamethasone suppression test (DST) resulted in AM cortisol of 12.9 mcg/dl. Two adequate 24hr Urinary cortisol measurements showed elevated cortisol excretion at 458 and 378mcg/24. Lab evaluation revealed elevated cortisol levels along with elevated adrenocorticotropic hormone (ACTH) levels(ACTH of 172 pg/ml with a cortisol level of 23.9 mcg/dl). A high dose DST demonstrated suppression of cortisol to 3.4 mcg/dl. MRI pituitary was performed which showed a clearright sided 7mm pituitary adenoma.Thyroid function tests performed were consistent with central hypothyroidism, with low levels of free thyroxine (FT4) at 0.67ng/dl along with an inappropriately low normal thyroidstimulating hormone (TSH) at 0.596 uIU/ml. Total T4 was low at 4 ug/dl in addition to a low total T3 of 66 ng/dl. Remaining labs revealed central hypogonadism along with slightly elevated prolactin of 16 ng/ml. He was not started on thyroid hormone.He then underwent transsphenoidal surgery for tumor removal. He developed post-operative adrenal insufficiency (cortisol 2.12 mcg/dl) 16 hours post-op after which he was started on hydrocortisone replacement, indicating remission. 12 hours post-op, his TSH was 0.656 uIU/ml with a free t4 of 0.79 ng/dl, both in the normal range. 36 hours post-op, TSH was 0.524 uIU/ml and free t4 was 1.15 ng/dl. Histopathological examination confirmed the diagnosis of an ACTH-secreting pituitary adenoma.At 4 weeks post-op, thyroid labs showed normal FT4 (1.07ng/dl) and TSH (2.06uIU/ml). Conclusion: Hypercortisolism causes a global inhibition of the thyroid axis, with decreased levels of TSH, T4, and T3 (1). Previous studies suggest the monitoring of thyroid function at 6 and 12 months after surgical cure of hypercortisolism. Our case suggests that the resolution of hypothyroidism occurs shortly after surgery for Cushing’s disease and the need for earlier monitoring.
Presentation: 6/3/2024
8533 Salt on the Kidneys A case of DDAVP induced arginine vasopressin resistance
Authors: Jordan M M , Islam J R , Hassan R 
Published: October 2024

Abstract
Disclosure: M.M. Jordan: None. J.R. Islam: None. R. Hassan: None.
A 63-year old female with a history of head trauma complicated by polyuria and excessive fatigue diagnosed with central DI and started on treatment with oral Desmopressin. She had no other known pertinent medical history. Patient was lost to follow-up with an eventual visit to the emergency department with complaints of bilateral leg cramps, nausea and persistent headaches. She was noted to have been initiated intranasal desmopressin in addition to oral DDAVP. On initial lab work, Sodium was 114 along with acute kidney injury. She was admitted to ICU and treated with hypertonic saline. DDAVP was withheld until sodium normalized and stabilization of renal functions. GFR still remained impaired on discharge at 40 mL/min/1.73m*2. She was then discharged on DDAVP with reestablished follow up in the endocrinology clinic with complaints of persistent polyuria. Once more, she was sent to the emergency room and was admitted for acute renal injury secondary to dehydration in the setting of polyuria and altered mentation. Upon review of her medications, the patient continued both oral and inhaled DDAVP. No other medications or supplements were reported. During this subsequent hospitalization, sodium remained between 131-135 with urine output 4.5L/ day despite increasing doses of oral DDAVP and oral sodium supplementation. At which point, suspicion for mixed DI was hypothesized (central DI and arginine vasopressin resistance). Other causes of polyuria were ruled out. Labs for persistent AKI revealed gross proteinuria. Renal biopsy was performed during hospitalization which showed acute to chronic vascular thrombotic microangiopathy and focal segmental glomerulosclerosis with collapsing features. Extensive workup for chronic infections, autoimmune conditions and hematological malignancies were negative. This showed concerns for possible DDAVP induced renal injury.
Presentation: 6/2/2024
8686 scRNA-seq of pituitary from letrozole-induced PCOS mouse model reveals abnormal prolactin secretion
Authors: De Robles G , Ujagar N , Del Mundo Z , Nicholas D 
Published: October 2024

Abstract
Disclosure: G. De Robles: None. N. Ujagar: None. Z. Del Mundo: None. D. Nicholas: None.
Polycystic ovary syndrome (PCOS) has a complex pathophysiology and is the most common endocrine disorder among reproductive-aged women. Ovarian hormonal dynamics are regulated via the secretion of the gonadotropin-releasing hormone (GnRH), which stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary gland. High serum levels of LH in PCOS patients indicate an increase in GnRH levels, but the mechanisms within the anterior pituitary at a cellular level are unclear. We performed single-cell mRNA sequencing (scRNA-seq) on the pituitaries of the letrozole-induced (LET) mouse model of PCOS to profile the functional genomics of endocrine cell populations relative to serum hormone levels. The population percentage of lactotropes significantly decreased; in contrast, two gonadotrope populations significantly increased in the LET mice compared to the placebo-treated mice. Consistent with these changes, an increasing trend of serum LH levels and a decreasing trend of serum prolactin (PRL) levels were observed in the LET mice, while no change occurred in serum growth hormone levels. A gene set enrichment analysis (GSEA) on the differentially expressed genes (DEGs) from the lactotropes revealed an association with negative regulation of protein kinase activity. These DEGs included Hspb1, Park7, Pcp4, and Ppia, which all share the function of mediating stress-induced apoptosis. A GSEA on the DEGs between the two gonadotrope clusters in the LET mice also confirmed a variation in biological pathways linked to ribosomal subunits, transcription regulation, and the regulation of steroid metabolic processes. Based on the scRNA-seq results of the anterior pituitaries of LET mice, alterations in the proportions of hormone-secreting cells may be a response to hyperandrogenism, in which functionally diverse gonadotropes could contribute to heterogeneity in reproductive phenotypes. Changes in the lactotrope population and PRL serum levels also support further research on the lactation hormone and its role in PCOS. PRL is involved in metabolic homeostasis and reproduction, and understanding its dysregulations may provide additional insight into the pathophysiology of PCOS.
Presentation: 6/3/2024
6622 Severe Primary Hypothyroidism in a Child Presented as a Pituitary Tumour; a case Report
Authors: Awadalla S S 
Published: October 2024

Abstract
Disclosure: S.S. Awadalla: None.
A 9-year-old patient showed up to the emergency department due to a headache that had been going on for a month without other symptoms and no neurological alterations. Complete blood count and glycemia were normal. A Cerebral MRI was requested and showed a pituitary adenoma. The patient was initially evaluated by neurosurgeons and referred to a pediatric endocrinologist. TSH, free T4, IGFI, and cortisol were evaluated, TSH was found to be high at 936 (normal, 0.4-4.2), free T4 &lt; 0.4; suggestive of severe primary hypothyroidism. The case was analysed with the neurosurgery department, and a joint decision to start therapy with LT4 was taken, whilst monitoring the evolution of the pituitary adenoma. TSH and Free T4 were normal, and the MRI of Sella Turcica three months later showed complete pituitary normality. The presentation of this case is of relevance as the primary modality of treatment is thyroid hormone supply and not surgery. Interprofessional team integration is recommended for the treatment of patients with this condition.
Presentation: 6/1/2024