bluuebunny/crossref_metadata_2025_split huggingface dataset:
8278 Myxedema Coma With COVID-19 Infection
Authors: Kalas R , Manohar V , Bapat N S , Kim Y 
Published: October 2024

Abstract
Disclosure: R. Kalas: None. V. Manohar: None. N.S. Bapat: None. Y. Kim: None.
Myxedema coma is a rare medical emergency that occurs in severe hypothyroidism with a mortality rate reaching 60%. The hallmarks include depressed mental status and hypothermia, but hypotension, hyponatremia, bradycardia, and hypoventilation can also occur. This complication can occur in patients with a longstanding history of severe hypothyroidism especially when precipitated by an acute event such as infection, myocardial infarction, or surgery. Prompt recognition and treatment of the condition is important to prevent fatal outcomes. We present a case of myxedema coma in the setting of COVID-19 infection and nonadherence to medication. A 91-year-old woman with history of hypothyroidism, hypertension, coronary artery disease, cardiomyopathy, and chronic obstructive pulmonary disease presented with dyspnea. Her home medications included levothyroxine 75 mcg daily, which she reported not taking for at least 3 weeks. Vital signs revealed a normal heart rate and blood pressure of 84 beats/min and 137/78 mmHg, but the patient was hypothermic to 35.7 °C. On exam, she was somnolent. Labs were notable for markedly elevated TSH level of 111 (0.380 - 4.700 uIU/mL), low free T4 level of 0.57 (0.93 - 1.70 ng/dL), random cortisol level of 25.5 (6.2-18.4 ug/dL), and positive SARS-COV-2 PCR test. Chest x-ray revealed bilateral lower lung parenchymal consolidations and arterial blood gas revealed a pH of 7.29 and pCO2 of 52.5 (35-45 mm Hg), indicating hypercapnia. She was treated for COVID pneumonia and given concern for COVID induced myxedema coma she was given IV levothyroxine 100 mcg for 2 days, after which the patient’s hypothermia and somnolence improved, with an improved repeat free T4 level 0.87 ng/dL. She was subsequently transitioned to oral levothyroxine 112 mcg daily and discharged after improvement of her COVID symptoms. Myxedema coma is a rare complication of decompensated hypothyroidism, frequently triggered by an infection. Thyroid hormone plays an important role in regulating both the innate and adaptive immune systems. As a result, individuals with hypothyroidism are at increased risk of acquiring infections, which can further lead to myxedema coma. COVID-19 infection has been associated with thyrotoxicosis, thyroiditis and hypothyroidism. Given the associated high mortality rate, regardless of the underlying precipitant, prompt diagnosis and early administration of thyroid hormone replacement therapy is crucial to improve outcomes.
Presentation: 6/3/2024
6855 Nationwide Analysis Of Mentorship In Endocrinology Fellowship
Authors: Toro-Tobon David , Billings Heather , Bancos Irina 
Published: October 2024

Abstract
Disclosure: D. Toro-Tobon: None. H. Billings: None. I. Bancos: None.
Background: Mentorship is crucial for training physicians' career development, yet evidence of its impact on endocrinology trainees is lacking. We assessed the current state of mentorship in endocrine fellowship training in the United States. Methods: We conducted a cross-sectional study between June and September 2023. Endocrine fellows were invited to complete an online questionnaire describing their mentorship experience and its influence on burnout, satisfaction, and scholarly productivity. Results: Of 153 participants (mean age 34, 69% women, 47% White, 20% Hispanic/Latino), 73% had a mentor. Having a mentor was not associated with age, gender identity, race, or ethnicity. Those without mentors were more commonly in two-year fellowships (63% vs. 81%, p=0.04), had less access to formal mentorship programs (48% vs. 21%, p&lt;0.01), cited insufficient faculty availability for mentoring (11% vs. 26%, p=0.01), and encountered more challenges finding mentors in their training programs (11% vs. 38%, p&lt;0.001). Mentored participants exhibited increased post-fellowship interest in academic practice (69% vs. 50%, p&lt;0.01), higher involvement in clinical research (65% vs. 49%, p=0.01), more fellowship-dedicated scholarly time (36% vs. 22%, &lt;0.001), a greater median number of publications (4.6 vs. 1.8, p&lt;0.01) and abstracts (7 vs. 3.7, p&lt;0.01), were more likely to have submitted a grant (29% vs. 5%, p=0.03) and had higher satisfaction with training (92% vs. 64%, p&lt;0.001). Mentors were mostly chosen by mentees (70%) and shared gender identity (61%) but often had a different race or ethnicity (71.8%). The majority found mentorship relationships satisfactory (87%), contributing to increased academic productivity (84%) and reduced mentee burnout and stress levels (60%). In bivariate analysis, all mentor attributes significantly influenced higher academic productivity and mentee satisfaction. The most divergent for academic productivity were improved communication, alignment with expectations, inspiration for goal attainment, and effective networking. For mentorship satisfaction, distinctions were found in communication enhancement, goal-oriented assistance, knowledge/skill enrichment, and personalized career path development. Traits like active listening and adapting communication styles were not linked to decreased burnout, but actively supporting work-life balance independently correlated with reduced burnout. Conclusion: Mentorship positively affects endocrine fellows' scholarly productivity and career development. Yet, a significant number lack mentors or access to programs. Mentor attributes, like effective communication, goal alignment, and networking support boost productivity and satisfaction. However, reducing mentee burnout hinges on actively fostering work-life balance.
Presentation: 6/3/2024
7715 A Case of Cerebral Infarction Resulting From Pituitary Apoplexy
Authors: Jenkins William Evan , Elmaaz Ahmed , Makdissi Antoine 
Published: October 2024

Abstract
Disclosure: W.E. Jenkins: None. A. Elmaaz: None. A. Makdissi: None.
Background: Acute cerebral infarction as a sequela of pituitary adenoma and apoplexy is a rare phenomenon with poor outcomes. The mechanism is typically direct mechanical compression of the internal carotid artery secondary to hemorrhage. There is a very small number of reported cases of non-hemorrhagic compression. We report a case of a pituitary adenoma causing tandem internal carotid-middle cerebral artery occlusion with resultant infarction, most likely due to non-hemorrhagic pituitary apoplexy. Clinical Case: A 76-year-old male with hypertension and type II diabetes mellitus presented to the emergency department with a sudden onset severe headache, left facial droop, and left-sided weakness. CT stroke study revealed a right-sided cavernous ICA occlusion and a tandem MCA occlusion with a large sellar mass extending into the right sphenoid and cavernous sinus. Ophthalmologic evaluation revealed right pupillary dilation and ophthalmoplegia concerning for orbital apex syndrome. Emergent thrombectomy, angioplasty, and stenting of the occlusion in the supraclinoid segment of the ICA were performed, and treatment with dual antiplatelet therapy was initiated. MRI confirmed a large 25x20x20 mm right paramedian sellar/suprasellar mass with encasement of the ICA, however there was no evidence of sellar hemorrhage. Given recent stenting and the patient's hemodynamic stability, the neurosurgical team opted for delayed surgical intervention. The patient was discharged with marked improvement in left-sided weakness, although his right pupil remained minimally reactive with visual perception only to light. Based on biochemical evaluation, the mass was deemed non-functional, as prolactin and IGF-1 were within normal limits. There was evidence of secondary hypothyroidism and hypogonadism. Transsphenoidal surgery was pursued, occurring 114 days from symptom presentation. Histopathology revealed foci of devitalized anterior pituitary consistent with infarction of a pituitary adenoma. He was started on IV hydrocortisone on the day of surgery and tapered to a daily replacement dose. Visual acuity in the right eye remained severely reduced after the operation. Conclusion: Our case displays that, while extremely rare, clinicians should be aware that pituitary adenomas can result in cerebral infarction secondary to mechanical compression of the internal carotid artery, typically caused by an apoplexy event, hemorrhagic or ischemic. Emergent medical and endovascular treatment of the infarction should take precedence, and if clinical stability allows, a delayed surgical approach to resect the pituitary mass may be appropriate.
Presentation: 6/2/2024
7518 A Case of Delayed Diagnosis of Acromegaly Associated with Uncontrolled Diabetes
Authors: Mahmoudabadi A , Patel S 
Published: October 2024

Abstract
Disclosure: A. Mahmoudabadi: None. S. Patel: None.
Background: Acromegaly is a rare disorder characterized by an excess secretion of growth hormone (GH) and increased circulating insulin-like growth factor 1 (IGF-1) levels, typically due to a GH-secreting pituitary adenoma. This consequently leads to complications such as acral and soft tissue overgrowth, visual disturbance, insulin resistance, and dyslipidemia. In this case, we describe a patient who presented to the endocrinology clinic for uncontrolled diabetes and was subsequently diagnosed with acromegaly. Clinical Case: This is a 47-year-old male with a history of heart failure, hypertension, and type 2 diabetes mellitus (DM) who presented to the clinic with uncontrolled DM. He had failed to achieve adequate blood sugar control despite being compliant with metformin, dapagliflozin, and insulin degludec. Physical examination revealed frontal bossing, prognathism, macroglossia, and a deep voice. On further questioning, he had noticed these changes since five years prior. Anthropometry and laboratory tests were as follows: Height, 180 cm; body weight 107.5 kg; body mass index (BMI), 33.05 kg/m2 and A1c level of 15.0%. Suspicion of acromegaly was confirmed based on biochemical and imaging findings. Fasting growth hormone (GH), at 58 mU/L (reference range 0-10), and insulin-like growth factor 1 (IGF-1), at 857 nmol/L (reference range 81-263), were markedly elevated. Pituitary magnetic resonance imaging (MRI) showed a sellar and suprasellar mass (2.6 × 2.2 × 2.2 cm) extending and compressing the optic chiasm. He eventually underwent a transsphenoidal adenomectomy with neurosurgery. Following surgery, his insulin requirements went from a total daily dose of about 100 units to an inpatient dose of 30 units by his last day of admission. Conclusion: Acromegaly is prevalent in less than 3% of patients with DM, but higher rates of DM are seen in acromegalic patients with higher IGF-1 levels and longer duration of disease. The diagnosis of acromegaly can often be delayed due to missed findings on routine physical examination. This can lead to increased morbidity, mortality, and complications such as uncontrolled DM, witnessed in our patient. Surgical management of acromegaly is the mainstay of treatment and can lead to improvement of glycemic control and insulin sensitivity. Fortunately, our patient could undergo surgery, but delayed diagnosis can prevent patients from surgery if the pituitary tumor becomes too large or unresectable. Ultimately, this case highlights the importance of a thorough physical examination and keeping a wide differential diagnosis when evaluating patients with uncontrolled DM, as failure to diagnose acromegaly at an early stage may have devastating consequences on patient outcomes.
Presentation: 6/3/2024
8774 An Uncommon Presentation Of A Large Silent Pheochromocytoma
Authors: Lozano M , Pinero-Pilona A 
Published: October 2024

Abstract
Disclosure: M. Lozano: None. A. Pinero-Pilona: None.
Background: The reported estimated incidence of pheochromocytoma is approximately 2-8 cases per 1 million people per year. Of those, silent pheochromocytomas will make up about 8%. Thus, biochemically silent and non-secreting pheochromocytomas are a very rare phenomenon. Clinical Case: A 74-year-old Caucasian female with significant past medical history of primary hypothyroidism, hypercholesterolemia, and nasal sinus carcinoma s/p surgery (in remission) presented to the clinic for endocrine evaluation of a right adrenal mass. The patient was asymptomatic and denied headaches, tachycardia, sweating, severe hypertension, diabetes, muscle weakness, easy bruising, or striae. The mass was initially diagnosed as an incidental finding after a contrast CT scan of the abdomen was performed for diverticulitis. The right adrenal enhancing mass was 2.3 x 3.9 x 4.1 cm in diameter. Subsequent MRI abdomen with and without contrast ordered by the referring physician showed that the adrenal mass had grown to 4.9 x 3.8 x 5.4 cm and was hyperenhancing in nature with central T2 hyperintense signal. Notably, multiple “parasitized and arborealized” vessels were detected within the mass. Such findings led us to suspect metastatic versus primary adrenal neoplasm such as cortical carcinoma as a working diagnosis. Other laboratory studies including plasma free metanephrines (&lt;10 pg/mL, normal 0-88 pg/mL), plasma normetanephrines (29.2 pg/mL, normal 0-285.2 pg/mL) and 24-hour urine collections (24 hr urine epinephrine - 3 ug/24 hr [normal 0-20 ug/24 hr]; 24 hr urine norepinephrine - 75 ug/24 hr [normal 0-135 ug/24 hr]; 24 hr urine VMA - 3 mg/24 hr [normal 0-7.5 mg/24 hr]) were negative for pheochromocytoma. As her mass was greater than 4 cm in diameter, surgical referral was then recommended to the patient. Right adrenalectomy was performed. Pathology report was consistent with pheochromocytoma as supported by immunohistochemistry. Ki-67 proliferation index was 0-10% (average 3-4%, rare hotspots 10%). Atrophy and vascular ectasia were present in residual non-neoplastic adrenal cortex and medulla. Histology showed a nested growth pattern, absence of composite tumor elements, absence of necrosis, and no atypical mitoses. The incidence of non-secreting pheochromocytomas has been quoted to be 0.000064% (1). Conclusion: The case illustrates an uncommon presentation of a large, silent pheochromocytoma with negative plasma metanephrines accompanied by negative urine studies, which have a negative predictive value close to 100% in ruling out a pheochromocytoma. Our case emphasizes the importance of considering pheochromocytoma on the differential of adrenal masses with high attenuation or high enhancement even when biochemical studies suggest otherwise. Reference: (1) Radojkovic, D., et al. "CLINICALLY" SILENT GIANT PHEOCHROMOCYTOMA. CASE REPORT." Acta Endocrinologica (1841-0987) 9.1 (2013).
Presentation: 6/1/2024
7743 A Case Study of Ectopic Adrenocorticotropic Hormone Secretion from Pancreatic Neuroendocrine Tumor
Authors: Wei K S , Huang J 
Published: October 2024

Abstract
Disclosure: K.S. Wei: None. J. Huang: None.
Introduction: Pancreatic neuroendocrine tumors (PanNETs) are uncommon cancers that account for less than 2% of pancreatic malignancies. Even rarer are ACTH-producing NETs which may only become symptomatic until after metastasis. This case study examines the distinct presentation and diagnostic complexities associated with ectopic adrenocorticotropic hormone (ACTH) secretion from a PanNET. Clinical Case:A 42 year-old male with hypertension and type 2 diabetes initially presented to the hospital with increased abdominal girth for one month, bilateral lower extremity edema for two weeks, and generalized abdominal pain. He had unremarkable surgical, family, and social histories. Patient was afebrile, normotensive, saturating well on room air, with exam notable for a distended abdomen and 2+ bilateral pitting edema. Admission labs were notable for potassium of 2.4 (ref: 3.5-5.1 mmol/L). MRI abdomen showed hepatomegaly with numerous heterogeneously enhancing masses and an ill-defined pancreatic tail mass with involvement of the spleen. Liver biopsy showed well-differentiated neuroendocrine tumor, grade 2. He was started on octreotide 20mg q4weeks and capecitabine/temozolomide q4weeks. Two months later, the patient was readmitted after presenting with back pain for two days, found to have acute compression fractures of T9-L1 without spinal PET activity. At follow-up visit with endocrinology, he endorsed easy bruising and muscle weakness and had hypertension (161/96 mmHg) with hypokalemia. Random cortisol was 43.7 (ref: 2.5-11.9 mcg/dL). ACTH was 124 (ref: 6-50 pg/mL) despite receiving chemotherapy. 24-hour urine cortisol was 3,049 (ref: 4-50 mcg/24 hrs). He was diagnosed with ectopic Cushing’s disease from ACTH-producing PanNET leading to osteoporosis and fracture of the vertebral bodies. For the ectopic Cushing’s disease, he was started on ketoconazole 200mg BID with plan to start osilodrostat once approved. For the fracture, he is scheduled for Zometa infusion and IR kyphoplasty. Conclusion: This case offers several important clinical insights. In patients with PanNET with Cushingoid exam findings, ACTH-producing PanNET should be high on the differential. Most ACTH NETs are aggressive often with liver metastases, whereby metastatic disease will have already occurred by the time the Cushingoid features develop. The initial severe hypokalemia and hypertension should have prompted investigation for mineralocorticoid excess from hypercortisolism, which may have led to an earlier diagnosis of ectopic ACTH Cushing’s disease, thereby decreasing the possibility of developing vertebral fractures, uncontrolled diabetes and hypertension. Ketoconazole or osilodrostat may be used to treat Cushing’s disease from ACTH NETs.
Presentation: 6/1/2024
7025 Acute Psychosis and the Diagnosis of Cushing’s Syndrome: Lessons Learned from a Patient with a Long History of Obesity
Authors: Modi Saman , Maria Belalcazar L 
Published: October 2024

Abstract
Disclosure: S. Modi: None. L. Belalcazar: None.
Background: Although the association of hypercortisolism and psychosis is well established, acute psychosis remains a very rare manifestation of Cushing’s syndrome, especially in the absence of previous psychiatric history. We present lessons learned from a patient in whom the diagnosis of Cushing’s syndrome was missed until the onset of acute psychosis helped identify his underlying endocrine disorder. Clinical Case: A 31-year-old male presented to the Emergency Department after being found down on the street. The patient had superficial lacerations that were suspected to be self-inflicted due to a suicide attempt, but later found to be the result of auditory hallucinations. He had no previous psychiatric history and no history of suicidal ideation. His medical history was positive for obesity since adolescence and a recent diagnosis of hypertension. His family noted that for the past several months he had been experiencing headache, fatigue, muscle weakness and, more recently, insomnia, restlessness, and confusion. Weight gain was noted, but of unknown magnitude. On admission, he was agitated and hallucinating. He was initially sedated with dexmedetomidine and started on quetiapine. Physical examination revealed Cushingoid features with truncal obesity (body mass index of 35 kg/m2), facial plethora, and dorsocervical fat pad; no abdominal striae were present. Labs showed mild hypokalemia. His AM cortisol was markedly elevated at &gt; 123 ug/dL (normal 4.5-23.0 ug/dL) with an ACTH level at 144 pg/mL (normal 7.2-63.3 pg/mL). MRI Brain showed a 1.9 cm pituitary macroadenoma with small suprasellar extension. With a diagnosis of Cushing’s disease, later confirmed by pathology, he underwent transsphenoidal resection. AM cortisol on post-operative day 3 was 3.2 ug/dL (normal 4.5-23.0 ug/dL). Maintenance-dose steroids were started due to evidence of post-surgical corticotroph suppression. Notably, there was marked improvement in his anxiety, paranoia, and confusion post-operatively. Quetiapine and blood pressure medications were discontinued after discharge. Conclusion: In this patient, the diagnosis of Cushing’s syndrome was missed when initially presenting with new onset hypertension in the setting of long-standing obesity. Despite months of symptoms compatible with the diagnosis, it was not until he developed acute psychosis and a careful history was obtained, that the diagnosis of Cushing’s syndrome was entertained. Psychosis is present in only 3-8% of reported cases of Cushing’s syndrome. This case illustrates the importance of including Cushing’s syndrome in the differential diagnosis of acute psychosis, especially in patients without previous psychiatric history. It also highlights the need of excluding secondary causes of hypertension in young adults, with particular attention to Cushing’s syndrome in those who present with obesity, even if long-standing.
Presentation: 6/1/2024
12224 Addressing Blood Glucose Fluctuations and Fasting Challenges in Sheehan Syndrome: A Case Study
Authors: Awadalla Huyam Awadalla Hassan , Kiani Amna Nadeem , Taha Wael , Solanki Naisargee Nilesh , Lattouf Ali , Shermetaro Angela , Taweel Adrianna 
Published: October 2024

Abstract
Disclosure: H.A. Awadalla: None. A.N. Kiani: None. W. Taha: None. N.N. Solanki: None. A. Lattouf: None. A. Shermetaro: None. A. Taweel: None.
Introduction: Sheehan's syndrome (SS) is a rare condition characterized by hypopituitarism resultingfrom ischemic necrosis of the pituitary gland due to severe postpartum hemorrhage.Patients may have hormonal insuﬃciencies, ranging from single pituitary hormoneinsuﬃciency to total hypopituitarism. The diagnosis of SS is often delayed due to itsnonspeciﬁc signs and symptoms, leading to many undiagnosed and untreated cases. Case Presentation:A 33-year-old African American female with a history of panhypopituitarism secondaryto Sheehan Syndrome presented with syncope, lightheadedness, and severehypoglycemia (blood glucose 12mg/dL). Despite regular food intake, she struggled withglycemic control, experiencing recurrent hypoglycemic episodes associated withnausea, vomiting, unintentional weight loss (25kg), and polydipsia/polyuria. Laboratoryﬁndings revealed low ACTH, sodium, cortisol, and elevated liver enzymes, consistentwith hypopituitarism. Cosyntropin stimulation test conﬁrmed adrenal insuﬃciency. MRIshowed an empty sella. Initially treated with high-dose hydrocortisone, then transitionedto lower maintenance doses, she continued to experience glycemic ﬂuctuations.Intravenous dextrose and insulin sliding scale were initiated. Upon discharge, she wasprescribed hydrocortisone and levothyroxine. Despite adjustments, hypoglycemiapersisted, managed with dietary modiﬁcations. This case underscores the challenges inmanaging Sheehan Syndrome-associated panhypopituitarism and the need for tailoredtreatment approaches to achieve metabolic stability. Conclusion: This case underscores the complexities of managing panhypopituitarism secondary toSheehan syndrome, emphasizing the importance of comprehensive hormonalreplacement therapy and thorough monitoring to achieve symptom control andmetabolic stability. Tailored treatment regimens and continuous assessments arecrucial to addressing individual hormone deﬁciencies and preventing associatedcomplications effectively in these patients.
Presentation: 6/1/2024