AM Cortisol Research Articles

Abstract #1408202: A Case of Rathke's Cleft Cyst with Multiple Associated Endocrinopathies

Rathke Cysts are cystic sellar or suprasellar lesions deriving from the remnants of Rathke’s pouch. During fetal development, Rathke’s pouch migrates from the oral ectoderm to what eventually develops as the sellar region. The pharyngohypophyseal stalk connecting Rathke’s pouch to the stomodeum is obliterated by growth of the sphenoid bone. Inadequate obliteration of the pharyngohypohyseal stalk results in formation of the rathke cyst. While most cases of Rathke cyst are asymptomatic, they may present with headache, vision loss, pituitary hormone deficiency, and diabetes insipidus. We present the case of a 44-year-old female with a history of cerebral palsy, secondary amenorrhea beginning at age 30, and blindness who presented to the hospital with generalized weakness and altered mental status. The degree and nature of visual impairment could not be assessed in the inpatient setting due to the patient’s altered mental status. She was found to have a urinary tract infection and was started on antibiotic therapy. Hospital course was complicated by hypotension refractory to fluid resuscitation. Further workup demonstrated low AM cortisol responsive to cosyntropin stimulation, and hypotension resolved with IV scheduled hydrocortisone. Pituitary lab follow-up demonstrated low estradiol with inappropriately normal gonadotropin levels, low Free T4 with inappropriately normal TSH, low IGF-1, and normal prolactin. MRI revealed a 2.4x1.7x2.2cm suprasellar mass consistent with Rathke cyst, with obliteration of the optic chiasm, pituitary parenchyma, and infundibulum. The patient’s adrenal insufficiency, panhypopituitarism, blindness, and amenorrhea were likely caused by mass effect on the optic chiasm and pituitary gland. Secondary adrenal insufficiency was managed with physiologic hydrocortisone dosage and secondary hypothyroidism was managed with oral levothyroxine. Outpatient neurosurgical intervention was recommended for cyst resection. This case represents a rare, symptomatic presentation of a Rathke cyst with vision loss and multiple endocrinopathies. Visual symptoms, which may include visual field defects, decreased visual acuity or oculomotor palsies, arise from mass effect on the optic chiasm or cavernous sinus. For these patients, surgical resection may recover visual function or prevent irreversible vision loss. Rathke cyst may also present with hypopituitarism. Restoration of pituitary function following resection is less common than resolution of visual symptoms. In patients presenting with visual disturbances, adrenal insufficiency, and hypopituitarism, a diagnosis of symptomatic Rathke cyst or other sellar mass should be considered.

Abstract #1401368: Does A Male Sheehan’s Like Syndrome Exist?

Panhypopituitarism is defined as a condition in which secretion of most or all hormones from the pituitary gland is inadequate or absent. Deficiency of pituitary hormones such as Adrenocorticotropic Hormone (ACTH) and Thyroid Stimulating Hormone (TSH) impairs the ability of the adrenal glands and thyroid gland to secrete hormones that are vital for survival. Hypopituitarism is a rare condition, and its incidence is approximately 4.2 per 100,000 per year. Sheehan syndrome is a form of pituitary necrosis secondary to infarction in setting of severe postpartum hemorrhage. Hemorrhagic pituitary apoplexy of pre-existing pituitary adenomas in setting of hypotension has been reported. We describe a unique case of hypopituitarism in a man without known pituitary adenoma after liver transplantation. A 48-year-old male underwent liver transplantation for cirrhosis. A few years after the transplant the patient developed dizziness, lightheadedness, polyuria, polydipsia, decreased libido, loss of muscle mass and fatigue. Post transplant he was on maintenance dose of Prednisone which was discontinued several years after the surgery. Testosterone replacement therapy with testosterone gel for fatigue was initiated by primary care provider, and he was referred to endocrinology for further evaluation. Hormonal profile revealed TSH 0.724 mcIU/mL (0.450-4.500), free T4 1.13 ng/dL (0.82-1.77), AM cortisol 5.2 mcg/dL (6.2-19.4), ACTH stimulated cortisol 11.4 mcg/dL after 30 min, 14.8 mcg/dL after 90 min, morning total testosterone 104.8 ng/dL (264-916), free testosterone 4.1 pg/mL (6.8-21.5), prolactin 2.1 ng/mL (4.0-15.2), LH 1.2 mIU/mL (1.7-8.6), IGF-1 26 ng/mL (75-216), FSH 1.6 mIU/mL (1.5-12.4), ACTH 19.6 pg/mL (7.2-63.3). Sodium was 143 mmol/L with urine osmolality 1135 mOsm/kg after overnight water deprivation so DI was successfully ruled out. An MRI of the brain demonstrated a very small pituitary gland within a small pituitary fossa. This was a significant change compared to the MRI performed soon after transplantation - it was unremarkable with normal sella and parasellar structures. The findings of empty sella on MRI and blood work consistent with hypogonadism, central adrenal insufficiency, hypoprolactinemia and growth hormone deficiency indicated a diagnosis of panhypopituitarism. Since ACTH stimulation test demonstrated partial adrenal insufficiency Hydrocortisone 20 mg daily was initiated. Patient was switched from gel to injectable testosterone with significant improvement in testosterone concentration. During a follow up visit patient reported feeling better but still endorsed fatigue and tiredness. Trial of growth hormone therapy resulted in resolution of his symptoms and improved wellbeing. This case describes a unique presentation of hypopituitarism after major surgery in a patient with intact pituitary gland possibly secondary to hypotension during surgery and the pathophysiology may be analogous to Sheehan syndrome. Early diagnosis of hypopituitarism is crucial as deficiency in ACTH and TSH can cause adrenal insufficiency and hypothyroidism, respectively, which could be life-threatening.

Abstract #1398468: Lymphocytic Hypophysitis Successfully Treated with Prednisone

Lymphocytic Hypophysitis is an inflammatory disorder of the pituitary gland that has classically been described in pregnant and postpartum women. It is the most common type of Primary Hypophysitis which refers to inflammation of the pituitary gland that is not secondary to other systemic diseases or drugs. This is a rare group of disorders with an estimated annual incidence of 2.4 in 10 million. We present the case of a young woman diagnosed with Lymphocytic Hypophysitis and successfully treated with prednisone. A 27-year-old previously healthy female presented with daily headaches and fatigue that began 4 months after an uncomplicated vaginal delivery. She was amenorrheic despite cessation of breast milk production. Physical exam was within normal limits. Laboratory evaluation revealed an AM cortisol of 1 mg/dl (4-22), Free T4 of 0.4 ng/dL (0.8-1.8), LH of 0.5 mIU/mL (1.9-12.5), and estrogen of 30 pg/ml (12.5-166, follicular), consistent with adrenal insufficiency, hypothyroidism, and hypogonadism. Prolactin was normal. She had no evidence of Diabetes Insipidus. MRI pituitary with and without contrast revealed an intensely and homogenously enhancing sellar mass measuring 2 x 2 x 1.3 cm with suprasellar extension and mass effect on the optic chiasm. She did not have any abnormalities in her visual fields or acuity. Lymphocytic Hypophysitis was felt to be the most likely diagnosis based on her clinical presentation and imaging features. Via shared decision-making, she was started on 40 mg of oral prednisone daily in addition to levothyroxine and oral combined contraceptive pills. On reevaluation 2 months later, her symptoms improved and a repeat MRI revealed a dramatic improvement in the appearance of the lesion following which prednisone was reduced to 30 mg with a plan for revaluation after 2 more months. Lymphocytic Hypophysitis should always be suspected in pregnant and postpartum women with neurological complaints of headaches or visual abnormalities and pituitary hormonal deficiency. The investigation involves obtaining an anterior pituitary hormonal profile including TSH with free T4, ACTH with cortisol, FSH, LH, estradiol, and prolactin. Serum sodium with plasma and urine osmolality can be used to evaluate diabetes insipidus in suspected cases. MRI pituitary with and without contrast frequently reveals a symmetric sellar lesion that enhances intensely and homogeneously with gadolinium. A pituitary adenoma, in contrast, enhances less than the normal pituitary tissue. A tool based on clinical and radiological features called the Gutenberg score can also aid in differentiating lymphocytic hypophysitis from an adenoma. Treatment involves management of hormonal deficiencies including Diabetes Insipidus and relief of symptoms of mass effect. Glucocorticoids can induce remission and possible recovery of hormonal function. Follow-up with serial imaging in a few months after initiation of glucocorticoids is essential. Diagnosis needs to be reconsidered if there is no improvement in the appearance of the lesion and a pituitary biopsy may be indicated.

Abstract #1413579: Rathke Cleft Cyst Unveiling Incidental Prolactin Producing Adenoma

Rathke cleft cysts (RCCs) are benign sellar and or/suprasellar lesions that arise from remnants of Rathke's pouch. Pituitary hormonal dysfunction associated with RCCs most often present as hormonal deficiencies due to compression. However pituitary hyper-secretion may coexist with RCC challenging diagnosis and management. A 37-year-old female presented with worsening headache, bilateral blurry vision and pressure-like eye pain for two weeks. She denied any galactorrhea or irregular periods. Her medications included as-needed butalbital-acetaminophen-caffeine and alprazolam. CT Head without IV contrast revealed a pituitary lesion measuring 1.9 cm extending near the inferior margin of the optic chiasm. Subsequent MRI Pituitary with and without IV contrast revealed an enhancing sellar/suprasellar solid lesion measuring 1.6 x 2.7 x 1.9 cm with small hypoenhancing components associated with expansion of the sella, rightward infundibulum deviation, mass effect on the optic chiasm and left cavernous sinus invasion. Pituitary secretion workup revealed an elevated serum prolactin level of 50.4 ng/mL (range 4.8 - 23.3 ng/mL). Repeat prolactin level was 75.7 mg/ml. Dilution studies 1:10 and 1:100 revealed prolactin levels of 78.3 ng/mL and 75.9 ng/mL respectively; absence of hook effect. Her elevated prolactin was attributed to stalk effect given the large size of her sellar mass and relatively minimally elevated prolactin level. Serum Alpha Subunit, ILGF-1, TSH, FT4, LF, FSH, AM cortisol and ACTH level were all normal. She underwent endoscopic transsphenoidal pituitary mass resection with pathology results revealing prolactin producing adenoma and RCC. Immunostains were strongly positive for chromogranin A and prolactin while negative for FSH, ACTH, TSH, beta hCG, GH. Prolactin levels 11 days post-resection remained elevated at 50.7 ng/mL. She continued to have regular periods without galactorrhea. Additionally, she expressed desire to attain pregnancy. This case illustrates the presence of a secreting pituitary prolactinoma in the setting of an RCC. Whether these two entities share a common pathophysiology or simply co-exist is unknown. In one study of 33 surgically treated RCC at presentation, 60% had gonadotroph deficiency, 36% had ACTH deficiency, 36% had TSH deficiency, 18% had ADH deficiency and 31% had hyperprolactinemia (1). It is possible that the majority of this patient 's sellar mass was comprised of RCC as a much higher prolactin level would have been expect for the size of her mass. Interesting, her sellar mass exhibited enhancement which is uncharacteristic for RCC, classical described as cystic lesions without calcification or enhancement. Given that her post-resection prolactin level remained elevated and she desires pregnancy, she may require dopamine agonist therapy.

PMON125 A Case of Hypothalamic Lipoma Causing Hyperprolactinemia in a Patient With Family History of Birt-Hogg-Dubé Syndrome

Abstract A 41year old female with a medical history significant for depression presented for evaluation of bilateral nipple discharge for 5 months. The patient reported that for the last 5 months she started noticing expressible nipple discharge. She reported no associated headaches, vision changes. She denied the use of vitamins, supplements, herbal remedies. No associated fatigue, changes in the shoe/ring size, heat/cold intolerance, tremors, recent weight changes. She denied neck enlargement, neck pain, dysphagia. The patient reported her menstrual cycles had always been heavy and irregular (every 33-50 days). She has never been pregnant. She has been on Sertraline for the last 4 years with no recent dose changes. Family history was significant for Birt-Hogg-Dubé (BHD) syndrome in father, brother, and sister. The patient has not been tested yet. Initial blood test revealed TSH 1.180 uiu/ml (0.45-4.5 uiu/ml), free T4 1.15 ng/dl (0.82- 1.77 ng/dl), T3 91ng/dl (71-180 ng/dl), FSH 3.8 mIU/ml, LH 3.7 mIU/ml, IGF-1 83 ng/ml (74-239 ng/ml), prolactin 107 ng/ml (4.79-23.3 ng/ml), monomeric prolactin 75.7 ng/ml, macroprolactin 23%, estradiol 16 pg/ml, AM Cortisol 6.5 ug/dl (6.2-19.4ug/dl). The urine pregnancy test was negative. Given low normal AM cortisol, a Cosyntropin stimulation test was done, which was normal. MRI Pituitary with contrast showed flattening of pituitary contour compatible with a partially empty sella turcica and an 8 mm fat intensity in hypothalamic region compatible with a lipoma, stable since last 4 years. The patient was referred to Neurosurgery for further evaluation. The patient remained asymptomatic and medical therapy was not indicated. Genetic testing for BHD was discussed. The patient will be followed in the clinic with a follow-up of prolactin levels and imaging as needed. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

RF13 | PMON83 Culture Negative Pituitary Abscesses: A Case Series

Abstract Introduction Pituitary abscesses are rare, representing less than 1% of pituitary lesions. Patients may present with pituitary hypofunction, headache, and/or vision changes, often without systemic or biochemical signs of infection, with diagnosis only made intraoperatively. Cases A 74-year-old man with history of diabetes and coronary artery disease presented with headache and left-eye ptosis. MRI revealed a 1.8 cm hypoenhancing cystic, hemorrhagic sellar mass extending into the left cavernous sinus. Pre-operative labs showed AM cortisol 1.1 ug/dL, testosterone 43 ng/dL (reference range 250-1100), FSH 15.3 mIU/mL, LH 4.5 mIU/mL consistent with adrenal insufficiency and hypogonadism. He underwent transsphenoidal pituitary resection (TSR) during which frank pus was demonstrated after incision into the dura overlying the pituitary. Surgical pathology showed necrosis and granulation-type reaction with acute inflammatory cell infiltrates. Gram stain and methenamine silver stains did not reveal definite micro-organisms while tissue bacterial cultures showed normal skin flora. He remained hemodynamically stable without fevers throughout the hospitalization and was discharged on empiric antibiotics and hydrocortisone. A 74-year-old female with history of a pituitary macroadenoma was admitted for worsening headaches. Labs were consistent with her known history of secondary adrenal insufficiency and hypogonadotropic hypogonadism. Repeat MRI showed characteristics suggestive of hemorrhage within a 1.8 cm intrasellar mass with inhomogeneous and peripheral enhancement after contrast. She underwent TSR and intraoperatively frank pus was encountered. Surgical pathology showed sinonasal mucosa with chronic inflammation. There was no growth in aerobic, fungal, or AFB cultures; anaerobic cultures grew rare commensal bacteria. She was discharged with a course of antibiotics and remains on hydrocortisone. A 42-year-old male presented with headache and was found to have a 2.5 cm sellar mass with rim enhancement elevating and compressing the optic chiasm on MRI. Labs were significant for AM cortisol 4.9 ug/dL and testosterone 8 ng/dL, FSH 0.4 mIU/mL, LH <0.2 mIU/mL consistent with adrenal insufficiency and hypogonadism. He underwent TSR and was found to have purulent debris in the sella. Pathology showed epithelial tissue fragments insufficient for diagnosis, and cultures grew few skin and oropharyngeal contaminants. He was discharged on hydrocortisone with a course of antibiotics. Conclusion We describe three patient cases presenting with headache and varying degrees of hypopituitarism, found to have purulent material emanating from the sella during transsphenoidal resection. None presented with clinical or biochemical systemic signs of infection. MRI imaging was variable, ranging from cystic, hemorrhagic features to peripheral enhancement. Surgical pathology and cultures were unrevealing for a definitive infectious source or other cystic lesion such as Rathke's cleft cyst. This case series demonstrates the potential nonspecific presentation of pituitary abscesses including negative cultures and pathology. It is important to keep this rare diagnosis in the differential for patients presenting with pituitary disease. Presentation: Sunday, June 12, 2022 12:30 p.m. - 12:35 p.m., Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

ODP284 Hyperinsulinism-Hyperammonaemia syndrome: a dive into the rare presentation and diagnostic challenges encountered in adults

Abstract Background Hyperinsulinemic-hyperammonemia, a rare form of congenital hyperinsulinemia, can seldom present in adulthood if failed to be diagnosed during infancy, enabling it to be difficult to identify, and predisposing affected individuals to neurological complications. Case A 20-year-old female with intellectual disability, seizure disorder and ornithine transcarbamylase deficiency was admitted for recurrent episodes of asymptomatic hypoglycemia. Her medications included risperidone, fluoxetine, levetiracetam, lacosamide, ferrous sulphate and acetaminophen. Physical examination including vital signs was unremarkable. Relevant labs included a fasting glucose of 46mg/dl [70-99]. Further work up of hypoglycemia revealed an IGF-1 of 215ng/dl [85-350] and AM Cortisol of 6.5mcg/dl [5-25]. Given a low AM cortisol level under stress, an ACTH stimulation test was done with appropriate response of cortisol of 24 following cosyntropin administration, ruling out adrenal insufficiency. The patient continued to have h ypoglycemia noted on several glucometer checks every 4 hours where she remained asymptomatic. She was further evaluated with a mixed meal study where no hypoglycemia was noted. A 72 -hour fast was performed which was terminated based on a venous blood sample glucose reading of 50 mg/dl confirmed after hypoglycemia was noted on a glucometer check. The labs showed elevated C-peptide levels of 4ng/ml [0.4-2], insulin of 4mIU/L [<25] and proinsulin level of 2.3pmol/l [3-20]. Levels of insulin and proinsulin were noted to be inappropriately normal in the setting of hypoglycemia. Beta hydroxybutyrate was low at 0.1mmol/L [<0.5] and glucagon inappropriately normal at 36pg/ml [50-100]. Sulfonylurea, meglitinide and autoimmune antibody screen were negative. CT abdomen and pelvis was negative for pancreatic abnormality. In the absence of evidence for acquired causes of hyperinsulinemic hypoglycemia, congenital cases were investigated. Based on that, further labs were obtained including ammonia levels which was elevated at 177.2 u/dl [15-45]. Accordingly, GLUD-1 gene mutation was sent, given high suspicion for hyperinsulinemic hyperammonemia syndrome, which resulted positive and confirmed the diagnosis. She was started on a protein restricted diet and diazoxide which regulated her blood glucose levels effectively. Discussion Hyperinsulinism/hyperammonemia (HI/HA) syndrome is a form of congenital hyperinsulinism caused by activating mutations of the GLUD 1 gene which encodes Glutamate Dehydrogenase, a key enzyme in the beta cell pathway of amino acid-stimulated insulin secretion. The resultant syndrome is characterized by fasting and protein induced hypoglycemia, elevated serum ammonia levels without typical hyperammonemic symptoms. Management includes effective blood glucose control with an insulin inhibitor such as diazoxide and a protein restricted diet with consideration to predominantly include carbohydrates and fat. Conclusion Hyperinsulinemia hyperammonemia is a rare form of congenital hyperinsulinemia typically diagnosed during infancy and should be considered as a possible differential diagnosis in patients presenting with new onset hypoglycemia, as timely diagnosis and intervention can prevent forthcoming neurological complications. Presentation: No date and time listed

RF25 | PMON76 Kissing carotid arteries: An unusual cause of male hypogonadotropic hypogonadism.

Abstract Background Aneurysms of the internal carotid arteries are a rare cause of pituitary dysfunction1. While there are reports of primary amenorrhea in females due to ectatic internal carotid arteries2, hypogonadism in a male due to "kissing internal carotid arteries" causing compression of the pituitary gland has not previously been reported. Clinical Case A 27-year-old male with history of Crohn's disease, obesity, depression and sleep apnea on CPAP presented to endocrinology clinic for evaluation of low testosterone levels diagnosed 9 months prior to his initial visit. At the time of initial evaluation patient was using intramuscular testosterone cypionate 120mg weekly with total testosterone of 2.43 ng/mL (2.50-9.50 ng/mL). Testosterone replacement therapy was discontinued at that time to assess the hypothalamic-pituitary-gonadal (HPG) axis. After 9 months without testosterone treatment, repeat labs demonstrated total testosterone 0.91 ng/mL, bioavailable testosterone 0.69 ng/mL (1.10-4.0 ng/mL), SHBG 8 nmol/L (10-89 nmol/L), LH 3.1 mIU/mL (2-12 mIU/mL), FSH 2.7 mIU/mL (1.5-10 mIU/mL), estradiol 23 pg/mL (6-44 pg/mL), IGF-1 193 ng/mL (85-310 ng/mL), prolactin 10 ng/mL (3-23 ng/mL), TSH 1.03 mIU/L (0.3-5.5 mIU/L), FT4 1.15 ng/dL (0.76-1.70 ng/dL), 8 AM cortisol 13.5 ug/dL (5.3-22.5 ug/dL) and ACTH 37 pg/mL (5-52 pg/mL). Semen analysis was also performed which was unremarkable. Pituitary MRI revealed symmetric ectatic cavernous portions of the internal carotid arteries compressing and distorting the normal anatomy of the anterior pituitary gland consistent with "kissing carotid arteries." MRA was performed which did not demonstrate aneurysm or malformation of the cavernous internal carotid arteries. Patient was started on subcutaneous semaglutide 0.25mg weekly which was titrated to 1mg weekly for treatment of obesity. Testosterone replacement therapy was not re-initiated given future fertility goals and normal semen analysis. Conclusion To our knowledge, this is the first reported case of kissing internal carotid arteries causing isolated hypogonadotropic hypogonadism in a male patient. References 1) Heshmati HM, Fatourechi V, Dagam SA, Piepgras DG. Hypopituitarism caused by intrasellar aneurysms. Mayo Clin Proc. 2001 Aug;76(8): 789-93. doi: 10.1016/S0025-6196(11)63222-9. PMID: 11499817 2) Sahin M, Dilli A, Karbek B, Unsal IO, Gungunes A, Colak N, Uçan B, Cakal E, Ozbek M, Delibasi T. Unusual cause of primary amenorrhea due to kissing internal carotid arteries. Pituitary. 2012 Jun;15(2): 258-9. doi: 10.1007/s11102-012-0393-9. PMID: 22492265. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 12:44 p.m. - 12:49 p.m.

PMON100 IgG4 hypophysitis with granulomatous histopathology

Abstract Background IgG4-related disease is characterized by a dense lymphoplasmacytic infiltrate rich in IgG4 plasma cells that may be accompanied by elevated serum IgG4 levels, presence of granulomatous histopathology with multinucleated giant cells has not been reported in patients with IgG4 related hypophysitis.Clinical case: A 39-year-old female with no significant past medical history until April of 2021, when she developed gradual onset of headaches. MRI brain showed a mass in the sella, she was treated for over a month with glucocorticoids by ENT and her headaches improved. She finished the course of glucocorticoids, and soon after, she had a recurrence of her symptoms. Repeat brain MRI revealed a large pituitary mass and she had her first endoscopic endonasal transsphenoidal resection on 8/2021 at an outside hospital. Pathology report of the surgery suggested that she had a colloid cyst of the pituitary and cultures grew actinomyces and streptococcus oralis, likely, as a consequence of contamination from an ethmoid sinus infection/surgical infection, she was treated with antibiotics. Surgery was also complicated by diabetes insipidus for which she is taking desmopressin tablets.She presented to our hospital in November 2021, with persistent symptoms (headaches and worsening vision), and a postoperative brain MRI showing an expansion of the lesion with compression of the optic chiasm, she was evaluated by neurosurgery who recommended repeat revision endoscopic endonasal transsphenoidal resection of this lesion.The patient underwent a second transsphenoidal surgery on 11/29/2021 at our institution. During admission TSH was 0.123 mcIU/ml (0.27-4.2mcIU/ml) with Free T4 0.52ng/dL (0.93-1.7ng/dL). She was discharged on hydrocortisone, desmopressin tablets, and levothyroxine.The pathology report of the second surgery revealed mixed chronic and acute inflammation with granulomatous components containing histiocytic clusters and multinucleated giant cells. Many plasma cells, rare eosinophils, and foci of neutrophils are present. The ratio of IgG4 to IgG is over 70%, with more than 10 IgG4 (+) cells per 10HPF. GMS and AFB were negative for fungi and mycobacteria.Patient's outpatient labs were consistent with panhypopituitarism with AM cortisol of 1.9mcg/dL, ACTH 19pg/mL (6-50 pg/ml), FSH 6.5 mIU/ml, LH 2.4 mIU/ml and estradiol <15pg/ml. TSH was 1.26 mcIU/ml (0.27-4.2mcIU/ml) with Free T4 0.8ng/dL (0.8-1.8ng/dL). IGF-1 level was 72ng/ml (79-259ng/ml). Prolactin was 7.0 ng/ml (3.0-30.0ng/ml). IgG4 serum level was 100.2mg/dL (4.0-86.0mg/dL), IgG1 serum level was 446mg/dL (382-929mg/dL). Conclusion This is a unique patient with panhypopituitarism that meets the criteria for IgG4 related hypophysitis but also has secondary granulomatous components developed after the rupture of the colloid cyst during the first surgery. The implications of these findings are unknown in terms of management and prognosis. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

PSUN282 Sertraline-Induced Hypoglycemia in a Non-Diabetic Patient

Abstract Background Sertraline is one of selective serotonin reuptake inhibitors (SSRIs) commonly prescribed for depression. Irrespective of diabetes status, SSRIs can cause glycemic dysregulation. Clinical Case 74-year-old man with depression was evaluated for hypoglycemia. His depression was managed with sertraline for more than 10 years. He did not have diabetes. Non fasting, laboratory studies done during annual evaluation showed blood glucose of 29 mg/dL but he didn't have any symptom of hunger, sweating, shaking or dizziness. Lab report was initially considered to be an error. Repeat blood glucose was 102 mg/dl. Subsequent labs done 6 months later also reported blood glucose of 27mg/dl. He suffered from a bicycle accident with head laceration in May 2021, his blood glucose on presentation to ED was 38 mg/dL). Follow up labs showed a fasting glucose 86 mg/dL, insulin level 4.2 IU/ml (1.9-23. 0 IU/ml), c-peptide 1.3 ng/ml (0.8-3.5 ng/ml), AM cortisol 22.6 mcg/dL (6.7-22.6 mcg/dl) and hemoglobin A1C 5.3%. Thyroid function test was normal. Sertraline was discontinued and he was on continuous glucose monitoring for 6 months during which there were no hypoglycemic episodes. The exact mechanism of sertraline-induced hypoglycemia remains unclear. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

LBODP011 Pembrolizumab Induced Hypophysitis And Resultant Isolated ACTH Deficiency Presenting As Secondary Adrenal Insufficiency.

Abstract Introduction Pembrolizumab is a novel human immunotherapeutic monoclonal antibody directed against PD-1 (programmed death receptor 1). It has been approved by the FDA for treatment of many malignancies including breast cancer. Although it has improved survival for many oncological conditions, it has been linked to a variety of endocrinopathies. We present a case of Pembrolizumab induced hypophysitis with isolated ACTH deficiency presenting as secondary adrenal insufficiency. Case presentation A 36 year old female with a history of breast cancer treated with chemotherapy and surgery, presented with intractable nausea and vomiting. She reported not being able to keep anything down for 4-5 days and had experienced multiple episodes of non-bilious, non-bloody emesis. She endorsed dizziness, but denied fever, chills, shortness of breath, abdominal pain, or problems with urination/bowel movements. She had been treated with Pembrolizumab with the last dose being 4 months prior to presentation. On arrival, vitals included temperature 98.4 F, BP 104/62 mm Hg, Heart rate 104 bpm, RR 16 with SpO2 100%. Labs were significant for WBC count 3.65 K/uL (3.81 - 8.94), Eosinophils 10.4% (0.1 - 6; she was noted to have eosinophilia prior to presentation), Hemoglobin 11.6 g/dL (11 - 14.9), Sodium 140 mmol/L (136-145), Potassium 3.4 mmol/L (3.4 - 5.1), Glucose 57 mg/dL (70 - 100), Lactate 0.7 mmol/L (0.2 -2), Lipase 23 U/L (13 - 60), Urine HCG negative, Urinalysis negative for nitrites and leukocyte esterase, TSH 1.22 uIU. ml (0.5 -5.7) and AM cortisol 0.4 ug/dL (6 - 18.4). Endocrinology was consulted and further work up was sought: ACTH <5 pg/ml (7.2 - 63) and Cortisol 30 - 60 minutes after cosyntropin stimulation 3.6 ug/dL. Prolactin, free T4, FSH and LH were within normal limits. MRI brain showed a prominent pituitary gland with enhancement and interval loss of posterior pituitary bright spot representing lymphocytic hypophysitis. She was started on Solu-Cortef and her symptoms resolved. She was discharged on hydrocortisone with education on sick day rules for secondary adrenal insufficiency. Discussion Adrenal insufficiency secondary to immunotherapy is a rare, emergent and dangerous condition. The key to successful management is early recognition. In patients treated with immunotherapy agents, non-specific symptoms such as nausea, vomiting, fatigue (which are common adverse effects of chemotherapy) should prompt urgent evaluation with hormonal workup. Evidence suggests that eosinophilia may be an early indicator before the onset of symptoms which was evident in our case. Radio-graphic imaging is helpful for diagnosis. Treatment entails high dose corticosteroids for acute crisis followed by physiological maintenance dosing. Patients should be educated on sick day rules for adrenal insufficiency. Presentation: No date and time listed

PMON324 Crooke Cell Corticotroph Adenoma: A rare but Real Possibility in Children

Abstract Background Cushing disease (CD) is uncommon in the pediatric population and is usually caused by benign pituitary corticotroph microadenomas. In some adults with CD, Crooke cell adenoma (CCA), a more aggressive histologic variant of corticotroph adenomas, has been described. CCA has rarely been reported in children as the etiology of CD and its course is not well described. Objectives To report a pediatric case of CCA, the youngest to our knowledge Case An 11-year-old African American female presented to the endocrinology clinic with concerns for diabetes, excessive weight gain and linear growth arrest. Workup for possible etiology showed: midnight salivary cortisol 0.924 (normal < 0.112 µg/dL), ACTH 119(6-48 pg/mL), morning cortisol 8.5 (normal < 1.8 µg/dL) post 1 mg dexamethasone mg/dL, consistent with the diagnosis of CD. Magnetic resonance imaging (MRI) showed a 4 mm pituitary microadenoma in the left anterior side of the adenohypophysis for which she underwent endoscopic endonasal transsphenoidal resection. Histopathologic examination revealed pituitary adenomatous tissue consisting of a uniform population of basophilic cells with granular cytoplasm, arranged in trabeculae and small nests with bundles encircling the nuclei, findings pathognomonic of CCA. Given persistence of hypercortisolemia, another transsphenoidal gross total resection of residual adenomatous tissue was performed 4 months later. This led to resolution of CD as evidenced by weight loss and linear growth. Twelve months following the second surgery, the patient experienced rapid weight gain and a decelerated linear growth accompanied by pubertal arrest. Another pituitary MRI showed a recurrent left sided adenoma (8×8×7 mm). Biochemical investigation this time again showed elevated midnight salivary cortisol and 24- hour urine free cortisol (UFC). In addition, AM cortisol was unsuppressed following 1 mg overnight dexamethasone administration. In response, repeat transsphenoidal gross total resection was performed, however residual microscopic disease in the cavernous sinus wall was highly suspected intraoperatively. A spine MRI did not show disseminated disease. Despite this, hypercortisolemia persisted both clinically and biochemically. The patient subsequently underwent proton beam radiation therapy in combination with adjuvant adrenolytic therapy with mitotane. The patient responded to these interventions with normalization of 24-hour UFC, resumption of linear growth, and pubertal progression. The treatment course was complicated by the development of isolated TSH deficiency requiring thyroid hormone replacement. Conclusion CCA is an aggressive entity described in the adult literature as a cause of CD. The current report adds to the limited pediatric cases of this disease. CCA can be equally aggressive in children and refractory to surgical treatment. Here, we show that it may respond to proton beam radiation and adrenolytic therapy. Pediatric endocrinologists should be aware of the rare occurrence of CCA in children and tailor treatment accordingly using a multi-disciplinary approach. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

PMON18 A Case of Hypophysitis and Hyperthyroidism Following COVID-19 Vaccine in a Patient Receiving Immune-Checkpoint Inhibitor Therapy

Abstract Introduction Immune Checkpoint inhibitors (ICI) have been associated with multiple endocrinopathies including hypothyroidism, hyperthyroidism, primary and secondary adrenal insufficiency, hypophysitis and type 1 diabetes. Unlike other adverse effects from ICI, endocrinopathies tend to be irreversible. There are limited reports on the interaction of Covid-19 vaccine in patients receiving ICI for cancer treatment. Clinical Case A 56 year old man with history of non-small cell lung cancer presents to the hospital with nausea, decreased appetite, fatigue and 30lb unintentional weight loss. He had been started on immunotherapy with pembrolizumab 4 months prior to symptom onset (total of 4 doses). His symptoms began the day after he received his first Covid-19 vaccine injection. At an outside hospital, his initial work up showed TSH of 0.02mcU/mL, free T3 of 8.3pg/mL and free T4 of 2.8ng/dL. Thyroid stimulating immunoglobulin (TSI) was negative and he did not undergo thyroid uptake scan due to recent contrast load for CT abdomen imaging. Patient was diagnosed with hyperthyroidism and started on methimazole 10mg daily. He presented to our hospital after two weeks at his oncologist's recommendation due to worsening symptoms and concern for failure to thrive. On admission, he was noted to have hypotension and tachycardia. Given the severity of his symptoms, we obtained an AM cortisol and ACTH. His baseline cortisol was 1.2mcg/dL, so he underwent a cosyntropin stimulation test. Patient was diagnosed with adrenal insufficiency given his subnormal response on cosyntropin stimulation test. He was treated with intravenous hydrocortisone 50mg every 8 hours and methimazole 20mg daily with dramatic clinical improvement within 24 hours. ACTH obtained prior to initiation of steroids subsequently resulted as undetectably low. Further hormonal work up including LH, FSH and IGF-1 were in the normal range with mildly elevated prolactin. MRI pituitary demonstrated a 4mm hypo-attenuation in the posterior pituitary. Discussion Thyroid dysfunction is the most common adverse effect occurring in up to 30% of patients on ICI. Although less common, hypophysitis has been documented in 0.6-3.2% of patients on ICI depending on the drug. Many patients present only with adrenal insufficiency especially in those treated with pembrolizumab. Additionally, not all cases will present with radiographic findings of enhancement or inflammation of the pituitary gland. We describe a patient who developed acute symptoms of hyperthyroidism and adrenal insufficiency within 24 hours of receiving his Covid vaccine. We hypothesize that the vaccination may have triggered ICI-induced hypophysitis and hyperthyroidism in our patient. Resolution is yet to be determined. Conclusion Hypopituitarism and hyperthyroidism can be life-threatening if undiagnosed and untreated. Patients on ICI should be closely monitored for adrenal insufficiency and other endocrinopathies after receiving Covid-19 vaccine. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

ODP631 Infectious Disease Causing Damage Of The Adrenal Glands, A Life Threating Event

Abstract Introduction Primary Adrenal Insufficiency (PAI) is not a common cause of adrenal insufficiency. The most common cause is Addison disease that is an autoimmune condition. Other causes include hemorrhage, infiltration, infections, necrosis and metastasis. We present a rare case of primary adrenal insufficiency caused by disseminated histoplasmosis. Case presentation 87 yo male from the Midwest with a history of HTN, HLD, CAD s/p CABG was admitted to our hospital for fatigue and 15 lbs weight loss. In the ED, he was found to have persistent hypoglycemia (BG in the 50s mg/dl after several vials of D50%). He was admitted to ICU for continuous D10% infusion. His laboratory showed Na 137mmol/L, K 3.7mmol/L. Further work up for hypoglycemia showed BG of 53 mg/dl with C-peptide of 0.92ng/ml and Insulin <1uIU/ml. Due to the concern of non-insulin dependent hypoglycemia, AM cortisol was done which was low7ug/dl. Immediately, he was started on high dose hydrocortisone. Head CT was negative for pituitary lesions. CT showed lung nodules and bilateral peripherally calcified adrenal lesions 3.6 & 2.6 cm homogenous, well defined borders (HU 20-30). Adrenal hormones work up showed normal metanephrines, Aldosterone <1ng/dl and PRA 1.35ng/ml/h (0.25-5.82). ACTH stim test revealed cortisol level of 9. 0 ug/dl, 9.4 ug/dl, and 9.2 ug/dl at baseline, 30min and 1hr respectively with a baseline ACTH of 539. Lung biopsy showed necrotizing granuloma and fungal spores compatible with histoplasmosis. He was started on amphotericin then transition to itraconazole for 1 year. Additionally, the dose of HC was decrease and Fludrocortisone 0.1mg daily was added. He refused adrenal biopsy at that point and wanted to continue current treatment with a plan to repeat imaging in 3 months and possible adrenal biopsy depending on CT results. On follow-up, patient regained weight and hypoglycemia resolved. Repeated adrenal CT showed shrinkage of the adrenal nodules bilateral. He was continued on PAI replacement. Discussion Histoplasmosis is a fungal infection caused by (H. capsulatum), found in soil contaminated with bird or bat droppings. Infection usually limited to respiratory disease in immunocompetent host but may cause disseminated infection in immunocompromised patient which can involve any organ system. Less commonly, disseminated type may occur in an immunocompetent host with the adrenal gland being the most common infected organ. Treatment involves systemic antifungal therapy; ketoconazole or itraconazole for mild-moderate forms and amphotericin B for 12-18 months for severe ones. Relapse rate is high; ∼ 7.5% and most patients require long-term glucocorticoid replacement. Because unrecognized disseminated histoplasmosis accompanying PAI usually results in a high mortality rate, considerable suspicion and appropriate investigations are necessary for correct diagnosis of this rare but treatable disease. Presentation: No date and time listed

ODP346 Prevalence and Predictors of Endocrinopathies Amongst Patients on Chronic Opioid Use for Non-Cancer Pain

Abstract Introduction Opioids are increasingly used for non-cancer pain control. Studies in cancer patients have shown that chronic opioid use could lead to secondary hypocortisolism and hypogonadism of varying degree. We seek to determine this association in an Asian cohort of patients with non-cancer pain and also examine the effect of opioids on other pituitary hormones comparing them to patients who are on non-opioid analgesia. Methods This is a cross-sectional study of patients recruited from pain clinic. Inclusion criteria were patients aged between 18-75 with non-cancer pain on opioids (morphine/oxycodone/fentanyl/tramadol) for more than 3 months. Patients with active cancer or intracranial pathology, who were already on hormone replacement and on long term glucocorticoids or had intra-muscular or intra-articular steroids in the preceding 3 months were excluded. Controls were age and sex matched. All recruited patients had a renal profile, albumin, cortisol, ACTH, fT4, TSH, FSH, LH, IGF-1, prolactin, testosterone (male) and oestrogen (female) drawn at 8am in a fasting state. Demographic data, menstrual history, pain type and pain score, opioid type and duration of use, were collected. Results Forty eight patients (28 opioid group and 20 controls), 52% men, 31%postmenopausal women, mean age: 55 ±13 years and mean BMI: 27±5 kg/m 2, were recruited. Opioid group had significantly higher pain score (6±2 vs 5±2, p=0. 09) and duration of pain (6.16 ± 5.87 vs 3.56 ± 3.35 years, p=0. 07) compared to controls. 75% of patents were on short acting opioids with a morphine equivalent daily dose (MEDD) of 31 ± 16 mg. There was a higher prevalence of hypocortisolism in the opioid group (50%) compared to control (30%). Of note, 14% of the opioid group had AM cortisol of <100nmol/L, which required replacement. The MEDD of more than 25mg was the only independent predictor of hypocortisolism with OR: 20.4 (95% CI: 1.1-39. 0, p=0. 04). 11% of patients (3 men, 2 post-menopausal women) had secondary hypogonadism. Pain score was significantly higher (7.8±1.5 vs 5.6±2.1, p=0. 03) and the duration of opioid was significantly longer (7.6±3 vs 3.2±4, p=0. 02) in the hypogonadism group. However, there was no independent predictive factor for hypogonadism. The was no sodium abnormality or other pituitary axes involvement in both groups. Conclusion With the increasing use of opioids for non-cancer pain, the prevalence of opioid endocrinopathies are expected to rise. Development of hypocortisolism is independently associated with a higher MEDD. Gonadal axis involvement was more common amongst men and postmenopausal women. Higher use of short acting opioids in our cohort may explain the lower prevalence of hypogonadism compared to previous studies. Further long term studies are needed to examine the need for and effects of hormone replacement in this group of patients. Presentation: No date and time listed

ODP326 Isolated Abducens Palsy as a Presenting Feature of Pituitary Apoplexy

Abstract Case Presentation A 27-year-old female with a history of T1DM presented to the ED for continued visual changes onset the past 10 days. The patient states that she was driving from Wisconsin to Arizona when she developed blurry vision localized to her right eye. She was previously evaluated by outpatient ophthalmology where she was diagnosed with R abducens palsy with no evidence of retinopathy. Associated symptoms included nausea, dizziness, and right sided HA localized behind her right eye and the base of her head. This HA was not relieved by Excedrin or Tylenol. Over the past 3 months, her menstrual periods have been lighter and irregular. Additionally, she has been lactating ever since the birth of her child 2.5 years ago. Hospital Course: Pt had stable vitals: T: 36.4 C, HR: 97, BP: 130/76, RR: 23, SPO2: 100%. Physical exam was WNL other than CN6 palsy. Lab workup was notable for: Na: 138, Cr: 1. 02. FT4 0.94, TSH 3.281, AM Cortisol 8.5, Random Cortisol 7.5, FSH 3.4, FG Glucose 329, and Prolactin 60.4. An MR Brain with and without contrast revealed an enlarged pituitary with a posterior 7mm lesion with small amount of hemorrhage given the high T1 signal. The patient was admitted for concerns of apoplexy and started on Hydrocortisone 50mg IV q12 x2 followed by Hydrocortisone 15mg qAM and 5mg qPM. 18 units of Lantus were started q24 hours along with Cabergoline 0.5mg tabs qhs Wednesday and Sunday. Discussion Pituitary Apoplexy is an endocrine emergency characterized by cortisol levels insufficient for normal body homeostasis. However, not all presentations of Apoplexy are typical. This case highlights isolated abducens palsy as the presenting feature of pituitary apoplexy. Due to the nature of the anatomy of the cavernous sinus, ocular palsies can be a simple physical findings that may have important clinical correlates that should be investigated further. Presentation: No date and time listed

PSUN266 A Case of Ipilimumab Induced New-Onset type1 Diabetes Mellitus in a Patient With Renal Cell Carcinoma.

Abstract A 50-year-old female with a recent diagnosis of Renal cell cancer (RCC) with hepatic metastasis and hypothyroidism was referred to the clinic for management of Diabetes Mellitus (DM). The patient was diagnosed with RCC in 2017 and was treated with immunotherapy Ipilimumab for two years. No family history of Diabetes Mellitus and denies history of corticosteroid usage. No previous episodes of Diabetic Ketoacidosis. She was diagnosed with GAD65 negative type 1 Diabetes Mellitus one year after starting Ipilimumab and was managed on a basal-bolus insulin regimen. She was on levothyroxine for the last two years for hypothyroidism and remained clinically and biochemically euthyroid. She attained menopause 10years ago. Physical examination is unremarkable with normal monofilament tests. Initial labs showed a Complete blood count within normal. The comprehensive metabolic panel showed Glucose 104mg/dl (74-106 mg/dl), Potassium 4.2 mmol/L (3.5 -5.0 mmol/L), Bicarb 25mmol/L (21-33 mmol/L).Hb A1C 6.5%, C-peptide 0.3ng/ml(0.8-3.85ng/ml), GAD 65, ia2 and insulin antibodies negative,TSH 3.420uIU/L (0.5-4.5 uIU/L), Free T4 1.16ng/dl (0.79-2.35 ng/dL), Total T3 78 (71-180ng/dl),Thyroid Peroxidase Antibodies(TPO) negative.Pituitary hormone analysis ruled out possible central, which showed FSH >200 IU/L, LH 78.6 IU/L, ACTH 31pg/mL(10-60pg/mL), Serum AM cortisol within normal. Her DM1 was well controlled with an insulin pump with DEXCOM for continuous glucose monitoring, requiring a total daily dose of around 15-20 units/day. The patient currently remains asymptomatic and will be followed in the clinic with labs. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

PSAT332 Immune Checkpoint Inhibitor Related Hypothyroidism - a Complication of Ipilimumab/ Nivolumab Therapy

Abstract Introduction Endocrine dysfunctions are among the most recognized immune related adverse drug events associated with immune checkpoint inhibitor (ICPi) therapy, with thyroid dysfunction being the most common. This case highlights the risk of thyroid dysfunction with mono and combined immunotherapy. Clinical Case We present a case of a 61 year old male with no significant endocrine history, who was diagnosed and treated for lung adenocarcinoma. His initial stage was cT4N0M0 Stage III-A based on CT chest, bronchoscope lymph node biopsies and PET/CT imaging. Initial MRI brain was also negative for metastasis. He was treated with neoadjuvant carboplatin/taxol with radiation therapy and subsequent right upper lobectomy with mediastinal lymph node dissection. Surgical pathology showed residual tumor present in chest wall structures but negative lymph nodes (ypT3N0MX). After two weeks of consolidative chemotherapy, the patient became intolerable to treatment and chemotherapy was discontinued. Surveillance CT chest scans did not reveal disease reoccurrence. Sixteen months post-surgery, a cystic lesion in the left cerebral hemisphere was found on CT after presenting with vomiting and gait instability. He underwent parietal craniotomy, with surgical pathology showing metastatic adenocarcinoma. Immuno-histochemistry was positive for PD-L1 expression. Post-operatively, he was treated with tumor bed directed gamma knife stereotactic radiosurgery and immunotherapy with ipilimumab/ nivolumab. His pretreatment TSH was normal (3.87 microU/mL; ref 0.270-4.200 microU/mL). Six days after immunotherapy he was admitted for generalized weakness, fatigue and chills where blood cultures and other infectious work up was negative. TSH increased to 6.12 µU/L. He was assessed as immunotherapy adverse reaction and was treated with 80mg prednisone therapy with a two week taper. He was then switched to nivolumab monotherapy. TSH repeated one month later was normal (3.86 µU/L) and his fatigue improved. However, surveillance TSH showed a gradual increase (5.34 µU/L at 4 months and 8.3 µU/L at 8 months), associated with fatigue. The patient was assessed as immunotherapy induced hypothyroidism and started on levothyroxine therapy. AM cortisol, ACTH, FSH and prolactin were within normal limits. Other values were testosterone 93 ng/dL (ref 87 -780 ng/dL); LH 1.4 mU/mL (ref 1.5–9.3 mU/mL), HbA1c 5.9%. Free T4 and T3 while on levothyroxine 25µg were 1.1ng/dL and 3.3ng/dL respectively. Thyroid peroxidase antibodies (TPO Ab) were undetectable. The patient is remaining on indefinite levothyroxine therapy. Conclusion Thyroid dysfunction is one of the most common ICPi related endocrinopathies, with the time of onset ranging from weeks to months post therapy. However, dysfunction can occur after one cycle as with our patient and combination therapy with ipilimumab/ nivolumab significantly increases the risk. The exact mechanism of ICI induced thyroid dysfunction is unclear. Many patients who develop ICPi related hypothyroidism do not have elevated TPO Ab, suggesting a TPO Ab independent pathway. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

PMON90 Pituitary Abscess, A rare cause of Hypopituitarism

Abstract Introduction Pituitary abscess is a rare condition, representing 0.2-0.6% of all pituitary lesions. The presentation can be non-specific, and imaging can mimic a pituitary adenoma, often making the diagnosis challenging. We present a case of a pituitary abscess from Staphylococcus epidermidis and Corynebacterium propinquum with resulting hypopituitarism and central diabetes insipidus (DI). Clinical case A 42-year-old man with a history of hypothyroidism secondary to thyroiditis presented to the emergency room with sudden onset headache, nausea, and emesis. There were associated symptoms of fatigue, weight loss, and sexual hypofunction for approximately six months. He did not have fever or leukocytosis. Brain MRI revealed a 2.5×1.8×1.6 cm sellar and suprasellar mass with rim enhancement and compression of the optic chiasm. Pre-operative pituitary hormonal evaluation showed central hypogonadism, growth hormone deficiency and secondary adrenal insufficiency: FSH 0.4 mIU/mL (n < 15mIU/mL), LH <0.2mIU/mL (n < 10 mIU/mL), AM Testosterone 8 ng/dL (n 250-1100 ng/dL), IGF-1 38 ng/ml (n 52-328 ng/mL), ACTH 5.6 pg/mL (n 7.2-63 pg/mL), AM cortisol 4.9 ug/mL (n 4-10 ug/dL). Prolactin was normal (14.7 ng/mL, n <15 ng/mL). TSH was elevated to 4.88 uU/mL (n 0.3-4.2 uU/mL) with a low FT4 of 0.5 ng/dL (n 0.6-1.5 ng/dL) on levothyroxine 75mcg daily. He was started on stress doses of hydrocortisone and underwent trans-sphenoidal pituitary resection. Intraoperative findings were significant for 3-5 mL of purulent debris in the sella suggestive of a pituitary abscess. He was started on Ceftriaxone, Metronidazole, and Vancomycin, with improvement in headache. Pituitary abscess cultures grew Staphylococcus epidermidis and Corynebacterium propinquum. Blood cultures were negative for any bacterial growth. Post-operative course was complicated by transient DI. The patient was discharged on Linezolid to complete six weeks of antibiotics, a physiological dose of hydrocortisone (20mg daily), and levothyroxine 88mcg daily. At outpatient Endocrine follow-up a month later, he was found to have a recurrence of DI and started on maintenance desmopressin with improvement in polyuria and polydipsia. Conclusion Pituitary abscesses are rare, life-threatening pituitary lesions. 70% of cases are primary pituitary abscesses, which develop in a previously healthy gland. Secondary pituitary abscesses arise within a pre-existing pituitary lesion and are less common. Clinical manifestations include headache, visual disturbance, and hypopituitarism. The diagnosis is challenging since classical signs of infection, such as fever and leukocytosis, are uncommon, and pre-operative radiological findings can be non-specific. The majority of cases are confirmed intra-operatively. Commonly isolated organisms are Gram-positive cocci (Staphylococcus and Streptococcus) and Gram-negative bacteria (Neisseria, Escherichia coli and Corynebacterium). This case highlights the importance of considering pituitary abscesses in the differential diagnosis of patients presenting with a sellar mass. Prompt recognition of a pituitary abscess will allow for rapid treatment with trans-sphenoidal evacuation, antibiotic therapy, and pituitary hormonal replacement when indicated. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

PMON122 Unveiling the Kraken- An Incidentally Found Silent Corticotroph Adenoma of the Pituitary Gland

Abstract Introduction Silent corticotroph adenomas (SCA) are an unusual and rare variant of non- functioning pituitary adenomas (NFA) that do not produce biochemical hypercortisolism or clinical Cushing's disease (CD), yet stain strongly for ACTH on immunohistochemistry. They represent 3-19% of non-functioning adenomas and 20% of corticotroph producing adenomas. SCAs are distinguished by their late presentation, frequent cavernous sinus involvement and earlier recurrence requiring multimodal management. Case We present a case of a 70 year old female with a remote history of breast cancer (2002) and uterine cancer (2016) in remission who was found to have an incidental soft tissue mass in the sella turcica on CT head after a fall in 2021. An MRI brain confirmed the mass as a 1.8×2.0×1.5 cm pituitary lesion with expansion to the sella. Patient had no symptoms related to pituitary hyperfunction or mass effect. Biochemical workup including IGF-1, prolactin, LH, FSH, and AM Cortisol level were all within normal limits. Ophthalmologic evaluation was normal. Repeat pituitary MRI 2 months later showed increasing homogeneously enhancing lesion on the left petrous ridge measuring 2.8×2.8×1.3 cm. There was extension into the cavernous sinus with involvement and encasement of the carotid artery. After multi-disciplinary evaluation including neurosurgery and ENT, patient elected to undergo transnasal endoscopic resection of pituitary tumor. The tumor was only partially resected due to its close association with the carotid artery. Final pathology was significant for monotonous proliferation of tumor cells with small round nuclei and amphophilic cytoplasm, characteristic of a pituitary adenoma. The tumor cells stained strongly positive for ACTH, and negative for all other hormone receptors. Further endocrine workup showed normal morning cortisol and ACTH and marginally elevated 24 hour urine cortisol measuring 47.6 mcg/g creatinine (ULN 42.3). Her clinical presentation was consistent with a SCA. A Dotatate PET/CT was ordered to be performed 3 months postoperatively to assess for SSTR receptors for potential targeted therapy against the residual tumor. Discussion We present the case of an elderly female who was incidentally found to have an invasive SCA precluding its complete resection. There are multiple theories regarding the lack of biological activity of SCAs including lack of enzyme in the tumor to cleve the active ACTH from the prohormone state, dysfunctional lysosomal activity leading to destruction of ACTH before secretion, origin from POMC positive pars intermedia cells instead of true corticotropic cells. These tumors have an increased rate of tumor invasion and recurrence making them difficult to treat. A potential targeted treatment may be somatostatin receptor ligands which will be seen on the dotatate PET/CT. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.