Hypopituitarism, a rare disorder, is defined as decreased production and secretion of one or more of the hormones that are normally secreted by the pituitary gland, resulting from the diseases of the pituitary gland itself or the hypothalamus. The clinical manifestations of this disorder are usually nonspecific and can lead to life-threatening complications and mortality. Here, we present a case of a 66-year-old female patient who was brought to the ER by her family with concerns of altered mentation. The altered mentation was found to be secondary to a severe hypoglycemic episode, which was later discovered to be due to underlying panhypopituitarism with secondary adrenal insufficiency. Endocrinology was consulted and recommended assessment of the hypothalamic-pituitary axis. The tests revealed low levels of serum insulin and C-peptide along with decreased levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, cortisol, free thyroxine (T4), and adrenocorticotropic hormone (ACTH). She was started on intravenous hydrocortisone and levothyroxine, which were later switched to oral hydrocortisone and levothyroxine after the stabilization of her blood glucose levels. She was later advised to follow up with endocrinology upon discharge. While evaluating a patient with hypoglycemia, it is important to keep hypopituitarism causing secondary adrenal insufficiency in mind as a differential diagnosis because it can be life-threatening if not recognized early and treated in a timely manner.
Introduction Pembrolizumab is a novel immunotherapeutic monoclonal antibody directed against PD-1 (programmed death receptor 1), which has been linked to endocrinopathies. We present a rare case of type 1 DM and Grave's disease noted in setting of Pembrolizumab use. Case presentation A 56 year old female with history of Hodgkin's lymphoma (being treated with Pembrolizumab), heart failure and type 2 DM was sent to the ED from oncology infusion clinic for labs concerning for DKA. She endorsed fatigue, light-headedness, polydipsia and polyuria. She had moderate to severe DKA with bicarbonate 9 mmol/L (22 - 31), anion gap 29 mmol/L (7 -17), venous Ph 7.16 (7.30 - 7.40), beta hydroxybutyrate 9.4 mmol/L (0 - 0.3) and blood glucose 451 mg/dL (70 - 100). She was admitted to the ICU and started on insulin drip. She had a 20 year history of type 2 DM and prior to this episode had been managed on Metformin 500 mg daily alone with good glycemic control (HbA1c 5.7 - 7.1%) and had never had DKA before. Of note, she also reported recent 75 pound weight loss which she attributed to lifestyle changes. GAD65 antibody assay was positive 5.49 nmol/L (<=0. 02 nmol/L). She was discharged on a basal bolus insulin regimen and continues to follow up with Endocrinology. On admission, she had thyrotoxicosis with TSH 0. 06 uIU/mL (0.50 - 5.70), fT4 1.8 ng/dL (0.9 - 1.7), and total T3 99 ng/dL (80 -200) while clinically euthyroid. Repeat TFTs in one week were consistent. TSI was elevated 1.8 (<=1.3 TSI Index). 10 days later, labs showed improvement TSH 0. 09 uIU/mL, fT4 1.2 ng/dL and total T3 130 ng/dL. As she was clinically euthyroid and noted to have improving levels, she was managed conservatively. However, one additional one month later, tests were repeated and showed progression to hypothyroid state - TSH 44.23 uIU/mL and fT4 0.4 ng/dL. She was started on Levothyroxine supplementation. Repeat testing showed normalization of TSH. Discussion Our patient had long standing history of well controlled Type 2 DM and no history of thyroid abnormalities yet presented with moderate to severe DKA and thyrotoxicosis due to Grave's disease shortly after initiating immune checkpoint inhibitor therapy. GAD65 antibody and TSI panel were positive indicating development of autoimmunity. Although rare, development of rare endocrinopathies such as insulin deficient diabetes and Grave's disease are important side effects of immunotherapy. Patients being treated with immunotherapeutic agents should be monitored closely with serial metabolic panel testing for the first twelve weeks after starting therapy. In addition, a low threshold should be maintained for testing for additional thyroid related endocrinopathies. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
Introduction - Euglycemic DKA is a notorious entity; previously thought to be primarily afflicting type 1 diabetics and rarely type 2 diabetics in a state of relative insulin deficiency, it has now become a major cause of concern and lead to the issuance of FDA warning in 2015 with regards to its link with SGLT-2 inhibitors. Although DKA is characterized by hyperglycemia, metabolic acidosis and ketogenesis, euglycemic DKA poses a diagnostic challenge as it remains disguised under the cover of euglycemia. Moreover, in the setting of recent SGLT-2 inhibitor use, this definition becomes even more of a paradox as SGLT-2 inhibitors, by the virtue of their action, promote ketogenesis thereby further adding to this enigma. Case presentation - A 67 year old male with hypertension and diabetes mellitus type 2 (on Metformin and Empagliflozin) presented to the emergency room with dizziness. He woke up to go to the bathroom that day and felt weak, dizzy and like he was going to fall. He endorsed nausea and vomiting but denied headache, fever, chills, chest pain, shortness of breath, abdominal pain, and problems with urination/bowel movements. He was afebrile and hemodynamically stable. On examination, left sided dysmetria, loss of coordination, and axial imbalance were noted. No motor/sensory deficits. Labs were significant for WBC count 10 k/mm cu (4 - 11), Creatinine 0.78 mg/dL (0.7 - 1.3), Glucose 279 mg/dL (70 - 99), Bicarbonate 21 mmol/L (21 -31), Anion gap 19 mmol/L (6 - 14), and Lactate 3.2 mmol/L (0.7 - 2). Urinalysis showed glucosuria (glucose >500 mg/dL) and ketonuria (ketones 20 mg/dl). CT head was negative but MRI brain showed left inferior cerebellar peduncle acute ischemic infarct. Stroke protocol was initiated and he transferred to telemetry. The next day, labs showed Glucose 166, Bicarbonate 13, Anion gap 21, and Ketones 5.6 mmol/L (<0.6). Since blood glucose levels remained less than 250 mg/dl with concurrent anion gap metabolic acidosis in the setting of recent Empagliflozin use, he was transferred to ICU for insulin infusion for management of euglycemic diabetic ketoacidosis. Subsequently, he was transitioned to a basal-bolus insulin regimen and transferred to the floors. Discussion - SGLT-2 inhibitors reduce renal tubular glucose reabsorption, causing glycosuria, and promote ketonemia directly by enhancing ketogenesis via glucagon secretion from the pancreatic alpha cells and indirectly by decreasing the renal clearance of ketone bodies. In the setting of acute stress, such as stroke in our patient, and recent SGLT-2 inhibitor use, the presence of ketonuria should be recognized as an early ominous warning sign for euglycemic DKA. A targeted approach detailing diagnostic and therapeutic interventions should be designed to halt its progression in its track before it transforms into the dreaded euglycemic DKA. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
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
Introduction - COVID-19 pandemic hit the world in 2019 and with its advent, began a race against time to curtail its destructive aftermath, which finally seemed plausible with effective vaccination. Malaise, fatigue, dizziness are the most commonly reported side effects of the vaccine. We present a series of two cases which shed light on such symptoms which often remain camouflaged under the background of expectation while indeed, may be linked to biochemical alterations in thyroid functioning causing a state of thyroid dysregulation - a syndrome of vaccine induced mild, self-limiting thyroiditis. Case presentation - Two healthy females presented with mild, non-specific symptoms of fatigue and dizziness days to weeks after receiving SARS-CoV-2 mRNA (severe acute respiratory syndrome coronavirus 2 messenger ribonucleic acid) vaccination. Lab work showed hyperthyroidism. They did not exhibit other clinical signs of overt hyperthyroidism. They were managed conservatively with serial hormonal measurements which stabilized over the next couple of months. Case 1 A 44 year old female presented for an annual visit and reported fatigue and dizziness for 2-3 days. TSH (thyroid stimulating hormone) was <0. 010 (normal 0.27 - 4.20 uIU/ml). She had received the SARS-CoV-2 mRNA vaccine 4 weeks earlier. TSH was repeated in 10 days and remained suppressed at <0. 010 while Free T4 was elevated at 1.92 (normal 0.5-1.6 ng/dL). At Endocrinologist appointment six weeks later TSH normalized at 3.734 and free T4 was low at 0.50. She was advised conservative management. Repeat lab testing in 6 week showed a return to euthyroid state. Case 2 A 29 year old female presented with dizziness and increased sweating. TSH was <0. 005 (normal 0.27 - 4.20 uIU/ml) and freeT4 2.62 (normal 0.5-1.6 ng/dL). She had received the SARS-CoV-2 mRNA vaccine 2.5 weeks earlier. Tests after one month: TSH 0. 013 and free T4 1. 06. ESR was 1 (normal 0-20 mm/hr). Labs showed a promising trend towards euthyroid state as the TSH had become detectable and the free T4 had normalized, and thus, she was recommended conservative management with repeat laboratory testing in 4-6 weeks. Discussion - Post-vaccination nonspecific, often overlooked, symptoms can stem from underlying biochemical abnormalities induced by the vaccines and their interactions with the thyroid gland. Due to the covert nature of these derangements owing to their co-incidentally similar symptomatology and occurrence immediately following vaccination, there is very limited data available on this topic. There is a need to detect, report and investigate this phenomenon to formulate monitoring guidelines, identify certain populations at risk and most importantly, investigate the effects of multiple vaccinations in a series, which is likely on the horizon given the trajectory of SARS-CoV-2 illness, as it can have a huge impact on the burden of thyroid disease in the general population. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
Introduction The relationship between medullary thyroid carcinoma and parathyroid adenoma is well recognized and has been described in connection with MEN syndromes; however, co-existing Grave's disease with underlying non medullary thyroid carcinoma and primary hyperparathyroidism remains a rare phenomenon. The basis of this entity remains yet to be deciphered. With this case we wish to highlight that synchronous abnormalities of thyroid and parathyroid should always be considered and further testing to evaluate for underlying genetic abnormalities should be offered on a case by case basis. In addition, since both Grave's disease and hyperparathyroidism contribute to hypercalcemia, their interplay must be considered in interpretation of serum calcium and parathyroid function. Case presentation A 44 year old male with no significant medical history presented to the PCP with chest pain and dyspnea on exertion. EKG showed sinus tachycardia. Labs showed Calcium 11.1 mg/dl (8.6 - 10.3), Albumin 4 g/dl (3.5 - 5.7), TSH <0. 010 uIU/ml (0.27 - 4.20), Free T4 3.71 ng/dl (0.5 - 1.6). Repeat labs confirmed these findings. Additional tests included: PTH 105.9 pg/ml (12 - 88), Ionized calcium 6.4 mg/dl (4.5-5.4), TPO antibody positive and TSI antibody positive. Propranolol was started and Endocrinology was consulted. Thyroid ultrasound showed hyperechoic gland and 24 hour radio-active Iodine uptake was abnormally increased to 67.8% (8 - 33%), consistent with Grave's disease. Options for treatment were discussed. Decision was made to start Methimazole to achieve euthyroid state followed by repeat PTH (104.1 pg/ml) and Calcium (calcium 10.6 mg/dL) testing. Due to persistent hypercalcemia with inappropriately elevated PTH, surgical intervention was planned. Pre-operative localization studies were ordered: thyroid ultrasound showed two hypoechoic thyroid nodules in the superior right thyroid lobe and inferior left thyroid lobe, and sestamibi scan did not show any focus of increased activity to suggest a parathyroid adenoma. Total thyroidectomy with parathyroid exploration was planned. Surgical pathology was consistent with three foci of papillary thyroid carcinoma measuring 5 mm, 3 mm and 1 mm in size in the right thyroid lobe and right inferior parathyroid adenoma. Post-operatively, thyroid hormonal supplementation was initiated and thyroid and parathyroid function panel normalized. Discussion Our patient had concurrent non medullary thyroid carcinoma and primary hyperparathyroidism. Concurrent thyroid carcinoma should always be considered in patients presenting with parathyroid abnormalities, and a complete pre-surgical screening evaluation must be done. Genetic testing should be considered. And since hyperthyroidism and hyperparathyroidism both can lead to hypercalcemia, their interplay must be considered in interpretation of serum calcium and parathyroid function. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
Introduction Primary hyperparathyroidism entails hyperfunctioning of the parathyroid gland and is characterized by hypercalcemia in the setting of inappropriately normal or elevated PTH. Evidence of nephrolithiasis is an indication for surgical intervention. We present a case of primary hyperparathyroidism presenting as recurrent nephrolithiasis. Case presentation A 57 year old female with past medical history significant for hypertension, pre-diabetes and recurrent nephrolithiasis presented to the ED with subjective fever, chills and dysuria. Of note, she had a long standing history of nephrolithiasis with multiple instances of cystoscopic lithotripsy and stent placement with recurrent UTIs over the past decade. She was noted to be in septic shock secondary to urosepsis. She was managed in the ICU with broad spectrum intravenous antibiotics and pressor support. Her workup revealed hypercalcemia with serum calcium 12 mg/dL (8.6 - 10.3), albumin 3.4 g/dL (3.5 - 5.7) in the setting of inappropriately elevated parathormone PTH at 120.4 pg/ml (12 - 88). Endocrinology was consulted. Extensive chart review revealed that she had a long standing history of hypercalcemia and prior urinary calculi analysis were consistent with calcium oxalate and calcium phosphate stones. She endorsed polyuria, polydipsia, constipation and low mood. Medications were reviewed and she had not been on any agents known to cause hypercalcemia. 25 Hydroxyvitamin D was low at 20 ng/ml (30 -100) and appropriately 24 hour urine calcium was low - suppressed at 157 mg (100 - 300). The Sestamibi scan did not show an adenoma. A parathyroid ultrasound showed a possible hypoechoic area bilaterally in the parathyroid region. She underwent parathyroid exploration with excision of right superior parathyroid adenoma. Pathology report showed hypercellular parathyroid tissue consistent with a parathyroid adenoma. Post operatively, calcium and PTH value normalized. Discussion Primary hyperparathyroidism is associated with nephrolithiasis and nephrocalcinosis. Nephrolithiasis is an indication for surgical intervention. Our patient had the classic signs of primary hyperparathyroidism for at least a decade; however, it was not diagnosed until she presented with urosepsis and ended up in the ICU. Primary hyperparathyroidism is often thought of as a disease commonly seen in the outpatient setting. However, a high radar of suspicion must be maintained in both inpatient and outpatient settings as this disorder, when left untreated can have dangerous consequences. Similarly, in patients presenting with nephrolithiasis, a thorough history and physical examination in addition to a complete review of systems and medication review must be carried out to effectively rule out primary hyperparathyroidism. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
Introduction Empagliflozin is an anti-diabetic agent belonging to the class of SGLT-2 inhibitors, which was approved by the U. S. Food and Drug Administration (FDA) in 2013. It has emerged as a popular choice of second line diabetic therapy owing to benefits of reduction in cardiovascular adverse events and delayed progression of kidney disease. However, in 2015, FDA issued a safety warning in connection to its use with euglycemic ketoacidosis and subsequently in 2016, started investigating its link with pancreatitis. We present a case of a type 2 diabetic started on Empagliflozin therapy 4 days prior to his presentation to the ER with nausea, vomiting and diarrhea when he was found to have concurrent euglycemic DKA and acute pancreatitis. Case presentation A 49 year old male with a history of diabetes mellitus type 2 presented to the ER with nausea, vomiting, diarrhea and fatigue. He reported these symptoms since starting a new anti-diabetic agent Empagliflozin four days ago. He denied fever, chills, chest pain, shortness of breath, abdominal pain, and urinary symptoms. He denied heavy alcohol use or binge drinking. Lab tests showed: WBC count 18.7 k/mm cu (4 -11), Glucose 229 mg/dL (70 - 99), Bicarbonate 7 mmol/L (21 - 31), Anion gap 30 mmol/L (6 -14), Lactate 1.8 mmol/L (0.7 - 2.5), Serum beta hydroxybutyrate level >4 mM (0. 02 - 0.27), Lipase 866 IU/L (11 - 82) and Venous blood pH 6.98 (7.30 - 7.45). Repeat blood glucose measurements remained < 250 mg/dl. Urinalysis showed > 500 mg/dl glucose. CT abdomen and pelvis showed moderate fat stranding consistent with acute pancreatitis. He was started on insulin infusion and admitted to the intensive care unit. He was subsequently discharged on a basal-bolus regimen with instructions to discontinue Empagliflozin. Discussion Acute pancreatitis and euglycemic DKA are grave clinical entities, associated with significant mortality. Our patient presented with nausea, vomiting, diarrhea and fatigue; he denied the characteristic abdominal pain yet was noted to have pancreatitis by laboratory and imaging studies. It is extremely important that pancreatitis be considered and ruled out in patients presenting with non-specific symptoms while on SGLT-2 inhibitor therapy. In addition, a high radar of suspicion should be maintained in both inpatient and outpatient settings for euglycemic DKA in patients on SGLT-2 inhibitor therapy presenting with non-specific symptoms, even in the absence of a classic identifiable triggering event, especially as there is evidence to suggest that pancreatitis may actually serve as a triggering factor for euglycemic DKA suggesting that, due to a cause-effect phenomenon, these two conditions may co-exist more often than expected. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
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