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
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