bluuebunny/crossref_metadata_2025_split huggingface dataset:
RF07 | PSUN359 Alpelisib-induced Diabetic Ketoacidosis
Authors: Majumdar Sachin , Parekh Jay , Ostas Anca , Tan Jia Wei , Mathialagan Karthik , Polisetty Lakshmi 
Published: November 2022

Abstract

Background
Alpelisib is an oral α-specific phosphatidylinositol 3-kinase (PI3K) inhibitor use in combination with fulvestrant to treat postmenopausal women with HR+/HER2−, PIK3CA-mutated, advanced or metastatic breast cancer that has acquired resistance to endocrine-based therapy. (1)Alpelisib interferes with the PI3K/Akt signalling pathway resulting in impaired peripheral glucose uptake, increased liver glycogenolysis, loss of beta-cell mass and insulin secretion dysfunction(2). Hyperglycemia is a frequent adverse effect of alpelisib but diabetic ketoacidosis (DKA) is considered a rare occurrence. We describe a patient without a previous history of diabetes who developed DKA after 2 months on alpelisib.Clinical caseA 81 year-old woman with metastatic ER+ PR – Her2 - breast cancer, presented with a 1 week history of nausea, vomiting, and polyuria. Her hemoglobin A1C was 5.5% on two separate occasions last year. She had started alpelisib at 300 mg/day 7 weeks prior to presentation. She presented with a blood glucose (BG) of 659 mg/dL, anion gap of 21, serum bicarbonate 17 mmol/L, beta-hydroxybutyrate 3.82 mmol/L (normal &lt; 0.27 mmol/L), serum osmolarity 319 mOsm/kg, serum creatinine 2.83 mg/dL (baseline 1.38 mg/dL), C-peptide 4.3 ng/mL (normal 1.1–4.4 ng/mL), negative GAD-65 antibodies and Islet Antigen 2 antibodies, septic workup were non-revealing, leading to the diagnosis of alpelisib-associated DKA. Alpelisib was held, and she was treated with intravenous insulin and hydration. DKA resolved in 12 hours, however, she had persistent hyperglycemia. She was started with insulin regimen of 0.2 units/kg and discharged with Humalog 75/25 5 units twice daily.

Conclusion
Patients with no pre-existing history of diabetes mellitus can also be at risk for DKA which may develop within weeks to months of initiation of alpelisib. Risk factors for development of DKA are yet to be identified, but would be useful to help tailor frequency of BG monitoring. This warrants further research. The hyperglycemic effects of alpelisib appear to be reversible upon drug discontinuation, however when DKA is the presenting syndrome, insulin therapy is indicated.

Reference
André F, Ciruelos E, Rubovszky G, Campone M, Loibl S, Rugo HS, Iwata H, Conte P, Mayer IA, Kaufman B, Yamashita T, Lu YS, Inoue K, Takahashi M, Pápai Z, Longin AS, Mills D, Wilke C, Hirawat S, Juric D; SOLAR-1 Study Group. Alpelisib for PIK3CA-Mutated, Hormone Receptor-Positive Advanced Breast Cancer. N Engl J Med. 2019 May 16;380(20): 1929-1940. doi: 10.1056/NEJMoa1813904. PMID: 31091374.
Nguyen P, Musa A, Samantray J. Alpelisib-Induced Diabetic Ketoacidosis. Cureus. 2021 May 1;13(5): e14796. doi: 10.7759/cureus.14796. PMID: 34084688; PMCID: PMC8166359.
Presentation: Saturday, June 11, 2022 1:36 p.m. - 1:41 p.m., Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSAT025 Functional Adrenocortical Oncocytic Neoplasm: A Rare Cause of ACTH Independent Cushing's Syndrome
Authors: Chang Alan , Shah Kajal , Hand Jane 
Published: November 2022

Abstract

Background
Adrenal oncocytomas (AOCs) or adrenocortical oncocytic neoplasms (ACONs) are extremely rare tumors of adrenal glands characterized by the presence of oncocytes, which are epithelial cells with eosinophilic cytoplasm. Only about 140 cases have been reported in literature so far. AOCs are more common in females (2.5: 1), more prevalent on the left adrenal gland (3.5: 1), and tumor size ranges from 3 to 17 cm. About two thirds of AOCs are reported to be nonfunctioning, and only less than 6% of functioning are cortisol secreting. The malignant potential of these tumors has been described quite variably in current literature. Based on the most recent systematic literature review, about 35% were found to be benign, 24% malignant, and 41% borderline, based on the Lin Weiss Bisceglia system. The mainstay of treatment is surgical resection. Here we describe a case where biochemical workup and pathology revealed a functional AOC with uncertain malignant potential.

Clinical Case
A 68 year old female with hypertension was found to have an incidental left 3 cm adrenal nodule on CT abdomen and pelvis during a workup for hematuria. The nodule was biopsied and initially found to be benign. Afterwards, she was referred to endocrinology where biochemical testing was consistent with ACTH-independent Cushing's syndrome. She had three elevated late night salivary cortisol - 0.10 mcg/dL, 0.14 mcg/dL, and 0.19 mcg/dL (≤0. 09 mcg/dL), three abnormal 1 mg dexamethasone suppression tests - 16.4 mcg/dL, 15.1 mcg/dL, and 17.1 mcg/dL (&lt;1.8 mcg/dL), two normal 24 hour urinary cortisol - 22.5 and 31.5 mcg/24h (4-50 mcg/24h), and ACTH &lt;5 pg/mL (6-50 pg/mL). She was then referred to surgery and was treated by laparoscopic adrenalectomy. Surgical pathology showed a 3.5 cm adrenal cortical tumor with oncocytes infiltrating into the periadrenal adipose tissue, with positive staining for synaptophysin and negative for P53. On Ki67 staining, some hot spots were greater than 5%. Therefore, the tumor was characterized as AOC with undetermined malignant potential or a low grade, oncocytic adrenocortical carcinoma. She was evaluated by oncology and radiation oncology, and it was decided to monitor the patient without systemic therapy or adjuvant radiation therapy. A surveillance approach was favored given that the risks of adjacent bowel and kidney toxicity outweighed the benefits of radiation.

Conclusion
We hereby report a case of AOC with undetermined malignant potential. This case highlights many challenges in the diagnosis, management and long-term surveillance of patients with AOCs, and need for further research.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
PSUN48 Serum leptin levels among chronic kidney diseased subjects with hypertensive heart disease: An observational cross-sectional study
Authors: Ofori Emmanuel Kwaku 
Published: November 2022

Abstract

Background
Chronic kidney disease (CKD) is one of the main health concerns in Sub-Saharan Africa. Leptin, a peptide hormone produced by the adipocytes have been observed to trigger complications such as cardiovascular diseases with significant mortality. The precise role of leptin in hypertension-mediated development of CKD is unknown. Research findings in this area have been inconsistent. The aim of the study was to evaluate serum leptin levels among CKD patients attending a tertiary referral hospital.

Methodology
An observational cross-sectional study. One hundred and eight (108) participants took part in the study. A structured questionnaire was used to gather their anthropometric and demographic characteristics. Blood samples were obtained and analyzed for leptin and other biochemical parameters.

Results
There were significant differences in the plasma levels of leptin, glucose (FBG), creatinine and triglyceride among CKD subjects compared with controls (p &lt;0.05 respectively). An inverse correlation was found for leptin vs estimated GFR (r = -0.505, p= 0.0001) among CKD subjects. In the CKD group, being at stage 5 made the largest unique contribution (beta = 0.47, p &lt; 0.0001) to the variance in serum leptin levels, followed by HDL, FBG, HHD diagnosis of more than 6 years, female gender and BMI respectively (p&lt; 0.05). In the control group, female gender made the largest unique contribution to circulating leptin levels (beta = 0.709, p &lt; 0.0001) followed by BMI (beta = 0.341, p &lt; 0.0001), and eGFR (beta = -0.222, p = 0.011).

Conclusion
Serum leptin levels were significantly higher among CKD subjects co-burdened with hypertension heart disease in Accra. Stage 5 CKD was the most significant predictor of serum leptin levels. These findings underscore the role of leptin in the biochemical complexities observed in CKD subjects. Therapeutic strategies targeting leptin reduction are welcomed in the management of CKD.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN63 Approach to hyperlipidemia management in Carnitine Palmitoyltransferase II deficiency
Authors: Anbari Raghda A , Ghayee Hans , Xhikola Majlinda , Kadiyala Sushma 
Published: November 2022

Abstract

Background
Carnitine Palmitoyltransferase II deficiency (CPT II) is a disorder of long-chain fatty-acid oxidation. Clinical presentations include a lethal neonatal form, severe infantile hepatocardiomuscular form, and myopathic form. The myopathic form is the most common disorder of lipid metabolism affecting skeletal muscle. Individuals with CPT II deficiency are unable to metabolize long-chain fatty acids and can have myalgia. The incidence of statin-induced muscle symptoms is 1.5% to 5%. Individuals with CPT II deficiency have been reported to have an increased incidence of statin-associated myopathy. Yet, it remains crucial to place patients with high ASCVD risk on the appropriate statin therapy.

Case Presentation
We present a 70-year-old male with medical history of CPT II deficiency (myopathic form), hyperlipidemia with significant hypertriglyceridemia, hypertension, type 2 diabetes mellitus, carotid artery stenosis, atrial fibrillation, and recurrent pancreatitis. Family history was positive for hyperlipidemia and premature coronary artery disease. After history of recurrent pancreatitis and severe myalgias, patient was diagnosed with CPT II deficiency at the age of 30 years. The myalgias were managed by increased carbohydrates intake for many years. Multiple low potency statins, and fenofibrate were attempted but he developed severe myalgia with elevated CPK levels. Eventually he was started on ezetimibe 10 mg daily with fish oil 2000 mg twice daily but his LDL-C continued to rise. CMP and TSH were within normal limits. Nuclear stress test was normal but his ASCVD risk score was 39%. Given the patient's CPT II deficiency and high risk for ASCVD score, statin was recommended for primary prevention. After a thorough discussion of risks and benefits of lipid-lowering therapy, the patient was started on pitavastatin 2 mg twice-weekly regimen and ezetimibe 10mg was continued. Eight weeks later, his LDL-C reduced from 132 mg/dl to 94 mg/dl (n &lt;129mg/dl), TG from 449 mg/dl to 307 mg/dl (n 0-149 mg/dl). As he experienced no myalgias, an extra tablet of pitavastatin a week was added until he reached a daily regimen. He continued to tolerate this treatment and his LDL-C improved to 66 mg/dl with normal CPK levels. Clinical Lesson: We present a case of CPT II deficiency and significant hyperlipidemia successfully managed with pitavastatin and ezetimibe, which helped to achieve a desirable LDL-C. Pitavastatin is not metabolized by hepatic CYP3A4 isoenzyme as other statins and is minimally metabolized by CYP2C9. In addition, patients with CPT II deficiency may benefit from avoiding extended episodes of exertion and high-fat diet. When treating patients with CPT II deficiency and hyperlipidemia, close follow-up and laboratory monitoring will be needed.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN250 Empagliflozin Induced Bladder Cancer in an Adult Patient With Latent Autoimmune Diabetes
Authors: Alzenaidi Ahlam , Alkhalidi Hisham 
Published: November 2022

Abstract

Sodium glucose cotransporter type 2 (SGLT2) inhibitor is a novel class of antidiabetic agent. The association of SGLT2 inhibitors and incidence of bladder cancer has not been well established due to few numbers of cases and not enough length of exposure. Here we describe a case of bladder cancer developed one year after empagliflozin exposure in a patient with latent autoimmune diabetes.

Case description
A 51-year-old man presented to our endocrine clinic with a one-year diagnosis of type 2 diabetes mellitus. His glycosylated hemoglobin (HbA1c) was 8% on maximum dose metformin and well adherence to diet. The patient had no significant past medical history and his body mass index was 23.6 kg/m2. Empagliflozin 25 mg daily was added to his regimen, in addition to sulfonylurea and dipeptidyl peptidase-4 (DPP-4) inhibitor drugs. The patient continued to have persistent hyperglycemia despite medical therapy with HbA1c ranged between 7.5-7.9%. After one year, he presented with fatigue, unintentional 7-kg weight loss and perianal pain. A transrectal ultrasound of the pelvis showed a 10-mm solid lesion in the urinary bladder. He underwent transurethral resection of bladder tumor; pathology showed a low grade papillary urothelial carcinoma with focal areas of high grade. Empagliflozin was discontinued and due to persistent hyperglycemia, further labs were requested. Fasting blood glucose of 265 mg/dl, HA1c of 7.9%, anti-GAD antibody was positive 37.52 u/ml (&lt;10.0), C-peptide of 0.51 ng/ml (0.37-1.47), insulin of 2.0 mu/ml (2.6-24.9). These findings suggested latent autoimmune diabetes with mild pancreatic reserve. Patient was then started on insulin therapy of Glargine and Aspart.

Conclusion
The use of SGLT2 inhibitors in patients with autoimmune diabetes may have a higher risk of bladder cancer as compared to patients with type 2 diabetes. An individualized selection of antidiabetic agent with consideration of proper diagnosis is recommended to prevent a serious consequence.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN251 Euglycemic DKA In A Patient Undergoing Major Surgery
Authors: Dapas Natalie , Baral Neelam , Sterrett Yamini , Sharma Meeta 
Published: November 2022

Abstract

Background
Euglycemic DKA represents a diagnostic challenge as a lack of hyperglycemia can lead to a delay in recognition and administration of appropriate treatment. We present a case of euglycemic DKA in the setting of starvation and surgical stress in a patient with type 2 diabetes without SGLT2 inhibitor use.

Clinical Case
A 61-year-old type 2 diabetic woman presented with a two-day history of vomiting associated with abdominal pain. She was previously treated with glipizide, metformin, and sitagliptin, which had been discontinued months ago due to poor oral intake. CT imaging demonstrated a 12.4×11.2×10.5 cm pelvic mass with ascites and omental nodularity in the setting of a history of prior right granulosa cell tumor and mature cystic teratoma status post total abdominal hysterectomy with bilateral salpingo-oophorectomy. The patient subsequently developed hematemesis on hospital day 7, for which she was made NPO. She underwent EGD which demonstrated severe esophagitis and duodenitis. She was given an oral diet for one day, prior to resuming NPO status on hospital day 10 for exploratory laparotomy and tumor debulking. On hospital day 11, the patient's labs were notable for an anion gap metabolic acidosis (pH 7.26, n 7.4; CO2 16 mmol/L, n 20-31 mmol/L; anion gap 15 mmol/L, n 5-15 mmol/L), elevated beta-hydroxybutyrate (5.5 mmol/L, n 0.02-0.27 mmol/L), and a blood glucose range of 141-233 mg/dL (n 65-140 mg/dL). The patient was not on any scheduled insulin other than a low dose correctional scale with Lispro subcutaneously pre-meals and had not used SGLT2 inhibitors. There was no suspicion for alcohol toxicity or other poisoning given that the patient had been hospitalized. The lactate level was normal. Thus, the patient met criteria for euglycemic DKA likely secondary to prolonged fasting, exacerbated by the stress of major surgery. The patient was started on an insulin drip with dextrose infusion until the metabolic parameters improved, and she was transitioned to subcutaneous insulin. In diabetic patients unable to tolerate enteral nutrition or with enteral nutrition delays due to surgery, initiation of parenteral nutrition may prevent progression to euglycemic DKA. Ultimately, her pathology was consistent with metastatic granulosa cell tumor, and she was discharged to subacute rehabilitation.

Conclusion
Euglycemic DKA may be overlooked due to normoglycemia leading to a delay in the diagnosis and appropriate management. It is a medical emergency and should be treated with an intravenous insulin infusion and dextrose. It can be prevented in diabetic patients undergoing major surgical stress by ensuring adequate nutritional support.Reference: Modi, A., Agrawal, A. and Morgan, F., 2017. Euglycemic diabetic ketoacidosis: a review. Current diabetes reviews, 13(3), pp.315-321.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN262 A Case of Hypoglycemia and Diabetic Ketoacidosis in an Adult with Down Syndrome
Authors: Lung John , Graves Brad 
Published: November 2022

Abstract

Introduction
Down syndrome is associated with a higher risk of autoimmune endocrinopathies including diabetes mellitus. Due to intellectual disabilities characteristic of Down syndrome, good glycemic control of insulin-dependent diabetes can be challenging with several reports of complications in the literature. We present an adult female with several admissions for hypoglycemia and DKA.

Case Presentation
A 52-year-old female with a notable past medical history of insulin-dependent diabetes mellitus, hypothyroidism, and Down syndrome with intellectual disability equivalent to a 12-year-old presented to the emergency department unresponsive with a point of care blood glucose of 21 mg/dL. Dextrose 10% was given by EMS en route to the ER with improvement in the blood sugars to 118 on arrival. Her hemoglobin A1c was 7.1%. Of note the patient was taking insulin detemir 24 units in the morning and 30 units in the evening and metformin 1g BID. She was not checking her blood sugars before self-injecting and was skipping meals while injecting insulin. Caregiver fatigue was also reported. She was admitted one month ago for similar hypoglycemia. She was taken off insulin and continued her metformin. Her blood glucose was at inpatient goals by discharge. One month later, the patient presented with altered mentation and a point of care blood glucose greater than 600 mg/dL. Her glucose on chemistry panel was 732 mg/dL, anion gap was 21 mEq/L, bicarbonate was 21 mmol/L, and her beta-hydroxybutyrate was 1.67 mmol/L. Calculated serum osmolality was 316 mOsm/kg. The patient was admitted for DKA with a possible component of hyperosmolar hyperglycemic nonketotic coma. She was placed on a DKA protocol with an insulin drip and isotonic fluids then switched to subcutaneous insulin once her anion gap closed. She was then placed on 20 units insulin detemir daily and discharged. The patient then presented 2 weeks later with 2 days of no oral intake complicated by septic shock of unclear origin. After discussion with the mother, the patient was transitioned to comfort care and died 4 days later.

Conclusion
Our case illustrates the difficulty of glycemic control in patients with Down syndrome and diabetes complicated by caregiver fatigue, intellectual disability, and a complex insulin regimen. Clinicians should aim for a balance between glycemic control and treatment regimen simplicity while avoiding hypoglycemia and ketoacidosis.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN266 A Case of Ipilimumab Induced New-Onset type1 Diabetes Mellitus in a Patient With Renal Cell Carcinoma.
Authors: Thota Geethika , Luo Hongxiu 
Published: November 2022

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 &gt;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.
PSUN273 Endocrine Management of Renal Transplant Patients: A Role in Successful Graft Survival? Updated Data
Authors: Mumtaz Mirrah , Joseph Jalaja , Abdelgyed Ehab , Mohamed Hadir , Conti David , Leinung Matthew 
Published: November 2022

Abstract

Introduction
Graft survival after renal transplantation is dependent upon multiple factors. Many patients undergoing renal transplantation have endocrine disorders, such as pre-existing diabetes and metabolic bone disease, and can develop post-transplant diabetes (PTDM) and hyperlipidemia. Diabetes, lipid abnormalities, and hypovitaminosis D have been associated negatively with patient and graft survival1, 2. Our kidney transplant program ranks among the top 3 programs in the country for its kidney transplant outcomes according to the data by the Scientific Registry of Transplant Recipients. We hypothesized that our multidisciplinary team management of these patients was one factor in this success. We reported our findings in 2017. Here we present follow up data through 2021 on this same cohort.

Methods
Over 20 years ago members of the Endocrine division began attending the transplant clinic in the Department of Surgery to facilitate patient care. In 2016 we identified all patients followed over the previous 3 years. Charts were reviewed after IRB approval and data collected retrospectively. Data for this cohort has been updated through 2021.

Results
A total of 241 patients were seen (of 626 total transplant recipients). There were 154 males, 87 females, and the average age at transplant was 47 years. Diabetes was present prior to transplant in 118 (46.6%) and an additional 51 (21%) developed PTDM. For patients with diabetes, the pre transplant A1c fell from 7.5 ± 1.6% to 7 ± 1.2% at 6 months (p = 0.13). At 6 months, the A1c was 6.45% for those who had developed PTDM. Pre-transplant, 79 (31%) were on some form of lipid lowering therapy. Post-transplant, 216 (90%) had hyperlipidemia: 186 (77%) were on a statin, in addition to 51(21%) on fish oil, 28 (12%) on gemfibrozil, and 4 (1.5%) on niacin. The average Vitamin D level within 1 year post-transplant was 19.9 ± 8, but increased to 33± 14 at most recent visits (P &lt; .01). Of 217 patients over the age of 40, 93 (43%) have had a DEXA: Osteoporosis was diagnosed in 43 patients and osteopenia in an additional 31. Of these patients, 34 are or have been on treatment (bisphosphonate).

Conclusions
We believe that multidisciplinary team management of post renal transplant patients can improve graft survival. While our improvement in A1c values at 6 months post-transplant was not statistically significant, the trend was clearly there even considering potential artefactual lowering of the A1c in renal failure patients. We did demonstrate improvement in Vitamin D levels and frequency of statin use. We also found that there remain some barriers for care (evidence, for example, by many patients not having Vitamin D levels or DEXA).
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.