bluuebunny/crossref_metadata_2025_split huggingface dataset:
DKA in Diet-Controlled Patient With Type 2 Diabetes and ESRD Precipitated by Acute COVID-19
Authors: Shafique Anum , Hamal Savyata , Huq Sabrina 
Published: May 2021

Abstract
Type 2 diabetes mellitus (T2DM) is the main factor for the global rise in end stage renal disease (ESRD), accounting for about 45% of the dialysis patient population in United States. Although T2DM is a common cause for ESRD, it is uncommon for well controlled T2DM patients on dialysis to develop DKA. The COVID-19 pandemic has highlighted infections as a precipitating cause of diabetic ketoacidosis (DKA) and stresses the importance of optimal glycemic control. We report a case of a previously diet controlled patient with T2DM and ESRD admitted with DKA and acute COVID-19. 46-year-old male with diet controlled T2DM, HIV (human immunodeficiency virus) on HAART (highly active antiretroviral therapy), ESRD secondary to HIV associated nephropathy was admitted from an outpatient dialysis unit with vomiting, chills and body aches. He was on metformin monotherapy prior to dialysis initiation. Regular self-monitored blood glucoses ranged 80-130mg/dl with HbA1C of 6% one month prior. Lab tests on admit revealed serum glucose 499mg/dl, elevated anion gap 21mmol/L, potassium 3.5mmol/L (3.5–5.0), HbA1C: 14.7%, elevated beta-hydroxybutyrate 5.6mmol/L(normal:&lt;=0.4), CD4 count 500 (489–1457/µL) with an undetectable HIV viral load however COVID-19 polymerase chain reaction was detectable. He was managed with cautious fluid resuscitation requiring a total of one-liter normal saline, higher potassium dialysate (3K+), and continuous insulin infusion with resolution of abdominal symptoms and DKA. No other infections or precipitating factors were found and acute COVID-19 infection was managed symptomatically. He was discharged on basal bolus insulin regimen on day seven of admit. Up to a third of patients with diabetes on dialysis do not require anti-hyperglycemic therapy, such as our case. Potential factors leading to reduced insulin requirements include reduced renal insulin clearance,reduced renal gluconeogenesis, protein-energy wasting, reduced body weight and accumulation of uremic toxins (guanidino compounds postulated to act as biguanide agents). Our case highlights that acute COVID-19 can precipitate DKA in previously well controlled T2DM patients on hemodialysis while being aware of the need for cautious fluid and potassium administration due to lack of osmotic diuresis in anuric dialysis patients. Close self-monitoring of blood glucose should be emphasized in patients withT2DM with ESRD, including diet controlled T2DM patients, in order to reduce hyperglycemic emergencies and inpatient admissions especially during COVID-19 pandemic.
Does a Supplement Cocktail a Day Keep the Doctor Away? An Unusual Case of Alcohol Induced Diabetes Mellitus: A Case Report and Review of Literature
Authors: Breault Kaley N , Arakaki Brittney H , Cabandugama Peminda K , Rowe Jordan M 
Published: May 2021

Abstract
Background: Currently there are no evidence-based medical recommendations to support the use of supplements in type 1 diabetes mellitus (DM), although there is some data that supports glucose lowering in type 2 DM with supplements such as cinnamon. Additionally, there is no evidence regarding the use of supplements in insulin-dependent DM secondary to pancreatic dysfunction from alcohol use disorder. Despite lack of clear evidence, it is estimated that more than 65% of Americans with DM use at least one dietary supplement for perceived health benefits. (1)Clinical Case: A 58-year old male presented with insulin-dependent DM secondary to pancreatic dysfunction from alcohol use disorder. Initial labs were significant for a low C-peptide of 0.13 ng/mL (0.80–3.85 ng/mL), A1c -9.4%, and blood glucoses ranging from 160–300 mg/dL. Patient’s DM regimen consisted of glargine 40 units nightly and aspart 12 units three times a day with meals. On a subsequent visit two months later, the patient stated that he had begun taking numerous supplements in hopes that these would improve his overall medical status. Supplements included Blood Boost Formula, Ultra K2 with MK-7, Chromium Picolinate, Male Enhancement, Super C Immune Complex, Nugenix Total-T, Niacinamide, Omega Q Plus Max, Cortisol Hormone Balancer, and Vitamin D3. Simultaneously, the patient self-discontinued all his maintenance medications except for his aforementioned insulin regimen due to the fear of negatively impacting his pancreas. Unexpectedly, his blood glucoses improved to a range of 90–150 mg/dL after being on these supplements without increasing his insulin dose. Upon literature review, three ingredients showed the most evidence for the possible explanation for his improvement in glucose control: L-arginine, nettle extract, and biotin with chromium. Conclusion: Literature review of in vivo and randomized, placebo-controlled studies demonstrated mechanisms of action for L-arginine, nettle extract, and biotin with chromium that indicate their potential role in lowering blood glucoses and increasing C-peptide levels in insulin-dependent DM secondary to pancreatic dysfunction from alcohol use disorder. Further investigations include exploring long-term impact on pancreatic function, glucose control, and insulin resistance. Reference: (1) Garrow, D., Egede, L. Association Between Complementary and Alternative Medicine Use, Preventive Care Practices, and Use of Conventional Medical Services Among Adults with Diabetes. Diabetes Care 2006 Jan; 29(1): 15–19.
Euglycemic Diabetic Ketoacidosis Post Bariatric Surgery in Type II DM in the Setting of SGLT2-Inhibitor Use
Authors: Alfares Khalid , Gidda Harish , Proudan Nikoletta 
Published: May 2021

Abstract
Introduction: Current AACE recommendations is to stop the SGLT-2 inhibitor at least 24 hours prior to elective surgery, planned invasive procedures, or anticipated severe stressful physical activity. However, case reports suggest that the pharmacologic effects of SGLT2 inhibitors persist beyond 5 half-lives of elimination (2–3 days), with glucosuria and ketonemia lasting as long as 9 to 10 days after discontinuation.
Case: A 51 year old female with a past medical history of hypertension, morbid obesity, DM type II, admitted to the hospital electively for bariatric surgery. Post-op day 1, she became tachypneic and lethargic. However, alert, oriented and responding appropriately. Lab work showed blood glucose levels &lt;200 mg/dl (70–200 mg/dl), pH 7.21 (7.35–7.45), anion gap of 36 (4–14 mol/L), bicarbonate of 3 (23–34 mmol/L), pCO2 of 6 (35–45) and Potassium of 2.6 (3.5–5.2 mmol). UA showed glucose &gt;500 mg/dl (0 mg/dl) and ketones 80 mg/dl (0 mg/dl). She was transferred to SICU. After reviewing her home medications, she was on Canagliflozin which was stopped 2 days prior to surgery and Glargine/Lixisenatide which was stopped 2 weeks prior to surgery as recommended by her endocrinologist. Patient was then diagnosed with euglycemic DKA. She was started on an insulin drip following potassium replacement and IV fluids. Over the course of few days, she started to feel better. Her PH, bicarb, anion gap and potassium all trended toward normal limits. She was transitioned off insulin drip to basal-bolus insulin regimen and then she was discharged on post-operative day 7 with the instruction to not take any SGLT2 inhibitors.
Discussion: SGLT-2 inhibitors is known to cause euglycemic DKA and ketosis. Our case brings to attention that discontinuation of SGLT2 inhibitor treatment 48 hours prior to surgery may not be adequate specially giving the half-life of the medication. The optimal timing of discontinuation remains unknown. Further studies are needed to evaluate if longer withholding period may be necessary (1).
1.Yehuda Handelsman, Robert R. Henry, Zachary T. Bloomgarden, Sam Dagogo-Jack, Ralph A. DeFronzo, Daniel Einhorn, Ele Ferrannini, Vivian A. Fonseca, Alan J. Garber, George Grunberger, Derek LeRoith, Guillermo E. Umpierrez, and Matthew R. Weir (2016) AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY POSITION STATEMENT ON THE ASSOCIATION OF SGLT-2 INHIBITORS AND DIABETIC KETOACIDOSIS. Endocrine Practice: June 2016, Vol. 22, No. 6, pp. 753–762.
Euglycemic DKA Associated With SGLT2 Inhibitors
Authors: TakallooBakhtiari Asieh , Butina Julio Piedra , Funderburk Sheri A Gillis , Brundavanam Hari V 
Published: May 2021

Abstract
Background: DKA associated with SGLT2 inhibitors also known as Euglycemic DKA (EDKA) is a rare condition characterized by milder degrees of hyperglycemia with a blood glucose level &lt; 200 mg/dl. Unfortunately, this unusual feature can often lead to missed or delayed diagnosis with potential life-threatening outcomes. Clinical Case: The patient is a 53-year-old Caucasian male with PMH of type 2 diabetes mellitus treating with Metformin and Empagliflozin. He presented to the emergency room with shortness of breath, flu-like symptoms, and decreased oral intake for a couple of days. Vital signs at presentation were: Temperature 98.2 °F, pulse rate 108 beats/min, respiratory rate 28 breaths/min, and blood pressure 134/72 mmHg. He was alert but ill-looking, moderately dehydrated with dry mucus membranes. The rest of the physical examination was unremarkable at the time of admission. In the initial blood work, sugar was found to be mildly elevated (163mg/dl), and hemoconcentration besides mild pre-renal acute kidney injury was detected. He was also found infected by the COVID-19 virus without hypoxemia or signs of pneumonia. Arterial blood gases showed metabolic acidosis with an elevated anion gap (PH 7.21, CO2 39.93mmHg, HCO3− 10mEq/L, anion gap 21mEq/L). Urine analysis was positive for ketones and glucose. After ruling out other causes of metabolic acidosis by screening for alcohols, salicylates, acetaminophen, lactic acid, and urine toxicology; the diagnosis of EDKA was made. He was treated with a 3L bolus of IV normal saline and an insulin drip with dextrose solution started as per the protocol based on his glucose levels and promptly admitted to the intensive care unit (ICU). Serial blood tests showed gradual resolution of ketoacidosis and anion gap normalized after 36 hours when insulin drip was stopped and replaced by subcutaneous insulin therapy. Conclusion: SGLT2 inhibitors increase the urinary excretion rate of glucose and subsequent fall in plasma glucose level. Thus, In the absence of exogenous insulin use, increase glucagon release resulting in upregulation of lipolysis and activation of the ketogenesis. Factors such as low oral intake, concurrent infection, and alcohol use can also exacerbate the process. Timely diagnosis of EDKA can be a challenge for physicians unfamiliar with this class of medications, additionally, ketone studies and blood gas analyses are not part of the routine workup for diabetic patients in the emergency department. We recommend all first-line care providers to consider ketosis in ill patients with diabetes and metabolic acidosis, despite the normal or near-normal serum glucose levels. EDKA is mainly a diagnosis of exclusion, but treatment is not different from DKA; correcting dehydration by using intravenous fluids and then, initiating insulin drip along with dextrose-containing solutions, and frequent monitoring of serum anion gap.
High Insulin Resistance in Pancreatic Adenocarcinoma
Authors: Murthi Swetha , Zarghamravanbakhsh Paria , Busta Agustin 
Published: May 2021

Abstract
Introduction: Diabetes mellitus and obesity is associated with increased risk of pancreatic cancer which has been postulated to be due to pancreatic beta cell dysfunction and increased insulin resistance. Pancreatic cancer also exerts its effect on pancreatic beta cells, reducing insulin secretion, affecting glucose uptake and increasing insulin resistance. We present a case of pancreatic adenocarcinoma with severe insulin resistance and uncontrolled diabetes which reversed after tumor removal.
Clinical Description: 79 year old male patient with no prior diagnosis of diabetes, history of hypertension, atrial fibrillation, cerebrovascular accident got admitted to the hospital with painless jaundice, dark colored urine and pruritus for a month. He also endorsed polyuria, polydipsia and weight loss for 2 months. He underwent Magnetic Resonance Cholangiopancreatography and was diagnosed with a 2.8 cm pancreatic head mass, consistent with adenocarcinoma along with intraductal papillary mucinous neoplasm. He was diagnosed with new onset of diabetes, A1c 12.6% during that hospitalization. He weighed about 75 kg and height 170cm (BMI 26.6). Labs showed normal renal function, deranged liver enzymes with direct hyperbilirubinemia, elevated transaminases and alkaline phosphatase. C-peptide level was 1.2 ng/ml for a blood glucose of 197 mg/dl. He was discharged on once daily insulin Glargine 25 units and mealtime insulin Lispro 10 units three times a day (TID) requiring 0.7 units/kg. During follow-up, his insulin requirement started to increase despite proper insulin injection technique and medication compliance. He required glargine 150 units/day and U500 insulin 50 units TID requiring about 4 units/kg. He underwent Whipple’s procedure, partial pancreas resection after a month of his diagnosis. Patient was started on clear liquid diet and his blood glucose started to get better on post-op day 1 with just correctional insulin. He was discharged on Repaglinide 0.5mg TID with each meal and all his insulin was discontinued. His blood glucose was in range of 80 to 160 mg/dl with Repaglinide during clinical follow-up with regular diabetic diet. His severe insulin resistance got reversed after the resection of pancreatic neoplasm.
Conclusion: The pathogenesis of pancreatic cancer associated diabetes has not been studied well. Basic science research found that adrenomedullin, an amionopeptide, is up-regulated in patients with pancreatic cancer and causes insulin resistance in β Cells. Cancer theories also found about metabolic reprogramming and metabolic cross talk happens between pancreatic cancer and peripheral tissue, inhibiting cellular glucose intake and inducing insulin resistance. More research is required to understand these paraneoplastic phenomenon caused by diabetogenic tumor-secreted product in pancreatic cancer associated diabetes.
Immunotherapy-Related Autoimmune Diabetes Mellitus and Exogenous Insulin Antibody Syndrome in a Patient With Metastatic Oral Squamous Cell Carcinoma
Authors: Bahlol Maimoona , Dai Yufei 
Published: May 2021

Abstract
Introduction: Exogenous insulin antibody syndrome (EIAS) is a rare condition characterized by wide glycemic excursions and recurrent hypoglycemia in the presence of high insulin antibody titers. It has been described in diabetic patients treated with exogenous insulin. Programmed death ligand 1 (PD-L1) inhibitors are known to cause autoimmune diabetes mellitus, but PD-L1-related EIAS has not yet been reported to our best knowledge. Case Description: A 63 years old Caucasian man with history of recurrent oral squamous cell cancer presented to emergency room with polyuria, polydipsia, nausea, and vomiting 3 months after initiation of immunotherapy (Durvalumab and cetuximab). He had no prior history of diabetes mellitus or hypoglycemia. He was admitted to hospital for management of diabetic ketoacidosis (Anion gap of 24 mEq/L, venous blood glucose of 805 mg/dL, Venous PH of 7.12, large urine ketone, A1C of 8.9%). After a brief hospital stay, the patient was discharged home on insulin glargine and metformin. His immunotherapy was resumed after hospital discharge. When the patient was seen by Endocrinologist in the clinic, metformin was discontinued and prandial insulin lispro was added. This basal-bolus insulin regimen improved his glycemic control initially. However, without significant changes in his lifestyle or medical condition, he developed worsening postprandial hyperglycemia and recurrent fasting hypoglycemia. Up-titration of his mealtime insulin did not lower postprandial hyperglycemia but possibly worsened fasting hypoglycemia. EIAS was suspected after reviewing his continuous glucose monitoring data. Further work up at this point revealed mildly elevated glutamic acid decarboxylase antibodies (5.9 units/mL, normal range 0.5 - 5.0) and markedly elevated insulin antibody level (77.0 µU/mL, normal range &lt;5). His blood C-peptide was undetectable when his venous blood glucose was 252 mg/dl. In addition, his total insulin level (198 uU/mL) was much higher than his free insulin level (38 uU/mL) following an insulin lispro injection. The patient was diagnosed with EIAS. Switching insulin lispro to insulin aspart while he was on a different immunotherapy medication (Pembrolizumab) immediately reduced his average blood glucose and reduced his total daily insulin dosage by more than 50%. This improvement in glycemic control with insulin aspart only lasted for about 1 week. Unfortunately, the patient’s squamous cancer progressed on immunotherapy. He was referred to hospice care and passed away. Conclusion: Evaluation for EIAS would be reasonable in insulin-treated diabetic patients who develop wide glucose excursions and unexplained fasting hypoglycemia while on immunotherapy.
Is Spontaneous Hypoglycemia a Feature of XLID Type Nascimento?
Authors: Mardini Amin A L , Singh Ishita 
Published: May 2021

Abstract
Introduction: X-linked intellectual disability (XLID) type Nascimento is a rare, under-diagnosed genetic disorder caused by intragenic mutations in the UBE2A gene. The syndrome was first described in 2006 by Nascimento et el. It is characterized by intellectual disability, dysmorphic facial features, skin anomalies, hypotonia, impaired speech, and seizures. To date, there is no literature to suggest that it affects glucose homeostasis.
Case: A 63-year-old male with a history of XLID (mutation in UBE2A pL112P variant), seizures, dementia, stage II CKD, polycystic kidneys, and hyperkalemia presented to the emergency department with altered mental status and blood glucose (BG) of 22 mg/dL. Mental status improved after correction of hypoglycemia.
He had multiple admissions for hypoglycemia, however, no history of diabetes mellitus, or use of hypoglycemia inducing medications. Home medications included Patiromer for hyperkalemia. Family history was remarkable for XLID type Nascimento in his brother and sister’s son. Imaging and laboratory studies conducted on prior admissions were inconclusive. Abdominal CT scan showed a 6mm cyst in the head of the pancreas, but no mass. A 72-hour fast after holding dextrose infusion did not yield a clear biochemical differential. BG 51 mg/dL, Insulin &lt;0.5 (3.0–25 mU/L), C-peptide 0.6 (1.1–4.4 ng/mL), pro-insulin 3.2 (0.0–10.0 pmol/L), β-hydroxybutyrate 0.2 (&lt;0.6 mmol/L). BG increased to greater than 25 mg/dL with 1 mg IV glucagon. Insulin antibody was negative (&lt;5 uU/ml). IGF-1, IGF-2 were low at 17 (49–188 ng/mL) and 142 (333-967ng/mL) respectively. Thyroid function and ACTH stimulation test were within normal limits. Aldosterone &lt;0.1(0.0–30 ng/dL), renin 0.195 (0.167–5.38 ng/mL/hr). Urine metabolic screen, urine amino acid screen, plasma amino acid screen and white cell lysosomal enzymes were normal for the nephew and not performed in our patient. The patient’s family requested not pursuing a repeat 72-hour fast, additional imaging or invasive procedures. Dexamethasone 0.5mg orally at bedtime was started which improved blood sugars and patient was discharged. He presented 2 weeks later with recurrent hypoglycemia. Dexamethasone was titrated to 1.5 mg with no improvement. Diazoxide 3mg/kg/day was subsequently started while dexamethasone was tapered and discontinued. Hypoglycemia did not recur.
Conclusion: This is the first case report describing spontaneous hypoglycemia in an individual with XLID type Nascimento. Our patient also had hyporeninemic hypoaldosteronism which raises the question of endocrine abnormalities as a manifestation of XLID type Nascimento and if hypoglycemia is an inborn error of metabolism in this patient.
Precipitation of Euglycemic DKA (euDKA) From the Initiation of SGLT2 Inhibitor (SGLT2i) and 0-Carb Diet Inpatient
Authors: Popli Rakesh , Chao Jing H 
Published: May 2021

Abstract
Background: SGLT2i are increasingly prescribed for their cardiorenal benefits. Nationally renowned endocrinologists have begun to actively discuss the need for guidelines on safe use of SGLT2i inpatient, with the most common indication being treatment for advanced heart failure (HF). However, no consensus has been reached to date. While in the hospital, patients with HF who are taking SGLT2i are at an increased risk for developing euDKA due to volume depletion, critical illnesses, and restricted dietary intake. We present a case of euDKA inpatient in a man admitted for HF treated with empagliflozin (EMPA).
Clinical Case: A 54-year-old man with HF and non-ischemic cardiomyopathy was admitted for decompensated HF. The patient was also newly diagnosed with T2D on admission when he presented with an elevated blood glucose (BG) of 395 mg/dL (n 62–125 mg/dL) and an elevated A1C of 13.6% (n 4–6%). Cardiologists initiated EMPA 25 mg PO daily on hospital day (HD) 2, in addition to MDI insulin. On HD3, a 0-carb diet was started for a planned FDG PET/CT scan to assess the etiology of cardiomyopathy. With an extremely limited food selection, the patient became largely fasting between HD3-6 while awaiting the PET scan, eating only eggs once a day. On HD6, patient developed chest pain and hypotension and was found to be in euDKA with AKI. Labs were notable for arterial pH 7.14 (n 7.35–7.45), CO2 12 meq/L (n 22–32 meq/L), anion gap (AG) 23 (n 4–12), BG 238 mg/dL (n 62–125 mg/dL), beta-hydroxybutyrate 7.29 mmol/L (n &lt;0.30 mmol/L), and an acute rise in creatinine from 0.8 to 1.4 mg/dL (n 0.51–1.18 mg/dL). In addition to stopping the EMPA, the patient required treatment with IV insulin and fluids for 24 hours, with resolution of euDKA, hypovolemia, and AKI. Patient was safely discharged on HD14 on MDI insulin and metformin.
Conclusion: While euDKA is increasingly recognized outpatient and perioperatively, it is under-recognized in the hospital setting. A study reported 94 patients at one center using SGLT2i inpatient experiencing no euDKA (1). However, hospitalized patients taking SGLT2i remain vulnerable to euDKA, especially with concurrent critical illnesses, volume depletion and restricted dietary intake. Zero-carb intake triggers energy production by ketosis, which greatly amplifies the risk of euDKA on SGLT2i. There are currently no guidelines for safe use of SGLT2i inpatient. When using SGLT2i inpatient, we advocate for clinicians to closely monitor patients’ symptoms and AG twice a day and consider holding SGLT2i with prolonged fasting of &gt;24 hours to readily prevent, diagnose and treat euDKA. We recommend educating clinicians on the side effects associated with SGLT2i, developing EMR alerts, and involving endocrinologists with inpatient use of SGLT2i in high-risk patients.
References: (1) Palermo, N.E. et al. Use of SGLT2 Inhibitors in Hospitalized Patients in an Academic Center. Diabetes 2020; 69(S1):1200-P.