bluuebunny/crossref_metadata_2025_split huggingface dataset:
Covid-19 and New Onset Diabetes: A Case Series
Authors: Saleem Marwa , Zahra Tasneem , Menon Vidya , Vargas-Jerez Julia , Sarwal Amara 
Published: May 2021

Abstract
Background: During the SARS CoV1 pandemic in 2003, there was much literature published about newly diagnosed diabetes mellitus (DM) in the patient population infected. This phenomenon has not been well established during this SARS CoV2 pandemic. In this case series, we aim to evaluate patients admitted to our facility with new onset DM who had a history of COVID-19 infection.
Method: This was a single center case series that included adult patients who presented to our facility with new onset DM during June-October 2020 who had a history of SARS CoV2 positive PCR and/or positive IgG antibody to SARS CoV2. Pregnant patients were excluded. Data was collected from the hospital electronic medical records. Diagnosis of diabetes was determined in these patients via hemoglobin A1C (HbA1C) level greater than 6.5%.
Results: Six patients fulfilled our diagnostic criteria. All patients were male with a median age of 54 years. The median BMI is 33.9, with 5 patients considered to be obese and 1 overweight. Other than the increased BMI, 2 patients with pre-DM and 3 patients who had a family history of DM, no other identifiable risk factors for DM were noted in this cohort.
Five patients required hospitalization for HHS or DKA and 1 patient was managed as an outpatient. Median random serum glucose on presentation was 761.5 mg/dl and median HbA1C on presentation was 11.5%. Significant dosages of parenteral insulin (0.45 U/Kg) was required for hospitalized patients during their inpatient stay along with immediately after discharge to control their hyperglycemia. Glutamic Acid Decarboxylase and Islet Cell antibodies were done for 2 of the patients and were negative.
Three of the patients who had follow up in 2 months showed improvement in their HbA1C (median of 7.1% [5.4–10.7]) and considerably diminished subcutaneous insulin requirement (0.2U/Kg). Two of these patients continued to follow up, and at 4 months from onset of DM, median HbA1C was 5.85% with insulin ceased. Of note, the patient who was lost to follow up was found to have an HbA1C improvement from 11.4% to 5.4% at the 2 month mark.
Discussion: Both SARS CoV1 and SARS CoV2 activates the RAAS, causing insulin resistance by altering insulin signaling and increasing oxidative stress leading to dysfunction of pancreatic beta calls. The inflammatory cytokine storm response seen in COVID-19 can also decrease skeletal muscle sensitivity to insulin and decrease peripheral glucose uptake. These mechanisms may be leading to the new-onset DM noticed in our COVID-19 patients. In addition, there may be a possible immune-mediated mechanism given the matched time line between the COVID-19 antibody life span and the duration of DM.
It is unknown whether this effect is permanent or temporary, although our results do support the latter. More studies that utilize a larger cohort and longer follow up are needed in order to get a better understanding of the mechanism of DM in COVID-19 infection.
Type ll Diabetic Patients’ Attitudes Toward Influenza and Covid-19 Vaccination
Authors: Gilfix Reisa , Elstein Jack , Elstein Eleanor 
Published: May 2021

Abstract
Influenza vaccination (fluv) is free and easily accessible to diabetics in Quebec. The importance of vaccination (v) during the Covid19 (CV19) pandemic has been widely discussed in the media. To ascertain the receptiveness of type 2 diabetics (T2D) to fluv during the CV19 pandemic and their acceptance of an eventual CV19 vaccine (CVv) we carried out telephone interviews with 34 unselected T2D pts in Montreal, Quebec post the 1st wave of CV19 in that region. Pts were asked if they planned taking the fluv and/or an eventual CVv, reasons for reticence to v, and attitudes toward and compliance with public health (PH) directives. They were also asked their primary source of health related information. Recent HbA1c and insulin use were recorded. Thirty four T2Ds were surveyed, 22 M 50–87 yrs (mean 69.2) and 12 F 49–84 yrs (mean 68.8). Eleven M and 5 F were on insulin. HbA1c ranged from 5.9–13.0 (mean 7.3). None of the pts had recently discussed v with a healthcare provider (HCP). One pt received his health related information from Facebook, the others from mainstream media. None had contraindications to v. None had been diagnosed with CV19. Past influenza history was unknown. Forty one percent (14/34) of pts, 11 M 50–86 yrs (mean 66.0) and 3 F 49–66 yrs (mean 59.0) did not plan to take the fluv. They explained their decisions as never having taken fluv (12 pts) or having been ill despite having taken it (2 pts). Neither accessibility nor cost were issues. Two F, 62 and 66 yrs, who refused fluv also refused CVv. Six M aged 60–86 yrs (mean 70.5) and 1 F aged 73 yrs were planning to wait to access real life safety (6pts) or efficacy (1pt) data before accepting CVv. All pts claimed to be following PH guidelines including social distancing, hand washing, and mask recommendations; 91.2% (31/34) fully agreed with PH policies, 2 were in moderate agreement and 1 thought PH policy was not strict enough. Of the latter 3 pts none planned on taking the fluv. One planned taking the CVv, 1 planned not to, and the 3rd planned to wait before deciding. Despite a long history of use, recommendations by experts, and free and easy accessibility, T2D pts questioned after the 1st wave of CV19 are not convinced of the fluv’s importance. Despite high case numbers and being themselves at high risk, not all T2Ds are willing to unequivocally accept a potential Health Canada sanctioned CVv. This study underlines the important work HCPs have ahead in educating and reassuring pts with regard to vaccination.
A Case of Euglycemic Diabetic Ketoacidosis Following Canagliflozin Therapy
Authors: Tuna Kubra M , Abdelmasih Randa , Abdelmaseih Ramy , Alsamman Mrhaf , Robbins Joseph 
Published: May 2021

Abstract
Introduction: Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus (DM). In general, DKA characterized by blood sugar over 250 mg/dL, anion-gap metabolic acidosis, and increased plasma or urine ketones. Approximately 2–3% of DKA patients can present with normal blood glucose levels (less than 250 mg/dl) which called euglycemic DKA. Some of the etiologies of euglycemic DKA include recent use of insulin, low caloric intake, alcoholism, chronic liver disease, and pregnancy. Very rarely, SGLT2 inhibitor use may be responsible for euglycemic DKA.
Case Presentation: Here we present a case of 44 years old female with a past medical history of DM type 2 who presented with acute onset of nausea and vomiting. Initial laboratory findings were remarkable for anion gap metabolic acidosis with a blood glucose level of 201 mg/dl. The patient was on long-acting insulin along with Canagliflozin and Metformin therapy over years and reported being compliant with medications. She was treated with intravenous insulin therapy which resolved acidosis as well as symptoms. The patient was discharged with recommendations of discontinuation of Canagliflozin.
Discussion: SGLT2 inhibitors are the novel class of oral antidiabetic drugs which widely used due to their favorable cardiovascular and renal outcomes independent of glycemic control. However, their side effects remain a concern. DKA is a rare but serious side effect of SGLT2 inhibitors with an incidence rate of 9.4% in type 1 DM and less than 0.2% in type 2 DM. Patients typically present with euglycemia or low-grade hyperglycemia which results in a diagnostic challenge for treating physicians. SGLT2 inhibitors increase urinary glucose excretion with a subsequent decrease in circulating insulin and an increase in glucagon, rendering a metabolic shift from glucose to fatty acid utilization. During times of intercurrent illness (decreased oral intake, sepsis) or metabolic stress (surgery), decreased carbohydrate intake coupled with the aforementioned changes will result in decreased insulin secretion and increased counter-regulatory hormones including adrenaline and cortisol, promoting lipolysis, fatty acid oxidation, and ketone production by the liver which ultimately leading to euglycemic DKA.
Conclusion: SGLT2 inhibitors induced euglycemic DKA treatment is identical to classic DKA with consideration of the lack of hyperglycemia. Appropriate patient counseling to ensure safe SGLT2 inhibitor therapy is crucial, including appropriate holding parameters during concomitant volume-depleting illnesses and decreased oral intake. Timely diagnosis of euglycemic DKA, and recognitions of other rare but lethal side effects to decrease overall morbidity and mortality.
Alpelisib Induced Hyperglycemic Ketoacidosis; Broadening the Adverse Effect Profile of an Emerging Cancer Therapy
Authors: Prasad Apurwa , Ali Faisal S , Thapa Pratikshya , Tuason John P W , Kim Keun Young 
Published: May 2021

Abstract
Introduction:
Alpelisib (PIQRAY) is a Phosphatidylinositol 3-Kinase Inhibitor (PIP-3K) recently approved by the united states food and drug administration (FDA) for hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA)-mutated, advanced, or metastatic breast cancer in post-menopausal women or men with an adjuvant to Fulvestrant. Hyperglycemia is a well-known side effect of Alpelisib. However, hyperglycemic ketoacidosis is a rare and life-threatening side effect.
Case Presentation:
A 63-year-old Caucasian woman with ER/PR+, HER2- metastatic breast cancer presented to the emergency room (ER) with polydipsia, polyuria, dryness of the mouth and skin, along with a 12-pound weight loss over a period of three weeks. Alpelisib was initiated three months prior to her presentation with Hba1c: 6.4% and random BG: 89 mg/dl at the time. Her initial lab work in the ER revealed blood glucose of 474 mg/dl, sodium 129 mmol/L, potassium 5.1 mmol/L, and an anion gap of 15 with a Co2 of 19 mmol/L, HCO3 of 20 mmol/L, and a blood ketones level of 2.6. Her urinalysis revealed glucosuria and ketonuria. She was admitted to the general medical floor and Alpelisib was held. In light of her insulin naivety and no history of diabetes mellitus, it was decided to treat her with subcutaneous insulin with hourly titration based on monitoring of serum glucose and electrolytes with IV hydration. She required a total of 31 units of regular insulin along with 15 units of long-acting insulin. Her ketosis resolved within 12 hours of admission. Endocrinology was consulted and she was discharged on long-acting insulin 15. On follow-up, Alpelisib was resumed, metformin added along with long-acting insulin. Despite anti-diabetic therapy, due to persistent hyperglycemia (fasting blood glucose &gt;300 mg/dl), Alpelisib was discontinued 3 weeks after presentation.
Conclusion:
Alpelisib-induced hyperglycemic ketoacidosis is an uncommonly reported adverse event with only 3 reported cases to the best of our knowledge. While there are guidelines available to manage Alpelisib induced hyperglycemia, there are no specific recommendations for patients presenting with hyperglycemia and ketoacidosis in terms of admission to intensive care unit (ICU) or general medical floor (GMF), use of the type, route, and dosage of insulin and continuation of insulin for the persistent elevation of FBG despite interruption of Alpelisib. Alternative approaches for the treatment of breast cancer should be considered with continual hyperglycemia despite appropriate management. Multidisciplinary discussion involving the oncologist as well as an endocrinologist can be useful for the management of persistent elevation of FPG even after substantial Alpelisib free days.
Alpelisib-Induced Diabetic Ketoacidosis- A Case Report
Authors: Rodriguez Lisette Patricia , Wiese-Rometsch Wilhelmine , Lorenzo Christian 
Published: May 2021

Abstract
Background: Alpelisib, in combination with Fulvestrant, was approved in 2019 by the Food and Drug Administration for treatment of HR+, HER2- advanced or metastatic breast cancer in patients with PIK3CA mutation. a This combination is currently on phase III of study. One of the most common side effects is hyperglycemia. Rarely, this can be severe enough to induce diabetes ketoacidosis, which is an indication for interrupting Alpelisib treatment.
Clinical Case: A 78 year old female presented to our emergency department with altered mentation. Her past medical history is significant for metastatic breast cancer, with known PIK3CA mutation, started on alpelisib three months prior. Concomitantly, despite not carrying a diagnosis of diabetes mellitus, the patient was started on metformin, due to the known side effect of hyperglycemia. Upon admission, the patient was found to be tachycardic and otherwise hemodynamically stable. Pertinent laboratory studies revealed an initial serum glucose of 600 (nl 70–100) mg/dL, potassium of 5.4 (nl 3.5–5.1) mmol/L, serum carbon dioxide of 8 (nl 21–32) mmol/L, calculated anion gap of 25 (nl &lt;12) mEq/L, and a serum beta-hydroxybutyrate &gt; 4.50(nl 0.02–0.27) mmol/l. ABG revealed a pH of 7.11, PaO2 of 102, pCO2 of 11, and a lactate of 4.0 mmol/L. Glycated hemoglobin was 10.7% (nl &lt;6.5%). EKG revealed sinus tachycardia with PACs, abnormal anterolateral T wave inversion, and a QTc of 519 msec. Initial troponin was elevated at 0.15 with a max troponin at 1.40 ng/mL. Urinalysis revealed glucosuria. Chest x-ray showed no acute cardiopulmonary process. Blood cultures were negative to completion. Patient was admitted for diabetic ketoacidosis and was started on DKA protocol which included aggressive hydration with sodium chloride and insulin drip. Alpelisib was discontinued immediately. Upon resolution of the anion gap metabolic acidosis, the patient’s encephalopathy significantly improved. She was transitioned to subcutaneous insulin. During the same hospitalization, the patient’s serum glucose rapidly normalized and she did not require insulin at the time of discharge.
Conclusion: Diabetic ketoacidosis is an unusual but life-threatening side effect of Alpelisib, even in patients without an underlying diagnosis of diabetes mellitus. This case suggests that such patients should have a close monitoring of glycemic control and intensification of their anti-diabetic medications if required, to prevent hyperglycemic crises.
Clozapine Induced Insulin Dependence
Authors: McCalmon Sean , Weide Lamont G 
Published: May 2021

Abstract
Background: Antipsychotic medications come with an array of potential side effects in a difficult-to-treat population, particularly if management of other comorbidities is required. A review of the literature shows some studies have discussed the possibility of antipsychotic medication inducing hyperglycemia by blocking pancreatic M3 receptors. Other studies have shown dramatic worsening of metabolic parameters in patients who already have Type 2 Diabetes Mellitus after starting Clozapine. Clinical Case: A 23 year old African American Male with a past history of treatment resistant Schizophrenia presented to the ED with hyperglycemia and altered mental status. Blood sugar 489 mg/dL, anion gap 28 mmol/L, bicarb 13 mmol/L, white Blood Cell count 9.0 x10^3/cmm. Urine positive for Ketones. Chest Xray and EKG were normal, there were no obvious signs of infection. This was the sixth admission for Diabetic Ketoacidosis (DKA) in the past 10 months. Antibodies obtained showed negative Glutamic Acid Decarboxylase Autoantibodies (&lt;5 IU/mL), Islet Cell Antibody IgG, Zinc Transporter 8 Antibody (&lt;10 U/mL), IA-2 (&lt;5.4 U/mL). C-peptide levels were in the low normal range (1.12 ng/mL) with a blood sugar 204 mg/dL. Prior to 10 months ago, the patient did not have a diagnosis of diabetes, with labs showing expected normal fasting blood sugar levels (90s mg/dL) and triglyceride levels of 150 - 200 mg/dL. One month after starting Clozapine for treatment resistant Schizophrenia, A1c doubled to 12.3%, Triglycerides increased to 1,378 mg/dL. The patient had been insulin dependent since the time of starting Clozapine. On this admission, Clozapine was held, DKA resolved with intravenous fluid, potassium replacement, and insulin drip. Repeat testing of c-peptide with blood glucose levels analyzed with the Homeostasis Model Assessment (HOMA) showed increasing HOMA%S (from 93% to 174%) and decreasing HOMA-IR with stopping Clozapine. Psychiatry recommended Clozapine as required treatment of his Schizophrenia, therefore the patient required chronic insulin. Conclusion: This case study shows Clozapine as the only major change in medications or lifestyle in this patient’s case. He demonstrated severe hyperglycemia and development of Diabetes Mellitus within a 4-week period of medication initiation as evidenced by multiple admissions for DKA, with low/normal C-peptide levels and insulin resistance. He has since been managed as a patient with Type 1 Diabetes. Clinicians should take a multidisciplinary approach to clinical surveillance during changes in schizophrenia treatment, particularly with second generation antipsychotics such as Clozapine, with attention to metabolic derangements including DKA.
Diabetes Induced Osmotic Demyelination of the Pons in a Patient on Peritoneal Dialysis
Authors: Mandava Sri , Pfeifer Lucas , D’Souza Gretel , Wilson Mark 
Published: May 2021

Abstract
Introduction: Osmotic demyelination of the pons as a result of uncontrolled diabetes is a rare event. Here we present a unique case of central pontine myelinolysis in a patient with poorly controlled type 2 diabetes mellitus in the setting of peritoneal dialysis.
Clinical Case: A 48-year-old male with a history of insulin-dependent diabetes mellitus, hypertension, non-ischemic cardiomyopathy, and end-stage renal disease, treated with peritoneal dialysis, presented to the hospital for slurred speech, inability to walk, and persistent hyperglycemia for 3 days. Approximately 2 years prior to admission, peritoneal dialysis was initiated for ESRD and poor cardiac function. The patient’s outpatient pharmacologic regimen was 30 units of glargine daily and glimepiride. On physical exam, there was evidence of aphasia, dysarthria, and muscle weakness (2/5 in bilateral upper and lower extremities) without muscle rigidity. Deep tendon reflexes were absent in the lower extremities, but sensation to light touch was intact throughout. On admission, the patient was found to be in a hyperosmolar hyperglycemic state without ketosis. Initial lab tests were significant for serum sodium: 138mmol/L (n=134–145 mmol/L), serum sodium corrected for hyperglycemia: 143 mmol/L, serum glucose: 419mg/dL (n=75–99 mg/dL), beta-hydroxybutyrate 2.1 mg/dL (n&lt;4.4 mg/dL), and serum osmolality: 330mosmol/kg (n=275–305 mosmol/kg). Urinalysis showed glucosuria without ketonuria. The cerebrospinal fluid analysis showed protein 57, glucose 109, and WBC 3. Lab studies for meningitis/encephalitis panel were negative. During his 2 years of dialysis, his HbA1C increased from 7.6% to 14.3% (n&lt;5.6%). CT brain without contrast showed midline hypoattenuation of the inferior pons without edema. Magnetic resonance imaging without contrast of the brain demonstrated a lobulated lesion in the pons measuring 1–2 cm that shows T2 hyperintensity without surrounding edema. He was then diagnosed with central pontine myelinolysis in the setting of chronic glycemic changes.
Conclusion: Osmotic demyelination of the pons is typically associated with rapid correction of hyponatremia. We describe osmotic demyelination of the pons as a result of poorly controlled diabetes with normal sodium. To our knowledge, this is the first report of this event in association with worsening diabetes after the initiation of peritoneal dialysis.
Diabetic Ketoacidosis and Acute Pancreatitis in Covid-19 Setting
Authors: Srinivasan Aswin , Wilson Branden , Pansuriya Tusharkumar , Qasmi Syed Talha , Kesavan Ramesh Babu 
Published: May 2021

Abstract
Introduction: Respiratory, kidney and gastrointestinal are some of the systems affected by COVID-19. Although COVID-19 has been studied as a lung pathogen, endocrine system involvement has rarely been studied. In this case report, we present a case of diabetic ketoacidosis (DKA) and acute pancreatitis in the setting of COVID-19.
Case Description: A 52-year-old female with a PMH of type 1 diabetes mellitus and hypothyroidism, presented to the ED with nausea, vomiting, fatigue and diffuse abdominal pain. She reports cosmetic surgery a few weeks prior and she started feeling these symptoms at the beginning of admission day of admission. On admission, WBC was 34.9, blood glucose was 496, lactic acid of 3.1. Arterial blood gas revealed pH of 6.96, PCO2 of 17 mEq/L, PO2 of 143, HCO3 of 5 and anion gap of 23. DKA protocol was initiated and was upgraded to ICU. She was found to be RT-PCR positive for SARS-CoV-2. She denied other symptoms, including melena, jaundice, hematochezia, hematemesis, cough, SOB or diarrhea. She also denied use of alcohol, tobacco or illicit drugs, prior hospitalizations, or family history of pancreatitis. The physical exam was significant for tenderness to palpation in epigastric region without guarding or rebound. Laboratory studies revealed lipase: &gt; 4000U/L, AST: 64 U/L, ALT: 57 U/L, ALKPHOS: 152 U/L, and total bilirubin: 1.1 mg/dL. Serum triglycerides and calcium levels were within normal limits. CT abdomen showed a severe peripancreatic inflammation and edema, moderate non-organized fluid surrounds pancreas. An abdominal ultrasound showed no calcified gallstone or gallbladder wall thickening. The common bile duct was 3 mm, normal size. Over the course of 24 hours, anion gap was 7, pH was 7.28, blood glucose was 158. For sepsis, lactic acid was 0.7 after initiation of azithromycin. For acute pancreatitis, she was treated conservatively with intravenous fluids, bowel rest and analgesia. Patient denied any upper respiratory symptoms and did not require oxygen so steroids were not started for COVID PNA. Her symptoms improved and she was discharged home. Discussion: Here we report a case of a patient who presented with DKA, found to have severe acute pancreatitis as well as SARS-CoV2 PCR positive. Few case reports have reported an association of DKA and acute pancreatitis. Although the exact mechanism by which SARS-CoV-2 is evolving, it is thought to be mediated by the Angiotensin-Converting Enzyme-2 which is present in intestine, and on islet cells of the pancreas. This injury may be due to cytopathic effect of viral replication or indirectly caused by the inflammatory response induced by the virus. Further studies are needed to better understand the pathophysiology behind AP in the setting of COVID-19.
Conclusion: This case highlights DKA and AP as a possible initiating presenting manifestation of COVID-19 infection