bluuebunny/crossref_metadata_2025_split huggingface dataset:
Can Anti-Hypertensives Cause Hypoglycaemia? - A Rare Presentation of Recurrent Hypoglycaemia Secondary to an ACE-Inhibitor
Authors: Kapoor Ashutosh , Banerjee Moulinath , Thant Aye Aye , Sankar Adhithya 
Published: May 2021

Abstract
Introduction: Angiotensin-converting enzyme (ACE) inhibitors are commonly prescribed Anti-hypertensives which are first line treatments in patients with Diabetes. We report a rare but significant side-effect of ACE inhibitor treatment, relevant to Diabetic and non-diabetic patients alike. Case Details: We report the case of a 79 year male, with a background of Hypertension (HTN), established on Ramipril and Bendroflumethiazide, who was admitted following an episode of unresponsiveness secondary to Hypoglycaemia, which was initially presumed secondary to Alcohol, the intake of which was minimal. He did not have a history of Diabetes Mellitus. 7 weeks later, he had a similar presentation and as found to be profoundly Hypoglycaemic. On arrival, his observations were unremarkable except for CBG 1.9 and GCS of 14/15, which responded well to IM glucagon, and IV Dextrose. Relevant investigations revealed significantly impaired renal functions and normal CT imaging. There was no history of alcohol intake or intoxication.
Management: Following acute management and stabilisation, he was admitted under the Endocrine and Diabetes team, who suspended his regular medications, including his ACE-I. As an inpatient, he underwent extensive biochemical investigations which were unremarkable followed by a prolonged 72 hours fasting test and an Oral Glucose Tolerance Test, wherein no significant drop in Blood Glucose was noted in both. Subsequently, there were no further episodes of hypoglycaemia and he remained asymptomatic whilst off his ACE-I and he was safely discharged. He was followed up in our Endocrine clinic and was found to have no episodes of Hypoglycaemia since discharge and remained asymptomatic. Discussion: We report the rare presentation of recurrent hypoglycaemia in a non- diabetic secondary to ACE-I. Hypoglycaemia may be defined by the Whipple’s triad, a classical triad of hypoglycaemic symptoms, low Blood Glucose levels and relief of symptoms following ingestion of glucose. The mechanism by which ACE-I treatment leads to hypoglycaemia remains unclear. It has been postulated that ACE-I related alterations in the Kininogen-Kinin system, are associated with hypoglycaemia. This mechanism may lead to an increase in Insulin sensitivity, mediated by increased muscle tissue uptake and diminished hepatic glucose production. Another proposed mechanism is the suppressive effect that ACE-inhibitors exhibit on the peripheral sympathomimetic overactivity, thus causing Hypoglycaemia. Exacerbating factors comprise of concurrent renal impairment, as in this case. The first case of ACE-I induced Hypoglycaemia was reported in 1985, with the usage of Captopril. To the best of our knowledge, this is one of the rare peculiar cases wherein an ACE-I has been implicated as the underlying aetiology causing Hypoglycaemia in a Non-Diabetic.
Capecitabine-Induced Hyperosmolar Hyperglycemic State
Authors: Yim Carly , Arnason Terra G , Hussein Nassrein 
Published: May 2021

Abstract
Capecitabine is an orally administered prodrug of 5-fluorouracil (5-FU) which is often used for treatment of solid tumour cancers such as breast cancer and gastrointestinal tumours. Common adverse effects include nausea, diarrhea, anorexia and erythrodysthesia (hand-foot syndrome). However, there have been case reports of metabolic disturbances linked to capecitabine including hyperlipidemia, and less commonly, hyperglycemia.
We report a case of a new diagnosis of persistent diabetes mellitus following an acute presentation of hyperosmolar hyperglycemic syndrome (HHS) subsequent to treatment with the chemotherapy agent, capecitabine. A 72 year old female with a history of metastatic breast cancer was admitted to hospital for management of hyperglycemic hyperosmolar state (HHS) after bloodwork from her family doctor revealed an elevated random blood glucose (40.2 mmol/L). Leading up to her presentation, the patient had completed 7 cycles of capecitabine treatment for her breast cancer. Prior to her capecitabine treatment, the patient did not have a history of diabetes mellitus. However, on admission, her hemoglobin A1C (HbA1C) was found to elevated into the diabetic range. Offending medications were considered and given the temporal dysglycemia following the patient’s chemotherapy regimen, capecitabine was thought to be a probable offending agent. The patient was acutely treated for HHS, and eventually transitioned to a basal-bolus insulin regimen at discharge. Her capecitabine was held pending review with her oncology team and she was closely followed up by her family doctor. The patient’s insulin regimen was ultimately titrated down to basal insulin only.
Given the increasing use of capecitabine therapy in breast cancer, it is important to recognize the risk of hyperglycemia and hyperglycemic emergencies as a potential adverse effect of this treatment. It highlights the need to ensure that blood glucose is monitored throughout treatment to prevent hyperglycemic emergencies.
Diabetic Myonecrosis: A Rare Condition That Present With Pain
Authors: Bicchi Amelia Guzman , Lubrano Heinsen Antonio E , Gomez-Daspet Joaquin , Tourtelot John 
Published: May 2021

Abstract
Diabetic myonecrosis is the term used for spontaneous ischemic necrosis of skeletal muscle, unrelated to atheroembolism or occlusion of major arteries. This is an uncommon manifestation of long-standing and poorly controlled diabetes mellitus.
A 65-year-old Hispanic female presented to the Hospital with one-week history of worsening right thigh pain. She denied associated fever, trauma, history of blood clots, past surgery, recent travel, ect. Patient has history of uncontrolled diabetes type 2, diabetic neuropathy and End-Stage Kidney Disease on hemodialysis for the last 3 years. Home medications include gabapentin 300 mg daily and insulin 70/30 20 units twice a day. On physical exam, vital signs appeared within normal limits. There was right medial and anterior thigh fullness, warmth and tenderness without erythema or fluctuance. Laboratory studies are pertinent for HbA1C 8.8% (n &lt;6.5%), C-reactive protein (CRP) 12.97 (n &lt;0.5 mg/dL), Erythrocyte sedimentary rate (ESR) &gt;130 (n 0–30 mm/hr), Creatinine: 6.2 (n 0.57–1.11 mg/dL), BUN 77 (n 6–20 mg/dL), CO2 19 (n 22–29 mEq/L) and albumin 2.7(n 3.5–5.0 gm/dL). Other labs including CPK, glucose, ANA panel and CBC are within normal limits. Patient was admitted with initial diagnosis of cellulitis without improvement in clinical status after 3 days of antibiotics. MRI of the right thigh showed proximal thigh muscle, cutaneous and subcutaneous edema. Right thigh muscle biopsy showed marked myonecrosis with surrounding endomysial edema, foci of histiocytes, fibroblasts, and regenerating muscle fibers. Histologic features, together with localized muscle pain, normal CPK, negative microbiologic studies and uncontrolled diabetes are consistent with diabetic myonecrosis. Insulin was adjusted for tight glucose control and patient was started on low dose aspirin with outpatient follow-up.
Diabetic myonecrosis presents with acute onset of painful swelling that evolves over days or weeks. The most common affected areas are the front and back of the thigh and calf. The pathophysiology is not well understood but appears related to thromboembolic events secondary to microvascular endothelial damage leading to tissue ischemia, which triggers an inflammatory cascade causing local tissue damage and ischemic necrosis. Common laboratory findings include elevated ESR, CRP and HbA1C level. Treatment involves symptomatic management, rest, glycemic control, analgesia and low-dose aspirin. The optimal approach is uncertain and current treatment is based upon published case reports and case series; there have been no randomized trials to compare approaches or specific agents. Close patient follow-up and tight glycemic control are key elements to prevent progression of this condition.
Do COVID-19 Apps Address Diabetes Mellitus and Health Equity Issues
Authors: Nguyen Brian , Lau Chap-Kay Kendra , Wu Gloria , Lubrin Dwight , Siu Vincent 
Published: May 2021

Abstract
Purpose: To evaluate if COVID-19 apps address risk factors such as diabetes, hypertension, race, gender, sexual orientation, language. Background: In 2019, there were 204 Billion app downloads and 3.7 billion downloads of ehealth apps. COVID-19 affects ethnic minority patients with diabetes, hypertension, and other risk factors. Spanish is the second most commonly used language after English in the U.S.. African Americans, Hispanic Americans, and Asian Americans are at an increased risk of COVID-19. LGBTQ+ communities are also at higher risk for COVID due to historically poor access to healthcare. Methods: The search term, “COVID,” in Google Play store and Apple App store was used to find the most popular COVID-19 apps. App inclusion criteria: 1) Contains COVID-19 information and/or COVID symptom tracker, 2) Marketed and designed for the general public, 3) Free, 4) Android (DROID): 100,000+ Downloads; Apple (iOS): highest star ratings. Apple does not provide a number of downloads. App features: COVID-19 information, COVID-19 symptom questionnaire (QN), Diabetes, Hypertension, Cardiovascular disease, Languages (Spanish, Chinese), Race, Gender, and Sexual Orientation. Results: The top 10 DROID apps in descending order are: 1) GuideSafe, 2) CO Exposure Notifications, 3) Care19 Diary, 4) Care19 Alert, 5) Crush COVID RI, 6) MI COVID Alert, 7) DC CAN, 8) CombatCOVID MDC, 9) CombatCOVID PBC, 10) Stronger than C19. The top 10 iOS apps in descending order are: 1) SlowCOVIDNC, 2) COVIDWISE, 3) COVID Alert Pennsylvania, 4) COVID Alert DE, 5) COVID Alert NY, 6) Covid Watch Arizona, 7) Apple COVID-19, 8) COVID Alert NJ, 9) COVID Trace Nevada, 10) CDC. Of the 20 apps: COVID 19 information: 20/20; COVID-19 symptom QN: 8/20; DM: 2/20; HTN: 1/20; CardioVasc: 2/20; Spanish: 11/20 (2/11 of the Spanish apps have Chinese as well). Race: 5/20. Gender: 8/20; Sexual Orientation: 3/20; Age: 10/20. Conclusion: 1) Most apps do not ask about important risk factors such as DM, HTN, and Race. 2) Smartphone apps are not uniform in their health education features. 3) Healthcare providers should continue to play an important role in public education despite the ubiquity of mobile apps.
Endoscopic Ethanol Ablation as Definitive Therapy for Suspected Insulinoma
Authors: Taneja Charit , Groff Andrew J , Lam Milay Luis 
Published: May 2021

Abstract
Introduction: Hypoglycemia is defined as plasma glucose &lt;70mg/dL, with autonomic and/or neuroglycopenic symptoms often occurring at levels less than 55mg/dL. Diagnostic workup of hypoglycemia unrelated to use of hypoglycemic agents is crucial as it is linked to increased mortality. After ruling out common culprits such as drugs (insulin, sulfonylureas), ethanol and malnutrition, further testing should be pursued for patients who meet the Whipple’s Triad: symptoms of hypoglycemia, documented low plasma glucose and relief of symptoms upon raising plasma glucose. We present the case of an 85-year old male with a suspected insulinoma who underwent endoscopic alcohol ablation as definitive therapy.
Case: An 85-year-old male with a history of metastatic prostate cancer was found to have recurrent episodes of asymptomatic hypoglycemia with fasting plasma glucose levels as low as 50-60s during an unrelated inpatient admission. He had no history of diabetes mellitus or insulin use. On further investigation, he was noted to have recurrent falls, though these symptoms could not be temporally linked to documented hypoglycemia as the patient was not monitoring blood sugars at home. Further workup revealed fasting plasma glucose of 58mg/dL and negative sulfonylurea screen. Plasma C-peptide and fasting plasma insulin levels during an episode of hypoglycemia were elevated at 6.42ng/mL and 38uIU/mL respectively. IGF-II and insulin autoantibody testing was negative. Abdominal imaging revealed a 1.3cm hypervascular pancreatic head lesion consistent with a neuroendocrine tumor, concerning for an insulinoma in view of his lab findings. Surgical removal of this lesion was not within the patient’s goals of care. Attempts at medical management included escalating doses of prednisone and subcutaneous octreotide; however, he continued to have hypoglycemic episodes despite therapy. His cardiac history precluded the use of other medical therapies. After careful evaluation, he underwent ultrasound-guided ethanol ablation of his neuroendocrine tumor as potential definitive therapy, with successful resolution of hypoglycemic episodes noted during his post-procedural hospital stay.
Discussion: Traditionally, insulinomas are primarily managed surgically. Poor surgical candidates can benefit from medical management including diazoxide, somatostatin analogs and verapamil among others. Ultrasound-guided ethanol ablation is a newer modality aimed achieving cure in selected patients, thus avoiding need for surgery. Our case highlights the challenges in management of insulinomas, especially in complicated patients like ours who are not surgical candidates and who may be resistant to medical therapy. Though there are not many studies on the long-term efficacy and outcomes with ethanol ablation of insulinomas, it appears to be a promising option and certainly deserves further study.
Euglycemic Diabetic Ketoacidosis Secondary to SGLT2-inhibitor Use in Combination With a Ketogenic Diet
Authors: Hester Joi C , Zimmerman Stacy , Nimmo Teresa Allison , Cunningham Wesley , Liu Joshua , Sukpraprut-Braaten Suporn , Pasquel Francisco J 
Published: May 2021

Abstract
Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are cardiorenal protective agents increasingly used in patients with diabetes. Cases of euglycemic diabetic ketoacidosis (euDKA) have been reported particularly among patients with type 1 diabetes. Our case is an example that highlights the role SGLT-2 inhibitors play in the development of euDKA in a patient with type 2 diabetes with confounding factors of strict adherence to a ketogenic diet and ankle fracture.
A 72-year-old female with a history of type 2 diabetes presented to the emergency department (ED) with right ankle pain and obvious deformity after a mechanical fall. Radiography of the right lower extremity confirmed distal fracture of the tibia and fibula. After reduction of her fracture in the ED, she was admitted in anticipation of an open reduction internal fixation. Her diabetes was controlled on empagliflozin monotherapy and adhering to a ketogenic diet. She monitored her blood ketones daily at home and reported values in the 3–4 mmol/L range. On admission, her basic metabolic panel (BMP) revealed a blood glucose of 148 mg/dL, bicarbonate of 20 mEq/L, anion gap of 18 mEq/L, Cr of 1.3 mg/dl, and eGFR of 40 mL/min. Her beta-hydroxybutyrate (BHB) was 5.09 mmol/L. The initial assessment was presumed starvation ketosis.
On hospital day three, she complained of continued nausea, polydipsia, and abdominal pain. Chart review revealed nocturia with approximately 3–4 voids per night. Repeat BMP showed a blood glucose of 152 mg/dL, bicarbonate of 16 mEq/L, anion gap still at 18 mEq/L, Cr 1.4 mg/dl, and eGFR of 37 mL/min. Since admission, all of her blood glucose levels ranged between 118–178 mg/dL. She denied dyspnea but exhibited Kussmaul respirations on physical exam. Repeat labs revealed a BHB of 8.92 mmol/L, and arterial blood gas (ABG) showed pH 7.2, pCO2 23, pO2 100, bicarbonate 8.6 mEq/L, consistent with high-anion gap metabolic acidosis, confirming the diagnosis of euDKA. Her empagliflozin had been held since admission, but she had not received any insulin up to this point due to euglycemia. She was immediately started on a weight-based dose of 12 units of insulin glargine with subsequent improvement of her BHB and anion gap.
This patient’s use of an SGLT2-inhibitor in combination with her being on a ketogenic diet, contributed to a nonregulated state of ketone production leading to euDKA in the perioperative period. As SGLT2-inhibitors become more readily available, it is important to educate physicians and patients about the risk of euDKA during fasting, ketogenic diets, and the perioperative period.
Euglycemic DKA in Patients on SGLT2 Inhibitor and Potentially Ketotic State
Authors: Khalifa Maram , Aftab Hassaan , Kantorovich Vitaly 
Published: May 2021

Abstract
Background: With mounting evidence demonstrating improved cardiovascular and renal outcomes with the use of sodium-glucose cotransporter-2 (SGLT2) inhibitors, this class of newest antidiabetic agents is rapidly gaining favor. SGLT2 inhibition lowers the renal threshold for glucose excretion, resulting in renal glycosuria, a shift in substrate utilization from carbohydrate to fat oxidation and hyperglucagonemia and thus poses the risk of developing euglycemic DKA as a rare but serious adverse effect. Clinical Cases: the first case is A 36-year-old female was diagnosed with type 2 DM with an HbA1c of 10% and was started on multi-agent antihyperglycemic therapy including metformin 500 mg BID, extended release exenatide 2 mg once a week and empagliflozin 25 mg once daily which were all initiated simultaneously. 2 days after starting regimen, she complained of nausea, vomiting and was unable to tolerate oral diet and fluids by day 4 which potentially predisposed to starvation ketoacidosis. She presented to the ED with normal vitals, grossly normal physical exam and labs were significant for beta-hydroxybutyrate of over 7 mmol/L (ref range &lt;0.28), bicarbonate of 10 mmol/L (22 - 33), anion gap 25 (7 - 17), arterial pH 7.16 (7.33 - 7.43), serum glucose 111 (7.33 - 7.43). GAD-65 antibody titer was &lt;5 IU/mL (&lt; 5). She was diagnosed with euglycemic DKA, transferred to ICU and started on DKA protocol to which she responded very well. Second patient is A 65 Years old male with past medical history of CAD, HTN, HDL, history of PE/DVT and Type 2 DM was on insulin and jardiance, started ketodiet while continuing taking the jardiance and stopped taking his insulin because his sugars were controlled presented to the ED with abdominal pain, nausea and vomiting, had relatively normal vitals and benign physical exam, labs showed Bicarbonate of 9 mmol/L (22 - 33), anion gap of 31 (7 - 17), venous pH of 7.07 (7.33 - 7.43) glucose was 189 (7.33 - 7.43), beta-hydroxybutyrate of over 7.7 mmol/L (ref range &lt;0.28), patient was admitted to the ICU and started on insulin on DKA protocol Conclusion: SGLT2 inhibitors may be associated with DKA due to their ketogenic effects secondary to enhanced lipolysis and increased glucagon to insulin ratio. although not expected, euglycemic DKA could be much more present in cases where there is predisposition to increase ketones generation w/without appropriate clearance eg. starvation, ketotic diet, AKI, etc. These should be monitored for and the patient needs to be educated about accordingly to prevent both adverse outcomes and potential decrease in drug use if not strongly indicated. also,It would be prudent for prescribing clinicians to advise patients to withhold potentially harming medications temporarily if they cannot maintain adequate oral intake.
Glycogenic Hepatopathy in a Patient with Pancreatogenic Diabetes
Authors: Baggett A Brooke , Jiwani Rahim Ali , Shahid Basma 
Published: May 2021

Abstract
Glycogenic hepatopathy is characterized by acute liver injury secondary to reversible accumulation of excess glycogen in hepatocytes. This phenomenon has been described in type 1 diabetes, with few cases reported in patients with type 2 diabetes. Glycogenic hepatopathy in the setting of pancreatogenic (type 3c) diabetes has yet to be reported.
A 57-year-old female with a history of insulin-requiring pancreatogenic diabetes mellitus secondary to alcohol-induced chronic pancreatitis status post distal pancreatectomy presented with recurrent admissions for abdominal pain, hyperglycemia, hyperosmolar hyperglycemic state (HHS), and unexplained elevation of liver transaminase levels. Glycemic control remained poor over many years with consistently elevated HbA1c in the setting of labile blood sugars, medication noncompliance, and lifestyle non-adherence.
The patient was admitted to the hospital with altered mental status and markedly elevated blood glucose (1,182 mg/dL) concerning for HHS. On admission, her liver function tests (LFTs) revealed elevated alkaline phosphatase (1,011 U/L, n &lt;150 U/L), AST (583 U/L, n &lt;34 U/L), and ALT (517 U/L, n &lt;55 U/L). Direct and total bilirubin were within normal limits. The patient underwent extensive workup including drug and toxin levels, autoimmune evaluation, serology for infectious causes, abdominal computed tomography scanning, right upper quadrant ultrasound, and magnetic resonance cholangiopancreatography (MRCP). All laboratory workup was negative, ultrasound was unremarkable, and MRCP showed no evidence of biliary or common bile duct dilatation. Throughout her hospitalization, LFTs gradually improved with optimization of blood glucose.
Less than one week later, the patient returned with blood glucose of 673 mg/dL and LFTs notable for alkaline phosphatase 789 U/L, AST 1,068 U/L, and ALT 299 U/L. Again, all testing was negative for causes of rapid increase in liver enzymes. Similar to previous admissions, her LFTs improved with resolution of hyperglycemia. Review of electronic medical record revealed a similar trend during previous admissions. The patient did not undergo liver biopsy; however, the parallel relationship of LFTs and hyperglycemia, in the absence of radiologic or laboratory evidence of alternate liver pathology, supports the diagnosis of glycogenic hepatopathy.
This is the first case of glycogenic hepatopathy reported in a patient with pancreatogenic diabetes. Due to the rarity of this condition and minimal literature of its occurrence in adult non-type-1 diabetics, glycogenic hepatopathy is likely infrequently considered when evaluating patients with recurrent hyperglycemia and elevated LFTs. This case accentuates the need for further research of this condition in non-type 1 diabetics as the prognosis and management differ from other forms of acute liver injury.