Urine Ketone Research Articles

2367-PUB: Metabolic Abnormalities after Coronary Angiogram in Patients Taking Sodium-Glucose Cotransporter 2 Inhibitors

Background: Some evidence suggests an association of SGLT2 inhibitors (SGLT2i) with an increased risk of euglycemic DKA (euDKA). The incidence and possible procedure-related triggers of metabolic abnormalities in patients taking SGLT2i after coronary angiography has not been well established. Methods: All patients with diabetes mellitus on a SGLT2i undergoing coronary angiography at a single center from November 2017 to November 2018 were reviewed for periprocedural characteristics and post-procedural metabolic abnormalities. Metabolic abnormalities were defined as: euDKA, DKA with hyperglycemia, or elevated urine ketones without confirmed acidosis. Results: A total of 44 patients with diabetes mellitus on a SGLT2i undergoing coronary angiogram were identified. There was one case of euDKA after angiography and one of hyperglycemic DKA. There was an additional two cases of patients with elevated urine ketones for whom DKA labs were not available. Baseline characteristics including age (p=0.71), type of SGLT2i (p=.20) and hemoglobin A1c (p=.49) were similar between the cases with metabolic abnormalities and those without. Similarly, procedural variables including indication for angiography (p=0.26), amount of contrast used (p=0.47), angiography outcome (p=0.87) and complications (p=0.40) were not statistically different between the groups. Conclusions: With a rare incidence and subtle clinical presentation, cases of euDKA may be missed after angiography, especially if acidosis is attributed to the preceding procedure without further workup. Continued case identification may help determine if specific procedural variables contribute to the development of euDKA. As the fasting state and stress of angiography can be triggers for ketosis, protocols should be developed for post-procedural screening and management in this population. Disclosure M. Shahid: None. S. Pickett: None. X. Jia: None. M. Alam: None. Y. Birnbaum: Other Relationship; Self; AstraZeneca. Other Relationship; Spouse/Partner; AstraZeneca, Boehringer Ingelheim International GmbH.

1277-P: Diabetes Management Supplies in Youth with Type 1 Diabetes: Don’t Leave Home Without Them!

Youth with type 1 diabetes (T1D) require 24/7 access to T1D management supplies. This study aims to characterize access to T1D supplies when youth are away from home. We emailed a comprehensive survey to 4756 parents of T1D Exchange participants <18 years old; 752 respondents completed the survey (83% completed by parents). Results were age-stratified: <6 (N=21), 6-12 (N=271) and 13-18 (N=459). The majority of youth carry rapid-acting insulin most of the time or always, yet the proportion decreases as age increases (Table 1). ≥80% of injection users carry an extra pen or syringe, while >55% of pump users carry an extra infusion set. Among CGM users, 100% of ≤6 years old vs. 67% of adolescents carry a receiver or phone; 33% of 13-18 years old never carry an extra sensor. 38% of youth ≤6 years old vs. 27% of teens carry blood or urine ketone testing supplies. In total, 64% reported carrying glucose tablets or gel; 87% carry another rapid acting carbohydrate. 64% of respondents carry glucagon, again decreasing across adolescence. Over 2/3 carry at least one form of T1D identification. Technology to optimize glycemic control and detect/prevent acute complications of T1D have improved. Yet, adolescents are less likely than younger T1D-affected youth, to carry supplies to detect, prevent and/or treat acute events. These findings call for novel and ongoing T1D emergency preparedness training to strike a balance between supervision and autonomy of adolescents. Disclosure M. Quinn: None. R. Bailey: None. N.C. Foster: None. J. Simmons: None. E. Eyth: None. H. Rodriguez: Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Bristol-Myers Squibb Company, Daiichi Pharm Corp, MannKind Corporation, Medtronic MiniMed, Inc. Research Support; Spouse/Partner; Medtronic MiniMed, Inc. Research Support; Self; Takeda Pharmaceutical Company Limited. Other Relationship; Self; Merck & Co., Inc., Novartis Pharmaceuticals Corporation, Novo Nordisk Inc. S. Corathers: None. C.J. Levy: Advisory Panel; Self; Novo Nordisk A/S, Sanofi. Employee; Spouse/Partner; Allergan. N.M. Sheanon: None. R.M. Wasserman: None. D. Sparling: None. D. Adkins: None. A. Albanese-O'Neill: None. D.J. DeSalvo: Consultant; Self; Dexcom, Inc., Insulet Corporation. Funding The Leona M. and Harry B. Helmsley Charitable Trust

Improving Compliance with Very Low Energy Diets (VLEDs) Prior to Bariatric Surgery-a Randomised Controlled Trial of Two Formulations.

Preoperative very low energy diets (VLEDs) improve access during bariatric surgery. Compliance with traditional VLED is variable, mainly due to gastrointestinal side effects. Formulite™ is a new formulation of VLED, with higher protein, soluble fibre and probiotics. To compare traditional VLED (Optifast™) with the new VLED (Formulite™) and assess compliance, weight loss, satisfaction, side effects and surgical access. This was a randomised double-blinded study involving patients scheduled for bariatric surgery. The primary outcome was compliance, assessed by urinary ketone concentration and proportion of patients in ketosis at 2weeks. Secondary outcomes were weight loss, satisfaction and patient reported outcomes, gastrointestinal side effects and operative conditions. There were 69 participants: 35 in the Formulite™ group and 34 in the Optifast™ group. Ketosis at 2weeks was achieved in both groups (88.5% vs 83.3%, Formulite™ vs. Optifast™, p = 0.602). Urinary ketones were higher with Formulite™ (1.5 vs 15mmol/L, p = 0.030). Total body weight loss percentage, hunger and operative conditions were similar in both groups. Formulite™ produced less flatulence (score 3 vs 2, p = 0.010) and emotional eating (score 2 vs 1, p = 0.037); however, Optifast™ ranked higher in terms of taste (score 4 vs 3, p = 0.001) and overall satisfaction (score 5 vs 7, p = 0.011). Compliance over 2weeks was high in both VLEDs with most subjects achieving ketosis. Overall satisfaction was moderately high, although variable. Whilst Formulite™ is a viable alternative to Optifast™, better formulations of VLED that addresses key adverse effects, whilst achieving ketosis, would be of significant value.

Diabetic ketoacidosis caused by fulminant type 1 diabetes during adjuvant chemotherapy for colon cancer: A case report.

Development of diabetic ketoacidosis (DKA) caused by fulminant type 1 diabetes (FT1D) during administration of uracil-tegafur (UFT) with leucovorin (LV) as adjuvant chemotherapy is extremely rare. Here, we report a case of DKA caused by FT1D during administration of UFT with LV as adjuvant chemotherapy for colon cancer. A woman in her 60s was transferred to the emergency medical center of our hospital with complaints of impaired consciousness and vomiting. She had undergone left hemicolectomy and D3 lymph node dissection for transverse colon cancer 8 months earlier. She was provided UFT with LV as adjuvant chemotherapy. Laboratory analysis revealed hyperglycemia, high anion gap metabolic acidosis and urinary ketones. She was diagnosed with DKA and was started on intravenous infusion of fluid and continuous subcutaneous insulin injections. Following admission, she was examined and diagnosed with FT1D. The present case describes an extremely rare case of DKA caused by FT1D during adjuvant chemotherapy with UFT + LV for colon cancer.

Biochemical Changes of Ketosis in Cows at Post Parturient Period

The present study was conducted to determine biochemical changes in apparently healthy control and ketotic cows. Fresh urine samples were collected from 350 post-parturient cows to screened urinary ketone bodies by using Modified Rothera's test and urine Diastix test. Total forty cows showing clinical signs of ketosis were included for biochemical studies (before and after treatment). It was observed that serum glucose was significantly (P<0.01) lower as compared to helthy animals. While, serum ketones and urine ketones levels were significantly (P<0.01) elevated. Similarly, total serum protein, globulin and albumin levels were significantly (P<0.05) higher in ketotic cows. It can be concluded that group treated with Decadurabolin (Nandrolone Decanoate) in association with parenteral dextrose give excellent recovery rate in Ketosis.

Diabetic ketoacidosis in children and adolescents with newly diagnosed type 1 diabetes in Tigray, Ethiopia: retrospective observational study.

Background: Diabetic ketoacidosis (DKA) is the most severe acute complication of type 1 diabetes mellitus which results in increased risk of morbidity and mortality especially in developing countries.Objective: To assess prevalence and associated factors of diabetic ketoacidosis in children and adolescents with newly diagnosed type 1 diabetes in hospitals of the Tigray region, Ethiopia.Methods: A facility based retrospective observational study design was conducted in newly diagnosed type 1 diabetic children and adolescents up to the age of 18 years who were registered in 13 general and two referral hospitals from January 1, 2013 to December 30, 2017. The diagnosis of diabetic ketoacidosis was made with the criteria below, Children presenting with polysymptoms, weight loss, vomiting, dehydration, and also the indirect signs or effects of acidosis on respiratory and central nervous systems like Kussmaul breathing, lethargy or coma and biochemically random blood sugar level >11 ml/L, glucosuria and urine ketone >+1 and diagnosed with type 1 diabetes for the first time. Descriptive, Mann–Whitney U and logistic regression analysis were carried out to describe and identify the associated factors with diabetic ketoacidosis.Results: More than three-quarters, 258/328 (78.7%) of the newly diagnosed type 1 diabetes patients, presented with diabetic ketoacidosis at initial diagnosis. Median age of diabetic ketoacidosis patients was 11 years. The patients with diabetic ketoacidosis were younger than nondiabetic ketoacidosis patients (11 vs 13 years, P=0.002). The mortality rate of diabetic ketoacidosis was 4.3%. Young age, presence of precipitating factors and symptoms of DKA/diabetes were found to be highly associated with diabetic ketoacidosis at initial diagnosis.Conclusions: The prevalence of diabetic ketoacidosis was alarmingly high. Young age group patients, precipitating factors and the presence of symptoms of diabetes/DKA like excessive drinking, vomiting and fatigue were highly associated with diabetic ketoacidosis.

Ketoacidosis in Euglycemic Patients With Type 2 Diabetes After Abdominal Surgery

Diabetic ketoacidosis is defined as hyperglycemia >250mg/dL with metabolic acidosis of arterial pH <7.3, serum bicarbonate <18 mEq/L with positive urine and serum ketones and an anion gap >10. Euglycemic ketoacidosis has been reported in patients with type 2 diabetes and in patients with type 1 diabetes. However, as a surgical complication, euglycemic ketoacidosis has not been reported. We report 2 cases from 2 teaching tertiary care centers of patients with type 2 diabetes who developed high-gap ketoacidosis in an intensive care unit while recovering from emergent abdominal surgery. Both patients developed altered mental status, metabolic acidosis with a bicarbonate level as low as 14mEq/L, and an anion gap > 18, without hyperglycemia. Both patients had β-hydroxybutyrate levels > 5mmol/L.

SAT-470 A Case of Acromegaly with Concomitant Hypercortisolism Presenting with Diabetic Ketoacidosis

Background: Acromegaly is a rare disorder with an annual incidence of 4-6 new cases per 1 million population.1 Impairment in glucose metabolism has been previously described in such disorder, but diabetic ketoacidosis is rare. Case: A 25 year old, male, presented at our emergency room with seizures. Laboratory data showed hyperglycemia (blood glucose 418 mg/dl), ketonuria (urine ketone +2), and pure high anion gap metabolic acidosis consistent with severe Diabetic Ketoacidosis. Hba1c was 12%. A normal fasting C-peptide 1.68 ng/ml (1.10-4.40 ng/ml) indicate residual insulin secretion, or maybe an inappropriately normal response in the presence of severe hyperglycaemia hyperglycemia. Features of acromegaly were noted and hormonal evaluation showed elevated IGF-1 level at 484.50 ng/ml (83-344 ng/ml), supporting the diagnosis. Random growth hormone was elevated at 5.7 ng/ml (<3 ng/ml). GH suppression testing with oral glucose load was not done due to unstable glucose levels. An elevated 24 hour urine cortisol 6208.0 nmol (100.0-379.0 nmol/24h) may be associated with uncontrolled diabetes, or an underlying subclinical Cushing’s disease contributing to further insulin resistance. Other hormones of the anterior pituitary reveal normal thyroid function, central hypogonadism and hyperprolactinemia at 828.50 uIU/ml (58.0-475.0 uIU/ml) likely due to hypophyseal stalk compression by the tumor. Cranial MRI with contrast showed an enhancing sellar mass measuring 23.7 x 22.3 x 18.0 mm (AP x T x CC) which extends inferiorly to the upper portion of the prepontine cistern. Resolution of ketoacidosis required 360 units of regular insulin per day, without achieving target blood glucose levels. Blood glucose level was successfully controlled with insulin and oral hypoglycemic agents. There was incomplete resection of the mass following transphenoidal surgery. Conclusion: This case highlights the concomitant presence of increased counter regulatory hormones (GH and cortisol) and IGF-l levels in Acromegaly leading to increased insulin resistance, which are uncommon, but important causes of Diabetic Ketoacidosis. Reference: Melmed, S. (2016). Williams textbook of endocrinology. Elsevier Health Sciences.

SUN-174 Severe Insulin Resistance and Diabetic Ketoacidosis after Brentuximab Vendotin and Cyclosporin Treatment

Introduction: Brentuximab Vendotin(BV) is antibody-drug conjugate that selectively delivers cytotoxic agent, monomethyl auristatin E, targeting cells expressing surface CD30, treatment approved for refractory Hodgkin’s lymphoma. Previous research suggested MDR1 inhibition (cyclosporine) can overcome BV resistance. Case: 23 year old male with relapsed and refractory classical Hodgkin lymphoma underwent clinical trial with BV and Cyclosporin( CyA). He was given one dose of BV( 1.8mg/kg) and CyA ( 725mg 2 times a day for 5 days). A week after BV and 3 days after the last dose of CyA, patient had acute onset of hyperglycemia and ketoacidosis; glucose 435 mg/dL, bicarbonate 14 mmol/L, anion gap 14( 8-14), beta hydroxybutyrate 40.3 mg/dL (0.0-3.0 mg/dL), urine ketone +3, C-peptide 9.0 ng/ml (0.8-3.5 ng/ml). Serum cyclosporine level was high as 453 ng/ml (150-300ng/ml) at the time of presentation, which was reduced to 116 ng/ml within a week. He had no previous diabetes history. His severe hyperglycemia and metabolic acidosis persisted after aggressive hydration and multiple daily insulin injections. He was started on modified intravenous insulin infusion protocol. Within 24 hours, his glycemic control was improved at goal requiring average 34 units/h of regular insulin with NPO status. This was transitioned to U500 regular insulin divided dose injection every 8 hours with holding criteria. 10 days after initial clinical presentation, patient's insulin requirement was abruptly reduced and eventually discontinued. Patient was discharged and glucose level remained within reference range (80-128 mg/dl) without additional medical management from follow-up. Patient had completed given clinical trial with reduced dose of BV and CyA, and there was no further similar episode. During the hospital course, underlying endocrine disease related to insulin resistance was ruled out including thyroid, glucagon, cortisol, catecholamine, or growth hormone excess. Autoimmune workup was negative except elevated ESR. Insulin autoantibody panels were negative. Pancreatitis and infections were also ruled out. Lymphocytes were reduced and monocytes were increased in CBC during the episode. Peripheral blood mononuclear cell (PBMC) analysis by flow cytometry showed that absolute B and T cell counts were low but in the residual CD4+ and CD8+ T cells, expression of CD25 and PD-1 was increased. Major portion of the PBMC did not stain with our standard immune phenotype panel, which may include plasma cells, NKT, or dendritic cells. Discussion: Adverse events ≥ Grade 3 hyperglycemia (12%) has been reported with BV treatment. On the other hand, CyA is known to be related to insulin resistance as well. This is the first case report of a patient who developed rare condition of severe insulin resistance and diabetic ketoacidosis in the context of hyperinsulinemia likely due to impaired insulin signaling induced by BV and CyA.

MON-132 DKA Accompanied with Concomitant Hypertriglyceridemia-Induced Acute Pancreatitis as Initial Presentation of Ketosis-Prone Diabetes

Background: Ketosis-prone diabetes (KPD) or Flatbush diabetes has been reported as an initial presentation of DKA; There are, however, limited presentations of this phenomenon with co-existing hypertriglyceridemia-induced acute pancreatitis with normal serum lipase. Clinical Case: A 29-year-old African-American man presented with a 2-week history of epigastric pain, nausea, and vomiting. Associated symptoms included nocturnal polyuria and polydipsia and 10 lbs unintentional wt loss. He had no previous known history of diabetes; no current use of medications and past medical history was significant for medically-complicated obesity. Vital signs were remarkable for BMI of 43.3. Physical exam was mostly unrevealing except for decreased skin turgor and dry oral mucosa. Baseline chemistry and serology showed HbA1c of 11.1%, blood glucose of 910 mg/dl, serum Bicarbonate 16 mg/dl, Potassium 5.7 mmol/K, Anion Gap 19 mEq/L, with positive serum and urinary ketones. Serum lipase of 100 U/L (0-160 U/L), triglycerides of 1575 mg/dL (<150 mg/dL). Additional work-up revealed fasting C-peptide level of 2.09 (1.1−4.4 ng/mL), GAD-65 Ab titers: <5.0 U/mL (0.0−5.0 units/mL), and negative ICA (<1.1). CT Abdomen and Pelvis was remarkable for focal pancreatitis with thickening in the peripancreatic space. Biochemical testing and clinical picture were consistent with ketosis-prone T2DM. Conclusions: KPD is a different subset of diabetes, characterized by unprovoked ketosis or new-onset DKA. However, patients lack the standard phenotypes of T1DM or LADA. The underlying pathophysiology of KPD is thought to be due to β-islet cell dysfunction. Phenotypes of KPD may be further broken down via the presence or absence of β-islet cell autoantibodies, as well as long-term β-cell reserve. In our case described, the patient had negative autoantibodies and residual β-cell function, which is classified as KPD subtype A−β+. Furthermore, free fatty acidbreakdown by pancreatic lipases results in hypertriglyceridemia or lipotoxicity resulting in acute pancreatitis. Initially, management is the same as for those with T1DM with ketoacidosis, and all patients should be maintained on insulin until C-peptide levels can then be retested in 2 to 10 weeks to assess trajectory and determine transient vs. long-term insulin requirements and dependency.

SUN-168 HAART-Induced Hyperglycemic Hyperosmolar Syndrome: A Rare Manifestation of HAART Therapy

Methods: Analysis of case report Objective: Increase awareness of Hyperglycemic complications secondary to HAART therapy) : 59-year-Old Hispanic Male with past medical History of pre-diabetes and recently diagnosed with HIV presented to the Emergency Department with the complaint of fatigue for 3 days associated with nausea for same duration. He denied any other complaints. Patient's blood glucose was 1900 mg/dl, serum bicarbonate level: 22, Blood pH: 7.38, serum acetone negative, and urine ketones negative. Serum osmolarity was 340 mmol/kg and HBA1c was 19%. Based on above laboratory Values, Diagnosis of Hyperglycemic Hyperosmolar Syndrome (HHS), was made and patient was admitted to Medical ICU started with Intravenous (IV) fluids and IV insulin Infusion. After normalization of blood sugar, patient transferred to the medical floor and provided with diabetic teaching and started on subcutaneous Insulin Injection. On review of past medical history, patient was diagnosed with HIV 6 weeks ago and was started with HAART therapy containing a Protease inhibitor (ritonavir) as one of drug in the combination therapy. Blood work 8 weeks ago showed HAB1C 6.2% and blood glucose 115 mg/dl showing temporal relation of the start of HAART therapy and sudden change in blood glucose and increased HBA1c. Infectious disease team was consulted and patient's HIV regimen was switched and Protease inhibitor ( Ritonavir) was stopped, Patient was discharged with a new HAART therapy and also subcutaneous Insulin. We followed the patient closely in outpatient management and over the course of 3 months, HBA1C and blood sugar came back to baseline and subcutaneous insulin was stopped. Conclusion 1. Protease inhibitors are commonly associated with Metabolic Syndrome. This is first case to our best of knowledge in which protease inhibitors has been linked to pure Hyperglycemic Hyperosmolar Syndrome. 2. Patients starting with HAART therapy should be further investigated for possible hyperglycemia secondary to protease Inhibitors. Abbreviation: HHS: Hyperglycemic Hyperosmolar Syndrome HAART: Highly Active Anti-Retroviral Therapy MICU: Medical Intensive Care Unit IVF: Intravenous Fluids

OR31-1 Sodium-Glucose Co-Transporter-2 Inhibitors and the Risk of Diabetic Ketoacidosis: Clinical and Biochemical Characteristics of 21 Cases

Background: Sodium-glucose cotransporter 2 inhibitors (SGLT2i’s) are the newest class of anti-hyperglycemic drugs. Their mechanism of action involves increasing urinary glucose excretion by preventing glucose reabsorption in the proximal renal tubules, yet they can also promote ketogenesis under certain circumstances. Numerous reports suggest an association between SGLT2i’s and diabetic ketoacidosis (DKA), but the medical literature remains sparse. Since the use of these drugs for diabetes has increased dramatically due to favorable cardiac outcomes, identification of patients at greatest risk for this life-threatening complication is essential. Therefore, in an effort to better understand the circumstances in which SGLT2i associated DKA occurs we reviewed all available cases at our hospital over a 5-year period. Patients and Methods: We retrospectively reviewed all cases of ketoacidosis associated with SGLT2i use at our hospital from 2013 to October 2018 using an electronic medical record search algorithm. Terms included canagliflozin, dapagliflozin, empagliflozin, SGLT2 inhibitors, metabolic acidosis, ketoacidosis, diabetes, and DKA. Patients that developed DKA without being treated with SGLT2i were excluded. Results: We identified 77 cases, 21 of which met criteria for DKA associated with SGLTi use. 64% were female and 36% were male, average age was 57.8 years, BMI 29.8 kg/m2, and mean diabetes duration was 11 years. The majority carried diagnoses of T2DM (94%) and 83.4% had no history of DKA prior to using an SGLT2i. The most common presenting symptoms were nausea, vomiting (38%), abdominal pain (28.5%) and altered mental status (19%). Common precipitants were poor oral intake (57.14%) and infection (23.8%). Average blood glucose concentrations at presentation were 329 + 36 mg/dl, interestingly, 52% of the episodes were euglycemic DKA (euDKA) with blood glucose <300 mg/dl. Average anion gap values were 25+1.4 mg/dl, bicarbonate 12.6+1.3 mg/dl and pH 7.17+0.03. All had positive urine ketones and average beta-hydroxybutyrate levels were 6.4 mmol/l. Latest hemoglobin A1c was 9.8+0.6%. A variety of drugs were prescribed along with an SGLT2i, and 62% of patients were using insulin. SGLT2i’s associated with DKA were canagliflozin (52%), empagliflozin (29%), and dapagliflozin (19%). No cases were fatal. Conclusion: We found that the majority of SGLT2i associated DKA cases occurred in older patients with type 2 DM without prior episodes of DKA. The most common presenting symptoms were nausea, vomiting, abdominal pain and altered mental status, while poor food intake and infection where the main precipitants. Clinicians should consider the possibility of ketoacidosis in SGLT2i-treated patients presenting with these symptoms, even in absence of marked hyperglycemia. If DKA is diagnosed, the SGLT2i should be discontinued and insulin therapy for DKA should be initiated.

SUN-176 Euglycemic Diabetic Ketoacidosis withSGLT2 Inhibitor Presenting as Chest Pain in a Patient with Coronary Artery Disease on a Ketogenic Diet

Background: Euglycemic diabetic ketoacidosis (DKA) is a known complication of sodium-glucose cotransporter 2 (SGLT2) inhibitors. We report an unusual case of euglycemic DKA caused by an SGLT2 inhibitor during self-introduction of a ketogenic diet; initial concern was for acute coronary syndrome. Clinical Case: A 61-year-old man with a history of type 2 diabetes with a hemoglobin A1c of 8.3%, coronary artery disease, hypertension, and hyperlipidemia presented to the emergency room with nausea and chest pain. The patient had a 30-year history of diabetes and was on oral therapy for years before starting insulin with an average daily dosage of 28 units. Three years ago, he started an SGLT2 inhibitor, improved his lifestyle and glycemic control, and was able to stop insulin. His home medications included empagliflozin 10 mg daily, metformin 500 mg twice a day, liraglutide 1.8 mg subcutaneously daily, rosuvastatin 5 mg daily, ezetimibe 10 mg daily, and omeprazole 40 mg daily. He reported several weeks of atypical chest pain and computed tomography angiography showed total occlusion of the mid-right coronary artery. He underwent an exercise stress test that showed echocardiographic changes that were positive for ischemia and subsequently was scheduled to undergo a left heart catheterization in 1 week. In the interim, he was highly motivated to change his lifestyle. He adopted a ketogenic diet, significantly limiting his daily carbohydrate. Five days later, he developed persistent and increased right-sided chest pain along with nausea, and presented to the emergency room. On review of systems, he reported hunger and his wife reported an odd breath odor. His vitals were stable. His troponin was negative and EKG showed inferior Q waves similar to prior EKGs. Given concern for acute coronary syndrome, he underwent cardiac catheterization, which showed the known complete total occlusion of RCA with collaterals, for which intervention was not performed. Review of additional labs showed: glucose 110 [70-100 mg/dL], bicarbonate 17 [22-29 mmol/L], anion gap 17 [6-14 mmol/L], betahydroxybutyric acid 4.1 [<0.3 mmol/L], large quantity of urinary ketones and glucose. He was diagnosed with euglycemic DKA and treated with insulin, fluids, and dextrose with resolution of ketoacidosis and chest pain. Conclusion: The use of SGLT2 inhibitors is increasingly favored in those with established cardiovascular disease, and carbohydrate-restrictive diets are a popular form of nutritional therapy. This case highlights severe carbohydrate restriction as an important risk factor that may predispose patients on SGLT2 inhibitors to euglycemic DKA that demonstrated with an unusual presentation of chest pain.

SUN-186 Insulin Antibody Associated Severe Insulin Resistance Leading to Uncontrolled Hyperglycemia

Background: Severe insulin resistance is unusual in young patients with type 1 DM and normal BMI. We report a case of severe insulin resistance attributed to the development of insulin antibodies. Clinical Case: An 18 year old male with uncontrolled Type 1 DM was admitted to psychiatry for management of a delusional disorder. His home insulin regimen consisted of degludec 56 units daily and aspart 30 units before meals. He weighed 75 kg with a BMI of 27.5 kg/m2. Initial blood work revealed hyperglycemia with glucose of 549 mg/dl, HbA1C of 10%, C-peptide of <0.1 ng/ml (0.9-7.1 ng/ml), and no evidence of urinary ketones, acidemia, hyperosmolarity or thyroid dysfunction. He was started on a basal bolus regimen with a total daily dose of 0.9 units/kg. His hyperglycemia persisted despite rising standing insulin doses and metformin 1000 mg twice daily was added with minimal improvement in glycemic control. Due to persistent hyperglycemia despite rising insulin doses, insulin antibody titers were measured and found to be elevated at 4.4 U/ml (<0.4 U/ml.) When his psychiatric symptoms stabilized, he was discharged on a basal bolus regimen with total daily dose of 2.6 units/kg and metformin 1000 mg twice a day with improved glycemic control. Conclusion: Development of insulin antibodies is known to occur in type 1 diabetics using animal preparations of insulin but far less commonly in patients receiving recombinant human insulin or insulin analogues. Factors related to their development include the type of insulin (animal insulin having higher immunogenicity), mode of delivery (increased levels seen with insulin pump use and more frequent injections) and predisposing genetic factors such as certain HLA types. In some individuals, these antibodies may be clinically insignificant while others may develop severe insulin resistance with highly variable glycemic control. Often these patients experience marked hypoglycemia at night yet are hyperglycemic during the day. Treatment options include switching insulin formulations, insulin sensitization with metformin or thiazolidinediones, stimulation of insulin production with sulfonylureas or GLP-1 receptor agonists and immunosuppression with glucocorticoids, mycophenolate or cyclophosphamide. In patients who fail these treatments, plasmapheresis has been described as an alternative. In conclusion, the presence of insulin antibodies should be considered in patients with severe hyperglycemia despite increasing doses of insulin.

Pilot study of a ketogenic diet in relapsing-remitting MS.

ObjectiveTo assess the safety and tolerability of a modified Atkins diet (KDMAD), a type of ketogenic diet (KD), in subjects with relapsing MS while exploring potential benefits of KDs in MS.MethodsTwenty subjects with relapsing MS enrolled into a 6-month, single-arm, open-label study of the KDMAD. Adherence to KDMAD was objectively monitored by daily urine ketone testing. Fatigue and depression scores and fasting adipokines were obtained at baseline and on diet. Brain MRI was obtained at baseline and 6 months. Intention to treat was used for primary data analysis, and a per-protocol approach was used for secondary analysis.ResultsNo subject experienced worsening disease on diet. Nineteen subjects (95%) adhered to KDMAD for 3 months and 15 (75%) adhered for 6 months. Anthropometric improvements were noted on KDMAD, with reductions in body mass index and total fat mass (p < 0.0001). Fatigue (p = 0.002) and depression scores (p = 0.003) were improved. Serologic leptin was significantly lower at 3 months (p < 0.0001) on diet.ConclusionsKDMAD is safe, feasible to study, and well tolerated in subjects with relapsing MS. KDMAD improves fatigue and depression while also promoting weight loss and reducing serologic proinflammatory adipokines.Classification of evidenceThe study is rated Class IV because of the absence of a non-KD control group.

By-products of lithotripsy: Are they related to abdominal fat and wave characteristics?

ObjectivesThis study aimed to evaluate the correlations between by-products of extracorporeal shock wave lithotripsy (ESWL) and some physical parameters such as abdominal fat, energy levels, and shock wave pulses.MethodsA total of 40 patients (20 men and 20 women), aged 37.18 ± 10.64 years, with renal or ureteral stones were recruited. All patients were treated with ESWL, and their abdominal fat was measured using an Omron body fat monitor and the body mass index (BMI). Parameters such as the levels of malondialdehyde (MDA), ketones, and protein in urine were measured before and after ESWL using a Bio Doctor Analyzer. The wave characteristics of the lithotripsy procedure and the wave pulses were determined.ResultsThe mean levels of urinary MDA and ketones showed statistically significant increases in post-ESWL compared with pre-ESWL values. The results showed significant elevations in MDA and ketones in both male and female patients. In addition, there was a significant correlation between MDA/ketones and energy levels and between ketones and BMI in female patients. The analysis also revealed that the shock wave pulse had an insignificant impact on the by-product parameters.ConclusionAn energy level of ≤4 J is recommended for overweight and obese patients undergoing ESWL. In addition, measurement of the post-ESWL MDA urinary level should be performed as a routine test, especially in obese male patients.

A cross-sectional survey based on blood VOCs, hematological parameters and urine indicators in a population in Jilin, Northeast China

The objective of this study was to examine whether long-term exposure to low-dose volatile organic compounds (VOCs) will have an effect on the health of non-occupational population. A total of 499 non-occupational participants aged more than 18 that live around Jilin Petrochemical Industrial Zone were chosen by stratified cluster random sampling. Their blood VOCs' levels, hematological parameters and urine indicators together with detailed questionnaire data were used to find possible relationships using binary logistic regression analysis. The detection rate of benzene in the blood was high in the non-occupational population around the industrial area, and it even reached 82.3% in males but no significant difference was recorded between male and female population. In addition, trichloroethane (male: 33.2% V female: 21.7%; p = 0.002), carbon tetrachloride (males: 20.3% V females: 7.5%; p < 0.001) and trichlorethylene (male: 34.9% V female: 24.7%; p = 0.004) all showed significant differences in gender, and without exception, the prevalence of males was higher in these three VOCs than of females. The changes in red blood cell (RBC), hematocrit (HCT) and basophils are correlated with carbon tetrachloride, trichloroethylene and chloroform, respectively. And RBC, HCT and basophils are statistically significant in male compared with female of the study population. The increase in trichlorethylene was associated with an increase of 1.723% (95% CI 1.058-2.806) in HCT. The increase in carbon tetrachloride showed a more significant correlation with an increase of 2.638% in RBC count (95% CI 1.169-5.953). And trichloromethane led to a 1.922% (95% CI 1.051-3.513) increase in basophils. The changes in urinary WBC, urine ketone (KET) and urinary bilirubin (BIL) showed significant correlation with benzene, carbon tetrachloride and dibromochloromethane, respectively. The correlation in females is more significant than in males. The increase of benzene in the female population increased urinary leukocyte count by 2.902% (95% CI 1.275-6.601). The effect of carbon tetrachloride on KET was particularly pronounced, resulting in an increase of 7.000% (95% CI 1.608-30.465). Simultaneously, an increase in dibromochloromethane caused an increase of 4.256% (95% CI 1.373-13.192) in BIL. The changes in RBC, HCT and basophils can only serve as an auxiliary indicator for disease diagnosis, so they have no significant clinical significance. However, the alteration of urinary WBC, KET and BIL has great clinical significances, and it is suggested that the monitoring of the above indicators from low-dose long-term exposure be strengthen in this area.

Is there any Relationship between Body Weight and Urine Ketones?

The objective of this study was to correlate normal body weight with urine ketones. When there is insufficient level of glucose in our body, body use fats as an alternate source of energy. The substance produced is known as ketones, this will be shown in our blood and urine. If the patients are diabetics, then urine contain ketones means we are not producing insulin. There is another condition in which we are not diabetics but can develop ketones. Life of a patient or an individual is highly affected by its weight. Cardiac vascular diseases are all due to the overweight than to normal. Pulmonary disorders are also the results of overweight. People were asked to collect their urine in a container and then we imposed the dipstick method and analyzed the results for the ketones in the urine and noted the readings of the people. A questionnaire was prepared and asked the people about weight and ketones presence in their urine. All the experiments were conducted when the persons were at normal conditions. None of them is using any medicines or certain kind of drugs. The data described us that there was not a scientific relationship between the human body weight and urine ketones. It was inferred that there was no relationship between the body weight and normal ketones in urine.

How Rice Likeliness is Associated With Ketones in Urine?

How Rice Likeliness is Associated With Ketones in Urine?

Is there any Relationship between Body Weight and Urine Ketones?

Is there any Relationship between Body Weight and Urine Ketones?