Hypoglycemia In Nondiabetic Patients Research Articles

Association Between the Blood Glucose Value at PACU Discharge and Postoperative Hypoglycemia in Nondiabetic Patients With Hyperglycemia After Hysteroscopic Surgery: A Retrospective Cohort Study

PurposeThe target glycemic control for nondiabetic patients in the postanesthesia care unit (PACU) after hysteroscopic surgery remains unclear. Our goal is to determine the optimal level of glycemic control by finding the relationship between blood glucose level (BGL) leaving the PACU and postoperative hypoglycemia in nondiabetic patients. DesignThis retrospective cohort study was conducted at a comprehensive tertiary hospital in Chongqing, China between June 2018 and December 2020. MethodsThe target independent and dependent variables were BGL leaving the PACU and postoperative hypoglycemia, respectively. The primary outcome was the incidence of hypoglycemia. Logistic regression was used to explore the association between discharge BGL and hypoglycemia. The optimal glycemic control range was determined by using the receiver operating characteristic (ROC) curve. FindingsPrior to insulin use, BGL in the insulin-using subgroup might be as high as 20 mmol/L. Hypoglycemia was related to the BGL while leaving the PACU (odds ratio (OR) 0.37 [95% confidence interval (CI) 0.22 to 0.65]). The best cut-off value (12.95 mmol/L) was determined by fitting the ROC curve. ConclusionsIf severe hyperglycemia develops during hysteroscopic surgery in individuals with 5% glucose as the mediator of uterine distention, the recommendation is to maintain blood glucose above 12.95 mmol/L when treated with insulin.

Differences in glycemic trends due to reconstruction methods after proximal gastrectomy from the perspective of continuous glucose-monitoring.

In recent years, clinicians have focused on the importance of preventing hypoglycemia. We evaluated the impact of different reconstruction procedures after proximal gastrectomy on glycemic variability in non-diabetic patients with gastric cancer. This prospective observational study was conducted between April 2020 and March 2023. Flash continuous glucose-monitoring, a novel method for assessing glycemic control, was used to evaluate the glycemic profiles after gastrectomy. A flash continuous glucose-monitoring sensor was placed subcutaneously at the time of discharge, and glucose trends were evaluated for 2weeks. The anastomotic methods for proximal gastrectomy were esophagogastrostomy in 10 patients and double-tract reconstruction in 10 patients. The time below this range (glucose levels < 70mg/dL) was significantly higher in the double-tract reconstruction group than in the esophagogastrostomy group (p = 0.049). A higher nocturnal time below this range was significantly correlated with an older age and double-tract reconstruction (p = 0.025 and p = 0.025, respectively). These findings provide new insights into reconstruction methods after proximal gastrectomy by assessing postoperative hypoglycemia in non-diabetic patients with gastric cancer.

Hypoglycemia in non-diabetic in-patients at a teaching referral hospital in Iran.

This study aims to investigate comorbidities, clinical features, laboratory values, and diagnoses in non-diabetic patients experiencing hypoglycemic episodes. A retrospective observational study was conducted at Shariati Hospital in Iran from 2016 to 2023. Seventy-four non-diabetic patients admitted with a diagnosis of hypoglycemia were included, while patients with diabetes were excluded. Demographic data, symptoms, and biochemical assessments were obtained from the hospital information system. Hypoglycemic episodes were identified based on low measured blood glucose, recorded medications for hypoglycemia treatment, or recorded codes indicating hypoglycemia. Hypoglycemia was defined as blood glucose below 70mg/dL (3.9 mmol/L) along with two other criteria of the Whipple triad. Statistical analysis was performed using SPSS software (version 26). Among the enrolled patients, 63.5% were female, and 13.5% were elderly (≥ 65 years). The most common comorbidities observed were cardiovascular disease (20.3%), psychological disorders (20.3%), hypothyroidism (14.9%), and hypertension (8.1%). The prevalent symptoms included weakness, loss of consciousness, sweating, palpitations, dizziness, and tremors. Non-diabetic hypoglycemia was caused by factitious disorders, insulinoma, organ failure, and infection, respectively. Due to the diverse range of clinical symptoms, hypoglycemia in non-diabetic patients may be diagnosed late, leading to misdiagnoses such as psychological disorders or seizures. It is crucial to consider the possibility of hypoglycemia in non-diabetic patients and determine its underlying cause. Given the poor prognosis associated with hypoglycemia, timely interventions are essential.

SAT173 Insulin Autoimmune Syndrome: A Rare Diagnosis With Unique Features

Abstract Disclosure: S. Naqvi: None. S. Syed: None. A.R. Kasireddy: None. S. Alshami: None. D. Edem: None. J.A. Henske: None. Introduction: Insulin Autoimmune Syndrome [IAS], or Hirata’s disease, is a rare cause of hypoglycemia. It is characterized by positive insulin autoantibodies in an insulin naïve patient and should be considered in the differential for post-prandial hypoglycemia. Case: A 48-year-old male presented with postprandial tremors, sweating, palpitations and episodes of incoherent speech and loss of consciousness at least 6 months prior to his presentation. He had no history of diabetes, however, was found to have severe symptomatic documented hypoglycemic episodes, with resolution of hypoglycemic symptoms upon treatment; fulfilling the Whipple’s triad. Outpatient workup for causes of his hypoglycemia ruled out insulinoma, use of diabetes medications or insulin, adrenal insufficiency, severe illness, infections, thyroid, liver or kidney dysfunction. He never had gastrointestinal or bariatric surgery. Given his symptoms and severity of hypoglycemic episodes, he was admitted for observation and 72 hour fast. Lab work during hypoglycemic episode revealed inappropriately elevated insulin and low to normal c-peptide levels, undetectable proinsulin, elevated beta-hydroxybutyrate, normal IGF-1, IGF-2, and a negative sulfonylurea screen. Importantly, his insulin: c-peptide ratio was more than 1 and his insulin antibodies were elevated, consistent with IAS. He denied any history of autoimmune disorders or use of any medications with sulfhydryl group. CGM sensor clearly showed the relationship between high glycemic index foods, glucose spikes, and drops in his blood glucose several hours later. Dietary counselling was provided, without much improvement. Trials of Acarbose and Octreotide were not tolerated due to side effects like rash. Prednisone 20 mg bid was started; Diazoxide was titrated to 200 mg tid with much improvement. He has been followed by our clinic, and tapered to prednisone 10 mg bid and Nifedipine 30 mg daily with resolution of his symptoms. Conclusions: Severe hypoglycemia in non-diabetic patients requires investigation utilizing a broad differential diagnosis and biochemical evaluation. The findings of post-prandial hypoglycemia and inappropriately high insulin, with low to normal c-peptide and proinsulin levels with an insulin: C-peptide [ICP] ratio &amp;gt;1 in a non-diabetic patient is consistent with IAS. An ICP ratio &amp;gt;1 is a clue that the half-life of insulin has been increased by circulating antibodies. Mechanistically, post-prandial hyperglycemia cause insulin secretion, however, circulating insulin antibodies neutralize its effect. Ongoing hyperglycemia leads to further high levels of insulin, followed by intermittent spontaneous decoupling of insulin-antibody complex and subsequent post-prandial hypoglycemia. IAS may spontaneously resolve over time but may require indefinite length of treatment and dietary modification until this occurs. Presentation: Saturday, June 17, 2023

THU276 The Use of Continuous Glucose Monitors for Management of Postbariatric Hypoglycemia

Abstract Disclosure: S. Jani: None. S. Bao: None. Postprandial hypoglycemia is a known complication of bariatric surgery. Mixed meal tolerance test performed in these patients often revealed hypoglycemia 1-3 hours after meals. Recent clinical studies using continuous glucose monitors (CGM) have shown the incidence of postbariatric hypoglycemia is much higher than previously identified. In addition to diet modification and medication treatment, CGM has become a more popular and useful tool in managing severe cases. We present a case of using CGM to manage postbariatric hypoglycemia. A 47 year old female with prior history of class 3 obesity treated with sleeve gastrectomy presented with hypoglycemia 2.5 years after her bariatric surgery. She complained of headache, anxiety, dizziness, and fatigue during a routine clinic visit, two hours after consuming a carbohydrate rich meal with simple sugars. Blood glucose was obtained and revealed severe hypoglycemia (glucose 38 mg/dL). This prompted an urgent referral to endocrinology. Review of glucose trends revealed multiple instances of postprandial hypoglycemia. Further labs suggested a low likelihood for insulinoma with no fasting hypoglycemia and HA1C normal at 5.3%. Postprandial hyperinsulinemic hypoglycemia was suspected clinically. Dietary modification with multiple small meals consisting of high protein, fiber and complex carbohydrates was recommended. Additionally, she was started on Libre 2 CGM for monitoring and prevention of severe hypoglycemia. Review of her CGM data during follow up visit demonstrated very low incidence of hypoglycemia and absence of severe hypoglycemia. Over time with continued use of her CGM and low incidence of hypoglycemia, she did not require medical therapy. Postprandial hypoglycemia after bariatric surgery can be severe and lead to disabling neuroglycopenic symptoms. With increased utilization of bariatric surgery, these postoperative complications will likely become more prevalent. In a Swedish nationwide study, the prevalence of postbariatric hypoglycemia was close to 0.2% in a cohort of 5040 patients. However, a more recent prospective study with a two-year observation of 333 patients after bariatric surgery using 2-hour glucose tolerance test revealed much higher prevalence of severe postprandial hypoglycemia (25.6%). Hypoglycemia was highest after gastric bypass surgery (32.6%), followed by sleeve gastrectomy (22.6%). Currently, there is no official guideline on utilization of CGM in management of hypoglycemia in nondiabetic patients. This case highlights the role of CGM in managing postbariatric hypoglycemia. CGM provides continuous glucose data, trends and alerts that can be a critical tool for patients to monitor, anticipate and prevent hypoglycemic events. Additionally, the real time data provided by CGM’s can help clinicians identify high risk patients who may benefit from the addition of medications to treat hypoglycemia. Presentation: Thursday, June 15, 2023

Severe hypoglycemia in non-diabetic patients

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Prevalence and predictive factors of factitious hypoglycemia in non-diabetic patients

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

“The Unusual Suspect” - Insulin Autoimmune Syndrome, an Extremely Rare Cause of Hypoglycemia

Background: Insulin autoimmune syndrome (IAS), also called Hirata syndrome, is a rare diagnosis which is characterized by hypoglycemia, normal or elevated fasting insulin level, and elevated anti-insulin antibody titers. Clinical Case: 45-year-old nondiabetic Caucasian female presented to the emergency department (ED) with chief complaint of near-syncope. She reported difficulty concentrating and feeling faint roughly 1 hour after consuming breakfast. Upon ED arrival, fingerstick glucose (FSG) was 47 mg/dL. Her symptoms resolved with ingestion of orange juice and repeat blood glucose (BG) 15 minutes later was 120 mg/dL. She reported similar symptoms in the last 5 years happening “every few months” without a predictable pattern; twice with witnessed loss of consciousness. Workup for syncope in the past included normal neurologic, cardiac, and tilt-table testing. She had no prior low FSG/BG recorded, no personal history of bariatric surgery or family history of diabetes mellitus and no access to antihyperglycemic medications. Past medical history included ulcerative colitis and medications included sulfasalazine and multivitamins. Pertinent review of systems was negative for weight loss, nausea, and diarrhea. Vital signs were within normal limits. Physical exam was unremarkable. Height was 165 cm, weight 67.8 kg and body mass index 24.9 kg/m2. Blood draw after overnight fast revealed BG of 78 mg/dL, C-peptide 0.7 ng/mL (ref range 0.8–3.5), insulin 10 µIU/mL (3–19), proinsulin <1.6 pmol/L (<8.0), insulin-like growth factor-2 (IGF-2) 339 ng/mL (180–580) and insulin antibody level 10.0 U/mL (0.0–0.4). She was managed conservatively with frequent small meals and patient has continued to do well without recurrence of symptoms. Conclusion: IAS is an exceedingly rare disease entity with about 460 cases described in literature, mostly in patients of Asian descent. Workup for hypoglycemia in non-diabetic patients should include insulin antibody titers to rule out IAS. There appears to be a genetic predisposition to developing IAS in patients with major histocompatibility complex (MHC) genes HLA-DQA1, HLA-DQB1 and HLA-DRB1. It is now being more frequently described in patients of non-Asian descent, particularly those with other autoimmune or plasma cell dyscrasias. It is also associated with drugs containing sulfhydryl groups and viral infections. Treatment should be tailored to severity of disease. Most drug induced IAS resolves after cessation of culprit drug. Conservative management is usually the first step with frequent, low carbohydrate meals with diazoxide or octreotide as adjunctive options. Immunosuppression (high-dose prednisolone or rituximab) and plasma exchanged are reserved severe or refractory cases.

Non- pancreatic neuroendocrine tumour presenting with hypoglycemia in an elderly patient.

Hypoglycemia is a common, symptom seen in individuals. Hypoglycemia in the elderly is both under-recognized and misdiagnosed due to nonspesific hypoglycemic symptoms and accompanying comorbidities in this population. In diabetic individuals, hypoglycemia is most commonly caused by administering insulin or sulphonylureas and insulin secretagogues. Other drugs, such as antibiotics or beta-blockers, have been reported to reduce blood glucose to abnormally low levels. Hypoglycemia in non-diabetic patients is considered a rare event, and the possible reasons may be reactive hypoglycemia, insulin-secreting tumours and other malignancies, hypopituitarism, hypocortisolism, alcohol abuse, inappropriate insulin self-administration, malnutrition, renal failure and sepsis. An 86- year- old male was admitted to the emergency department with hypoglycemia diagnosed with non-pancreatic neuroendocrine tumour (NET) on lung secreting insulin. No surgical intervention or chemotherapy was planned due to patients age and comorbidities so best supportive care was planned. We used prednisone for symptomatic treatment of hypoglycemia and the patient has been followed up periodically. In this period he had no hypoglycemic attack. For patients with hypoglycemia who are unable/decline to receive any further treatment, low dose glucocorticoid is a good choice to achieve normoglycemia. It seems to be more cost effective compared to other treatment options. Furthermore hospitalisation rates may decrease due to decreased hypogylcemic attacks.

Ciprofloxacin and risk of hypoglycemia in non-diabetic patients

BackgroundFluoroquinolones have been associated with hypoglycemia in patients taking diabetic medications, most commonly due to drug-drug interactions and other associated risk factors. Except for four published case reports, there are no studies that have found positive associations between ciprofloxacin and hypoglycemia. In all but one of the cases, ciprofloxacin was taken with other hypoglycemic drugs. Recently, the Eritrean National Pharmacovigilance Centre received a serious case of hypoglycemia with recurrent episodes in a young and healthy patient without diabetes following use of oral ciprofloxacin. The aim of the present study is therefore to assess the causal relationship between ciprofloxacin and hypoglycemia in patients without diabetes using the World Health Organization-Uppsala Monitoring Centre global adverse drug reaction database (VigiBase®).MethodsA search was made on the World Health Organization global adverse drug reaction database (August 15, 2018) using “ciprofloxacin” as the drug substance and “hypoglycemia” as the reaction term. Cases that used hypoglycemic drugs (patients with diabetes) concurrently with ciprofloxacin and those with a completeness score below 50% were excluded to control for confounders and to improve the strength of the data. Hill criteria were used to assess causation.ResultsA total of 35 cases of hypoglycemia reported since 1989 from 17 countries in patients without diabetes associated with ciprofloxacin use with a median time to onset of 4 days were retrieved. The cases have a median age of 64 years (interquartile range, 50–85) with a similar male–to-female ratio. Ciprofloxacin was the only suspect and the sole drug administered in 48.5% of the cases. In ten cases, hypoglycemia abated following withdrawal of ciprofloxacin, and reaction recurred in one case on the subsequent rechallenge. Hypoglycemia was marked as “serious” in 20 cases, and the outcome was fatal in two cases.ConclusionsThis assessment found a suggestive causal link between use of ciprofloxacin and hypoglycemia in patients without diabetes.

MON-145 An Unusual Cause of Hypoglycemia in a Non-Diabetic Elderly Male

Introduction: Hypoglycemia (HYPO) in non-diabetic patients is an unusual scenario and presents a diagnostic challenge, resulting in serious consequences for patients. We describe the case of an elderly non-diabetic male who developed severe persistent HYPO. Case: A 78-year-old male with history of macroprolactinoma taking bromocriptine, Hashimoto's hypothyroidism, initially treated with low dose L-thyroxine, followed by Graves' hyperthyroidism, Parkinson’s disease (PD), osteopenia was noted to have hypoglycemia (54 mg/dL) on routine lab work. When questioned, he admitted to having had years of lightheaded episodes, "feeling jittery", which improved within minutes after eating sugary foods. His wife mentioned that he “loved to eat sweets” and high simple carbohydrate meals(CARBS). Physical exam - orthostatic hypotension and mild resting tremors, both attributed to PD. Continuous glucose monitoring (CGMS) was performed for 2 weeks which documented HYPO overnight while sleeping, fasting and between meals. The HYPO was associated more frequently with sweet bedtime snacks. Laboratory- Glucose tolerance test was stopped due to HYPO with symptoms. ACTH=19 pg/mL (nl 0-47), AM Cortisol 19.4 microg/dL (nl 5.3-22.5), fasting blood glucose 83 mg/dL(nl 70-99), fasting insulin 6.9 mIU/L( nl 0-24.9), proinsulin 16.9 pmol/L ( nl <=18.8 pmol/L), c-peptide 1.39 ng/mL( nl 0.81-3.85), beta-OH butyrate 0.072 mmol/L( nl 0.020-0.270). Islet cell Ab was normal. Gastric emptying study was negative. Although the dose of bromocriptine was reduced due to HYPO, it continued. He was advised to decrease intake of CARBS, eat small, high protein and fat meals with frequent snacks. On subsequent visits, he reported less hypoglycemic episodes with improved energy level and general well-being, which was confirmed by CGMS. Discussion: Although a wide range of diseases can cause HYPO in nondiabetic patients, differences in characteristics between non-diabetic HYPO and diabetic HYPO have not been well studied. Common underlying diseases associated with HYPO include malignancies, cerebrovascular diseases, infection, major organ failure, and alcohol-related disorders. In addition, comorbidities linked with HYPO include sepsis, kidney diseases, and alcohol dependence, pneumonia, liver diseases and insulin abuse. Malnutrition, alcohol, infection, and post gastrectomy are the leading causes of nondiabetic hypoglycemia. In addition, methimazole use has been associated with insulin autoimmune syndrome resulting in HYPO due to interaction of sulfhydryl group with disulfide bond in the insulin molecule Conclusion: Clinicians should be aware of the potential for hypoglycemia in non-diabetic patients, due to other etiologies, which can also result in severe and possibly life-threatening sequelae. An in-depth evaluation, including the use of CGMS can assist in determining underlying causes.

MON-139 Hyperinsulinemic Hypoglycemia In A Patient Of Chronic Calcific Pancreatitis : A Medical Oxymoron

Introduction Hypoglycemia is rare in persons without diabetes due to normal physiological defences and thus a thorough evaluation is warranted in such cases. Neurogenic symptoms occur initially followed by neuroglycopenic symptoms like cognitive impairment, behavioural changes, psychomotor abnormalities and rarely seizures and coma. Causes of hypoglycemia in non diabetic patients include hepatogenous hypoglycemia, critical illness, alcohol and multiple drugs. Major causes of hypoglycemia in a seemingly healthy individual, after excluding drug intake, include hyperinsulinemic hypoglycemia caused by Insulinomas, Nesidioblastosis, Insulin autoimmune syndrome; and IGF2 secreting tumors. Management includes removal of the tumor, if found, or medical management with Diazoxide and frequent feeds. Octreotide can be used in patients with suspected Insulinoma. Medical management is difficult and frequent feeds can lead to obesity. Chronic calcific pancreatitis, on the other hand, usually leads to hyperglycemia due to pancreatic diabetes which is generally brittle. Hypoglycemia can occur in such patients but is generally a result of antidiabetic therapy. However, it is rare to have hyperinsulinemic hypoglycemia in patients who are not on antidiabetic medication and diagnosis can be delayed. Here we present a case of hyperinsulinemic hypoglycemia in a patient of chronic calcific pancreatitis. Case A 47 year old female with history of repeated episodes of slurred speech, confusion, disorientation and abnormal limb movements for last 3 years. She had been treated as seizure disorder with antiepileptics and was incidentally found to be hypoglycemic during one of these episodes. She was subsequently referred to us for further evaluation. At presentation she was conscious, oriented and had no history suggestive of any chronic illness or drug intake other than antiepileptics. Investigations showed RBS of 85 mg/dl and HbA1c of 3.2%. During prolonged fasting test, she developed hypoglycemia within 10 hours with RBS of 26 mg/dl with concomitant serum Insulin level of 15.47 µU/ml (cutoff < 3 µU/ml with hypoglycemia) and C-peptide level of 2.07 ng/ml (cutoff < 0.2 ng/ml with hypoglycemia). These were consistent with hyperinsulinemic hypoglycemia. CT abdomen showed features of chronic calcific pancreatitis, no focal pancreatic lesion was found. 68Ga DOTATATE PET/CT scan was negative for any functional lesion. She was started on Diazoxide and advised frequent feeds. She improved symptomatically with diazoxide with recurrence of symptoms off it. She was given a trial of octreotide due to non-availability of diazoxide. She improved with octreotide and was started on long acting octreotide. Conclusion Hyperinsulinemic hypoglycemia should be excluded in all patients with unexplained seizure disorder, even if the clinical probability for the same is low, as in our patient.

MON-134 Use of CGMS for Evaluating Hypoglycemia in Non-Diabetic Patients

Introduction: Continuous Glucose Monitoring System (CGMS), is a tool for measuring blood glucose (BG) levels in patients with Diabetes Mellitus (DM). Post-prandial Hypoglycemia (PPH) is a known complication of Roux-en-Y gastric bypass (RYGB). We present two cases of PPH following RYGB, confirmed by CGMS. Case 1: 70-year-old non-diabetic male, with RYGB 20 yrs. ago, presented with episodes of tremors, generalized weakness and blurring of vision, lasting about 10-15 min, occurring after eating simple carbohydrate foods. Onset and duration of episodes were unclear. In clinic, a POCT BG was 40 mg/dl with symptoms after eating doughnuts prior to the visit. VS- BP 122/58 Sitting, BP 108/57 Standing, P 87/m, Wt. 70.9 kg, BMI 22.mkg/m². Labs: BG 74 mg/dL, Sulphonylurea screen-negative, Cortisol AM 15.4 ug/dL, ACTH 23 pg/mL, C-Peptide 1.31 ng/mL (nl 0.81 - 3.85), Fasting Insulin 4.5 mIU/L (nl 0.0 - 24.9), IGF-I 76 ng/mL (nl 41 - 279), IGF-II 299 ng/mL (nl 267 - 616), BOH-butyrate 0.377 mmol/L (nl 0.020 - 0.270); IA-2 Ab <0.8U/mL (nl <0.8 U/mL). CGMS for 15 days-multiple episodes of PPH. Patient was advised to follow high protein, low carbohydrate diet, later started with Acarbose therapy. CGMS was repeated 3 months later, with marked reductions in PPH. Case 2: 32-year-old male, with RYBG 5 years ago, resulting in 150 lbs. weight loss, presented to clinic for progressive episodes of hypoglycemia. He did not test BG on a regular basis, but when tested occasionally in the morning, reported BG were 90-199 mg/dl, unless he skipped a bedtime snack. Patient reported having one episode when he woke up in the middle of the night “jittery and sweaty,” and BG was 37 mg/dl. His symptoms resolved after juice. He reports not being able to eat large meals and has been eating frequent small meals. He noted symptoms of hypoglycemia, when he eats simple carbohydrates. He also reported some high BG levels (170-180 mg/dl) although he is not previously known to have DM. VS-BP 115/67, HR 67; no orthostasis; Wt 287 lbs, BMI 45. Kg/m². POCT Glucose 64, Fasting Labs: BG 86 mg/dL, HbA1C 5.8%, C-Peptide 1.48 ng/mL, BOH-butyrate 0.7 mmol/L, Cortisol AM 12.2 ug/dL, Insulin Fasting 8.0 mIU/L, Proinsulin 2.4 pmol/L (nl ≤8.0), Insulin Antibody <0.4U/mL (nl 0.0-0.4 U/mL). CGMS for 2 weeks demonstrated repeated PPH and nocturnal hypoglycemia. Diet changes were recommended. Discussion: CGMS compared to blood glucose monitoring, is more efficacious in recording hypoglycemic events, especially if hypoglycemia occurs between testing times, or in usual settings like PPH. Current guidelines recommend use of CGMS in DM patients with hypoglycemic unawareness, nocturnal hypoglycemia, postprandial hyperglycemia. In our cases, CGMS was proven to be effective in diagnosing PPH in RYBG patients. CGMS is also an efficient device to measure therapeutic responses and avoiding hypoglycemia, as well as improving quality of life.

SUN-184 Sertraline-Induced Hypoglycemia in Nondiabetic Patients

Background SSRI’s are effective for treatment of depressive disorders by reducing serotonergic function and hence altering neuroendocrine function. The effects of sertraline on blood glucose in non-diabetic patients was demonstrated in this case. Case 39 year-old African-American female with a medical history of GERD, hypertension, marijuana abuse, and panic attacks on trazadone presented with tremors, insomnia, and diaphoresis. Her symptoms began two days after she started sertraline. Physical examination and EKG were unremarkable. Initial blood glucose was 56. Laboratory results indicated HbA1C 4.5%(4.8 – 6.0%), beta-hydroxybutyrate 0.6mmol/L(0.02 – 0.27mmol/L), TSH 0.81uIU/ml(0.27 – 4.62uIU/mL), and insulin 20.8uU/mL(2.6 – 24.9uU/mL). Her sulfonylurea screen and urine toxicology were negative. UA was positive for glucose and ketones. She discontinued sertraline and was given glucose supplements which improved glucose to 226 and she had a full recovery. Discussion We believe this was SSRI-induced hypoglycemia because of her recent introduction of sertraline. WHO reports more than 440 cases annually of SSRI-induced hypoglycemia and over 100 with sertraline.2 One way SSRI’s increase risk of hypoglycemia is by impairing hormonal counter-regulatory response (CRR) of epinephrine and glucagon.3 Sertraline induces linear pharmacokinetics with changes in drug concentration in proportion to change in dose through inhibition of neuronal reuptake of serotonin (5-HT). Study by Sanders et al. found sertraline treatment lasting longer than 6-20 days resulted in increased epinephrine and restored the blunted adreno-medullary response seen in acute administration.3 Another way sertraline can induce hypoglycemia is by regulation of liver receptors through 5-hydroxytryptamine activation and inhibition of potassium channels, resulting in increased insulin sensitivity and production and reduced gluconeogenesis. Study by Gomez et al. showed rats pre-medicated with sertraline neutralized hyperglycemia post-glucose load1 indicating that symptoms can resolve with discontinuation of sertraline and glucose supplementation. Conclusion and Follow-Up Results Sertraline-induced hypoglycemia is becoming more prevalent in non-diabetic patients. Correction of sertraline-induced hypoglycemia by discontinuing the medication and adding glucose can resolve hypoglycemia and the associated side-effects. References1Gomez R. Acute effect of different antidepressants on glycemia in diabetic and non-diabetic rats. Braz J Med Biol Res. 2001;34:57–64. 2Khoza S. Glucose dysregulation associated with antidepressant agents: an analysis of 17 published case reports. IJCP. 2011;33:484–492. 3Sanders N. The selective serotonin reuptake inhibitor sertraline enhances counterregulatory responses to hypoglycemia. AJP: Endocrinology and metabolism. 2008;294(5):E853-60.

MON-LB026 Critical Illness Associated Fatal Hypoglycemia in a Non-Diabetic Male

Introduction: Hypoglycemia in non-diabetic patients can be diagnostically challenging. It can have various etiologies including medications, tumors, post gastric bypass surgery, alcohol use, critical illness, liver/renal disease and adrenal insufficiency. We present a case of a 55-year old male with persistent, refractory hypoglycemia in the absence of Diabetes Mellitus (DM). Case Description: Patient is a 55-year old male with past medical history of Congestive Heart Failure with ejection fraction of 30%, Chronic Kidney Disease, Atrial Fibrillation, and alcohol abuse. He presented with sudden onset severe abdominal pain. Admission vitals were stable except oxygen saturation of 70% on room air. Labs were significant for lactic acid of 5.3 mmol/L and Acute Kidney Injury (AKI). CT scan of the abdomen was unremarkable. The patient was admitted to the ICU for severe acute hypoxic respiratory failure and mesenteric ischemia. On hospital day-3, he became unresponsive. At that time, his labs revealed blood sugar of less than 10 mg/dl and worsening renal failure. The patient was given multiple ampules of Dextrose 50% and infusion of dextrose 5% was started. He was initiated on Continuous Renal Replacement Therapy (CRRT) as well. Despite this, his blood sugar remained in the 40’s. His IV fluids were switched to Dextrose 10% and eventually to Dextrose 20% because of persistent hypoglycemia, also requiring intermittent IV Glucagon. He had no family or personal history of DM. HbA1c was 5.6%. Cortisol, Pro-insulin, Insulin, C-peptide levels were normal. Sulfonylurea screen was negative. Liver Function Tests were normal. Endoscopic Ultrasound did not reveal any pancreatic mass. Paracentesis of ascitic fluid was suggestive of underlying liver cirrhosis. It was then determined that the patient’s hypoglycemia was likely secondary to critical illness along with underlying severe hepatic and renal failure. The patient’s overall prognosis was poor and his condition declined rapidly. He refused any further intervention and opted for hospice care. Conclusion: Patients with critical illness especially those with underlying advanced liver/renal disease, malnutrition and advanced age may develop profound hypoglycemia even in the absence of diabetes. These patients should have frequent monitoring of blood sugar levels. Prompt support for decompensated disease is vital for overall survival.

Hypoglycemia in non-diabetic patients: clinical features and causes

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

A study on etiological spectrum of hypoglycemia in nondiabetic patients in a rural medical teaching institution

INTRODUCTION: Awareness regarding etiological distribution of nondiabetic hypoglycemia is poor among physicians. No study of etiological spectrum of hypoglycemia is found in rural West Bengal. We conducted this study to identify different causes of hypoglycemia in nondiabetics in a rural area of the western part of West Bengal. METHODS: Nondiabetic patients admitted in general medical ward with clinical or laboratory features of hypoglycemia with blood sugar level RESULTS: A total of 55 patients were included in this study. The most common cause of hypoglycemia was alcoholism (27.27%). Next common cause was steroid withdrawal (18.18%), especially in rheumatic patients. The third common cause was sepsis (12.73%), followed by panhypopituitarism (10.91%). Sheehan syndrome was seen in three cases. Hypoglycemia was detected in one chronic kidney disease (CKD) patient after hemodialysis (HD) and two CKD patients without HD. Hypoglycemia developed in one case of fulminant hepatitis, two cases of decompensated cirrhosis (hepatitis B and alcoholic), and two cases of congestive cardiac failure. Hypoglycemia developed in two cases of primary adrenocortical insufficiency due to tuberculosis and histoplasmosis of bilateral adrenal glands. All patients had fasting hypoglycemia except one case of dumping syndrome due to Billroth II gastrojejunostomy surgery. Other rare causes were insulinoma, malnutrition, and malignancy. CONCLUSION: Knowledge regarding different causes of hypoglycemia will increase the alertness and suspicion of possible hypoglycemia in appropriate situations. It will also help to identify underlying disorders in cases of hypoglycemia.

Hospitalization with hypoglycemia in patients without diabetes mellitus: A retrospective study using a national inpatient database in Japan, 2008-2012.

We aimed to examine prevalence, patient characteristics, etiology, and clinical outcomes of hospitalized patients who had hypoglycemia without a diagnosis of diabetes mellitus, using a Japanese nationwide database.This was a retrospective observational study using a national database of acute-care inpatients in Japan. Nondiabetic patients aged ≥15 years who were hospitalized for hypoglycemia were eligible. We estimated the annual numbers of hospitalized cases in Japan. We also investigated the patient characteristics, and risk factors of in-hospital mortality.We identified 8684 eligible patients out of 22.7 million discharge records between July 2008 and March 2013. The average age was 70.0 years and the average body mass index (BMI) was 19.9 kg/m2. Most frequently recorded underlying diseases were malignancies, cerebrovascular diseases, pneumonia, renal failure, and heart failure. The estimated annual numbers of hospitalizations because of hypoglycemia in nondiabetic patients were 5000 to 7000. In-hospital mortality was 14.9%, and predictive factors for poor survival included older age, community hospital, low BMI, coma at admission, urgent admission, renal failure, heart failure, pneumonia, sepsis, chronic liver diseases, and malignancies.Patients without diabetes mellitus but with hypoglycemia had multiple comorbidities and high in-hospital mortality. Clinicians should carefully investigate the etiology of hypoglycemia in nondiabetic patients, and treat the underlying diseases.

The contribution of fast test in the diagnostic approach of hypoglycemia in non-diabetic patients

The contribution of fast test in the diagnostic approach of hypoglycemia in non-diabetic patients

A rare cause of hypoglycemia in a type 2 diabetic patient: insulinoma

Recurrent episodes of hypoglycemia in patients with diabetes are often associated with the ongoing treatment regimen. However, despite changes in treatment modalities, assessment of the causes of hypoglycemia in nondiabetic patients in the presence of severe and recurrent hypoglycemia is very important. The treatment that had been provided for 6 years in a 67-year-old female patient with type 2 diabetes mellitus was discontinued due to hypoglycemic episodes that presented for the previous 2 years. The patient experienced persistent hypoglycemia after cessation of the treatment and was hospitalized for further examination. Spontaneous hypoglycemia with a final diagnosis of insulinoma was established following histopathologic evaluation and was relieved postoperation. Insulinoma is rarely encountered as a cause of hypoglycemia in patients with type 2 diabetes. Insulin-secreting tumors should be considered where hypoglycemic episodes occur despite discontinuation of insulin and other antidiabetic treatment with endogenous hyperinsulinemia being noncompliant with the blood glycemic levels.