Journal articles on the topic 'Hypoglycemia'
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Abrahamsson, Niclas, Britt Edén Engström, Magnus Sundbom, and F. Anders Karlsson. "Hypoglycemia in everyday life after gastric bypass and duodenal switch." European Journal of Endocrinology 173, no. 1 (July 2015): 91–100. http://dx.doi.org/10.1530/eje-14-0821.
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DesignGastric bypass (GBP) and duodenal switch (DS) in morbid obesity are accompanied by marked metabolic improvements, particularly in glucose control. In recent years, episodes of severe late postprandial hypoglycemia have been increasingly described in GBP patients; data in DS patients are scarce. We recruited three groups of subjects; 15 GBP, 15 DS, and 15 non-operated overweight controls to examine to what extent hypoglycemia occurs in daily life.MethodsContinuous glucose monitoring (CGM) was used during 3 days of normal activity. The glycemic variability was measured by mean amplitude of glycemic excursion and continuous overall net glycemic action. Fasting blood samples were drawn, and the patients kept a food and symptom log throughout the study.ResultsThe GBP group displayed highly variable CGM curves, and 2.9% of their time was spent in hypoglycemia (<3.3 mmol/l, or 60 mg/dl). The DS group had twice as much time in hypoglycemia (5.9%) and displayed CGM curves with little variation as well as lower HbA1c levels (29.3 vs 35.9 mmol/mol,P<0.05). Out of a total of 72 hypoglycemic episodes registered over the 3-day period, 70 (97%) occurred in the postprandial state and only about one-fifth of the hypoglycemic episodes in the GBP and DS groups were accompanied by symptoms. No hypoglycemias were seen in controls during the 3-day period.ConclusionBoth types of bariatric surgery induce marked, but different, changes in glucose balance accompanied by frequent, but mainly unnoticed, hypoglycemic episodes. The impact and mechanism of hypoglycemic unawareness after weight-reduction surgery deserves to be clarified.
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Büyükkaya Besen, Dilek, Hamdiye Arda Sürücü, and Cansu Koşar. "Self-reported frequency, severity of, and awareness of hypoglycemia in type 2 diabetes patients in Turkey." PeerJ 4 (December 13, 2016): e2700. http://dx.doi.org/10.7717/peerj.2700.
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ObjectivesHypoglycemia is a common side effect of insulin therapy in type 1 and type 2 diabetes. Limited data exist on the frequency of hypoglycemic events in type 2 diabetic patients in Turkey. Our study investigated self-reported hypoglycemic events and awareness of hypoglycemia in Turkish patients with type 2 diabetes.MethodsPeople with type 2 diabetes older than 18 years of age were recruited from the two university hospital diabetes clinics. The frequency and severity of hypoglycemia and awareness of hypoglycemia during the preceding year were determinated using questionnaires by the face-to-face interview method.ResultsIn this study of 187 patients with type 2 diabetes, 83.4% had impaired awareness of their hypoglycemia, and 62% reported that they had missed some of the symptoms of hypoglycemia. Of the patients reporting hypoglycemic symptoms and severity level, 84.1% experienced mild hypoglycemia, 60% moderate, and 15.5% severe hypoglycemia in the past year. No significant association was made between hypoglycemia awareness and age, body-mass index (BMI), years of diabetes, dose of insulin, duration of insulin use, number of meals, or amount of snacking. A significant correlation was found between A1c levels and hypoglycemia awareness and severity of hypoglycemia. A significant correlation was found between dose of insulin, amount of snacking, and severity of hypoglycemia. No significant association was made between severity of hypoglycemia and age, BMI, years of diabetes, duration of insulin use, or the number of meals. However, the group with severe hypoglycemia had diabetes longer, and the average daily dose of insulin use was higher than in other groups.ConclusionsAccording to the study results, the percentage of patients with impaired awareness of hypoglycemia is high, and 62% of patients reported that they had missed some of the symptoms of hypoglycemia in type 2 diabetes. In addition, the percentage of severe hypoglycemic events is not low. Impaired awareness of hypoglycemia is a major risk factor for severe hypoglycemic events. Patients should be educated about the danger of hypoglycemia. Education should be improved, and a determined attempt should be made to eradicate the problem.
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Beattie, Sarah. "Hypoglycemia." Nurse Practitioner 48, no. 10 (October 2023): 17–23. http://dx.doi.org/10.1097/01.npr.0000000000000100.
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Abstract: Primary care NPs are central to the management of diabetes mellitus, which carries with it the risk of hypoglycemia. Fully understanding risk factors, prevention strategies, and treatment assist in reducing hypoglycemic events. This article details hypoglycemia, risk factors for hypoglycemia, prevention strategies, and appropriate treatment plans.
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Parilo, Miguel A. "Gatifloxacin-Associated Hypoglycemia." Journal of Pharmacy Technology 18, no. 6 (November 2002): 319–20. http://dx.doi.org/10.1177/875512250201800605.
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Objective: To report a case of prolonged hypoglycemia associated with glyburide and gatifloxacin use. Case Summary: An 82-year-old white woman with diabetes mellitus type 2 and chronic renal insufficiency developed postoperative pneumonia. She had previously been on long-term glyburide therapy. Protracted hypoglycemia after institution of gatifloxacin developed despite discontinuation of oral hypoglycemic therapy. After 2 days of intravenous dextrose, sustained normoglycemia was achieved. Discussion: Hypoglycemic reactions with glyburide and fluoroquinolone antibiotics have been reported, but not with gatifloxacin. Although drug administration error cannot be excluded, no documentation exists to support this. The onset of hypoglycemia soon after administration of gatifloxacin and reports of similar interactions favor the hypothesis that hypoglycemia was induced by a gatifloxacin–glyburide interaction. Conclusions: Fluoroquinolone-associated hypoglycemia has been documented, and an interaction of gatifloxacin and glyburide appears probable. Patients with diabetes should be monitored for the development of resistant hypoglycemia, especially if they are on concomitant oral hypoglycemic medications.
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Singh, Dolat, Hamid Nawaz Ali Memon, Tariq Zaffar Shaikh, and Syed Zulfiquar Ali Shah. "HYPOGLYCEMIA." Professional Medical Journal 22, no. 04 (April 10, 2015): 408–13. http://dx.doi.org/10.29309/tpmj/2015.22.04.1316.
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Objective: To determine the frequency and severity of hypoglycemia in patientswith liver cirrhosis. Study Design: Cross sectional case series study. Period: Six months.Setting: Liaquat University Hospital Hyderabad. Methods: All the patients of liver cirrhosis,of >12 years of age and of either gender were evaluated for hypoglycemia by assessing theglycemic status through random or fasting blood glucose level. The severity of liver cirrhosiswas identified according to the Child-Pugh classification whereas the severity of hypoglycemiawas grouped in mild, moderate and severe categories. The data was entered and saved inSPSS and frequency and percentage was calculated for hypoglycemia in patients with livercirrhosis. The stratification was done for age, gender, hypoglycemia and severity of the diseaseand hypoglycemia. The chi-square test was applied between categorical variables at 95%confidence interval and p -value ≤0.05 was considered as statistically significant. Results:During six months study period, total 100 cirrhotic subjects were studied for hypoglycemia,of which 59% were males and 41% were females. The mean ± SD for age in all (100)cirrhotic patients was 42.33 ± 8.87 while the mean ± SD for age in male cirrhotic patientswas 44.06±11.45 where as in female cirrhotic subjects it was 39.92±12.55 respectively. Thehypoglycemia was observed in 67%, of which 45(67.2%) were males and 22(32.8%) werefemales. The mean random blood glucose level in male and female hypoglycemic cirrhoticpatients was 67.88±8.43 and 65.62±6.75 while the mean fasting blood glucose level in maleand female hypoglycemic cirrhotic patients was 52.93±5.31 and 53.64±8.73 respectively. Outof sixty seven hypoglycemic cirrhotic subjects 45(67%) were males and 22(33%) were females.Of sixty seven, 32(47.8%) had moderate hypoglycemia while 30/67(44.8%) were in Child-Pughclass B (p<0.05). Conclusions: The hypoglycemia was detected in patients with liver cirrhosis,hence frequent blood glucose monitoring is one of the most important way to detect mildhypoglycemia and prevent serious and severe episodes.
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Hekimsoy, Zeliha, Sevinç Biberoǧlu, Abdurrahman Çömlekçi, Oktay Tarhan, Cem Mermut, and Kadir Biberoǧlu. "Trimethoprim/sulfamethoxazole-induced hypoglycemia in a malnourished patient with severe infection." European Journal of Endocrinology 136, no. 3 (March 1997): 304–6. http://dx.doi.org/10.1530/eje.0.1360304.
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Abstract Hypoglycemia resulting from the combination of sulfonylurea and sulfonamides is a recognized drug interaction. Hypoglycemia induced by sulfonamides alone may be encountered less frequently. Because of their structural similarities to sulfonylureas. sulfonamides are liable to facilitate hypoglycemia by increasing insulin release in susceptible individuals. Sulfonamides can potentiate the hypoglycemic effect of sulfonylurea agents when given in combination. We describe a malnourished patient with severe infection who developed hypoglycemia during high-dose trimethoprim/sulfamethoxazole therapy. Elevated C-peptide concentrations during the hypoglycemic episode indicate that hypoglycemia resulted from increased endogenous insulin secretion. As malnourished patients are prone to hypoglycemia, we suggest that they should be monitored carefully if they are on sulfonamide therapy. European Journal of Endocrinology 136 304—306
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Johnson, Jeffrey A., Joanne E. Kappel, and M. Nabi Sharif. "Hypoglycemia Secondary to Trimethoprim/Sulfamethoxazole Administration in a Renal Transplant Patient." Annals of Pharmacotherapy 27, no. 3 (March 1993): 304–6. http://dx.doi.org/10.1177/106002809302700309.
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OBJECTIVE: To report a case of trimethoprim/sulfamethoxazole (TMP/SMX)-induced hypoglycemia in an immunosuppressed renal transplant patient. DATA SOURCES: English-language journal articles and reference texts identified via a MEDLINE search and a bibliographic review of pertinent data sources. DATA SYNTHESIS: Hypoglycemia resulting from the combination of sulfonylureas and sulfonamides is a recognized drug interaction. Hypoglycemia induced by sulfonamides alone may be encountered less frequently. Previously reported cases of TMP/SMX-induced hypoglycemia postulated that the sulfonamide mimics hypoglycemic sulfonylurea agents and stimulates pancreatic islet cells to secrete insulin. We report a case of hypoglycemia following the administration of high-dose TMP/SMX in a renal transplant patient. Elevated C-peptide concentrations following the hypoglycemic episode indicate that hypoglycemia resulted from increased endogenous insulin secretion. CONCLUSIONS: Hypoglycemia has been a rarely encountered result of TMP/SMX use. Patients receiving TMP/SMX, particularly those with impaired renal function and those receiving high doses, should be monitored closely for hypoglycemia.
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Haywood, Samuel C., Adam J. Bree, Erwin C. Puente, Dorit Daphna-Iken, and Simon J. Fisher. "Central but not systemic lipid infusion augments the counterregulatory response to hypoglycemia." American Journal of Physiology-Endocrinology and Metabolism 297, no. 1 (July 2009): E50—E56. http://dx.doi.org/10.1152/ajpendo.90673.2008.
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This study tests the hypothesis that lipids could act as an alternative fuel source in the brain during insulin-induced hypoglycemia. Male Sprague-Dawley rats were subjected to hyperinsulinemic (5 mU·kg−1·min−1) hypoglycemic (∼50 mg/dl) clamps. In protocol 1, intralipid (IL), a fat emulsion, was infused intravenously to prevent the fall in free fatty acid levels that occurs in response to hyperinsulinemic hypoglycemia. Intravenous lipid infusion did not alter the counterregulatory responses to hypoglycemia. To test whether IL could have central effects in mediating the counterregulatory response to hypoglycemia, in protocol 2 the brains of precannulated rats were intracerebroventricularly (icv) infused with IL or artificial cerebrospinal fluid (aCSF) as control. Unexpectedly, the epinephrine and glucagon response to hypoglycemia was significantly augmented with icv IL infusion. To determine whether central IL infusion could restore defective counterregulation, in protocol 3 rats were made recurrently hypoglycemic (RH) for 3 days and on the 4th day underwent hyperinsulinemic hypoglycemic clamps with icv IL or aCSF infusion. RH rats had the expected impaired epinephrine response to hypoglycemia, and icv IL infusion again significantly augmented the epinephrine response in RH rats to normal. With regard to our experimental model of hypoglycemic counterregulation, we conclude that 1) systemic lipid infusion did not alter the counterregulatory response to hypoglycemia, 2) the icv infusion of lipids markedly increased CSF FFA levels and paradoxically augmented the epinephrine and glucagon responses, and 3) the blunted sympathoadrenal response in recurrently hypoglycemic rats was completely normalized with the icv lipid infusion. It is concluded that, in the setting of insulin-induced hypoglycemia, increased brain lipids can enhance the sympathoadrenal response.
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Mete, Türkan, and Mustafa Cesur. "Non-diabetic hypoglycemia." Intercontinental Journal of Internal Medicine 1, no. 4 (November 29, 2023): 94–105. http://dx.doi.org/10.51271/icjim-0021.
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Glucose is the main substrate utilized by the brain, and therefore numerous counterregulatory mechanisms exist to maintain plasma glucose concentration. This makes it rare for hypoglycemia to develop in people who are not taking hypoglycemic drugs, such as insulin or sulfonylureas, for diabetes. The symptoms of hypoglycemia are nonspecific. The presence of Whipple’s triad is necessary for diagnosis. When symptoms occur spontaneously, the patient can be evaluated for hypoglycemia. If this is not possible, then a 72-hour fasting test or a mixed meal tolerance test can be performed to create conditions for symptoms to occur. Non-diabetic hypoglycemia is mainly divided into two main groups: insulin-mediated (hyperinsulinism) and insulin-independent. The main causes of hypoglycemia due to endogenous hyperinsulinism are insulinoma and islet cell hyperplasia (nesidioblastosis), post-bariatric surgery, and autoimmune hypoglycemia with the presence of anti-insulin antibodies. Other important causes of hypoglycemia include hypoglycemic drugs, non-islet cell tumors, hormonal deficiencies (primary adrenal insufficiency, anterior pituitary insufficiency), and critical illnesses (liver/kidney failure). In this article, we provide an overview of the pathogenesis and treatment of hypoglycemia.
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Chakraborty, Abhishek, and Monika Deb. "Hypoglycemia in breastfed neonates: a hospital-based study." International Journal of Contemporary Pediatrics 10, no. 4 (March 27, 2023): 479–83. http://dx.doi.org/10.18203/2349-3291.ijcp20230722.
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Background: Neonates has well-coordinated adaptation system which maintains the blood sugar at certain safe level in extra uterine life. However certain intrauterine risk factors alter this adaptation system leading to hypoglycemia in early post-natal period. Most of the time hypoglycemic episodes are transient but sometimes there may be recurrent or prolonged hypoglycemia leading to permanent insult in brain and neurological deficit in post-natal life. Aims and objective of the study was to find out incidence of hypoglycemia in exclusively breastfeed neonates and the risk factors associated with this in the post-natal ward of a tertiary care centre in North-East India. Methods: This is a prospective study conducted for a period of six month, where 112 exclusively breastfeed neonates who were shifted immediately to post-natal ward were included. Capillary blood sugar was checked at 1, 3, 6, 12, 24, 48 and 72 hours of life. Neonates with capillary blood glucose less than 40 were considered hypoglycemic. All the hypoglycemic babies were extensively evaluated for different intrauterine and post-natal risk factors. Results: Incidence of hypoglycemia was 16% (18 out of 112 babies). Significant numbers (30.5%) of LBW babies had hypoglycemia, where as 6.5% of normal birth weight babies had hypoglycemia. 38.8% of preterm babies had hypoglycemia where as 11.95% of term babies had hypoglycemic episodes. 71.4% (5 out of 7 babies) of neonates born from diabetic mother. All the large for date infants of diabetic mother had hypoglycemia. Conclusions: Our study came to a conclusion that incidence of hypoglycemia is not very uncommon finding in exclusively breastfeed neonates especially those with risk factors. Routine capillary blood glucose screening is utmost important to pick up the babies with hypoglycemia to prevent immediate and long-term complication.
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Zahed, Karim, Farzan Sasangohar, Ranjana Mehta, Madhav Erraguntla, Mark Lawley, and Khalid Qaraqe. "Investigating the Efficacy of Using Hand Tremors for Early Detection of Hypoglycemic Events: A Scoping Literature Review." Proceedings of the Human Factors and Ergonomics Society Annual Meeting 62, no. 1 (September 2018): 1211–15. http://dx.doi.org/10.1177/1541931218621278.
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Diabetes is a prevalent condition affecting millions of patients globally. Some diabetic patients suffer from a deadly condition called Hypoglycemia (sudden drop in blood glucose levels). Continuous Glucose Monitors (CGMs) have been the most pervasive tool used to track blood glucose levels but these tools are invasive and costly. While early detection of hypoglycemia has been studied, current approaches do not leverage tremors; which are a primary symptom of hypoglycemia. A scoping review was conducted to understand the relationship between tremors and hypoglycemia, and to document any efforts that utilized tremor signatures non-invasively to detect hypoglycemic events. Findings suggest that hypoglycemic tremors are a medium frequency tremor, more resistant to hypoglycemic impairment than other symptoms, and have not been fully explored yet. This paper also documents the work in progress to utilize a novel wearable device that predicts the onsets of hypoglycemia using hand tremor sensing.
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Singh, Kuldeep, and Anjali M. Kher. "Clinico-biochemical profile of hypoglycemia in neonates admitted in NICU." International Journal of Contemporary Pediatrics 6, no. 1 (December 24, 2018): 20. http://dx.doi.org/10.18203/2349-3291.ijcp20184694.
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Background: In high risk neonates’ incidence of hypoglycemia is up to 30%. There is limited evidence-based consensus regarding screening and management of neonates at risk of hypoglycemia. This study was undertaken to know the incidence, clinical profile, sequential blood glucose level upto 72 hours and short-term outcome of neonatal hypoglycemia.Methods: Blood sugar was screened at admission, after feed or D10 bolus, 6, 12, 24, 48 and 72 hours of age. Detailed maternal history and neonatal history, clinical manifestation, management and short-term outcome of hypoglycemic neonates were noted. Statistical analysis of data was done by SPSS 22.0 software.Results: 200 neonates with blood glucose less than 40mg/dl at admission to NICU in which 47 had repeat episode of hypoglycemia. Incidence of hypoglycemia at admission was 22.49% and 5.29% was incidence of repeat episode of hypoglycemia. Pre-term (p=0.005), low birth weight (p=0.020) and SGA (p=0.012) had repeat episode of hypoglycemia. GDM (p=0.040), birth asphyxia (p=0.046) and early septicaemia (p=0.0001) were common risk factors for hypoglycemia. Poor feeding, jitteriness and respiratory abnormality were common presentation of hypoglycemic neonates. The blood glucose levels at admission were less than 30 mg/dl in neonates who later had repeat episode of hypoglycemia. Most hypoglycemic episode after admission occurred within 24 hours of life.Conclusions: LBW especially Preterm SGA neonates are at increased risk of hypoglycemia. Maternal and neonatal risk factors are GDM and birth asphyxia, early septicaemia. Screening for hypoglycemia is essential for high-risk neonates.
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Shahid, Madhia, Gabriel Q. Shaibi, Hayley Baines, Pamela Garcia-Filion, Zoe Gonzalez-Garcia, and Micah Olson. "Risk of hypoglycemia in youth with type 2 diabetes on insulin." Journal of Pediatric Endocrinology and Metabolism 31, no. 6 (June 27, 2018): 625–30. http://dx.doi.org/10.1515/jpem-2018-0014.
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Abstract Background: The objective of this study was to ascertain the risk of hypoglycemia among youth with type 2 diabetes (T2D) on insulin therapy. Methods: Twenty-two youth with T2D on insulin therapy (M=12, F=10, age=14.4±4.0 years) were enrolled from a single pediatric endocrine practice. They were followed-up for 3 months with weekly phone calls and monthly in-person visits to review blood glucose logs and document any signs or symptoms of hypoglycemia (defined as finger stick glucose of ≤70 mg/dL). Episodes of hypoglycemia were categorized into five categories: severe, documented symptomatic, asymptomatic, probable symptomatic and relative hypoglycemia. In addition to examining the risk of hypoglycemia, the degree to which hypoglycemia was associated with patient demographics (e.g. age, gender and body mass index [BMI]) or clinical factors (i.e. duration of diabetes, duration of insulin treatment, glycemic control or insulin dose and regimen) was determined. Results: Nine hypoglycemic events occurred during the study period in five patients with an incidence rate of nine events per 5.3 patient-years. Of the hypoglycemic events, five were symptomatic and four were asymptomatic. No severe hypoglycemic events occurred. Hypoglycemia was not associated with age, ethnicity, duration of insulin treatment, insulin dose or initial hemoglobin (HbA1c). However, a significant difference in BMI was noted, with T2D youth who experienced hypoglycemia having a lower BMI than those who did not experience hypoglycemia. Conclusions: The results of this study suggest that the risk of hypoglycemia in youth with T2D on insulin therapy is low.
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de Galan, Bastiaan E., Saskia J. Rietjens, Cees J. Tack, Sieberen P. van der Werf, C. G. J. (Fred) Sweep, Jacques W. M. Lenders, and Paul Smits. "Antecedent Adrenaline Attenuates the Responsiveness to But Not the Release of Counterregulatory Hormones during Subsequent Hypoglycemia." Journal of Clinical Endocrinology & Metabolism 88, no. 11 (November 1, 2003): 5462–67. http://dx.doi.org/10.1210/jc.2003-030407.
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Abstract Hypoglycemia unawareness is thought to be the consequence of recurrent hypoglycemia, yet the underlying mechanism is still incompletely understood. The aim of the present study was to determine the role of antecedent elevated adrenaline in the pathogenesis of hypoglycemia unawareness. Sixteen healthy volunteers (eight of either sex) participated in two experiments, performed in random order and at least 3 wk apart. During the morning, three consecutive doses of 0.04, 0.06, and 0.08 μg·kg−1·min−1 of adrenaline or matching placebo (normal saline) were infused for the total duration of 1 h. Three hours later, a hyperinsulinemic (360 pmol·m−2·min−1) two-step hypoglycemic (5.0–3.5–2.5 mmol·liter−1) clamp study was performed. During hypoglycemia, hypoglycemic symptoms, counterregulatory hormones, cardiovascular responses, and cognitive function were monitored. Hypoglycemia induced similar responses of autonomic and neuroglycopenic symptoms, counterregulatory hormones, and lengthening in reaction time on the choice reaction time task, irrespective of antecedent infusions. However, prior adrenaline was associated with higher exogenous glucose requirements at hypoglycemic nadir (10.1 ± 1.3 vs. 7.3 ± 1.3 μmol·kg−1·min−1, P = 0.017), an attenuated hypoglycemia-induced fall in blood pressure (mean arterial pressure, −13 ± 2 vs. −8 ± 2 mm Hg, P = 0.006), and preserved cognitive function as assessed by the symbol digit test during hypoglycemia, when compared with prior placebo. We conclude that elevated adrenaline attenuates the responsiveness to, but not the release of counterregulatory hormones during subsequent hypoglycemia. As such, adrenaline’s role in the development of hypoglycemia unawareness is limited.
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Sandoval, Darleen A., Deanna L. Aftab Guy, M. Antoinette Richardson, Andrew C. Ertl, and Stephen N. Davis. "Acute, same-day effects of antecedent exercise on counterregulatory responses to subsequent hypoglycemia in type 1 diabetes mellitus." American Journal of Physiology-Endocrinology and Metabolism 290, no. 6 (June 2006): E1331—E1338. http://dx.doi.org/10.1152/ajpendo.00283.2005.
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Exercise-induced hypoglycemia can occur within hours after exercise in type 1 diabetes mellitus (T1DM) patients. This study tested the hypothesis that an acute exercise bout causes (within hours) blunted autonomic and metabolic responses to subsequent hypoglycemia in patients with T1DM. Twelve T1DM patients (3 W/9 M) were studied during a single-step, 2-h hyperinsulinemic (572 ± 4 pmol/l) hypoglycemic (2.8 ± 0.1 mmol/l) clamp 2 h after either a hyperinsulinemic euglycemic (AM EUG) or hypoglycemic clamp (AM HYPO) or after sitting in a chair with basal insulin infusion (AM CON) or 90 min of moderate-intensity exercise (50% V̇o2 max, AM EX). Both AM HYPO and AM EX significantly blunted epinephrine responses and muscle sympathetic nerve activity responses to subsequent hypoglycemia compared with both control groups. Endogenous glucose production was significantly lower and the exogenous glucose infusion rate needed to maintain the hypoglycemic level was significantly greater during subsequent hypoglycemia in AM EX vs. CON. Rate of glucose disposal (Rd) was significantly reduced following AM HYPO. In summary, within 2.5 h, both moderate-intensity AM EX and AM HYPO blunted key autonomic counterregulatory responses. Despite this, glucose Rdwas reduced during afternoon hypoglycemia following morning hypoglycemia, indicating posthypoglycemic insulin resistance. After morning exercise, endogenous glucose production was blunted, but glucose Rdwas maintained during afternoon hypoglycemia, thereby indicating reduced metabolic defenses against hypoglycemia. These data suggest that exercise-induced counterregulatory failure can occur very rapidly, increasing the risk for hypoglycemia in T1DM within hours.
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Serik, S. A., and V. I. Strona. "Hypoglycemia and cardiac arrhythmias in diabetes mellitus." Ukrainian Therapeutical Journal, no. 3—4 (December 30, 2022): 69–79. http://dx.doi.org/10.30978/utj2022-3-69.
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The article provides an assessment of cardiovascular risks associated with episodes of hypoglycemia in patients with diabetes mellitus. The analysis has been performed for the experimental and clinical data on cardiac arrhythmias during induced hypoglycemia in animal models and in patients with diabetes. The pathogenetic mechanisms of the development of life‑threatening heart rhythm disorders during hypoglycemic states (in particular, changes in autonomic nervous system activation and in the serum level of potassium) have been considered. The nature of electrocardiographic changes preceding the development of arrhythmias during hypoglycemia is described and factors affecting QT interval duration during hypoglycemia are given. The authors highlight the results of clinical studies of spontaneous hypoglycemia in terms of the arrhythmias’ specific features in daytime and nocturnal hypoglycemia, and different mechanisms of the cardiac arrhythmias’ development at different periods of the day. Clinical data have been presented as regards the drug‑induced hypoglycemia during administration beta‑adrenergic receptor blockers, angiotensin‑converting enzyme inhibitors, fluoroquinolones, as well as mechanisms of dysglycemic effects of these drugs. It has been noted that β‑blockers can mask symptoms of catecholamine‑mediated hypoglycemia. It has been established that among hypoglycemic agents, insulin secretion stimulators (sulfonylureas, meglinides) and insulin have the highest risk of serious hypoglycemia. However, the use of basal and prandial insulin analogues was associated with a lower frequency of hypoglycemia compared to human insulin. It was emphasized that hypoglycemia should be avoided in clinical practice to improve prognosis and prevent arrhythmias. For this, it is necessary to individualize target glycemic values with their mitigation in high‑risk patients, to use the safest insulin and non‑insulin hypoglycemic agents, and to implement new technologies (pumps, continuous glucose monitoring) more widely. It is extremely important to take into account comorbidity and the effects on hypoglycemia risk of drugs used for the treatment of concomitant diseases.
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Davis, S. N., and D. Tate. "Effects of Morning Hypoglycemia on Neuroendocrine and Metabolic Responses to Subsequent Afternoon Hypoglycemia in Normal Man1." Journal of Clinical Endocrinology & Metabolism 86, no. 5 (May 1, 2001): 2043–50. http://dx.doi.org/10.1210/jcem.86.5.7495.
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There is general agreement that prior hypoglycemia blunts subsequent hypoglycemic counterregulatory responses. However, there is considerable debate concerning the timing and number of prior hypoglycemic episodes required to cause this blunting effect. The aim of this study was to determine whether one episode of hypoglycemia could modify neuroendocrine, metabolic, and symptom responses to hypoglycemia induced 2 h later. A total of 24 (12 male and 12 female) young, healthy, overnight-fasted subjects participated in a series of glucose clamp studies. A total of 16 individuals underwent 2 randomized studies of either identical 2-h morning and afternoon hyperinsulinemic (490 ± 60 pmol/L) hypoglycemia (2.9 ± 0.1 mmol/L) separated by 2 h or, at least 2 months later, 2-h morning and afternoon hyperinsulinemic (492 ± 45 pmol/L) euglycemia (5.1 ± 0.1 mmol/L). A total of 8 other subjects participated in a single experiment that consisted of 2-h morning hyperinsulinemic (516 ± 60 pmol/L) euglycemia (5.1 ± 0.1 mmol/L) and 2-h afternoon hyperinsulinemic (528 ± 66 pmol/L) hypoglycemia (2.9 ± 0.1 mmol/L) also separated by 2 h. Morning hypoglycemia significantly (P < 0.01) reduced (33–55%) the responses of epinephrine, norepinephrine, glucagon, GH, cortisol, and pancreatic polypeptide during afternoon hypoglycemia. Hypoglycemic symptoms (primarily neuroglycopenic) were also significantly (P < 0.01) reduced during afternoon hypoglycemia. Plasma glucose, insulin, nonesterified fatty acids, glycerol, lactate, β-hydroxybutyrate (P < 0.01), GH, and cortisol (P < 0.05) levels were significantly increased at the start of afternoon hypoglycemia following morning hypoglycemia. Morning hypoglycemia created an insulin-resistant state during afternoon hypoglycemia. Despite blunted neuroendocrine responses, glucose infusion rates required to maintain hypoglycemia and increases in glucose oxidation were significantly attenuated during afternoon compared with morning hypoglycemia. This was in marked contrast to euglycemic control experiments where glucose infusion rates and nonoxidative glucose disposal were significantly increased during afternoon relative to morning studies. We conclude that in normal man one episode of prolonged, moderate, morning hypoglycemia can produce substantial blunting of neuroendocrine and symptomatic responses to subsequent near-term hypoglycemia, and the induction of posthypoglycemic insulin resistance can compensate for blunted neuroendocrine responses by limiting glucose flux and specifically glucose oxidation during subsequent near-term hypoglycemia.
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Sharma, Suresh K., and Ravi Kant. "Awareness of Symptoms and Early Management of Hypoglycemia among Patients with Diabetes Mellitus." Journal of Diabetes and Endocrinology Association of Nepal 1, no. 1 (September 28, 2018): 12–17. http://dx.doi.org/10.3126/jdean.v1i1.21190.
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Background: Hypoglycemia mostly occurs in diabetic patients on medications. Lack of awareness on hypoglycemic symptoms among patients may delay its identification and treatment. The symptoms of hypoglycemic symptoms among patients may delay its identification and treatment. Neglecting the symptoms of hypoglycemia and delaying treatment could cause poorer outcomes or morbidity. The present study was aimed to assess the awareness of symptoms of hypoglycemia and knowledge in early management of hypoglycemia among patients with diabetes.Methods: A Cross sectional study was done among 500 diabetes mellitus patients attending the outpatient department of AIIMS, Rishikesh, Uttarakhand in 2017. Patient with diabetes for over five years and who were on insulin treatment were included in the study. After obtaining an informed consent, knowledge on the symptoms and early treatment of hypoglycemia were collected. The data were analyzed by frequency and percentage.Results: The study included 500 diabetic patients, of which 55.5% were females. The common symptoms of hypoglycemia known to the study subjects were dizziness (84.4%), weakness (74.1%), and drowsiness (68.1%). Overall, 322 (64.4%) diabetic patients had good knowledge on hypoglycemia (knowledge of at least three symptoms of hypoglycemia together with at least one precipitating factor and at least one remedial measure). Regarding management of hypoglycemia, 49% patients preferred taking glucose powder or sugar with water as an immediate measure. Higher age, illiteracy, low socioeconomic status was associated with poor knowledge whereas treatment with insulin along with oral hypoglycemic agents was associated with good knowledge on hypoglycemia.Conclusion: Although the knowledge on the symptoms, remedial measures, and prevention of hypoglycemic episodes was good among the type 2 diabetic patients in the study, there were gap in knowledge on important aspects like precipitating factors, target levels etc., which need to be addressed by health care workers through regular educational programs.Jour of Diab and Endo Assoc of Nepal 2017; 1(1): 12-17
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Jackson, Lesley, Fiona L. R. Williams, Ann Burchell, Michael W. H. Coughtrie, and Robert Hume. "Plasma Catecholamines and the Counterregulatory Responses to Hypoglycemia in Infants: A Critical Role for Epinephrine and Cortisol." Journal of Clinical Endocrinology & Metabolism 89, no. 12 (December 1, 2004): 6251–56. http://dx.doi.org/10.1210/jc.2004-0550.
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Abstract The purpose of this study was to define plasma catecholamine responses as part of the counterregulatory hormonal reaction to hypoglycemia in infants after a regular 3- to 4-h feed was omitted. Hormone levels were assessed once, at the end of the fast or at hypoglycemia. The 121 infants were subdivided into three groups for analysis: normoglycemia (n = 94, 78%); transient hypoglycemia (n = 11, 9%); or severe and persistent hypoglycemia (n = 16, 13%). The severe and persistent hypoglycemic group had significantly higher levels of cortisol and epinephrine than the normoglycemic group. Norepinephrine and glucagon levels did not differ between the groups. Human GH levels were higher in the transiently hypoglycemic group but not in the severe and persistent hypoglycemic group. Prefeed blood lactate levels differed significantly among the groups and were highest in the severe and persistent groups. Multiple regression analysis showed that cortisol levels were significantly higher in infants who had severe and persistent hypoglycemia. The counterregulatory hormonal response in infants to severe and persistent hypoglycemia was limited to elevations in only cortisol and epinephrine levels but did not involve glucagon or human GH. This limited hormonal response may also contribute to the frequent occurrence of hypoglycemia in these infants.
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Makhlina, E. "ESTIMATION OF TYPE 1 DIABETES COMPENSATION BY RESULTS OF GLUCOSE LONG MONITORING." Health and Ecology Issues, no. 3 (September 28, 2008): 56–60. http://dx.doi.org/10.51523/2708-6011.2008-5-3-11.
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Recently in diabetology there were started actively implementing new modern technologies. One of such directions in continuous glucose monitoring system (CGMS). The purpose of the present work is revealing of hypoglycemia fluctuations during the day by CGMS, detection of frequency and duration of hypoglycemic reactions and registration of post hypoglycemic hyperglycemias. The provided data analysis has shown that the period of hyperglycemia made up the basic period of time not depending on patients age. The given fact is caused by chronic insulin overdose due to latent hypoglycemias and a syndrome of the damaged glycemia counter-regulation.
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Hilleman, Daniel E., Syed M. Mohiuddin, Ismail S. Ahmed, and Joann M. Dahl. "Cibenzoline-Induced Hypoglycemia." Drug Intelligence & Clinical Pharmacy 21, no. 1 (January 1987): 38–40. http://dx.doi.org/10.1177/10600280870211p104.
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Antiarrhythmic-induced hypoglycemia is an ill-defined phenomenon. Sporadic cases have been reported with disopyramide, a class IA antiarrhythmic agent. We report a case of cibenzoline-induced hypoglycemia in an elderly male with a history of ischemic heart disease, congestive heart failure, ventricular arrhythmias, and chronic obstructive pulmonary disease. Cibenzoline is a class I antiarrhythmic agent currently undergoing clinical investigation in the U.S. The initial hypoglycemic episode occurred after two years of successful treatment with cibenzoline. Blood glucose during the first hypoglycemic episode was 40 mg/dL. The hypoglycemia was associated with central nervous system depression, hyperkalemia, electrocardiographic abnormalities, and respiratory distress. Rechallenge with cibenzoline resulted in recurrence of symptoms and a blood glucose level of 21 mg/dL. A second rechallenge resulted in symptoms suggestive of hypoglycemia, but cibenzoline was discontinued before frank hypoglycemia and hyperkalemia recurred. Hypoglycemia occurred during periods of fasting, which most likely ruled out reactive-type hypoglycemia. Insulinoma was ruled out by the presence of normal fasting blood glucose and plasma insulin levels. It was concluded that this patient's hypoglycemia was secondary to cibenzoline. Hypoglycemia is a rare and sporadic adverse effect associated with antiarrhythmic therapy. However, the severity of these reactions warrants increased awareness of their occurrence in patients presenting with symptoms of hypoglycemia who are receiving disopyramide or cibenzoline.
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Sanders, Nicole M., Charles W. Wilkinson, Gerald J. Taborsky, Salwa Al-Noori, Wendi Daumen, Aryana Zavosh, and Dianne P. Figlewicz. "The selective serotonin reuptake inhibitor sertraline enhances counterregulatory responses to hypoglycemia." American Journal of Physiology-Endocrinology and Metabolism 294, no. 5 (May 2008): E853—E860. http://dx.doi.org/10.1152/ajpendo.00772.2007.
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Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed for patients with comorbid diabetes and depression. Clinical case studies in diabetic patients, however, suggest that SSRI therapy may exacerbate hypoglycemia. We hypothesized that SSRIs might increase the risk of hypoglycemia by impairing hormonal counterregulatory responses (CRR). We evaluated the effect of the SSRI sertraline on hormonal CRR to single or recurrent hypoglycemia in nondiabetic rats. Since there are time-dependent effects of SSRIs on serotonin neurotransmission that correspond with therapeutic action, we evaluated the effect of 6- or 20-day sertraline treatment on hypoglycemia CRR. We found that 6-day sertraline (SERT) treatment specifically enhanced the epinephrine response to a single bout of hypoglycemia vs. vehicle (VEH)-treated rats ( t = 120: VEH, 2,573 ± 448 vs. SERT, 4,202 ± 545 pg/ml, P < 0.05). In response to recurrent hypoglycemia, VEH-treated rats exhibited the expected impairment in epinephrine secretion ( t = 60: 678 ± 73 pg/ml) vs. VEH-treated rats experiencing first-time hypoglycemia ( t = 60: 2,081 ± 436 pg/ml, P < 0.01). SERT treatment prevented the impaired epinephrine response in recurrent hypoglycemic rats ( t = 60: 1,794 ± 276 pgl/ml). In 20-day SERT-treated rats, epinephrine, norepinephrine, and glucagon CRR were all significantly elevated above VEH-treated controls in response to hypoglycemia. Similarly to 6-day SERT treatment, 20-day SERT treatment rescued the impaired epinephrine response in recurrent hypoglycemic rats. Our data demonstrate that neither 6- nor 20-day sertraline treatment impaired hormonal CRR to hypoglycemia in nondiabetic rats. Instead, sertraline treatment resulted in an enhancement of hypoglycemia CRR and prevented the impaired adrenomedullary response normally observed in recurrent hypoglycemic rats.
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Heller, Simon R., Mark Peyrot, Shannon K. Oates, and April D. Taylor. "Hypoglycemia in patient with type 2 diabetes treated with insulin: it can happen." BMJ Open Diabetes Research & Care 8, no. 1 (June 2020): e001194. http://dx.doi.org/10.1136/bmjdrc-2020-001194.
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There are many misconceptions about the prevalence and effects of hypoglycemia in people with type 2 diabetes (T2D), including hypoglycemia does not occur or does not have adverse consequences in T2D. This narrative review aims to help dispel these myths. Around 25% of people with T2D taking insulin for >5 years were found to have severe hypoglycemic events, which is comparable to the severe hypoglycemia rate in adults with type 1 diabetes (T1D) diagnosed within 5 years. The total number of hypoglycemic events among insulin-treated T2D, including severe hypoglycemia, is as high or higher than among those with T1D. Recent evidence suggests serious consequences of hypoglycemia may, in some respects, be greater in individuals with T2D, particularly regarding effects on the cardiovascular system. Hypoglycemia is generally patient-reported. Issues with hypoglycemia unawareness, limited glucose testing, limited recall, lack of event logging and fear of failure or shaming limits the number of hypoglycemic episodes reported by people with diabetes. Barriers to healthcare provider inquiry and reporting include lack of knowledge regarding the problem’s magnitude, competing priorities during patient visits, lack of incentives to report and limitations to documentation systems for adequate reporting. All people with diabetes should be encouraged to discuss their experiences with hypoglycemia without judgment or shame. Glucose targets, testing schedules (blood glucose or continuous glucose monitoring) and treatment plans should be reviewed often and individualized to the minimize risk of hypoglycemia. Finally, people with T2D on insulin should always be encouraged to have oral glucose and rescue medication immediately available.
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Mohamed, Ashraf, Christine Bolen, Jennifer Morgan, Patricia Ann Rice, Meredith Speas, Ahmed Abdelmonem, and Carolyn Russo. "Reducing Morning Hypoglycemia Among Children Undergoing Treatment for Acute Lymphoblastic Leukemia." JCO Oncology Practice 17, no. 6 (June 2021): e901-e907. http://dx.doi.org/10.1200/op.20.00652.
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PURPOSE: Hypoglycemia has been observed in children receiving acute lymphoblastic leukemia (ALL) therapy, and it can negatively affect patient outcomes. We documented a 4%-6% prevalence of hypoglycemia among patients in the two clinics in this study. We aim to reduce morning hypoglycemia in children on chemotherapy for ALL at two community pediatric oncology clinics (A and B) by 50% in 9 months. METHODS: We used the Institute for Healthcare Improvement (IHI) Model for Improvement as the framework. Prolonged hours of fasting for procedural sedation, gaps in the caregivers' knowledge of hypoglycemia risk, and a lack of awareness of the new mercaptopurine administration guidelines were the most likely contributing factors for hypoglycemia. We developed a hypoglycemia prevention educational program for staff and caregivers followed by a knowledge assessment tool. RESULTS: Each month, the average number of patients seen in both clinics was 43. The monthly average of blood glucose tests in these patients was 94. After implementing the intervention, the percentage of caregivers who received hypoglycemia education reached 88%. Of those, 78% scored ≥ 75% in the knowledge reassessment resurvey. The combined average hypoglycemic episodes in the two clinics decreased by 46%. A higher reduction in hypoglycemic episodes was observed in clinic A (75%) compared with clinic B (17%). CONCLUSION: Implementing hypoglycemia education led to a significant drop in hypoglycemic episodes among children on ALL therapy. Despite using a similar approach, one of the two clinics showed a more than fourfold improvement compared with the other.
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Abs, Roger, Louis Verbist, Marleen Moeremans, Pierre Blockx, Ivo De Leeuw, and Jozef Bekaert. "Hypoglycemia owing to inappropriate glucagon secretion treated with a continuous subcutaneous glucagon infusion system." Acta Endocrinologica 122, no. 3 (March 1990): 319–22. http://dx.doi.org/10.1530/acta.0.1220319.
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Abstract A selective glucagon deficiency was documented in a 36-year-old female patient suffering from severe hypoglycemic attacks. The extremely low fasting plasma glucagon levels could not be stimulated by hypoglycemia. The increase in plasma glucagon during stimulation with arginine did not prevent hypoglycemia provoked by the simultaneous insulin secretion. Treatment consisting of a continuous sc glucagon infusion system resulted in correction of both postabsorptive and postprandial hypoglycemia. Further lowering of the glucose level during an arginine test could be the hallmark of this hypoglycemic syndrome characterized by an inappropriate glucagon secretion. This case report would indicate that epinephrine cannot prevent hypoglycemia when glucagon release is completely deficient.
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Yukina, M. Yu, N. F. Nuralieva, E. A. Troshina, and V. A. Ioutsi. "Clinical case of factitious hypoglycemia." Meditsinskiy sovet = Medical Council, no. 7 (May 29, 2020): 130–36. http://dx.doi.org/10.21518/2079-701x-2020-7-130-136.
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Hypoglycemic syndrome (HGS) is a significant decrease glucose in blood, manifested by neurological symptoms, and stopped by the introduction of glucose. Among the many causes of HGS the special place is taken by the factitious hypoglycemia, as one of the variants of Munchausen syndrome. Hypoglycemia in such cases is achieved by the intentional introduction of hypoglycemic drugs. The most commonly used medications are sulfonylurea derivatives, which are affordable, inexpensive and legal. The close collaboration of clinicians with the laboratory service plays a key role in the diagnosis of factitious hypoglycemia. Since the results of biochemical and hormonal analyzes in patients with hypoglycemia due to reception of oral hypoglycemic medications and pancreatogenous HGS are identical, the only way to differentiate these conditions is by detection of insulin secretagogue substances in the blood (or urine).The determination of oral hypoglycemic medications in cases of suspicion of artificial reception is not implemented in Russia. Factitious hypoglycemia in most cases is the diagnosis of exclusion, and its confirmation if often based on detection of medications among the personal effects of patient. This is a significant difficulty given the ethical standards. However, since 2018 we conduct in our Centre the determination of 7 oral hypoglycemic medications (glibenclamide, gliquidone, gliclazide, glimepiride, glipizide, nateglinide and repaglinide) in patient’s blood using the liquid chromatography–tandem mass spectrometry (LC-MS). This article presents a clinical case of a patient without diabetes mellitus taking glibenclamide and detection of this drug using highly selective LC-MS.
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Kim, Mina, Zhao-Xue Yu, Bertil B. Fredholm, and Scott A. Rivkees. "Susceptibility of the developing brain to acute hypoglycemia involving A1 adenosine receptor activation." American Journal of Physiology-Endocrinology and Metabolism 289, no. 4 (October 2005): E562—E569. http://dx.doi.org/10.1152/ajpendo.00112.2005.
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It has been suggested that the developing brain is less vulnerable to the adverse effects of hypoglycemia than the mature brain; however, this issue remains controversial. We also do not know the magnitude or duration of hypoglycemia needed to trigger hypoglycemic brain injury during development. To address this issue a series of in vivo and in vitro studies were performed. First, we established an acute model of insulin-induced hypoglycemia in mice by administering 3 U/kg of neutral-protamine Hagadorn insulin subcutaneously. When we examined degenerating neurons in hippocampus and striatum by TUNEL labeling, injury was observed after 4 h of hypoglycemia in postnatal day ( P)7 mice, and we observed more cell injury in animals rendered hypoglycemic at P 7 than at P21. Studies of hippocampal slice cultures revealed that reduction in glucose concentration induced more neuronal injury in slices prepared from P3 and P7 than from P14 and P21 mice. Treatment of slices with an adenosine A1 receptor (A1AR) antagonist reduced the hypoglycemic damage, whereas agonists increased damage, particularly in slices prepared from very young pups. This suggests a critically important role for A1ARs, which was further demonstrated by the reduction of hypoglycemic damage in hippocampal slices prepared from A1AR−/− mice. Furthermore, insulin-induced hypoglycemia in P7 A1AR−/− mice did not increase TUNEL-positive cells, but a major increase was seen in A1AR+/− mice. These observations show that the developing nervous system is indeed sensitive to acute hypoglycemic injury and that A1AR activation contributes to damage induced by hypoglycemia, particularly in immature mouse brain.
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Shum, Kathy, Karen Inouye, Owen Chan, Julian Mathoo, Debra Bilinski, Stephen G. Matthews, and Mladen Vranic. "Effects of antecedent hypoglycemia, hyperinsulinemia, and excess corticosterone on hypoglycemic counterregulation." American Journal of Physiology-Endocrinology and Metabolism 281, no. 3 (September 1, 2001): E455—E465. http://dx.doi.org/10.1152/ajpendo.2001.281.3.e455.
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This study aimed to differentiate the effects of repeated antecedent hypoglycemia, antecedent marked hyperinsulinemia, and antecedent increases in corticosterone on counterregulation to subsequent hypoglycemia in normal rats. Specifically, we examined whether exposure to hyperinsulinemia or elevated corticosterone per se could impair subsequent counterregulation. Four groups of male Sprague-Dawley rats were used: 1) normal controls (N) had 4 days of sham antecedent treatment; 2) an antecedent hypoglycemia group (AH) had 7 episodes of hyperinsulinemic hypoglycemia over 4 days; 3) an antecedent hyperinsulinemia group (AE) had 7 episodes of hyperinsulinemic euglycemia; and 4) an antecedent corticosterone group (AC) had 7 episodes of intravenous corticosterone to simulate the hypoglycemic corticosterone levels in AH rats. On day 5, hyperinsulinemic euglycemic-hypoglycemic clamps were performed. Epinephrine responses to hypoglycemia were impaired ( P< 0.05 vs. N) after antecedent hypoglycemia and hyperinsulinemia. This correlated with diminished ( P < 0.05 vs. N) absolute glucose production responses in AH rats and diminished incremental glucose production responses in AE rats. Paradoxically, norepinephrine responses were increased ( P < 0.05 vs. N) after antecedent hypoglycemia. Glucagon and corticosterone responses were unaffected by antecedent hypoglycemia and hyperinsulinemia. In AC rats, incremental but not absolute glucose production responses were decreased ( P < 0.05 vs. N). However, neuroendocrine counterregulation was unaltered. We conclude that both antecedent hypoglycemia and hyperinsulinemia impair epinephrine and glucose production responses to subsequent hypoglycemia, suggesting that severe recurrent hyperinsulinemia may contribute to the development of hypoglycemia-associated autonomic failure.
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Matveyenko, Aleksey V., MaryAnn Bohland, Maziyar Saberi, and Casey M. Donovan. "Portal vein hypoglycemia is essential for full induction of hypoglycemia-associated autonomic failure with slow-onset hypoglycemia." American Journal of Physiology-Endocrinology and Metabolism 293, no. 3 (September 2007): E857—E864. http://dx.doi.org/10.1152/ajpendo.00283.2007.
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Antecedent hypoglycemia leads to impaired counterregulation and hypoglycemic unawareness. To ascertain whether antecedent portal vein hypoglycemia impairs portal vein glucose sensing, thereby inducing counterregulatory failure, we compared the effects of antecedent hypoglycemia, with and without normalization of portal vein glycemia, upon the counterregulatory response to subsequent hypoglycemia. Male Wistar rats were chronically cannulated in the carotid artery (sampling), jugular vein (glucose and insulin infusion), and mesenteric vein (glucose infusion). On day 1, the following three distinct antecedent protocols were employed: 1) HYPO-HYPO: systemic hypoglycemia (2.52 ± 0.11 mM); 2) HYPO-EUG: systemic hypoglycemia (2.70 ± 0.03 mM) with normalization of portal vein glycemia (portal vein glucose = 5.86 ± 0.10 mM); and 3) EUG-EUG: systemic euglycemia (6.33 ± 0.31 mM). On day 2, all groups underwent a hyperinsulinemic-hypoglycemic clamp in which the fall in glycemia was controlled so as to reach the nadir (2.34 ± 0.04 mM) by minute 75. Counterregulatory hormone responses were measured at basal (−30 and 0) and during hypoglycemia (60–105 min). Compared with EUG-EUG, antecedent hypoglycemia (HYPO-HYPO) significantly blunted the peak epinephrine (10.44 ± 1.35 vs. 15.75 ± 1.33 nM: P = 0.01) and glucagon (341 ± 16 vs. 597 ± 82 pg/ml: P = 0.03) responses to next-day hypoglycemia. Normalization of portal glycemia during systemic hypoglycemia on day 1 (HYPO-EUG) prevented blunting of the peak epinephrine (15.59 ± 1.43 vs. 15.75 ± 1.33 nM: P = 0.94) and glucagon (523 ± 169 vs. 597 ± 82 pg/ml: P = 0.66) responses to day 2 hypoglycemia. Consistent with hormonal responses, the glucose infusion rate during day 2 hypoglycemia was substantially elevated in HYPO-HYPO (74 ± 12 vs. 49 ± 4 μmol·kg−1·min−1; P = 0.03) but not HYPO-EUG (39 ± 7 vs. 49 ± 4 μmol·kg−1·min−1: P = 0.36). Antecedent hypoglycemia local to the portal vein is required for the full induction of hypoglycemia-associated counterregulatory failure with slow-onset hypoglycemia.
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Yukina, Marina Yu, Nurana F. Nuralieva, Ekaterina A. Troshina, Nikolay S. Kuznetsov, and Nadezhda M. Platonova. "The hypoglycemic syndrome (insulinoma): pathogenesis, etiology, laboratory diagnosis (review, part 1)." Problems of Endocrinology 63, no. 4 (September 19, 2017): 245–56. http://dx.doi.org/10.14341/probl2017634245-256.
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Hypoglycemic syndrome is a cluster of symptoms developing due to imbalance in the glucose homeostasis system leading to hypoglycemia and that is corrected by glucose administration. A rapid and significant drop of glucose blood level may lead to life-threatening condition, hypoglycemic coma. Chronic hypoglycemia leads to irreversible changes in the central nervous system, while forced frequent meals with high carbohydrate content in order to correct hypoglycemia significantly increases body weight, until morbid obesity develops. Hence, the hypoglycemic syndrome is a topical problem of contemporary medicine. Insulinoma is the most common cause of pancreatogenous hypoglycemia in patients without diabetes mellitus. Exogenous administration of hypoglycemic agents, severe multiple organ and tumor pathologies, sequelae of bariatric surgery, deficiency of contrainsular hormones, genetically determined enzyme disorders and autoimmune diseases may also cause the hypoglycemic syndrome. The primary diagnostic tasks determining the choice of the treatment approach involve confirming the hypoglycemic syndrome and determining its etiology. The test after 3-day-long fasting and other tests are used for this purpose. In this review, we discuss the main causes and features of pathogenesis of the hypoglycemic syndrome, as well as criteria of differential diagnosis and the possibility of introducing new diagnostic tests and markers.
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Chen, Nai-Ching, Chien-Liang Chen, and Feng-Chih Shen. "The Risk Factors of Severe Hypoglycemia in Older Patients with Dementia and Type 2 Diabetes Mellitus." Journal of Personalized Medicine 12, no. 1 (January 7, 2022): 67. http://dx.doi.org/10.3390/jpm12010067.
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Background: The adequate glycemic control and risk factors for hypoglycemia in older patients with dementia and type 2 diabetes mellitus (T2DM) remain unclear. This study aimed to analyze the status of glycemic control and determine the risk of hypoglycemia among these groups. Methods: A hospital admission record due to hypoglycemia through an emergency room with glucose supplementation in the Chang Gung Memorial Hospital was identified as a hypoglycemic event. Patients with dementia and T2DM without hypoglycemic events throughout the study period were defined as the control group. We gathered patients aged ≥65 years with a diagnosis of Alzheimer’s dementia (AD) and T2DM between 2001 and 2018 in the Chang Gung Research Database (CGRD). We extracted data included medication use, diagnoses, and biochemistry data from hospital records. Results: A total of 3877 older patients with dementia and T2DM with regular visits to the outpatient department were enrolled in this study. During the two-year follow-up period, 494 participants (12.7%) experienced hypoglycemia. Multivariable logistic multivariable regression models for hypoglycemic events showed that metformin had a protective effect (odds ratio (OR) = 0.75, p = 0.023), insulin had the highest risk (OR = 4.64, p < 0.001). Hemoglobin A1c (HbA1c) levels were not correlated with hypoglycemic events (OR = 0.95, p = 0.140). Patients with hypoglycemic episodes had a significantly higher proportion of ≥2 Charlson Comorbidity Index scores than those without hypoglycemic episodes (83.2% versus 56.4%, p < 0.001). Conclusions: Drug regimen affects hypoglycemic episodes but not HbA1c in older patients with dementia and T2DM. In addition, patients with more comorbidities experience an increased risk of hypoglycemia.
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Clus, Simona, Gabriela Creteanu, and Amorin Popa. "Silent Hypoglycemia in Patients with Diabetes." Internal Medicine 15, no. 6 (December 1, 2018): 21–28. http://dx.doi.org/10.2478/inmed-2018-0042.
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AbstractIntroduction. Iatrogenic hypoglycemia increases cardiovascular morbidity sometimes even with fatalities, and also increases cognitive disorders in most people with type 1 diabetes (T1D) and type 2 diabetes (T2D). Hypoglycemia is characterized by unawareness if the sympathoadrenal response is attenuated during the night, in autonomic neuropathy or in elderly patients. Therefore, hypoglycemia is a limiting factor in the glycemic management of diabetes.Methods. We aimed to analyze the hypoglycemic events and the time spent with low glucose level (glucose <3.9 mmol/l) in patients with diabetes (T1D, T2D) with insulin therapy (basal or basal-bolus), in ambulatory or hospital setting. The glucose variability was assessed via the interstitial glucose concentration, measured with a Continuous Glucose Monitoring (CGM) system over 72 hours.Results. The incidence, severity and duration of hypoglycemia are not correlated with HbA1c, disease’s duration and patient’s age. In patients with T1D, severe hypoglycemia is more frequent in patients with a long duration of diabetes. In this analysis, the type of basal analog insulin did not influence the presence of hypoglycemia (p=0.7), but the duration of nocturnal hypoglycemia was longer with insulin glargine U100 than with insulin detemir. The basal regimen is more protective for hypoglycemia than basal-bolus insulin.Conclusions. The study suggested that hypoglycemic events are common, silent and prolonged in 1/3 of patients with T1D and T2D. The CGM system is beneficial for all patients with T1D and for patients with T2D with hypoglycemic risk and complications, to adjust medication in order to prevent cardiovascular events.
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A, Prameela, and Nirmala M. "A descriptive study to assess the awareness on management of hypoglycaemia among diabetic clients in PSG hospitals." Journal of Scientific and Innovative Research 10, no. 2 (June 30, 2021): 28–33. http://dx.doi.org/10.31254/jsir.2021.10201.
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Diabetes Mellitus (DM) is a foremost health problem in the globe. Diabetes mellitus describes a metabolic disorder of manifold etiologies characterized by chronic hypoglycemia with disturbances of carbohydrate, fat and protein metabolism. Creating alertness on signs and symptoms among diabetic clients may lessen the complications. The objectives were to assess the knowledge of diabetic clients regarding management of hypoglycemia and to find the association between the knowledge of diabetic clients on management of hypoglycemia and their selected demographic variable. The descriptive survey design was adopted by selecting 60 samples using purposive sampling technique. Out of sixty samples, 32(53.4%) were male and 28(46.6%) of the samples were female. Most of the samples 23 (38.33%) belongs to age group between 31-40 years. More than half of the samples, 40(66.66%) were using hypoglycemic agents. 33(55%) were taking medication once a day. 18 ((30%) samples were having the history of hypoglycemic symptoms. whereas, 7(11.66%) of them were not confident about the hypoglycemic symptoms. Only 24(40%) of them were conscious about the selfmanagement of hypoglycemia. The study highlights that the diabetes mellitus clients 13(21.6%) were having adequate knowledge, 39(65%) were having moderately adequate knowledge and 8(13.3%) had inadequate knowledge on management of hypoglycemia. The study concluded that it helped to identify the knowledge regarding hypoglycemia on diabetes mellitus patients and created awareness on hypoglycemic conditions using information booklet will enhance the patients to reduce the complications.
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Hong, Susana, Lubaina Presswala, Yael T. Harris, Isabela Romao, Daniel W. Ross, Hugo Andrade Paz, Meng Zhang, Kenar D. Jhaveri, Vipul Sakhiya, and Steven Fishbane. "Hypoglycemia in Patients with Type 2 Diabetes Mellitus and Chronic Kidney Disease: A Prospective Observational Study." Kidney360 1, no. 9 (July 9, 2020): 897–903. http://dx.doi.org/10.34067/kid.0001272020.
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BackgroundGlycemic management in patients with type 2 diabetes mellitus (T2DM) and CKD can become complicated. One factor that may affect treatment is hypoglycemia. Hypoglycemia risk may be increased by several biologic processes in CKD. The objective of this study was to determine the frequency, severity, and risk factors for hypoglycemia in patients with T2DM and CKD.MethodsThe design was a prospective observational study. A continuous glucose monitor (CGM) was worn by 80 patients for up to 14 days; glucose was measured every 15 minutes. Patients with T2DM and eGFR <45 ml/min were enrolled. Patients on dialysis were excluded. The primary outcome was to assess the frequency of hypoglycemic episodes during the study period. Hypoglycemic episodes were defined as a reduced glucose concentration (<70 mg/dl) lasting ≥15 minutes. Secondary outcomes included assessment of severity of hypoglycemia and risk factors for its development.ResultsA total of 80 patients wore the CGM for a mean of 12.7±2.9 days. Hypoglycemic events occurred in 61 of 80 patients (76%) with glucose <70 mg/dl, and 49 of 80 (61%) with glucose <60 mg/dl. Prolonged hypoglycemic events (CGM glucose <54 mg/dl for ≥120 consecutive minutes) occurred in 31 patients (39%) with 118 total events. Most hypoglycemic episodes occurred overnight, from 1:00 am to 9:00 am. By multivariate analysis, lower hemoglobin A1c and treatment with insulin were two modifiable risk factors for hypoglycemic events.ConclusionsPatients with T2DM and CKD have frequent periods of hypoglycemia that can be severe and prolonged. Hemoglobin A1c does not portray the full scope of hypoglycemia risk. This study illustrates the need for careful monitoring of glucose levels in patients with T2DM and CKD.
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Syed, Shumail, and Alain Joseph Taylon. "Losartan Induced Hypoglycemia in the Absence of Diabetes Mellitus - a Concealed Diagnosis." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A391. http://dx.doi.org/10.1210/jendso/bvab048.796.
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Abstract Background: Losartan has been shown to attenuate symptomatic and hormonal responses to hypoglycemia in prior studies. This results predominantly from blocking AT-II receptors blunting the hypoglycemia-induced rise in plasma epinephrine predisposing them to hypoglycemia unawareness. To our knowledge, however there are no case reports describing losartan induced hypoglycemia in a nondiabetic patient. This abstract is the first description of a patient without diabetes mellitus experiencing severe hypoglycemia induced by the ARB, Losartan. Clinical Case: A 51- year old nondiabetic female was found to be somnolent and in acute respiratory failure. Blood sugar was 34 mg/dL. She received D10 by EMS while coming to the hospital. She was intubated and treated for atypical pneumonia based on bilateral interstitial infiltrates. She remained persistently hypoglycemic around 62 mg/dL. Her most recent A1c was 4.4%. Thyroid function was within normal limits. AM cortisol was 16.8 mcg/dL so there was no concern of adrenal insufficiency. She had no history of gastric bypass surgery. She underwent a 72-hour fast and developed symptomatic hypoglycemia. Her venous blood glucose at this time was 49 mg/dL. Her hypoglycemia panel obtained at this time showed C-peptide 0.7 ng/mL, total insulin 2.9 microU/mL, proinsulin 3.1 pmol/L, IGF 45 ng/mL and BHOB 13.5 mmol/L. Her oral hypoglycemic agent screen was negative. Based on levels that were obtained during the hypoglycemic episode, this correlated to a non-diagnostic study for conventionally described causes of hypoglycemia including exogenous insulin, insulinoma, NIPHS, PGBH, oral hypoglycemic agent, insulin autoimmune or IGF-mediated. Her medication list was analyzed again. We learnt that she had recently been started on losartan about a month prior to this admission for her heart failure management. On further review, the patient mentioned that she was noticing these hypoglycemic events in the last month and that seemed to coincide with when she was started on losartan. We subsequently held losartan which resulted in profound improvement in her glycemic control and her blood sugars improved to a range of 110–140 mg/dL consistently. She was discharged from hospital off losartan. Blood sugar was stable on repeat testing outpatient after discharge. Conclusion: This is the first case that demonstrates the role of losartan in causing severe hypoglycemia in patients without a history of diabetes mellitus. Discontinuation of losartan resulted in prompt improvement of hypoglycemia. Reference: (1) Deininger E, Oltmanns KM, Wellhoener P, Fruehwald-Schultes B, Kern W, Heuer B, Dominiak P, Born J, Fehm HL, Peters A. Losartan attenuates symptomatic and hormonal responses to hypoglycemia in humans. Clin Pharmacol Ther. 2001 Oct;70(4):362–9. PMID: 11673752.
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Boeder, Schafer C., Justin M. Gregory, Erin R. Giovannetti, and Jeremy H. Pettus. "SGLT2 Inhibition Increases Fasting Glucagon but Does Not Restore the Counterregulatory Hormone Response to Hypoglycemia in Participants With Type 1 Diabetes." Diabetes 71, no. 3 (December 2, 2021): 511–19. http://dx.doi.org/10.2337/db21-0769.
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Individuals with type 1 diabetes have an impaired glucagon counterregulatory response to hypoglycemia. Sodium—glucose cotransporter (SGLT) inhibitors increase glucagon concentrations. We evaluated whether SGLT inhibition restores the glucagon counterregulatory hormone response to hypoglycemia. Adults with type 1 diabetes (n = 22) were treated with the SGLT2 inhibitor dapagliflozin (5 mg daily) or placebo for 4 weeks in a randomized, double-blind, crossover study. After each treatment phase, participants underwent a hyperinsulinemic-hypoglycemic clamp. Basal glucagon concentrations were 32% higher following dapagliflozin versus placebo, with a median within-participant difference of 2.75 pg/mL (95% CI 1.38–12.6). However, increased basal glucagon levels did not correlate with decreased rates of hypoglycemia and thus do not appear to be protective in avoiding hypoglycemia. During hypoglycemic clamp, SGLT2 inhibition did not change counterregulatory hormone concentrations, time to recovery from hypoglycemia, hypoglycemia symptoms, or cognitive function. Thus, despite raising basal glucagon concentrations, SGLT inhibitor treatment did not restore the impaired glucagon response to hypoglycemia. We propose that clinical reduction in hypoglycemia associated with these agents is a result of changes in diabetes care (e.g., lower insulin doses or improved glycemic variability) as opposed to a direct, physiologic effect of these medications on α-cell function.
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Whitley, Nathaniel T., Kenneth J. Drobatz, and David L. Panciera. "Insulin overdose in dogs and cats: 28 cases (1986–1993)." Journal of the American Veterinary Medical Association 211, no. 3 (August 1, 1997): 326–30. http://dx.doi.org/10.2460/javma.1997.211.03.326.
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Objective— To characterize the frequency, medical history, clinical signs, methods of treatment, and outcome of insulin-induced hypoglycemia and to identify predisposing factors. Design— Retrospective study. Animals— 8 dogs and 20 cats with diabetes mellitus that developed hypoglycemia because of insulin overdose. Procedure— Medical records of dogs and cats receiving insulin for treatment of diabetes mellitus were reviewed. Medical records of dogs and cats that had an episode of hypoglycemia were reviewed in detail. Results— Overdosing of insulin was more common in cats than in dogs. Median weight of diabetic cats that became hypoglycemic was significantly greater than that of the hospital population of diabetic cats at diagnosis. Eighty percent of cats that became hypoglycemic were receiving insulin doses > 6 U/injection, administered once or twice daily. Dose and type of insulin did not correlate with duration or severity of hypoglycemia. In 7 of 8 dogs and 10 of 20 cats, management factors or concurrent medical problems were considered to be predisposing causes for insulin overdose. Two dogs and 2 cats did not have clinical signs of hypoglycemia, despite documented low concentrations of glucose in their blood. Clinical Implications— Diabetic cats, especially if obese, are at greater risk of insulin overdose than are diabetic dogs. The reason for overdose may not be evident. Diabetic dogs and cats may become hypoglycemic without developing autonomic warning signs of hypoglycemia, or these signs may not be recognized (hypoglycemia unawareness). (J Am Vet Med Assoc 1997;211:326–330)
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Lyu, Young Sang, Jin Hwa Kim, and Sang Yong Kim. "Differential Diagnosis of Hypoglycemia." Korean Journal of Medicine 96, no. 6 (December 1, 2021): 484–92. http://dx.doi.org/10.3904/kjm.2021.96.6.484.
Full textAbstract:
Hypoglycemia is common but can lead to life-threatening consequences. Accurate diagnosis is important to establish the appropriate treatment strategy. Most cases of hypoglycemia are caused by hypoglycemic agents, although it can occur in individuals without diabetes. A systemic and comprehensive diagnostic approach is required to diagnose hypoglycemia in patients without diabetes. It is important to perform appropriate blood testing during an episode of hypoglycemia. This review will focus on the definition, differential diagnosis, causes, and treatment of hypoglycemia, particularly in people without diabetes.
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Yukina, Marina Y., Diana A. Davtyan, Ekaterina A. Troshina, and Nurana F. Nuralieva. "Autoimmune hypoglycemia." Obesity and metabolism 15, no. 3 (November 23, 2018): 9–13. http://dx.doi.org/10.14341/omet9536.
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Autoimmune hypoglycemia is a condition caused by the interaction of endogenous antibodies to insulin or the insulin receptor. Awareness of autoimmune hypoglycemia is important, since the syndrome can cause severe neuroglycopenic symptoms, and should be considered in differential diagnosis of hypoglycemic syndromes. Timely establishment of the correct diagnosis will help to avoid unnecessary surgical interventions in patients who can be successfully treated with conservative support.
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Hanley, James F., Darin D. Willardsen, and Robert Biberdorf. "Profound Hypoglycemia in a Mail-Order Pharmacy Customer as a Result of a Dispensing Error." Hospital Pharmacy 37, no. 7 (July 2002): 734–36. http://dx.doi.org/10.1177/001857870203700714.
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Accidental hypoglycemia is most commonly associated with the inadvertent ingestion of oral hypoglycemic drugs, and profound hypoglycemia can result in significant morbidity and mortality. Dispensing errors involving sulfonylureas are usually cited as the cause, and these errors have historically been related to sound-alike compounds or proximity errors. We present the case of a patient who received sulfonylureas meant for a different patient through the mail and simply complied with the instructions on the medication bottle, with the result of severe hypoglycemia. This case demonstrates the need for clinicians to properly assess all patients with profound hypoglycemia, evaluating them for inadvertent ingestion of hypoglycemic agents. Furthermore, pharmacies that provide mail-order prescription services must ensure patient safety through quality-control mechanisms.
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K.C., Indu. "Causes of Hypoglycemia in Hospitalized Diabetic Patients Referred to Endocrine Department of a Tertiary Level Hospital of India." Medical Journal of Shree Birendra Hospital 15, no. 1 (July 5, 2016): 26–31. http://dx.doi.org/10.3126/mjsbh.v15i1.15018.
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Introduction: Diabetes mellitus (DM) results from relative deficiency or reduced effectiveness of endogenous insulin leading to both micro-vascular and macro-vascular complications. Treatment goal is intensive therapy as early as possible in patients with both type-1 and type-2 diabetes to bring the HbA1c to less than 7%. Occurrence of hypoglycemia in a diabetic patient is a common side effect of treatment. This study was aimed to find the causes of Hypoglycemia in diabetes patients. Methods: It was hospital based cross-sectional observational study on admitted diabetes patients with other co-morbid conditions who were on either oral hypoglycemic agents (OHA) or Insulin. Cause of hypoglycemia was elicited by history taking and analysis. Results: Out of 36 diabetics included in this study, seven had severe hypoglycemia, 22 had moderate to mild hypoglycemia. Most of them had various comorbidities. The causes of hypoglycemic episodes were varied. Conclusion: Hypoglycemia can occur despite cautious treatment protocol especially in diabetics with organ dysfunction, which can be prevented by alert and well-coordinated medical team.
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Antonova, K. V., O. V. Lagoda, and M. M. Tanashyan. "Hypoglycemia in type 2 diabetes mellitus patients — cerebral, cognitive, psychosocial and clinical aspects." Diabetes mellitus 25, no. 3 (June 23, 2022): 288–98. http://dx.doi.org/10.14341/dm12840.
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The review article describes modern approaches to hypoglycemia in diabetes mellitus (DM) patients, its clinical and laboratory diagnostics, and its current classification. Hypoglycemia has the highest impact on cardiovascular morbidity and mortality, including stroke. Cerebral damage in neuroglycopenia, as well as neurological aspects in this group of patients, are discussed. The authors describe glycopenia’s influence on cerebral metabolism, counter-regulatory response, and impaired hypoglycemia recognition, as well as modern neuroimaging techniques that may enhance differential diagnostics in complex cases. The epidemiology of neurocognitive disorders in DM patients and their association with hypoglycemic conditions is outlined, together with psychosocial aspects of its consequences — both for the patient and relatives and for the medical professionals. The search for ways to reduce the burden of hypoglycemia from the standpoint of an effective and safe strategy for treating patients with type 2 diabetes does not lose its relevance, and therefore data on the prevalence of hypoglycemic conditions of varying severity when using certain classes of hypoglycemic drugs are presented. A therapeutic approach that maximizes metabolic control while reducing hypoglycemia to a minimum may determine further possibilities for personalized DM management.
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Hollinger, B. R., and R. M. Bryan. "Beta-receptor-mediated increase in cerebral blood flow during hypoglycemia." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 4 (October 1, 1987): H949—H955. http://dx.doi.org/10.1152/ajpheart.1987.253.4.h949.
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We tested the hypothesis that beta-adrenergic receptor stimulation is involved with the increase in regional cerebral blood flow (rCBF) during hypoglycemia. Rats were surgically prepared with the use of halothane-nitrous oxide anesthesia. A plaster restraining cast was placed around the hindquarters, and anesthesia was discontinued. Hypoglycemia was produced by an intravenous injection of insulin (15 U/kg); normoglycemic control rats were given saline. Propranolol (1.5 mg/kg) was administered to some control and some hypoglycemic rats to block the beta-adrenergic receptors. Regional CBF was measured using 4-[N-methyl-14C]iodoantipyrine. Plasma glucose in the normoglycemic and hypoglycemic groups was approximately 6 and 1.4 mumol/ml, respectively. Regional CBF increased during hypoglycemia in rats that were not treated with propranolol. The increase varied from approximately 60 to 200% depending on the brain region. During hypoglycemia, propranolol abolished the increase in rCBF in the hypothalamus, cerebellum, and pyramidal tract. In other regions the increase in rCBF was only 33-65% of the increase in hypoglycemic rats that were not treated with propranolol. We conclude that beta-receptor stimulation plays a major role in the increase in rCBF during hypoglycemia.
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She, Rui, Naba Hassan Al-sari, Ismo Matias Mattila, Anne-Sophie Sejling, Jens Pedersen, Cristina Legido-Quigley, and Ulrik Pedersen-Bjergaard. "Decreased branched-chain amino acids and elevated fatty acids during antecedent hypoglycemia in type 1 diabetes." BMJ Open Diabetes Research & Care 11, no. 3 (June 2023): e003327. http://dx.doi.org/10.1136/bmjdrc-2023-003327.
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IntroductionHypoglycemia is a major limiting factor in achieving recommended glycemic targets for people with type 1 diabetes. Exposure to recurrent hypoglycemia results in blunted hormonal counter-regulatory and symptomatic responses to hypoglycemia. Limited data on metabolic adaptation to recurrent hypoglycemia are available. This study examined the acute metabolic responses to hypoglycemia and the effect of antecedent hypoglycemia on these responses in type 1 diabetes.Research design and methodsTwenty-one outpatients with type 1 diabetes with normal or impaired awareness of hypoglycemia participated in a study assessing the response to hypoglycemia on 2 consecutive days by a hyperinsulinemic glucose clamp. Participants underwent a period of normoglycemia and a period of hypoglycemia during the hyperinsulinemic glucose clamp. Plasma samples were taken during normoglycemia and at the beginning and the end of the hypoglycemic period. Metabolomic analysis of the plasma samples was conducted using comprehensive two-dimensional gas chromatography with time-of-flight mass spectrometry.ResultsIn total, 68 metabolites were studied. On day 1, concentrations of the branched-chain amino acids, leucine (p=3.8×10−3) and isoleucine (p=2.2×10−3), decreased during hypoglycemia. On day 2, during hypoglycemia, five amino acids (including leucine and isoleucine) significantly decreased, and two fatty acids (tetradecanoic and oleic acids) significantly increased (p<0.05). Although more metabolites responded to hypoglycemia on day 2, the responses of the single metabolites were not statistically significant between the 2 days.ConclusionsIn individuals with type 1 diabetes, one episode of hypoglycemia decreases leucine and isoleucine concentrations. Antecedent hypoglycemia results in the decrement of five amino acids and increases the concentrations of two fatty acids, suggesting an alteration between the two hypoglycemic episodes, which could indicate a possible adaptation. However, more studies are needed to gain a comprehensive understanding of the consequences of these alterations.Trial registration numberNCT01337362.
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Moin, Abu Saleh Md, Hassan Kahal, Ahmed Al-Qaissi, Nitya Kumar, Thozhukat Sathyapalan, Stephen L. Atkin, and Alexandra E. Butler. "Amyloid-related protein changes associated with dementia differ according to severity of hypoglycemia." BMJ Open Diabetes Research & Care 9, no. 1 (April 2021): e002211. http://dx.doi.org/10.1136/bmjdrc-2021-002211.
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IntroductionHypoglycemia in type 2 diabetes (T2D) may increase risk for Alzheimer’s disease (AD), but no data on changes in AD-related proteins with differing degrees of hypoglycemia exist. We hypothesized that milder prolonged hypoglycemia would cause greater AD-related protein changes versus severe transient hypoglycemia.Research design and methodsTwo prospective case-control induced hypoglycemia studies were compared: study 1, hypoglycemic clamp to 2.8 mmol/L (50 mg/dL) for 1 hour in 17 subjects (T2D (n=10), controls (n=7)); study 2, hypoglycemic clamp to 2.0 mmol/L (36 mg/dL) undertaken transiently and reversed in 46 subjects (T2D (n=23), controls (n=23)). Blood sampling at baseline, hypoglycemia and 24-hour post-hypoglycemia, with proteomic analysis of amyloid-related proteins performed.ResultsIn control subjects, the percentage change from baseline to hypoglycemia differed between study 1 and study 2 for 5 of 11 proteins in the AD-related panel: serum amyloid A1 (SAA1) (p=0.009), pappalysin (PAPPA) (p=0.002), apolipoprotein E2 (p=0.02), apolipoprotein E3 (p=0.03) and apolipoprotein E4 (p=0.02). In controls, the percentage change from baseline to 24 hours differed between studies for two proteins: SAA1 (p=0.003) and PAPPA (p=0.004); however, after Bonferroni correction only SAA1 and PAPPA remain significant. In T2D, there were no differential protein changes between the studies.ConclusionsThe differential changes in AD-related proteins were seen only in control subjects in response to iatrogenic induction of hypoglycemic insults of differing length and severity and may reflect a protective response that was absent in subjects with T2D. Milder prolonged hypoglycemia caused greater AD-related protein changes than severe acute hypoglycemia in control subjects.Trial registration numbersNCT02205996, NCT03102801.
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Tkacs, Nancy C., Yanhua Pan, Ramesh Raghupathi, Ambrose A. Dunn-Meynell, and Barry E. Levin. "Cortical Fluoro-Jade Staining and Blunted Adrenomedullary Response to Hypoglycemia after Noncoma Hypoglycemia in Rats." Journal of Cerebral Blood Flow & Metabolism 25, no. 12 (May 18, 2005): 1645–55. http://dx.doi.org/10.1038/sj.jcbfm.9600152.
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Intensive insulin therapy in patients with type 1 diabetes mellitus reduces long-term complications; however, intensive therapy is also associated with a three-fold increase in hypoglycemic episodes. The present study in conscious rats characterizes the physiologic and neuropathologic consequences of a single episode of moderate hypoglycemia. In this model, intravenous insulin is used to reduce plasma glucose to 30 to 35 mg/dL for 75mins. This single hypoglycemic insult acutely induces hypoglycemia-associated autonomic failure (HAAF), with epinephrine responses to hypoglycemia reduced more than 36% from control. Neuropathology after this insult includes the appearance of dying cells, assessed with the marker Fluoro-jade B (FJ). After hypoglycemic insult, FJ+ cells were consistently seen in subdivisions of the medial prefrontal cortex, the orbital cortex, and the piriform cortex. There was a significant correlation between depth of hypoglycemia and number of FJ+ cells, suggesting that there is a critical threshold below which vulnerable cells begin to die. These data suggest that there is a population of cells that are vulnerable to moderate levels of hypoglycemia commonly experienced by patients with insulin-treated diabetes. These cells, which may be neurons, are primarily found in cortical regions implicated in visceral perception and autonomic control, raising the possibility that their loss contributes to clinically reported deficits in autonomic and perceptual responses to hypoglycemia.
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Urlaeva, Inna. "Hypoglycemia, an obstacle to achieving glycemic control. Importance of blood glucose self-monitoring." Clinical review for general practice 2, no. 7 (September 7, 2021): 40–44. http://dx.doi.org/10.47407/kr2021.2.7.00087.
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Hypoglycemia is a well-known factor, limiting the patient's ability to achieve adequate glycemic control, and capable of causing a number of car-diovascular diseases (CVDs). Recurrent hypoglycemia may result in severe, potentially fatal complication of diabetes mellitus (DM), the impaired hypoglycemia awareness, raising the risk of severe hypoglycemia up up to six times. Measuring blood glucose levels is a universally accepted com-ponent of glycemic control and one of the strategies for prevention of hypoglycemia, along with the structured patient education in DM manage-ment and the use of modern hypoglycemic medications. Prevention of severe hypoglycemia may be important for prevention of CVDs in patients with DM.
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Mohamed, Ashraf Mahmoud, Christine Marie Bolen, Jennifer Morgan, Patricia Rice, Meredith Speas, and Carolyn Russo. "A quality improvement initiative for reducing morning hypoglycemia in children undergoing treatment for acute lymphoblastic leukemia." Journal of Clinical Oncology 37, no. 27_suppl (September 20, 2019): 240. http://dx.doi.org/10.1200/jco.2019.37.27_suppl.240.
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240 Background: Hypoglycemia has been observed in children receiving Acute Lymphoblastic Leukemia (ALL) therapy. It affects patients’ outcome. The current quality initiative was piloted at two of the St Jude affiliate clinics. Each month about 10% of children with ALL develop hypoglycemia in those two clinics. Methods: Data was collected for the eight months prior to intervention. Root Cause Analysis (RCA) using fish bone diagram, and Pareto chart to find out the most likely causes of hypoglycemia. Prolonged hours of fasting for procedures, giving 6MP at night on empty stomach, seem to further prolong hours of fasting, and lack of awareness of the new 6MP administration guidelines were the top likely causes. Interventions based on RCA: Developed Hypoglycemia educational brochure addressing causes and prevention of hypoglycemia for care givers followed by knowledge assessment tool, in addition two educational sessions for staff. Plan, Do, Study, Act (PDSA) was used to guide implementation. 4 PDSA cycles were done. Results: Combined monthly average number of ALL patients seen in both centers was 43 (range 38-51) patients with monthly average of 94 (range 71-141) blood glucose samples drawn from them. Process Measure 1: % care givers received hypoglycemia education after 1st cycle was 16.3% which increased to 88% after PDSA cycle # 4. Process Measure 2: % of caregivers scored above 75% in the knowledge of morning hypoglycemia after education were 78%. Outcome Measure: At the end of intervention the average monthly patients with hypoglycemia decreased from 9.4% to 7.8% representing 17% reduction. Hypoglycemic episodes dropped from 6% to 4.2%, showing 30% reduction in hypoglycemic episodes. More reduction in hypoglycemic episodes was observed in clinic 1 (68%) compared to 22% reduction in clinic 2. Conclusions: Using quality improvement methodology in implementing hypoglycemia education led to drop in hypoglycemia episodes among children on ALL therapy. Despite using similar approach, yet one of the two clinics showed higher improvement compared to the other. This may reflect the possible impact of local institutional factors on implementation.
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Monzon, Alexandra D., Ryan McDonough, Christopher C. Cushing, Mark Clements, and Susana R. Patton. "Examining the Relationship between Nighttime Glucose Values in Youth with Type 1 Diabetes and Parent Fear of Nighttime Hypoglycemia." Pediatric Diabetes 2023 (April 14, 2023): 1–7. http://dx.doi.org/10.1155/2023/9953662.
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Objective. Youth with type 1 diabetes mellitus (T1D) are at risk for experiencing nighttime hypoglycemia, and many parents report significant anxiety at night regarding glucose management. Limited data exist examining continuous nighttime glucose levels as a predictor of parent fear of nighttime hypoglycemia. The present study aimed to examine the relationship between parent fear of nighttime hypoglycemia and nighttime blood glucose levels as measured by continuous glucose monitors (CGMs). Methods. A sample of 136 parents/caregivers of youth with T1D completed a one-time survey and youth provided 14 days of CGM data. We conducted regression models with mean nighttime glucose value, glycemic variability, and the percent of nighttime glucose values in the hypoglycemic, target, and hyperglycemic range as the independent variable and parents’ fear of nighttime hypoglycemia as the dependent variable. Results. Overnight hypoglycemia measured via CGM did not predict parents’ fear of nighttime hypoglycemia; however, average youth nighttime glucose levels and nighttime glycemic variability were significant predictors of parents’ fear of nighttime hypoglycemia. Conclusions. The results of the present study indicate that parents of youth with T1D may report higher fear of hypoglycemia if they observe increased fluctuations in their child’s nighttime glucose levels, regardless of how often their child’s glucose levels are in the hypoglycemic range. The results suggest that clinicians may consider screening for parent fear of nighttime hypoglycemia in families of youth who present with large variability in their glucose values overnight.
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Pratipanawatr, Thongchai, Bancha Satirapoj, Boonsong Ongphiphadhanakul, Sompongse Suwanwalaikorn, and Wannee Nitiyanant. "Impact of Hypoglycemia on Health-Related Quality of Life among Type 2 Diabetes: A Cross-Sectional Study in Thailand." Journal of Diabetes Research 2019 (October 23, 2019): 1–8. http://dx.doi.org/10.1155/2019/5903820.
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Type 2 diabetes mellitus (T2DM) is one of the most common chronic diseases. Patients are generally advised lifestyle changes with antihyperglycemic agents prescribed. The major drawback of prescribing antihyperglycemic agents is the risk of hypoglycemia which subsequently impacts on health-related quality of life (HRQoL). This study is aimed at examining association between previous history of hypoglycemia and HRQoL. The study was a multicenter cross-sectional study, conducted from February 2013 to March 2015 at 5 tertiary care hospitals in Thailand (Srinagarind, Phramongkutklao, Ramathibodi, King Chulalongkorn Memorial, and Siriraj hospitals). The study population were males or females diagnosed with type 2 DM according to ADA criteria, 30 years of age or older, who had been treated with sulfonylurea (SU) monotherapy or SU and metformin combination for at least 6 months. Prespecified medical factors were extracted from medical records 12 months prior to patients’ enrolment. The experience of hypoglycemia questionnaire was used to collect and measure severity of hypoglycemia experienced during the previous 6 months. HRQoL was assessed using the 3-level version of EuroQol-5-dimension (EQ-5D-3L) and visual analogue scale (EQ-VAS) questionnaires. Of 659 eligible patients surveyed, 202 patients (30.65%) had experienced symptoms of hypoglycemia. HRQoL was significantly lower among patients reporting at least one of hypoglycemic symptoms, measured by EQ-VAS scores (mean±SD; 73.66±13.18, 73.56±15.10, or 68.93±14.76 vs. 77.01±13.02, one-way ANOVA; p=0.006) and EQ-5D-3L index scores (0.62±0.47, 0.68±0.38, or 0.58±0.51 vs. 0.79±0.31, one-way ANOVA; p<0.001) for mild, moderate, or severe/very severe hypoglycemic patients compared with patients without hypoglycemic symptoms. After adjusting for confounding factors in a multiple linear regression model, patients with hypoglycemic symptoms either mild, moderate, or severe/very severe demonstrated significantly higher impairment for EQ-VAS and EQ-5D indexes than those who did not experience hypoglycemic symptoms. In conclusion, our study showed decreased HRQoL determined by EQ-5D and EQ-VAS in patients reporting symptoms of hypoglycemia compared with patients not reporting hypoglycemic symptoms, relative to severity of hypoglycemia.