Altered glucose kinetics occurs with aging: a new outlook on metabolic flexibility.

Our purpose was to determine how age affects metabolic flexibility and underlying glucose kinetics in healthy young and older adults. Therefore, glucose and lactate tracers along with pulmonary gas exchange data were used to determine glucose kinetics and respiratory exchange ratios [RER = carbon dioxide production (V̇co2)/oxygen consumption (V̇o2)] during a 2-h 75-g oral glucose tolerance test (OGTT). After an 12-h overnight fast, 28 participants, 15 young (21-35 yr; 7 men and 8 women) and 13 older (60-80 yr; 7 men and 6 women), received venous primed-continuous infusions of [6,6-2H]glucose and [3-13C]lactate with a [Formula: see text] bolus. After a 90-min metabolic stabilization and tracer equilibration period, volunteers underwent an OGTT. Arterialized glucose concentrations ([glucose]) started to rise 15 min post glucose consumption, peaked at 60 min, and remained elevated. As assessed by rates of appearance (Ra) and disposal (Rd) and metabolic clearance rate (MCR), glucose kinetics were suppressed in older compared to young individuals. As well, unlike in young individuals, fractional gluconeogenesis (fGNG) remained elevated in the older population after the oral glucose challenge. Finally, there were no differences in 12-h fasting baseline or peak RER values following an oral glucose challenge in older compared to young men and women, making RER an incomplete measure of metabolic flexibility in the volunteers we evaluated. Our study revealed that glucose kinetics are significantly altered in a healthy aged population after a glucose challenge. Furthermore, those physiological deficits are not detected from changes in RER during an OGTT.NEW & NOTEWORTHY To determine metabolic flexibility in response to an OGTT, we studied healthy young and older men and women to determine glucose kinetics and changes in RER. Compared to young subjects, glucose kinetics were suppressed in older healthy individuals during an OGTT. Surprisingly, the age-related changes in glucose flux were not reflected in RER measurements; thus, RER measurements do not give a complete view of metabolic flexibility in healthy individuals.

Remote patient monitoring for management of diabetes mellitus in pregnancy is associated with improved maternal and neonatal outcomes.

BACKGROUND: Diabetes mellitus is a common medical complication of pregnancy, and its treatment is complex. Recent years have seen an increase in the application of mobile health tools and advanced technologies, such as remote patient monitoring, with the aim of improving care for diabetes mellitus in pregnancy. Previous studies of these technologies for the treatment of diabetes in pregnancy have been small and have not clearly shown clinical benefit with implementation. OBJECTIVE: Remote patient monitoring allows clinicians to monitor patients' health data (such as glucose values) in near real-time, between office visits, to make timely adjustments to care. Our objective was to determine if using remote patient monitoring for the management of diabetes in pregnancy leads to an improvement in maternal and neonatal outcomes. STUDY DESIGN: This was a retrospective cohort study of pregnant patients with diabetes mellitus managed by the maternal-fetal medicine practice at one academic institution between October 2019 and April 2021. This practice transitioned from paper-based blood glucose logs to remote patient monitoring in February 2020. Remote patient monitoring options included (1) device integration with Bluetooth glucometers that automatically uploaded measured glucose values to the patient's Epic MyChart application or (2) manual entry in which patients manually logged their glucose readings into their MyChart application. Values in the MyChart application directly transferred to the patient's electronic health record for review and management by clinicians. In total, 533 patients were studied. We compared 173 patients managed with paper logs to 360 patients managed with remote patient monitoring (176 device integration and 184 manual entry). Our primary outcomes were composite maternal morbidity (which included third- and fourth-degree lacerations, chorioamnionitis, postpartum hemorrhage requiring transfusion, postpartum hysterectomy, wound infection or separation, venous thromboembolism, and maternal admission to the intensive care unit) and composite neonatal morbidity (which included umbilical cord pH <7.00, 5 minute Apgar score <7, respiratory morbidity, hyperbilirubinemia, meconium aspiration, intraventricular hemorrhage, necrotizing enterocolitis, sepsis, pneumonia, seizures, hypoxic ischemic encephalopathy, shoulder dystocia, trauma, brain or body cooling, and neonatal intensive care unit admission). Secondary outcomes were measures of glycemic control and the individual components of the primary composite outcomes. We also performed a secondary analysis in which the patients who used the two different remote patient monitoring options (device integration vs manual entry) were compared. Chi-square, Fisher's exact, 2-sample t, and Mann-Whitney tests were used to compare the groups. A result was considered statistically significant at P<.05. RESULTS: Maternal baseline characteristics were not significantly different between the remote patient monitoring and paper groups aside from a slightly higher baseline rate of chronic hypertension in the remote patient monitoring group (6.1% vs 1.2%; P=.011). The primary outcomes of composite maternal and composite neonatal morbidity were not significantly different between the groups. However, remote patient monitoring patients submitted more glucose values (177 vs 146; P=.008), were more likely to achieve glycemic control in target range (79.2% vs 52.0%; P<.0001), and achieved the target range sooner (median, 3.3 vs 4.1 weeks; P=.025) than patients managed with paper logs. This was achieved without increasing in-person visits. Remote patient monitoring patients had lower rates of preeclampsia (5.8% vs 15.0%; P=.0006) and their infants had lower rates of neonatal hypoglycemia in the first 24 hours of life (29.8% vs 51.7%; P<.0001). CONCLUSION: Remote patient monitoring for the management of diabetes mellitus in pregnancy is superior to a traditional paper-based approach in achieving glycemic control and is associated with improved maternal and neonatal outcomes.

Euglycemic diabetic ketoacidosis associated with ST segment elevation myocardial infarction following SGLT-2 inhibitor therapy.

Sodium-glucose cotransporter-2 (SGLT-2) inhibitors are the latest approved class of oral antidiabetic agents that inhibit renal SGLT-2 receptors and increase urinary glucose excretion in the luminal membrane of the proximal tubule. Diabetic ketoacidosis (DKA) is a triad of hyperglycemia, ketosis, and a high anion gap with metabolic acidosis. We present the case of 61 years-old men with severe euglycemic DKA (EDKA) complicated ST-segment elevation myocardial infarction following SGLT-2 inhibitor therapy for type 2 diabetes mellitus. Atypical presentation of ketoacidosis without hyperglycemia can delay diagnosis and may result in catastrophic complications. Quick diagnosis, appropriate clinical and biochemical assessment, and effective treatment protocols ensure successful resolution of EDKA.

Trimetazedine with hyperinsulinimea-euoglycemia, N-acetyl cysteine, and vitamin C: A new approach concept for management of aluminum phosphide poisoning.

Aluminum phosphide (AlP) is commonly used as a powerful suicidal tool. The exact mechanism of acute toxicity has not been well defined despite high mortality rates as well as its supportive treatment including rapid decontamination and institution of resuscitative measures. The current study aimed to investigate a new combination therapy using trimetazidine, N-acetyl cysteine, vitamin C, and hyperinsulinemia-euglycemia to manage acute AlP poisoning. Acute AlP-induced cardiotoxicity, hemodynamic changes, and hepatotoxicity were evaluated using electrocardiogram, creatinine kinase MB iso-enzyme, troponin-1, blood pressure, random blood glucose level, liver function tests, and histopathological changes in both the heart and liver in a rabbit model of AlP poisoning. The results showed that the new regimen therapy ameliorates the toxic effect of AlP with significant improvement in survival, cardiovascular and hemodynamic parameters in addition to histopathological changes. These results highlight the strong cardioprotective, antioxidant, hepatoprotective effects of the new combined therapy along with correction of hemodynamic changes and hyperglycemia as a potential target in the management of acute AlP poisoning.

Establishment and operation of glucose clamp technique in mice.

Glucose metabolism plays a central role in energy supply and metabolism regulation in various tissues and organs. Besides, insulin is the sole hormone lowering blood glucose in the body, and islet function and insulin sensitivity are the key steps modulating glucose metabolism. Since the development of glucose clamp technology, it has been recognized as the gold standard for evaluating insulin metabolism. The main categories include hyperinsulinemia-euglycemia clamp, hyperglycemia clamp, and hyperinsulinemia-hypoglycemia clamp. These can be done on either anesthetized mice or conscious and unrestricted mice. This protocol focuses on the establishment and operation of the mouse glucose clamp technique, including preparation of instrument consumables, surgical operations, clamping procedures, and precautions, serving as reference and guidance.

"The Bitter Truth of Sugar"-Euglycemic Diabetic Ketoacidosis due to Sodium-glucose Cotransporter-2 Inhibitors: A Case Series.

Diabetic ketoacidosis (DKA) is an acute and major complication of diabetes mellitus (DM), both type I and type II. Biochemically, DKA consists of a triad of blood sugar levels greater than 250 mg/dL, ketonemia of greater than 3 mmol/L and/or significant ketonuria, and a blood pH less than 7.3 with an increased anion gap. Currently, the sodium-glucose cotransporter-2 inhibitors (SGLT-2i) are widely used in management of type II diabetes. There have been several reports of an association between euglycemic diabetic ketoacidosis (EuDKA) and SGLT-2i agents. We present three different patients who were on SGLT-2i therapy who developed recurrent EuDKA postprocedure or sepsis. We believe that prolonged treatment (5-6 days) with intravenous (IV) insulin with glucose until resolution of glycosuria can be considered as an inexpensive marker of resolution of EuDKA. Moreover, the recommended duration for discontinuation of these drugs prior to elective procedures should be longer than 3 days. How to cite this article: Shah M, Pathrose E, Bhagwat NM, Chandy D. "The Bitter Truth of Sugar"-Euglycemic Diabetic Ketoacidosis due to Sodium-glucose Cotransporter-2 Inhibitors: A Case Series. Indian J Crit Care Med 2022;26(1):123-126.

Abnormal blood glucose and the relationship with clinical outcome in acutely ill children admitted to the emergency unit of a Nigerian Tertiary Hospital.

BACKGROUND: Dysglycemia (hyper- or hypoglycemia) is frequently seen in acutely ill children and may be associated with poor outcome. OBJECTIVE: To determine and compare clinical characteristics and outcomes of children admitted for acute illnesses presenting with euglycemia and dysglycemia. A prospective cohort study was conducted in Emergency Pediatric Unit (EPU), of Usmanu Danfodiyo University Teaching Hospital (UDUTH), Sokoto. SUBJECTS AND METHODS: Children aged ≤15 years, admitted for acute illnesses were enrolled consecutively for a 6-month period. An Accu-Chek Active glucometer was used to check blood glucose of subjects at admission, and based on the result; subjects were categorized as either euglycemic or dysglycemic. The clinical characteristics and outcomes (discharged or died) were compared in the two groups. Statistical analysis involved Chi square test and logistic regression. RESULTS: The median age of 376 subjects was 24 months (range: 1-156 months). Forty-four subjects (11.7%) had dysglycemia, consisting of 36 (9.6%) with hyperglycemia, and 8 (2.1%) with hypoglycemia, whereas 332 (88.3%) had euglycemia. The clinical characteristics associated with hyperglycemia were presence of fever (p = 0.001), and convulsion (p = 0.04), whereas hypoglycemia; coma and hepatomegaly (p = 0.01). Forty subjects (40/376, 10.6%) died. The proportion of those that died in the dysglycemic group (10/44, 22.7%) was significantly higher than that in the euglycemic group (30/332, 9%) (p = 0.006). Subjects who had hyperglycemia were 2.6 times less likely to survive (OR = 2.64, 95% CI: 1.02--6.79, P = 0.05) compared to their euglycemic counterparts. Hypoglycemia was not significantly associated with death outcome (p = 0.13). CONCLUSION: Dysglycemia, particularly hyperglycemia, was significantly associated with increased mortality in acutely ill children. We recommend routine bedside glucose estimation for all acutely ill children at admission to the emergency unit, to detect dysglycemia, treat hypoglycemia promptly, monitor closely, and treat aggressively the underlying conditions in children with hyperglycemia to prevent attendant high mortality.

The Precious Few Grams of Glucose During Exercise.

As exercise intensity exceeds 65% of maximal oxygen uptake carbohydrate energy sources predominate. However, relative to the meager 4-5 g blood glucose pool size in a postabsorptive individual (0.9-1.0 g·L-1 × 5 L blood = 18-20 kcal), carbohydrate (CHO) oxidation rates of 20 kcal·min-1 can be sustained in a healthy and fit person for one hour, if not longer, all the while euglycemia is maintained. While glucose rate of appearance (i.e., production, Ra) from splanchnic sources in a postabsorptive person can rise 2-3 fold during exercise, working muscle and adipose tissue glucose uptake must be restricted while other energy substrates such as glycogen, lactate, and fatty acids are mobilized and utilized. If not for the use of alternative energy substrates hypoglycemia would occur in less than a minute during hard exercise because blood glucose disposal rate (Rd) could easily exceed glucose production (Ra) from hepatic glycogenolysis and gluconeogenesis. The goal of this paper is to present and discuss the integration of physiological, neuroendocrine, circulatory, and biochemical mechanisms necessary for maintenance of euglycemia during sustained hard physical exercise.

Glucose Homeostasis and the Neonatal Brain: A Sweet Relationship.

Glucose is the primary substrate for energy metabolism in the brain and although the brain is dependent on a constant glucose supply for normal function, both local energy stores and the supply of alternate substrates are limited. In utero, the placenta provides a continuous supply of glucose to the fetus while transition to extrauterine life marks an abrupt change in substrate delivery and a major change in glucose metabolism where insufficiencies and disruptions can occur. Hypoglycemia is one of the most common biochemical disturbances in the neonatal period, affecting a wide range of neonates. Prolonged or persistent low plasma glucose concentrations can lead to neonatal brain injury and abnormal neurological outcomes. This article discusses fetal and neonatal metabolic adaptation, the physiology of glucose homeostasis, hypoglycemic brain injury (HBI), and neurodevelopmental long-term outcomes.

Creating happiness in the diabetes care clinic.

Happiness is an essential part of human health. The purpose of health care, including diabetes care, is to achieve happiness, or euthymia. Happiness, can also be viewed as a means to achieving good health, as well as a technique to overcome challenges, encourage team work and ensure better adherence to therapy. This opinion piece shares simple ways of achieving happiness in the diabetes care clinic. It lists best practices related to environment communication style, communication content, and inter-consultation contact. If integrated into daily practice, these will help create a happy health care ecosystem, which in turn will enhance patient satisfaction.

Proteomic Analysis of Restored Insulin Production and Trafficking in Obese Diabetic Mouse Pancreatic Islets Following Euglycemia.

For the treatment of patients with prediabetes or diabetes, clinical evidence has emerged that ß-cell function can be restored by glucose-lowering therapeutic strategies. However, little is known about the molecular mechanisms underlying this functional adaptive behavior of the pancreatic ß-cell. This study examines the dynamic changes in protein expression and phosphorylation state associated with (pro)insulin production and secretory pathway function mediated by euglycemia to induce ß-cell rest in obese/diabetic db/db islet ß-cells. Unbiased quantitative profiling of the protein expression and phosphorylation events that occur upon ß-cell adaption during the transition from hyperglycemia to euglycemia was assessed in isolated pancreatic islets from obese diabetic db/db and wild-type (WT) mice using quantitative proteomics and phosphoproteomics together with bioinformatics analysis. Dynamic changes in the expression and phosphorylation of proteins associated with pancreatic ß-cell (pro)insulin production and complementary regulated-secretory pathway regulation were observed in obese diabetic db/db islets in a hyperglycemic environment, relative to WT mouse islets in a normal euglycemic environment, that resolved when isolated db/db islets were exposed to euglycemia for 12 h in vitro. By similarly treating WT islets in parallel, the effects of tissue culture could be mostly eliminated and only those changes associated with resolution by euglycemia were assessed. Among such regulated protein phosphorylation-dependent signaling events were those associated with COPII-coated vesicle-dependent ER exit, ER-to-Golgi trafficking, clathrin-coat disassembly, and a particular association for the luminal Golgi protein kinase, FAM20C, in control of distal secretory pathway trafficking, sorting, and granule biogenesis. Protein expression and especially phosphorylation play key roles in the regulation of (pro)insulin production, correlative secretory pathway trafficking, and the restoration of ß-cell secretory capacity in the adaptive functional ß-cell response to metabolic demand, especially that mediated by glucose.

Continuous glucose monitoring following pancreatectomy with islet autotransplantation in children.

Aim was to determine whether CGM could accurately monitor blood glucose concentration in the immediate postoperative period following pancreatectomy with IAT in children. CGM was used in nine patients undergoing IAT at our institution between April 2015 and September 2016 (eight total pancreatectomy and one subtotal pancreatectomy). MAD and MARD of CGM values compared to time-matched serum blood glucose were calculated during the first 5 days of ICU admission. Goal range was defined as 70-140 mg/dL and out-of-range was >140 mg/dL or <70 mg/dL. Of 89 time-matched measures found, 75% of CGM values were within 15 mg/dL, and 51% were within 10 mg/dL, compared to serum glucose. MAD was 11.6 mg/dL, and MARD was 10.6%. CGM values did not differ from serum glucose (P=.74). By Clarke error grid analysis, 100% of paired values were in clinically acceptable zones. By surveillance error grid analysis, 96% of paired values were within clinically acceptable agreement. CGM is a reliable tool in monitoring glycemic control in the immediate postoperative period following pancreatectomy with IAT in children.

[The blood glucose value not necessarily indicates correctly the cellular metabolic state]. / A vércukorértékek nem feltétlenül jellemzik megfeleloen a sejtanyagcsere-állapotot.

In clinical recommendations the normalized blood glucose level is declared as the main target in therapy of diabetes mellitus, i.e. the achievement of euglycemia is the main therapeutic goal. This approach suggests, that the normal blood glucose value is the marker of the normal carbohydrate metabolism (eumetabolism), and vice versa: hyperglycemia is associated with abnormal metabolism (dysmetabolism). However the question arises, whether identical blood glucose values do reflect the same intracellular biochemical mechanisms? On the basis of data published in the literature authors try to answer these questions by studying the relations between the short/longterm blood glucose level and the cellular metabolism in different clinical settings characterized by divergent pathophysiological parameters. The correlations between blood glucose level and cellular metabolism in development of micro-, and macroangiopathy, in the breakthrough phenomenon, as well as during administration of metabolic promoters, the discrepancies of relation between blood glucose values and cellular metabolism in type 1, and type 2 diabetes mellitus, furthermore association between blood glucose value and myocardial metabolism in acute and chronic stress were analyzed. Authors conclude, that the actual blood glucose values reveal the actual cellular metabolism in a very variable manner: neither euglycemia does mandatorily indicate eumetabolism (balance of cellular energy production), nor hyperglycemia is necessarily a marker of abnormal metabolic state (dept of cellular energy production). Moreover, at the same actual blood glucose level both the metabolic efficacy of the same organ may sharply vary, and the intracellular biochemical machinery could also be very different. In case of the very same longterm blood glucose level the metabolic state of the different organs could be very variable: some organs show an energetically balanced metabolism, while others produce a significant deficit. These inconsistencies between blood glucose level and cellular metabolism can be explained by the fact, that blood glucose value is a transport parameter, reflecting the actual steady state of glucose transport from the carbohydrate pools into the blood, and that from the blood into the tissues. Without knowing the speed of these transports of opposite direction, the blood glucose value per se can not reveal the quantitative and qualitative characteristics of cellular metabolism. Orv. Hetil., 2017, 158(11), 409-417.

Efficacy and Safety of Long-term Ketogenic Diet Therapy in a Patient With Type 1 Diabetes.

Fewer than 1% of patients with type 1 diabetes achieve normal glycemic control (glycated hemoglobin [HbA1c] < 5.7%/ < 39 mmol/mol). Additionally, exogenous insulin administration often causes "iatrogenic hyperinsulinemia," leading to whole-body insulin resistance and increased risk of cardiovascular complications. We present data on the clinical efficacy and safety of a long-term (10-year) ketogenic diet (≤50 g carbohydrates/day) therapy in a patient with type 1 diabetes. The use of a ketogenic diet resulted in successful glycemic control, assessed by HbA1c (5.5%; 36.6 mmol/mol), continuous glucose monitoring median glucose (98 mg/dL; 5.4 mmol/L), and glucose time-in-range of 70 to 180 mg/dL (90%) without acute glycemic complications. In conjunction, there was a 43% decrease in daily insulin requirements. Low-density lipoprotein cholesterol increased, whereas small-dense low-density lipoprotein was in the normal range (<90 nmol/L). No adverse effects were observed on thyroid function, kidney function, or bone mineral density. This case report demonstrates that a long-term ketogenic diet in a person with type 1 diabetes has considerable therapeutic benefits.

Sodium-Glucose Cotransporter 2 Inhibitor-Induced Euglycemic Diabetic Ketoacidosis: The Other Side of the Coin!

Euglycemic diabetic ketoacidosis (EDKA) though rare is a life-threatening complication of sodium-glucose cotransporter 2 (SGLT2) inhibitors. With their increasing use in the management of type 2 diabetes mellitus (T2DM) due to long-term beneficial effects, the incidence of this complication is on the rise. We report a case of a 58-year-old lady with a history of T2DM on multiple anti-diabetes medications including dapagliflozin for one year, who during intercurrent illness developed EDKA. Her blood sugar on admission was 203 mg/dL, and arterial blood gas showed high anion-gap metabolic acidosis (HAGMA) with ketonuria and ketonemia (blood beta-hydroxybutyric (BOHB) acid level: 5.4 mmol/L). Low carbohydrate intake, dehydration resulting from repeated vomiting, and skipping the previous two days' dose of insulin could have precipitated this condition. She was treated with intravenous fluids, insulin, 5% dextrose infusion, and potassium supplements with complete resolution of acidosis after about 90 hours. This case signifies the importance of awareness of the link between the use of SGLT2 inhibitors and EDKA and early recognition of this complication to reduce morbidity and mortality. Furthermore, it also emphasizes the need for clinicians to educate their patients taking these drugs to stop them during the intercurrent illness to prevent them from developing EDKA.

Euglycemic Ketoacidosis and Lactic Acidosis Associated With Metformin Toxicity.

In patients with diabetes, diabetic ketoacidosis (DKA) is a well-documented potential complication, usually presenting with hyperglycemia, anion gap acidosis, and positive ketones. Metformin toxicity in the setting of acute renal failure is also a well-known cause of lactic acidosis. However, metformin-induced euglycemic ketoacidosis is less well-known or studied. We report a case of metformin toxicity in the setting of acute renal failure with both lactic acidosis and ketosis and an initial confounded clinical presentation of sulphonylurea-induced hypoglycemia. A high index of suspicion for metformin-associated lactic acidosis (MALA) and metformin-associated lactic acidosis with euglycemic ketoacidosis (MALKA) should be in place in patients who are taking metformin and presenting with acute renal failure and euglycemia.

Hyperglycemia Stimulates the Irreversible Catabolism of Branched-Chain Amino Acids and Generation of Ketone Bodies by Cultured Human Astrocytes.

Astrocytes are considered to possess a noticeable role in brain metabolism and, as a partners in neuron-glia cooperation, to contribute to the synthesis, bioconversion, and regulation of the flux of substrates for neuronal metabolism. With the aim of investigating to what extent human astrocytes are metabolizing amino acids and by which compounds are they enriching their surroundings, we employed a metabolomics analysis of their culture media by 1H-NMR. In addition, we compared the composition of media with either 5 mM or 25 mM glucose. The quantitative analysis of culture media by 1H-NMR revealed that astrocytes readily dispose from their milieu glutamine, branched-chain amino acids, and pyruvate with significantly high rates, while they enrich the culture media with lactate, branched-chain keto acids, citrate, acetate, ketone bodies, and alanine. Hyperglycemia suppressed the capacity of astrocytes to release branched-chain 2-oxo acids, while stimulating the generation of ketone bodies. Our results highlight the active involvement of astrocytes in the metabolism of several amino acids and the regulation of key metabolic intermediates. The observed metabolic activities of astrocytes provide valuable insights into their roles in supporting neuronal function, brain metabolism, and intercellular metabolic interactions within the brain. Understanding the complex metabolic interactions between astrocytes and neurons is essential for elucidating brain homeostasis and the pathophysiology of neurological disorders. The observed metabolic activities of astrocytes provide hints about their putative metabolic roles in brain metabolism.

Starvation Ketoacidosis in a Young Healthy Female After Prolonged Religious Fasting.

Ketone bodies are important energy sources for the body and are produced by the liver when the body is in a deficiency state of glucose, which is used in the peripheral tissues to provide energy. There are several ketone bodies that are produced by the liver, of which two are important: acetoacetate and beta-hydroxybutyrate. Even though ketone bodies are always present in the body, they are minimal when a person is not fasting. Ketone bodies are produced by the oxidation of fatty acids to fulfill the metabolic needs of tissues, especially the brain. The biochemical reactions of forming ketone bodies are triggered by a lack of insulin and an elevated glucagon level in the blood. Both cause unopposed lipolysis and free fatty acid oxidation resulting in the production of ketone bodies and eventually high anion gap metabolic acidosis. We present a case of young healthy female who presented with euglycemic ketoacidosis after involving prolonged fasting for her religious ceremony. She also physically exerted quite more during her fasting. With a detailed history and excluding other possibilities, we made the diagnosis of starvation ketoacidosis. She improved well with the treatment and established her pre-morbid condition in our review.

Insulin-euglycemia therapy in acute aluminum phosphide poisoning: a randomized clinical trial.

Introduction: Aluminum phosphide is a pesticide that is used in developing countries. Aluminum phosphide poisoning has a high mortality rate and there is no known antidote. This study aimed to evaluate the safety and efficacy of insulin-euglycemia therapy in the management of patients with acute aluminum phosphide poisoning.Methods: This trial was prospectively registered in the Pan African Clinical Trials Registry (PACTR202008534546951). A total of 108 patients were randomly allocated to two groups. The intervention group received insulin-euglycemia therapy in addition to standard treatment (norepinephrine and supportive care); the control group received standard treatment plus placebo. The main outcome measures were survival, blood pressure, and laboratory investigations.Results: The two groups had similar baseline parameters. Insulin-euglycemia therapy was associated with a significant reduction in mortality compared with that in the control group (64.8 percent and 96.3 percent, respectively; P value <0.001). Patients randomized to insulin-euglycemia also required lower doses of vasopressors (median was 7 mg versus 26 mg in control group; P value 0.006) and fewer patients needed intubation (61.1 percent versus 81.5 percent in the control group; P value 0.019). Insulin-euglycemia therapy significantly improved blood pressure (systolic, diastolic, and mean arterial pressure) (median at 6h post-admission was 80 mmHg, 55 mmHg and 65 mmHg compared with 20 mmHg, 10 mmHg and 13 mmHg in the control group respectively; P value <0.001) and bicarbonate and lactate concentrations.Conclusion: Insulin-euglycemia therapy appears to be a safe and effective treatment option for patients with aluminum phosphide poisoning. Vasopressor only therapy was associated with very poor outcomes in acute aluminum phosphide poisoning.

Diabetic ketoacidosis.

Diabetic ketoacidosis (DKA) is a form of a hyperglycemic emergency mainly characterized by the triad of hyperglycemia, ketosis, and anion gap metabolic acidosis. DKA may be the initial presentation in approximately 25-40 % of patients with type 1 diabetes. It may also occur in at least 34% of patients with type 2 diabetes. DKA has economic as well as medical implications. This review aims to explore and discuss diabetic ketoacidosis, its pathophysiology, clinical presentation, diagnosis, and management, including nuances in special populations such as pediatrics, obstetrics, and patients with chronic kidney disease.