A Comprehensive Monograph on Glucose (Dextrose) as a Therapeutic Agent (DrugBank ID: DB09341)

I. Introduction: The Fundamental Role and Medical History of Glucose

[A. Overview of Glucose: From Universal Fuel to Essential Medicine]

Glucose, a simple sugar with the chemical formula $C_6H_{12}O_6$, is the most abundant monosaccharide in nature and serves as the primary source of energy for the vast majority of living organisms.[1] Its biological significance is rooted in its central role in cellular metabolism. In plants and most algae, glucose is generated through photosynthesis from water and carbon dioxide, using energy from sunlight.[1] In humans, it is produced endogenously through hepatic gluconeogenesis and mobilized from storage via the breakdown of glycogen (glycogenolysis).[1] Circulating in the bloodstream as "blood glucose," it provides the essential fuel for cellular respiration, powering a myriad of physiological processes.[4]

Beyond its fundamental biological role, glucose is a cornerstone of modern medical therapy. It is identified in pharmaceutical contexts by multiple DrugBank identifiers, including DB09341 for its unspecified form (commonly known as dextrose) and DB01914 for the specific D-glucose isomer.[5] In recognition of its critical importance in healthcare, glucose, formulated as an intravenous sugar solution, is included on the World Health Organization's List of Essential Medicines, both as a standalone agent and in combination with sodium chloride.[1] This designation underscores its indispensable status for treating life-threatening conditions and providing nutritional support in health systems worldwide.

[B. Historical Milestones: Discovery, Characterization, and Therapeutic Application]

The journey of glucose from a natural substance to a purified, life-saving pharmaceutical agent spans several centuries and involves key breakthroughs in chemistry and medicine. The first isolation of glucose is credited to the German chemist Andreas Marggraf, who obtained it from raisins in 1747.[1] Nearly half a century later, in 1792, Johann Tobias Lowitz discovered glucose in grapes and, importantly, distinguished it from cane sugar (sucrose).[1] The name "glucose" itself was coined in 1838 by Jean-Baptiste Dumas, deriving from the Greek word

gleûkos, meaning "sweet wine" or "must".[1]

The structural elucidation of glucose was a monumental achievement in organic chemistry, largely attributed to the work of Hermann Emil Fischer between 1891 and 1894. Fischer meticulously established the stereochemical configuration of all known sugars, correctly predicting their possible isomers and validating Jacobus Henricus van 't Hoff's theories on the three-dimensional arrangement of atoms in carbon-bearing molecules.[1] This foundational research, which earned Fischer the 1902 Nobel Prize in Chemistry, defined the critical difference between the stereoisomers D-glucose and L-glucose, establishing that only the D-form is biologically active and metabolized by living organisms.[1]

The understanding of glucose's role in metabolism was further advanced by a series of Nobel Prize-winning discoveries. These include Otto Fritz Meyerhof's work on glucose metabolism (1922), Arthur Harden and Hans von Euler-Chelpin's research on sugar fermentation (1929), and the discoveries by Carl and Gerty Cori and Bernardo Houssay regarding glycogen conversion and the pituitary gland's role in glucose regulation (1947).[1]

The therapeutic application of intravenous (IV) fluids began to take shape in the 1830s, initially with the use of saline-like solutions to treat dehydration in cholera patients.[10] While experiments with various substances, including sugar solutions, were conducted, the widespread and sophisticated use of IV glucose did not emerge until much later. The development of total parenteral nutrition (TPN) in the 1960s and 1970s marked a significant turning point, establishing dextrose as the core carbohydrate source for patients unable to receive nutrition orally, a practice that has saved countless lives.[10]

[C. The Parallel Evolution of Glucose Monitoring: A Prerequisite for Safe Therapy]

The history of glucose as a therapeutic agent is inextricably linked to the parallel evolution of technologies designed to measure its concentration in the body. The safe and effective administration of glucose, particularly in high-risk scenarios like TPN or in the management of diabetes, would be impossible without accurate and timely monitoring. The emergence of glucose as a cornerstone of modern medicine is not the result of a single discovery but rather the culmination of three parallel and interdependent historical streams: fundamental chemistry, clinical application, and diagnostic technology. The advancement of each stream was a prerequisite for the others.

The earliest attempts at glucose quantification date back to the mid-1800s and focused on measuring glucose in the urine (glycosuria).[12] This practice was commercialized and made more convenient with the development of Benedict's copper reagent in 1908 and the subsequent introduction of the Clinitest tablet by Ames in 1945.[12] These methods, while revolutionary for their time, provided only a semi-quantitative and lagging indicator of blood glucose levels.

A paradigm shift occurred in 1965 with the invention of the Dextrostix, the first blood glucose test strip.[12] This innovation moved monitoring from urine to blood, providing a more direct and immediate assessment of a patient's glycemic state. This technology paved the way for the first glucose meters in the 1970s and, critically, the launch of home blood glucose meters in the 1980s.[12] The ability for patients to self-monitor blood glucose (SMBG) empowered them to actively manage their condition, particularly in response to hypoglycemia, and enabled the intensive insulin therapy regimens that were proven to reduce long-term complications in landmark clinical trials.

The modern era of glucose monitoring is defined by continuous glucose monitoring (CGM) systems. The first professional CGM device was approved in 1999, allowing clinicians to review several days of blinded glucose data.[12] This technology rapidly evolved into real-time, patient-facing systems that provide a dynamic view of glucose levels and trends, often integrated with insulin pumps to create "hybrid closed-loop" systems.[12] CGM has revolutionized the management of diabetes and dramatically improved the safety of therapies that carry a risk of severe hypoglycemia or hyperglycemia, including the administration of glucose itself.[12] Without the ability to monitor, the therapeutic use of glucose would be dangerously unguided.

II. Physicochemical Characteristics

[A. Chemical Identity and Structure]

Glucose is a monosaccharide with the molecular formula $C_6H_{12}O_6$.[1] It is classified as an aldohexose, a term indicating it possesses six carbon atoms and an aldehyde functional group (

$-CHO$) in its acyclic form.[1] In pharmaceutical and clinical contexts, it is commonly referred to as Dextrose, which specifically denotes the naturally occurring D-glucose stereoisomer.[5]

In aqueous solution, glucose exists in a dynamic equilibrium between its open-chain (acyclic) structure and a more stable cyclic (ring) structure.[1] The cyclic form, known as glucopyranose, predominates at physiological pH and is formed by an intramolecular reaction between the aldehyde carbon and the hydroxyl group on the fifth carbon atom.[1] This structural duality is fundamental to its chemical reactivity and biological function.

The stereochemistry of glucose is of paramount importance. The distinction between D-glucose and its synthetic enantiomer, L-glucose, is critical, as biological systems are highly stereospecific. The metabolic machinery of the body, including key enzymes like hexokinase, is configured to recognize and process only D-glucose. L-glucose cannot be phosphorylated by hexokinase and is therefore not a substrate for glycolysis, rendering it biologically inert from an energy metabolism perspective.[1]

The unique stereochemistry of D-glucose, specifically the equatorial orientation of its hydroxyl groups (with the exception of the anomeric hydroxyl) in its most stable cyclic conformation ($\beta$-D-glucopyranose), is a key determinant of its biological supremacy. This specific spatial arrangement makes it less prone to non-specific, damaging glycation reactions with the amine groups of proteins compared to other aldohexoses.[1] Glycation is a known mechanism of protein damage, exemplified by glycated hemoglobin (

$HbA_{1c}$), which serves as a clinical marker for long-term hyperglycemia. The relative stability of D-glucose minimizes the time it spends in its more reactive open-chain form, thereby reducing the rate of spontaneous cellular damage. This suggests that the very structure making glucose a stable and useful pharmaceutical also conferred an evolutionary advantage, favoring its selection as the primary metabolic fuel for most life on Earth.

[B. Physical Properties and Pharmaceutical Relevance]

In its purified solid state, D-glucose is a white crystalline solid.[3] Its physical properties are highly relevant to its diverse applications in pharmaceutical formulations. It is odorless and possesses a sweet taste, which makes it palatable for use in oral liquid and solid dosage forms and allows it to function as a sweetening agent in various products.[18]

One of its most critical properties is its high solubility in water; it is freely soluble, which is essential for its formulation as aqueous intravenous solutions, sometimes at very high concentrations.[18] Conversely, it is only slightly soluble in ethanol and is insoluble in ether.[19]

The following table summarizes the key physicochemical data for glucose.

Table II.A: Key Physicochemical Properties of Glucose

Property	Value / Description	Relevance to Pharmaceutical Use	Source(s)
Molecular Formula	$C_6H_{12}O_6$	Defines the basic elemental composition.	1
Molar Mass	Approx. 180.16 g/mol	Essential for calculating molarity and osmolarity of solutions.	18
IUPAC Name	D-glucose	The systematic chemical name for the naturally occurring isomer.	3
Common Names	Dextrose, Blood Sugar	Dextrose is the common name in pharmaceutical and food industries.	8
Physical Form	White crystalline powder	The standard form for use as a raw material and excipient.	19
Solubility	Freely soluble in water; slightly soluble in ethanol	High water solubility is critical for creating IV and oral liquid formulations.	18
Melting Point	146 °C (for α-D-glucose monohydrate)	A key physical constant for identification and quality control.	3
Density	Approx. 1.54 - 1.56 g/cm³	Relevant for bulk powder handling and formulation development.	3
Stereoisomers	D-glucose (biologically active), L-glucose (biologically inert)	Only the D-isomer is metabolized for energy, a critical distinction for therapeutic use.	1

III. Comprehensive Pharmacology

[A. Pharmacodynamics and Mechanism of Action]

The pharmacodynamic profile of glucose is uniquely dual-natured. It functions primarily as the body's main energy substrate, but also acts as a sophisticated signaling molecule that orchestrates metabolic homeostasis.

[1. Primary Role as an Energy Substrate]

The fundamental mechanism of action for therapeutic glucose is to serve as a direct source of cellular energy. It provides the fuel for the synthesis of adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide (NADH), the universal energy currencies of the cell, through a highly regulated series of metabolic pathways.[1]

• Glycolysis: This initial metabolic pathway takes place in the cytoplasm and begins with the phosphorylation of D-glucose to glucose-6-phosphate by the enzyme hexokinase. This step is the rate-limiting reaction; it effectively "traps" glucose within the cell and activates it for subsequent breakdown.[4] This process is stereospecific, as hexokinase cannot act on the L-glucose enantiomer, which explains the biological inertness of L-glucose.[5] Glycolysis ultimately converts one six-carbon glucose molecule into two three-carbon pyruvate molecules, with a net production of ATP and NADH.[4]
• Citric Acid Cycle and Oxidative Phosphorylation: In the presence of oxygen (aerobic conditions), the pyruvate generated from glycolysis is transported into the mitochondria. There, it is further oxidized through the citric acid cycle (or Krebs cycle) and the electron transport chain (oxidative phosphorylation) to produce carbon dioxide, water, and a substantial yield of ATP. The complete aerobic metabolism of a single glucose molecule can generate up to 36 ATP molecules, providing an efficient source of energy for all body tissues.[4]
• Energy Storage: When glucose intake exceeds immediate energy demands, the body stores it for future use. In the process of glycogenesis, glucose is converted into glycogen, a polymeric form, and stored primarily in the liver and muscles. For longer-term storage, glucose can be converted into fatty acids and stored as fat in adipose tissue.[4] These energy reserves are mobilized via glycogenolysis (breakdown of glycogen) or gluconeogenesis (synthesis of glucose from non-carbohydrate precursors) when blood glucose levels fall.[1]

[2. Role as a Signaling Molecule]

Beyond its function as a simple fuel, glucose is a critical signaling molecule that actively regulates systemic energy homeostasis.[5] Its concentration in the blood directly influences a cascade of physiological responses. Glucose can regulate gene transcription, modulate enzyme activity, and control the activity of specialized glucoregulatory neurons in the brain, which sense and respond to changes in energy availability.[4]

A primary example of its signaling role is the regulation of insulin secretion. An increase in blood glucose levels following a meal leads to glucose uptake by pancreatic beta-cells. The subsequent metabolism of this glucose increases the intracellular ATP/ADP ratio, which triggers a series of events culminating in the release of insulin into the bloodstream.[4] Insulin then facilitates glucose uptake by peripheral tissues, such as muscle and fat, thereby lowering blood glucose levels in a classic negative feedback loop.

The route of glucose administration fundamentally alters this hormonal response. Oral glucose administration is significantly more effective at stimulating insulin secretion than an equivalent intravenous dose.[4] This phenomenon, known as the "incretin effect," is due to the release of gut-derived hormones, such as glucagon-like peptide-1 (GLP-1), in response to glucose in the intestinal lumen. These incretin hormones potentiate the glucose-stimulated insulin secretion from the pancreas.[4] This physiological mechanism is not merely an academic detail; it forms the basis for major classes of modern antidiabetic medications, including DPP-4 inhibitors and GLP-1 receptor agonists, which leverage the incretin system to improve glycemic control.[24] Thus, the basic pharmacology of glucose absorption is directly linked to the mechanism of action of these advanced therapeutics.

[B. Pharmacokinetics: Absorption, Distribution, Metabolism, and Excretion (ADME)]

The pharmacokinetic profile of exogenous glucose is highly dependent on its route of administration, which dictates its absorption, bioavailability, and subsequent physiological effects.

• Absorption:
• Oral Route: When consumed orally, complex carbohydrates are first broken down into monosaccharides by pancreatic and intestinal glycosidases.[4] Glucose is then actively absorbed across the intestinal epithelium. This process is mediated primarily by two key membrane transporters: the sodium-dependent glucose transporter 1 (SGLT1) located on the apical (luminal) side of intestinal cells, and the facilitated glucose transporter 2 (GLUT2) on the basolateral side.[4] Following oral administration of a glucose solution or formulation, peak plasma concentrations are typically reached within 40 minutes.[4]
• Intravenous Route: Administration via IV injection bypasses the gastrointestinal tract entirely, resulting in 100% bioavailability by definition.[4] This allows for rapid and complete delivery of glucose into the systemic circulation, which is critical in emergency situations like severe hypoglycemia.
• Distribution: Once in the bloodstream, glucose is distributed throughout the body and taken up by various tissues. This uptake is facilitated by a family of glucose transporter (GLUT) proteins. Different tissues express different isoforms of these transporters (e.g., GLUT1, GLUT2, GLUT3, GLUT4), each with unique kinetic properties. This tissue-specific expression allows for the fine-tuned regulation of glucose uptake and utilization based on metabolic needs.5 For example, GLUT4, found in muscle and adipose tissue, is insulin-sensitive, meaning its translocation to the cell surface is stimulated by insulin. The mean volume of distribution for intravenously administered glucose is approximately 10.6 L.5
• Metabolism: As detailed in the pharmacodynamics section, glucose is extensively and rapidly metabolized by virtually all tissues in the body.4 The primary metabolic fate is oxidation via glycolysis, the citric acid cycle, and oxidative phosphorylation to produce carbon dioxide, water, and ATP.4 It can also be stored as glycogen or converted to fat. In some organisms, glucose can also serve as a precursor for the synthesis of other essential biomolecules, such as vitamin C (ascorbic acid).4
• Excretion: Under normal physiological conditions, glucose is not significantly excreted from the body. It is freely filtered from the blood by the renal glomeruli, but it is almost completely reabsorbed back into the circulation in the proximal tubules by SGLT transporters.4 Renal excretion of glucose (glycosuria) only occurs when the concentration of glucose in the blood exceeds the kidney's maximum reabsorptive capacity (the renal threshold), a hallmark of uncontrolled hyperglycemia.4 The plasma half-life of exogenously administered intravenous glucose is very short, estimated to be around 14.3 minutes, reflecting its rapid distribution and uptake by tissues for metabolism.4

The following table provides a consolidated summary of the key pharmacokinetic parameters for exogenous glucose.

Table III.B: Summary of Pharmacokinetic Parameters for Exogenous Glucose

Parameter	Value / Description	Route of Administration	Source(s)
Bioavailability	Variable; depends on GI health	Oral	4
	100%	Intravenous	4
Time to Peak (Tmax)	Approx. 40 minutes	Oral	4
Volume of Distribution (Vd)	10.6 L (mean)	Intravenous	5
Metabolism	Extensive cellular metabolism via glycolysis and aerobic respiration.	Both	4
Elimination Half-Life	Approx. 14.3 minutes (plasma)	Intravenous	4
Route of Elimination	Primarily metabolized; renal excretion only occurs above the renal threshold.	Both	4
Key Transporters	SGLT1, GLUT2 (Absorption); Various GLUT isoforms (Tissue Uptake)	Oral (Absorption) / Both (Uptake)	4

IV. Clinical Applications and Therapeutic Indications

The clinical utility of glucose is diverse, ranging from a life-saving emergency treatment to a fundamental component of long-term nutritional support and a key agent in diagnostic testing.

[A. Management of Hypoglycemia]

The primary and most critical therapeutic indication for glucose is the treatment of hypoglycemia (low blood sugar).[3] Hypoglycemia is a common and potentially dangerous complication for individuals with diabetes, particularly those treated with insulin or insulin secretagogues like sulfonylureas.[24] Prompt correction of low blood glucose is essential to prevent severe neuroglycopenic symptoms, including confusion, seizures, loss of consciousness, and in rare cases, death.

For conscious individuals experiencing mild-to-moderate hypoglycemia, typically defined as a blood glucose level below 70 mg/dL, the standard evidence-based approach is the "Rule of 15".[26] This guideline recommends the immediate consumption of 15 grams of a fast-acting carbohydrate. After ingestion, the individual should wait 15 minutes and then recheck their blood glucose. If the level remains low, the 15-gram dose should be repeated.[26]

The choice of formulation is critical and depends on the clinical scenario:

• Oral Tablets and Gels: These formulations are the preferred first-line treatment for conscious patients capable of self-administering. They are valued for their precise dosing, portability, and stability at various temperatures, making them ideal for individuals to carry for immediate use.[26] Glucose tablets typically contain 4 grams of carbohydrates each, requiring a dose of 3 to 4 tablets to meet the 15-gram recommendation.[27] Oral gels, which do not require chewing, can be particularly advantageous for children, individuals with dental issues, or in situations where blood glucose is dropping rapidly.[28]
• Intravenous (IV) Dextrose: This route is reserved for severe hypoglycemic episodes where the patient is unconscious, unable to swallow safely, or has failed to respond to oral treatment.[25] In these emergency settings, a typical dose of 10 to 25 grams of dextrose (e.g., 20 to 50 mL of a 50% Dextrose Injection) is administered intravenously to rapidly restore blood glucose levels.[30]
• Special Populations (Neonates): In newborns, particularly those at risk (e.g., infants of diabetic mothers, late preterm infants), oral 40% dextrose gel has emerged as an effective intervention for both the prevention and treatment of neonatal hypoglycemia.[31] Administered at a dose of approximately 0.5 mL/kg and massaged into the buccal mucosa to prevent aspiration, this approach has been shown to reduce the need for more invasive IV therapy and decrease the incidence of mother-infant separation for treatment.[31]

[B. Parenteral Nutrition (PN)]

In patients who are unable to meet their nutritional requirements through oral or enteral routes, parenteral nutrition (PN) is a life-sustaining therapy. Glucose, in the form of sterile dextrose solutions, serves as the primary carbohydrate source and the main contributor of calories in these formulations.[4]

While essential, the administration of PN presents a significant clinical challenge: TPN-associated hyperglycemia. The direct infusion of a high glucose load into the systemic circulation frequently overwhelms the body's regulatory capacity, leading to elevated blood glucose levels. This complication is remarkably common, with some estimates suggesting it occurs in up to 90% of patients receiving PN, depending on the diagnostic threshold used.[34]

Effective risk management is critical, as uncontrolled PN-associated hyperglycemia is linked to a substantially increased risk of adverse outcomes, including infections (such as pneumonia), acute renal failure, and mortality.[37] The consensus recommendation from major clinical societies is to maintain blood glucose levels within a target range of 140–180 mg/dL (7.8–10.0 mmol/L) for most hospitalized patients receiving PN.[34] Strategies to achieve this target include:

1. Careful monitoring of blood glucose levels.
2. Optimizing the PN formulation by limiting the daily dextrose content (e.g., to 150–200 g/day).[38]
3. Administering insulin, which can be given via a separate IV infusion, subcutaneously, or added directly to the PN admixture.[34]

[C. Diagnostic Applications]

Glucose is a key agent in the diagnosis of disorders of glucose metabolism. The Oral Glucose Tolerance Test (OGTT) is a standard procedure used to diagnose prediabetes, type 2 diabetes, and gestational diabetes.[39] The test involves measuring a patient's fasting blood glucose, followed by the ingestion of a standardized drink containing a specific amount of glucose (typically 75 grams). Blood glucose levels are then measured at set intervals (e.g., one and two hours) to assess the body's ability to clear the glucose load from the circulation, providing a dynamic measure of insulin sensitivity and secretion.[39]

[D. Investigational and Off-Label Uses]

The clinical trial landscape for Dextrose, unspecified form (DB09341) reveals its use in a diverse range of research settings, often extending beyond its primary indications. This diversity highlights the multifaceted role of glucose in medicine, where it can function not only as a therapeutic agent but also as a metabolic tool or a necessary component of supportive care. A superficial review of trial indications can be misleading; for instance, the presence of DB09341 in trials for both hypoglycemia and hyperglycemia is not a contradiction. In hypoglycemia trials, it is the active therapeutic agent being tested. In contrast, in trials for hyperglycemia, sepsis, or obesity, it typically serves as a metabolic probe to induce a specific physiological state for study, a caloric component of a broader nutritional intervention, or a control substance. Understanding this distinction is crucial for accurately interpreting its role in clinical research.

• Neurological Disorders: A completed clinical trial (NCT00004451) investigated the effects of glucose administration on cognitive function in healthy young and elderly individuals, as well as in patients with Parkinson's Disease (DBCOND0092599), suggesting research interest in its potential to modulate brain energy metabolism and function.[40]
• Sepsis and Blood Stream Infections: In a completed Phase 3 trial (NCT01223690) for sepsis (DBCOND0044705), D-glucose was used in combination with the antibiotic clarithromycin.[41] In this context, its role was likely as a caloric component of the intravenous fluids providing supportive care to critically ill patients, rather than as a direct treatment for the infection itself.
• Metabolic Research: Dextrose is frequently used in basic and clinical science to study metabolic pathways. For example, it is listed in an active (but not recruiting) trial on obesity (DBCOND0015947, NCT02653092) to investigate the "Reprometabolic Syndrome".[42] In another trial (DBCOND0048846, NCT00005889) investigating high blood sugar, dextrose is a component of the intravenous nutrition used to study gluconeogenesis in very low birth weight infants.[43] In these cases, glucose is the tool used to challenge or sustain the metabolic system under investigation.

The following table provides a structured overview of the varied clinical trials involving Dextrose (DB09341), clarifying its specific role in each context.

Table IV.D: Overview of Clinical Trials for Dextrose (DB09341) by Indication

Indication	DrugBank Condition ID	Status	Phase	Trial Identifier (NCT#)	Trial Title / Purpose	Role of Glucose	Source(s)
Hypoglycemia	DBCOND0020360	Completed	0	NCT02866435	Identifying the Brain Substrates of Hypoglycemia Unawareness in Type 1 Diabetes	Metabolic Probe	44
PD - Parkinson's Disease	DBCOND0092599	Completed	Not Available	NCT00004451	Randomized Study of the Effects of Glucose on Cognition	Therapeutic / Modulator	40
Blood Stream Infections	DBCOND0044705	Completed	3	NCT01223690	Clarithromycin as Immunomodulator for the Management of Sepsis	Nutritional Component	41
Obesity	DBCOND0015947	Active, Not Recruiting	Not Available	NCT02653092	Reprometabolic Syndrome Mediates Subfertility in Obesity	Nutritional / Metabolic Probe	42
High Blood Sugar	DBCOND0048846	Unknown Status	Not Available	NCT00005889	Gluconeogenesis in Very Low Birth Weight Infants Who Are Receiving Nutrition By Intravenous Infusion	Nutritional Component	43

V. Pharmaceutical Formulations and Manufacturing

The choice of glucose formulation is a critical determinant of its clinical utility and safety profile. The physical form—ranging from a highly concentrated intravenous liquid to a simple chewable tablet—directly corresponds to a specific medical need, from life-threatening emergencies to routine nutritional support and pharmaceutical manufacturing. Glucose as a "drug" is not a single entity but rather a portfolio of products where the formulation is precisely tailored to the clinical scenario, route of administration, and urgency of the condition.

[A. Intravenous Preparations]

Intravenous dextrose solutions are essential in hospital and emergency settings. The most potent of these is 50% Dextrose Injection, USP, a sterile, nonpyrogenic, and highly hypertonic solution (osmolarity of 2.53 mOsmol/mL) containing 0.5 g/mL of dextrose monohydrate.[30]

• Indications: Its primary indications are the emergency treatment of severe, insulin-induced hypoglycemia (insulin shock) and, following appropriate dilution, to serve as a concentrated source of carbohydrate calories in parenteral nutrition regimens for patients with restricted oral intake.[30]
• Administration and Safety: Due to its high concentration and osmolarity, 50% Dextrose Injection must be administered slowly and with caution to avoid serious complications such as significant hyperglycemia, hyperosmolar syndrome, mental confusion, and loss of consciousness.[30] To minimize the risk of venous irritation, phlebitis, and thrombosis, such hypertonic solutions should ideally be infused into a large central vein via a central venous catheter. While peripheral vein administration is possible, it requires a slow infusion rate through a small-bore needle into a large vein to mitigate these risks.[30]
• Packaging: To facilitate its use in various clinical settings, 50% Dextrose Injection is supplied in single-dose containers, including fliptop vials and pre-filled syringes such as the Abboject® and Ansyr® systems.[30]

[B. Oral Formulations for Rapid Glucose Delivery]

For the management of mild to moderate hypoglycemia in conscious individuals, a variety of oral formulations are available over-the-counter.

• Oral Gels: These products typically contain a 40% dextrose solution in a gel base formulated with water, glycerin, flavorings, and preservatives.[33] Prominent brand names include Glutose 15, Dex4, and various store brands (e.g., Walgreens). A standard dose is designed to deliver 15 grams of glucose in a single-use tube or packet.[28] The gel is squeezed directly into the mouth and swallowed. For neonates, the gel is massaged onto the buccal mucosa to ensure absorption while minimizing the risk of aspiration.[33]
• Oral Tablets: These are chewable tablets composed primarily of dextrose, along with binders and flavoring agents to improve palatability and stability.[28] Common brands include TRUEplus, Dex4, and Leader. The tablets typically contain 4 grams of fast-acting carbohydrates each, with a standard recommended dose being four tablets to achieve a total of approximately 15-16 grams of glucose.[27] They are highly valued for their convenience, portability, precise dosing, and long shelf life.[27]

[C. Glucose as a Pharmaceutical Excipient]

Beyond its direct therapeutic roles, dextrose is a versatile and widely used excipient in the pharmaceutical industry, incorporated into a vast array of drug formulations.[20] Its useful physicochemical properties allow it to perform several functions:

• Diluent: In capsules and powder formulations.
• Binder: In tablet formulations, adding cohesiveness to form a compact mass.
• Sweetening Agent: In oral liquids and chewable tablets to improve palatability.
• Bulking and Coating Agent: In solid dosage forms.
• Viscosity-Increasing Agent: In oral syrups and solutions.[20]

[D. Manufacturing Processes for Pharmaceutical-Grade Dextrose]

Pharmaceutical-grade dextrose is produced on an industrial scale, primarily through the enzymatic hydrolysis of starch.[49] Corn starch is the most common source material. The manufacturing process is a multi-step procedure designed to yield a highly purified product:

1. Liquefaction: The starch slurry is treated with enzymes, such as α-amylase, at high temperatures to break the long-chain starch molecules into smaller fragments.[49]
2. Saccharification: The liquefied starch is then treated with a second enzyme, glucoamylase, which completes the hydrolysis by breaking down the fragments into individual glucose molecules.[49]
3. Purification and Decoloration: The resulting glucose syrup undergoes several purification steps to remove impurities. This includes filtration to remove insoluble materials and treatment with activated carbon to remove colored compounds and other organic impurities.[50]
4. Concentration: The purified syrup is concentrated by evaporating excess water.[50]
5. Crystallization and Drying: The concentrated, supersaturated syrup is cooled under controlled conditions to induce crystallization. The resulting crystals (dextrose monohydrate) are separated from the remaining liquid via centrifugation and then dried to produce the final powder product.[50]

VI. Safety Profile, Interactions, and Risk Management

The safety profile of glucose is highly dependent on the formulation, route of administration, and the underlying clinical condition of the patient. While oral glucose for hypoglycemia is generally safe, intravenous administration of concentrated solutions carries significant risks that require careful management.

[A. Adverse Effects and Contraindications]

• Intravenous Administration: The most significant adverse effects are associated with the infusion of hypertonic dextrose solutions. Rapid or excessive administration can lead to fluid and/or solute overload, resulting in the dilution of serum electrolyte concentrations, overhydration, congested states, and potentially life-threatening pulmonary edema.[4] The high osmolarity can also cause venous irritation, phlebitis (inflammation of a vein), and thrombosis (blood clot formation), particularly when infused through a peripheral vein.[30] Other potential adverse effects include hyperosmolar syndrome, hyperglycemia, and electrolyte disturbances like hypokalemia and hypophosphatemia.[53]
• Oral Administration: Oral glucose products are generally very well tolerated.[26] The primary concern is the potential for a rare but serious allergic reaction. Symptoms of hypersensitivity include skin rash, hives (urticaria), angioedema (swelling of the face, lips, tongue, or throat), difficulty breathing or swallowing, and in severe cases, anaphylaxis.[25]

Contraindications:

• Oral glucose formulations should never be given to an individual who is unconscious, having a seizure, or is otherwise unable to swallow safely, due to the high risk of choking and aspiration.[25]
• A known hypersensitivity to glucose or any component of the formulation is a contraindication. Since most pharmaceutical dextrose is derived from corn, patients with a severe corn allergy should use it with caution.[25]
• Intravenous dextrose is contraindicated in patients with pre-existing severe dehydration or in those with diabetic coma who already have marked hyperglycemia.[53]

[B. Toxicity and Management of Overdose (Hyperglycemia)]

An overdose of exogenous glucose, or a failure of the body's endogenous regulatory mechanisms, results in hyperglycemia (high blood sugar).[6] While there is no specific toxic dose, any blood glucose level above 180 mg/dL is generally considered unhealthy.[16]

• Early Symptoms: The initial symptoms of hyperglycemia are often subtle and develop slowly. They include polydipsia (excessive thirst), polyuria (frequent urination), polyphagia (increased hunger), blurred vision, and fatigue or weakness.[56]
• Severe Complications: If left untreated, severe hyperglycemia can progress to life-threatening metabolic emergencies:
• Diabetic Ketoacidosis (DKA): This condition occurs when a severe lack of insulin prevents cells from using glucose for energy. The body begins to break down fat for fuel, producing acidic byproducts called ketones. The accumulation of ketones leads to metabolic acidosis. Hallmarks of DKA include nausea, vomiting, abdominal pain, deep and rapid breathing (Kussmaul respirations), and a characteristic fruity or acetone-like odor on the breath.[56]
• Hyperosmolar Hyperglycemic State (HHS): This condition is characterized by extremely high blood glucose levels (often exceeding 600 mg/dL) and severe dehydration, but without significant ketone production. It typically occurs in individuals with type 2 diabetes who still have some insulin production. HHS can lead to profound neurological changes, including confusion, lethargy, and coma.[58]
• Management: The management of severe hyperglycemia and its complications is a medical emergency that requires hospitalization. Treatment focuses on intravenous fluid replacement to correct dehydration and electrolyte imbalances, along with the carefully controlled administration of insulin to gradually lower blood glucose levels.

[C. Drug and System Interactions]

The concept of "drug interaction" for glucose is fundamentally different from that of most other drugs. While direct pharmacokinetic interactions are minimal, the clinical use of glucose is profoundly influenced by physiological (pharmacodynamic) interactions with a wide range of medications and by critical technical interferences with certain medical devices. These latter two categories are of far greater clinical significance.

• Pharmacodynamic Interactions: These are the most common and clinically relevant interactions. They involve other drugs that independently alter the body's glucose homeostasis.
• Hypoglycemia-Inducing Agents: Medications such as insulin, sulfonylureas (e.g., glyburide, glipizide), and meglitinides are designed to lower blood glucose. Their use is the primary reason a patient might require therapeutic glucose to treat a resulting hypoglycemic episode. The interaction is one of opposing physiological effects.[24]
• Hyperglycemia-Inducing Agents: A number of commonly prescribed drugs can raise blood glucose levels, potentially increasing insulin requirements in patients with diabetes or inducing hyperglycemia in susceptible individuals. These include corticosteroids, thiazide diuretics, sympathomimetic agents, and some atypical antipsychotics.[59]
• Alcohol: The interaction with alcohol is complex and unpredictable. Alcohol can cause hypoglycemia by impairing hepatic gluconeogenesis, especially when consumed on an empty stomach or after exercise. Conversely, some alcoholic beverages contain carbohydrates that can initially raise blood glucose. This dual potential makes alcohol consumption particularly risky for individuals with diabetes.[25]
• Pharmacokinetic Interactions: These are less common and generally of minor clinical significance.
• Testosterone: Some evidence suggests that testosterone esters (propionate, undecanoate) may decrease the serum concentration of dextrose.[4]
• Magnesium: Intravenous dextrose administration can increase the renal clearance of magnesium, potentially decreasing the serum levels of magnesium-containing supplements or medications.[53]
• Critical System/Device Interference: A life-threatening interaction can occur in patients on peritoneal dialysis who are using solutions containing icodextrin (brand name Extraneal).[63] Icodextrin is metabolized in the body to maltose. Certain types of blood glucose monitors and test strips, specifically those that use the glucose dehydrogenase pyrroloquinolinequinone (GDH-PQQ) or glucose-dye-oxidoreductase (GDO) enzymes, cannot distinguish between glucose and maltose. This leads to falsely elevated blood glucose readings. A dangerously low blood sugar (true hypoglycemia) could be masked by a falsely normal or high reading on the meter, leading to the withholding of necessary treatment. Alternatively, a falsely high reading could prompt the administration of excess insulin, causing severe, iatrogenic hypoglycemia. This is not a drug-drug interaction but a critical drug-device interaction that requires specific education for patients and healthcare providers to use only glucose-specific monitoring systems.[63]

The following table summarizes the most clinically important interactions affecting glucose administration and monitoring, categorized by their mechanism to provide a risk-stratified, practical guide.

Table VI.C: Clinically Significant Interactions Affecting Glucose Administration & Monitoring

Interacting Agent/Class/System	Type of Interaction	Effect on Glucose/Monitoring	Clinical Significance & Management	Source(s)
Insulin, Sulfonylureas	Pharmacodynamic	Increased risk of hypoglycemia	High. These drugs are the primary cause of hypoglycemia requiring glucose treatment. Patient education on symptoms and management is critical.	24
Corticosteroids, Thiazide Diuretics	Pharmacodynamic	Increased risk of hyperglycemia	Moderate. May increase insulin/antidiabetic drug requirements. Monitor blood glucose closely when starting or stopping these agents.	59
Alcohol	Pharmacodynamic	Unpredictable; can cause both hypoglycemia and hyperglycemia	Moderate to High. Risk of severe hypoglycemia, especially on an empty stomach. Advise patients to limit intake and monitor glucose carefully.	60
Icodextrin / GDH-PQQ Monitors	System/Device Interference	Falsely elevated blood glucose readings	High (Life-threatening). Can mask true hypoglycemia or lead to insulin overdose. Contraindicated. Use only glucose-specific monitors and test strips.	63
Testosterone Esters	Pharmacokinetic	May decrease serum dextrose concentration	Minor. Clinical significance is likely low, but be aware of potential for lower glucose levels.	4
Magnesium Salts	Pharmacokinetic	Dextrose may increase renal clearance of magnesium	Minor. Monitor magnesium levels in patients on long-term IV dextrose and magnesium supplementation.	53

VII. Expert Analysis and Concluding Remarks

[A. Synthesis: The Dual-Edged Sword of Glucose as Nutrient and Drug]

This comprehensive analysis reveals glucose to be a unique entity in the pharmacopeia, occupying a multifaceted role that transcends the typical definition of a drug. It is simultaneously an essential nutrient fundamental to life, a life-saving emergency medication, a precise diagnostic tool, a versatile metabolic probe in clinical research, and a ubiquitous pharmaceutical excipient. This duality means that its safety and efficacy are profoundly context-dependent. The clinical utility of glucose is not defined by the molecule alone but is inextricably linked to the patient's underlying physiological state (e.g., diabetes, critical illness, neonatal status), the urgency of the medical need, and, critically, the specific pharmaceutical formulation being employed. A 50% dextrose IV injection for a comatose patient and a 4-gram chewable tablet for an ambulatory individual with mild hypoglycemia represent two ends of a therapeutic spectrum, both using the same active molecule but with vastly different risk-benefit profiles and administration protocols.

[B. Critical Insights into Clinical Management Challenges]

Several critical challenges in the clinical management of glucose therapy emerge from the available evidence. The first is the management of TPN-associated hyperglycemia, a common and dangerous complication that requires a proactive, multi-pronged approach involving careful formulation, vigilant monitoring, and judicious insulin use to prevent increased morbidity and mortality. The second major challenge lies in patient education for the self-treatment of hypoglycemia. The availability of numerous over-the-counter products necessitates clear guidance on the "Rule of 15," the recognition of symptoms, and the appropriate use of different formulations to ensure timely and effective correction of low blood sugar without causing rebound hyperglycemia.

Furthermore, the analysis highlights the importance of recognizing non-obvious risks that exist at the intersection of pharmacology and medical technology. The potential for life-threatening errors resulting from the interaction between icodextrin metabolites and certain glucose monitoring systems is a stark reminder that safety considerations must extend beyond traditional drug-drug interactions. This specific failure point underscores a broader principle: as medical care becomes more technologically integrated, clinicians must be vigilant for potential interferences between drugs and the devices used to monitor their effects. The concept of "drug interactions" for glucose must therefore be broadened to prioritize these significant pharmacodynamic and drug-device conflicts over minor pharmacokinetic effects.

[C. Future Directions in Glucose-Based Therapeutics and Delivery Systems]

The field of glucose management continues to evolve rapidly, driven by technological innovation. Future directions will likely focus on optimizing delivery systems and integrating them more seamlessly with monitoring technology. This includes the development of novel oral formulations for hypoglycemia that may offer faster absorption, improved palatability, or enhanced stability.

However, the most significant advancements lie in the realm of automated insulin delivery. The increasing sophistication and accuracy of continuous glucose monitoring (CGM) systems are paving the way for more advanced "closed-loop" or "artificial pancreas" systems. These systems use algorithms to interpret real-time CGM data and automatically adjust insulin delivery via an insulin pump, aiming to maintain glucose levels within a target range with minimal patient intervention. This technology represents the next frontier in mimicking the function of a healthy pancreas and directly addresses the core challenges of both hypoglycemia and hyperglycemia. As these systems become more widespread, the role of exogenous glucose will remain critical as a rescue therapy for algorithm-induced or behavior-induced hypoglycemia, reinforcing its position as an indispensable tool in the management of diabetes. The history of glucose therapy has been a story of parallel advancements in chemistry, medicine, and technology, and its future will undoubtedly continue along this integrated path.

Works cited

1. Glucose - Wikipedia, accessed July 25, 2025, https://en.wikipedia.org/wiki/Glucose
2. Carbohydrates - MedlinePlus, accessed July 25, 2025, https://medlineplus.gov/carbohydrates.html
3. Glucose Chemical Formula - Structure, Properties, Uses, Sample ..., accessed July 25, 2025, https://www.geeksforgeeks.org/chemistry/glucose-chemical-formula-structure-properties-uses-sample-questions/
4. Glucose: Uses, Interactions, Mechanism of Action | DrugBank Online, accessed July 25, 2025, https://go.drugbank.com/drugs/DB09341
5. D-glucose: Uses, Interactions, Mechanism of Action | DrugBank Online, accessed July 25, 2025, https://go.drugbank.com/drugs/DB01914
6. Blood Glucose | Blood Sugar | Diabetes - MedlinePlus, accessed July 25, 2025, https://medlineplus.gov/bloodglucose.html
7. Hypoglycemia | DrugBank Online, accessed July 25, 2025, https://go.drugbank.com/indications/DBCOND0020360
8. Dextrose, unspecified form - Search Results | DrugBank Online, accessed July 25, 2025, https://go.drugbank.com/unearth/q?searcher=drugs&utf8=%E2%9C%93&query=DEXTROSE&search_type=drugs&button=
9. Dextrose (D-Glucose) | Goldfrank's Toxicologic Emergencies, 11e, accessed July 25, 2025, https://accessemergencymedicine.mhmedical.com/content.aspx?bookid=2569§ionid=210262251
10. Intravenous therapy - Wikipedia, accessed July 25, 2025, https://en.wikipedia.org/wiki/Intravenous_therapy
11. The history of IV therapy - Integrated medicine Clinic, accessed July 25, 2025, https://integratedmedicine.co/iv-therapy-articles/the-history-of-iv-therapy/
12. Introduction: History of Glucose Monitoring - Role of Continuous ..., accessed July 25, 2025, https://www.ncbi.nlm.nih.gov/books/NBK538968/
13. Introduction: History of Glucose Monitoring | Compendia - American Diabetes Association, accessed July 25, 2025, https://diabetesjournals.org/compendia/article-abstract/2018/1/1/144616
14. A Brief History of Diabetes Technology, accessed July 25, 2025, https://afontechnology.com/2023/07/07/a-brief-history-of-diabetes-technology/
15. Continuous Glucose Monitoring (CGM): What It Is - Cleveland Clinic, accessed July 25, 2025, https://my.clevelandclinic.org/health/articles/continuous-glucose-monitoring-cgm
16. Glucose Monitoring Devices - Content - Health Encyclopedia - University of Rochester Medical Center, accessed July 25, 2025, https://www.urmc.rochester.edu/encyclopedia/content?contenttypeid=85&contentid=p00339
17. Glucose: Structure, Functions, properties, Applications and Difference - Testbook, accessed July 25, 2025, https://testbook.com/chemistry/glucose
18. byjus.com, accessed July 25, 2025, https://byjus.com/chemistry/glucose/
19. Describe the properties of glucose. - Formula & Characteristics | CK-12 Foundation, accessed July 25, 2025, https://www.ck12.org/flexi/chemistry/Polysaccharides/describe-the-properties-of-glucose/
20. Glucose liquids | Cargill Pharmaceutical, accessed July 25, 2025, https://www.cargill.com/pharmaceutical/pharma-products/glucose-liquids
21. C PharmDex ® glucose monohydrates (Dextrose) - Cargill, accessed July 25, 2025, https://www.cargill.com/pharmaceutical/pharma-products/glucose-monohydrates-dextrose
22. DEXTROSE ANHYDROUS BioPharma - Roquette, accessed July 25, 2025, https://www.roquette.com/innovation-hub/pharma/product-profile-pages/dextrose-anhydrous-biopharma
23. go.drugbank.com, accessed July 25, 2025, https://go.drugbank.com/drugs/DB01914#:~:text=Glucose%20can%20act%20as%20precursors,the%20activity%20of%20glucoregulatory%20neurons.
24. Diabetes & Oral Medication: Types & How They Work - Cleveland Clinic, accessed July 25, 2025, https://my.clevelandclinic.org/health/articles/12070-oral-diabetes-medications
25. Glucose Uses, Side Effects & Warnings - Drugs.com, accessed July 25, 2025, https://www.drugs.com/mtm/glucose.html
26. www.webmd.com, accessed July 25, 2025, https://www.webmd.com/drugs/2/drug-3875/glucose-oral/details
27. Can glucose tablets help with managing hypoglycemia? - Medical News Today, accessed July 25, 2025, https://www.medicalnewstoday.com/articles/glucose-tablets-for-hypoglycemia
28. Comparing Top Brands of Glucose Tablets and Gels - Healthline, accessed July 25, 2025, https://www.healthline.com/diabetesmine/glucose-tablets-and-gels-for-diabetes-top-brands-explained
29. Leader Glucose Tablets - 10 Count - Mayo Clinic Store, accessed July 25, 2025, https://store.mayoclinic.com/leader-glucose-tablets-10-count.html
30. 50% Dextrose Injection, USP Concentrated Dextrose for Intravenous ..., accessed July 25, 2025, https://labeling.pfizer.com/ShowLabeling.aspx?id=4422
31. Glucose Monitoring in the Healthy Newborn Clinical Pathway — Inpatient | Children's Hospital of Philadelphia, accessed July 25, 2025, https://www.chop.edu/clinical-pathway/glucose-monitoring-healthy-newborn-clinical-pathway
32. Dextrose, unspecified form Completed Phase 4 Trials for Acute Pain Treatment - DrugBank, accessed July 25, 2025, https://go.drugbank.com/drugs/DB09341/clinical_trials?conditions=DBCOND0003831&phase=4&purpose=treatment&status=completed
33. 40% Glucose gel - Newborn use only, accessed July 25, 2025, https://www.seslhd.health.nsw.gov.au/sites/default/files/groups/Royal_Hospital_for_Women/Neonatal/Neomed/neo18glucose40.pdf
34. Management of Hyperglycemia in Hospitalized Patients Receiving Parenteral Nutrition, accessed July 25, 2025, https://www.frontiersin.org/journals/clinical-diabetes-and-healthcare/articles/10.3389/fcdhc.2022.829412/full
35. The Role of Glucose in TPN and Its Effect on Energy Levels - Pharmko, accessed July 25, 2025, https://www.pharmko.com/blog/the-role-of-glucose-in-tpn-and-its-effect-on-energy-levels
36. TPN and Diabetes - AmeriPharma® Specialty Care, accessed July 25, 2025, https://ameripharmaspecialty.com/tpn/tpn-and-diabetes/
37. Understanding the Risks of Hyperglycemia in TPN Therapy - Pharmko, accessed July 25, 2025, https://www.pharmko.com/blog/understanding-the-risks-of-hyperglycemia-in-tpn-therapy
38. Glycemic Management of Hospitalized Patients Receiving Nutrition Support | Diabetes Spectrum, accessed July 25, 2025, https://diabetesjournals.org/spectrum/article/35/4/427/147871/Glycemic-Management-of-Hospitalized-Patients
39. Diabetes - Diagnosis and treatment - Mayo Clinic, accessed July 25, 2025, https://www.mayoclinic.org/diseases-conditions/diabetes/diagnosis-treatment/drc-20371451
40. PD - Parkinson's Disease Completed Phase Trials for Dextrose, unspecified form (DB09341), accessed July 25, 2025, https://go.drugbank.com/indications/DBCOND0092599/clinical_trials/DB09341?phase=&status=completed
41. Blood Stream Infections Completed Phase 3 Trials for Dextrose, unspecified form (DB09341) - DrugBank, accessed July 25, 2025, https://go.drugbank.com/indications/DBCOND0044705/clinical_trials/DB09341?phase=3&status=completed
42. Obesity Active Not Recruiting Phase Trials for Dextrose, unspecified form (DB09341), accessed July 25, 2025, https://go.drugbank.com/indications/DBCOND0015947/clinical_trials/DB09341?phase=&status=active_not_recruiting
43. High Blood Sugar Unknown Status Phase Trials for Dextrose, unspecified form (DB09341), accessed July 25, 2025, https://go.drugbank.com/indications/DBCOND0048846/clinical_trials/DB09341?phase=&status=unknown_status
44. Hypoglycemia Completed Phase 0 Trials for Dextrose, unspecified form (DB09341), accessed July 25, 2025, https://go.drugbank.com/indications/DBCOND0020360/clinical_trials/DB09341?phase=0&status=completed
45. Glutose 15 (gel) Paddock Laboratories, Inc. - Drugs.com, accessed July 25, 2025, https://www.drugs.com/otc/100061/glutose-15.html
46. Glucose chewable tablets - Cleveland Clinic, accessed July 25, 2025, https://my.clevelandclinic.org/health/drugs/18081-glucose-chewable-tablets
47. Dextrose Monohydrate: What is it and where is it used? - Drugs.com, accessed July 25, 2025, https://www.drugs.com/inactive/dextrose-monohydrate-484.html
48. Dextrose for food, pharmaceutical, and industrial applications, accessed July 25, 2025, https://independentchemical.com/blogs/dextrose-for-food-pharmaceutical-and-industrial-applications-20105.aspx
49. Pharmaceutical Applications of Glucose Syrup from High Quality Cassava Flour in Oral Liquid Formulations, accessed July 25, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC8803456/
50. CN104911235A - Medical dextrose monohydrate production ..., accessed July 25, 2025, https://patents.google.com/patent/CN104911235A/en
51. US6527868B2 - Dextrose in powder form and a process for the preparation thereof - Google Patents, accessed July 25, 2025, https://patents.google.com/patent/US6527868B2/en
52. What Is Glucose? - IFIC, accessed July 25, 2025, https://ific.org/resources/articles/what-is-glucose/
53. D50W, DGlucose (dextrose) dosing, indications, interactions ..., accessed July 25, 2025, https://reference.medscape.com/drug/d50w-dglucose-dextrose-342705
54. Dextrose (oral route) - Side effects & dosage - Mayo Clinic, accessed July 25, 2025, https://www.mayoclinic.org/drugs-supplements/dextrose-oral-route/description/drg-20406063
55. www.nhsinform.scot, accessed July 25, 2025, https://www.nhsinform.scot/illnesses-and-conditions/blood-and-lymph/hyperglycaemia-high-blood-sugar/
56. High blood sugar (hyperglycaemia) - NHS, accessed July 25, 2025, https://www.nhs.uk/conditions/high-blood-sugar-hyperglycaemia/
57. Hyperglycemia | High Blood Sugar | Diabetes - MedlinePlus, accessed July 25, 2025, https://medlineplus.gov/hyperglycemia.html
58. Hyperglycemia in diabetes - Symptoms & causes - Mayo Clinic, accessed July 25, 2025, https://www.mayoclinic.org/diseases-conditions/hyperglycemia/symptoms-causes/syc-20373631
59. Hyperglycemia: Symptoms, Causes, and Treatments - Yale Medicine, accessed July 25, 2025, https://www.yalemedicine.org/conditions/hyperglycemia-symptoms-causes-treatments
60. Drug-induced disorders of glucose metabolism. Mechanisms and management - PubMed, accessed July 25, 2025, https://pubmed.ncbi.nlm.nih.gov/8884164/
61. Insulin and Alcohol/Food Interactions - Drugs.com, accessed July 25, 2025, https://www.drugs.com/food-interactions/insulin.html
62. www.rxlist.com, accessed July 25, 2025, https://www.rxlist.com/dextrose/generic-drug.htm#:~:text=Dextrose%20has%20moderate%20interactions%20with,magnesium%20citrate
63. baxter, accessed July 25, 2025, https://www.glucosesafety.com/
64. Baxter's glucosesafety.com, accessed July 25, 2025, https://www.glucosesafety.com/mp/index.html