Introduction

Blood glucose monitoring (BGM) is a cornerstone of diabetes management, enabling detection of glycemic patterns in response to diet, physical activity, medications, and underlying pathological processes. Accurate and timely glucose assessment is essential, as both hyperglycemia and hypoglycemia can lead to acute, life-threatening emergencies and long-term microvascular and macrovascular complications.[1][2] According to the International Diabetes Federation, an estimated 589 million adults aged 20 to 79 years were living with diabetes in 2024, a figure projected to rise to 852.5 million by 2050, underscoring the growing clinical importance of reliable glucose monitoring across all healthcare settings. [International Diabetes Federation. IDF Diabetes Atlas, 11th ed. Brussels: International Diabetes Federation; 2025]

Glycemic status can be assessed through multiple modalities. Capillary blood glucose (CBG) testing using point-of-care glucometers remains widely used for self-monitoring of blood glucose outside clinical facilities, while laboratory-based venous plasma glucose measurement and hemoglobin A1c (HbA1c) testing serve diagnostic and long-term glycemic evaluation purposes. Continuous glucose monitoring (CGM) systems, which measure interstitial fluid glucose and provide real-time trend data, have become increasingly integral to diabetes care. The 2026 American Diabetes Association (ADA) Standards of Care now recommend CGM use at the onset of diabetes and at any time thereafter for adults with diabetes on insulin therapy, on noninsulin therapies that can cause hypoglycemia, and on any diabetes treatment in which CGM aids management, substantially expanding the role of continuous monitoring.[3][4]

Regardless of the monitoring method employed, the accuracy and reliability of glucose measurements depend on adherence to established quality control practices, including internal quality control (IQC), external quality assessment (EQA), and laboratory safety protocols. Effective BGM extends beyond generating numerical data; it requires interpretation within the context of each patient’s clinical presentation and integration into individualized treatment plans by a coordinated interprofessional healthcare team.[1][2]

Pathophysiology

Dietary carbohydrates are broken down in the gastrointestinal tract into simpler sugars, primarily glucose, which is absorbed in the small intestine and transported via the bloodstream to cells throughout the body, including the liver. In response to rising postprandial blood glucose levels, pancreatic beta-cells secrete insulin, which facilitates cellular glucose uptake in insulin-sensitive tissues (skeletal muscle, liver, and adipose tissue), inhibits hepatic gluconeogenesis, and promotes glucose storage as glycogen (glycogenesis) and, to a lesser extent, as fat through de novo lipogenesis.[1]

The body maintains blood glucose homeostasis within a narrow range of approximately 3.9 to 5.5 mmol/L (70 to 99 mg/dL) through the opposing actions of insulin and counter-regulatory hormones. When blood glucose falls, pancreatic alpha-cells secrete glucagon, which stimulates hepatic glycogenolysis and gluconeogenesis to raise blood glucose levels. Other counter-regulatory hormones, including cortisol, epinephrine, and growth hormone, further support glucose mobilization during fasting, stress, and the early-morning hours (the dawn phenomenon).[5] In addition to direct glucose sensing by beta-cells, postprandial insulin secretion is augmented by the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), which are released from enteroendocrine cells in the gut in response to nutrient ingestion. Beyond their insulinotropic effect, incretins suppress glucagon secretion, delay gastric emptying, and promote satiety, thereby contributing to overall glucose regulation.[6] This tightly regulated balance between insulin-mediated glucose disposal, incretin-augmented insulin release, and counter-regulatory glucose production is central to normal glycemic control.

In diabetes mellitus, this homeostatic mechanism is disrupted. In type 1 diabetes, autoimmune destruction of pancreatic beta-cells results in absolute insulin deficiency. In type 2 diabetes, a combination of insulin resistance in peripheral tissues and progressive beta-cell dysfunction leads to relative insulin deficiency and impaired glucose utilization.[1] A diminished incretin effect, in which the glucose-lowering response to GLP-1 and GIP is attenuated, further contributes to postprandial hyperglycemia in type 2 diabetes and has become a key therapeutic target for glucagon-like peptide-1 receptor agonist (GLP-1 RA) and dual GLP-1/GIP receptor agonist therapies.[6] In both forms of diabetes, the resulting imbalance between insulin action and counterregulatory hormone activity leads to hyperglycemia. Patients with impaired glucose homeostasis and persistently elevated fasting blood glucose are at high risk of developing overt diabetes mellitus and its associated microvascular and macrovascular complications.[1][7]

Certain organs, notably the brain, kidneys, liver, and erythrocytes, do not require insulin for glucose uptake and are therefore particularly vulnerable to fluctuations in blood glucose levels. The brain is critically dependent on a continuous glucose supply; acute, chronic, or recurrent hypoglycemia can result in significant neurological morbidity, including cognitive impairment, seizures, and loss of consciousness.[8] Conversely, sustained hyperglycemia contributes to oxidative stress and the formation of advanced glycation end products, driving the microvascular and macrovascular complications of diabetes.[7][9]

Glucose is present in both the blood and the interstitial fluid; however, interstitial glucose levels may lag behind blood glucose, particularly during periods of rapid glycemic change. This physiological relationship is directly relevant to clinical practice, as CBG testing measures plasma glucose, while CGM systems measure interstitial fluid glucose. Understanding these compartmental differences and the underlying pathophysiology of glucose regulation is essential for accurate interpretation of monitoring data and appropriate clinical decision-making.[3][Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]  

Diagnostic Tests

Capillary Blood Glucose Test

A blood drop is usually collected from a fingertip prick. Blood samples can also be obtained from alternative sites, such as the earlobe, heel, forearm, and palm. Alternate-site testing yields results similar to finger-prick testing, especially during fasting and at postprandial time points. Using alternate sites may be less painful for the patient but may require a deeper lancet. The manufacturer’s instructions for the glucometer should be consulted to determine whether the device is approved for alternate-site testing.[3]

The equipment used in CBG testing includes a lancet to prick the skin, a glucometer, and test strips. Modern glucometers require a very small blood sample (0.3-1 µL), and many incorporate Bluetooth connectivity to synchronize data with paired smartphone applications. These applications record glucose measurements and provide trend data; some also offer options to log diet, medications, and physical activity, which can assist the healthcare team in developing and adjusting individualized management plans.[3][Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]  

Healthcare professionals should be aware of the differences in accuracy among blood glucose meters. Only meters approved by the US Food and Drug Administration (FDA) or comparable regulatory agencies and proven to be accurate should be used. Test strips should be unexpired, purchased from a pharmacy or licensed distributor, and properly stored. People with diabetes should be advised against purchasing or reselling pre-owned or secondhand test strips, as these may yield incorrect results.[3] Two widely used accuracy standards are the International Organization for Standardization (ISO) standard ISO 15197:2013 and the FDA guidance. Under FDA guidance for home use, 95% of results must fall within 15% of the reference value across the usable glucose range; for hospital (point-of-care) use, the criteria are stricter, requiring 95% of results to fall within 12% for blood glucose levels greater than or equal to 75 mg/dL and within 12 mg/dL for levels less than 75 mg/dL.[3]

Most currently available glucose meters use an enzymatic reaction linked to an electrochemical reaction, employing either glucose oxidase or glucose dehydrogenase.[3] Several physiologic and pharmacologic factors can interfere with glucose readings. Glucose oxidase–based monitors are sensitive to ambient oxygen levels; arterial blood or supplemental oxygen therapy may produce falsely low readings, whereas low oxygen tension (high altitude, hypoxia, or venous samples) may yield falsely elevated results. Glucose dehydrogenase–based monitors are generally not oxygen-sensitive. Other interfering substances include maltose, galactose, xylose, acetaminophen, dopamine, vitamin C, and N-acetylcysteine. Altered hematocrit levels affect meter accuracy: high hematocrit may yield falsely low readings, whereas low hematocrit may yield falsely high readings.[3][10] Temperature extremes outside a meter’s acceptable operating range may also compromise accuracy.[3]

Advantages: A small blood sample volume, a range of alternative testing sites, rapid testing time, an easy-to-read display, lower pain than venipuncture, and the ability to share data with healthcare providers via connected applications.[3][Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]  

Disadvantages: While manufacturers often provide low-cost or subsidized glucometers, test strips, and accessories carry a significant cost burden. Test strips are time-limited, have short expiry dates, and are affected by variables such as temperature, humidity, and sample quality. The clinical status of the patient, including hypoglycemia, anemia, altered hematocrit, hypotension, or critical illness, may affect the reliability of the results. Performing BGM alone does not lower blood glucose levels; for it to be useful, the information must be integrated into clinical and self-management treatment plans.[3][8]

Venous (Plasma) Blood Sample

Venous blood is collected via venipuncture, and the sample is processed in a clinical laboratory with appropriate quality control procedures. Laboratory-based glucose testing is required for the definitive diagnosis of diabetes mellitus and provides results with greater analytical precision than point-of-care devices. However, point-of-care glucose results that do not correlate with the patient’s clinical status should be confirmed by laboratory-based testing, particularly for asymptomatic hypoglycemic events in the hospital setting.[1][11]

Advantages: Offers superior analytical accuracy and precision compared with CBG testing when the laboratory meets established industry standards and serves as the reference standard for diabetes diagnosis.[1][11] 

Disadvantages: A more painful procedure than capillary testing, a risk of local tissue damage, the requirement for phlebotomy-trained personnel, and unsuitability for frequent specimen collection or real-time self-monitoring.[11][4]

Continuous Glucose Monitoring

CGM involves applying a small, water-resistant, disposable sensor, typically on the back of the upper arm or abdomen. The sensor measures glucose in the subcutaneous interstitial fluid via an electrochemical reaction—most commonly using glucose oxidase immobilized on an electrode surface, which generates a current proportional to glucose concentration.[3] [Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]

Depending on the device, sensors can remain in place for 10 to 15 days. CGM data can be shared with family members and healthcare providers via smartphone applications, and devices can send alarms or alert messages, including during episodes of hypoglycemia or hyperglycemia.[3]

The ADA (2026) recognizes 3 categories of CGM devices: real-time CGM (rtCGM), which provides a continuous data stream with adjustable alarms and alerts and is available by prescription; over-the-counter CGM (OTC-CGM), which lacks alarms and alerts and is available without a prescription for individuals not taking medications that increase hypoglycemia risk; and professional CGM, which is owned and applied by healthcare professionals to generate glucose data, either blinded or unblinded, over a short monitoring period.[3] Intermittently scanned CGM (isCGM) is no longer considered a current category, though it is still referenced as an older option. Most currently prescribed CGM devices have converged to offer similar features: no swiping required, a continuous data stream, and adjustable alarms and alerts.[3][12]

The choice of a CGM device should be individualized to the patient's clinical needs, lifestyle habits, and personal preferences.[13] CGM features can be categorized into essential features, including accuracy, safety, and regulatory approval; major drivers of choice, including approved indications, alert capabilities, integration with insulin delivery systems, data-sharing functionality, and adjunctive versus nonadjunctive use; and additional features that improve patient experience, including sensor size, calibration requirements, water resistance, and note-entry options.[13] For individuals with physical, psychological, or occupational barriers to regular finger-prick testing, a factory-calibrated CGM system with nonadjunctive use should be considered as a first choice.[13]

Clinical accuracy of CGM systems is evaluated using metrics such as the mean absolute relative difference and consensus error grid analysis. At least 95% of measured values are expected to fall within zones A and B of the Clarke–Parkes error grid.[13] [Volcansek S et al. The evolving role of continuous glucose monitoring in hospital settings: bridging the analytical and clinical needs. Diabetology. 2026;7(1):6.] The FDA’s integrated CGM (iCGM) designation signifies a high level of accuracy, reliability, and safety. This designation currently includes devices from Dexcom (G6, G7), Abbott (Libre 2 Plus, Libre 3 Plus), Medtronic (Simplera), and Senseonics (Eversense 365).[3][13] Real-world CGM accuracy can be affected by factors specific to the sensor, such as day-of-wear, sensor-to-sensor variation, insertion site, and compression artifacts, as well as by physiological conditions, such as rapid changes in glucose levels during exercise.[13]  

Use of CGM is now recommended at diabetes onset and anytime thereafter for children, adolescents, and adults with diabetes who are on insulin therapy, on noninsulin therapies that can cause hypoglycemia, and on any diabetes treatment where CGM helps in management. In people on insulin therapy, CGM devices should be used as close to daily as possible for maximal benefit. People using CGM must also have access to BGM at all times, including when CGM accuracy is in question, during sensor warm-up, when there is a disruption in transmission, or when glucose levels are changing rapidly (>2 mg/dL/min).[14][8]

Advantages: CGM provides continuous, real-time glucose data with trend information (rate and direction of change) rather than single-point measurements; reduces the need for frequent fingerstick testing; enables detection of nocturnal and asymptomatic hypoglycemia; has demonstrated improvements in glycemic control across diabetes types; supports integration with insulin delivery systems; allows remote data sharing with the care team; and in hospital settings, can reduce nursing workload, exposure to infectious patients, and use of personal protective equipment.[3][Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025] [Volcansek S et al. The evolving role of continuous glucose monitoring in hospital settings: bridging the analytical and clinical needs. Diabetology. 2026;7(1):6.][4][8]

Disadvantages: Glucose appears in the blood before it appears in the interstitial fluid. Therefore, CGM readings may lag behind blood glucose values during periods of rapid glycemic change. This physiological lag means that sole reliance on CGM may not always provide reliable readings during periods of rapid glycemic change and may necessitate confirmatory BGM in certain clinical situations.[3][Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]

Both irritant and allergic skin reactions may occur at the sensor site. The complete adhesive composition may not be disclosed in product labeling, and reactions may only be revealed through actual use.[3][13] Several interfering substances may affect CGM accuracy, including acetaminophen (at doses above 1000 mg every 6 hours in some systems), high-dose ascorbic acid, hydroxyurea, and, in implantable systems, mannitol, sorbitol, and tetracycline antibiotics. Healthcare professionals should review patients’ medication histories to identify potential drug interactions.[3][13] Cost remains a barrier for some individuals, although the expanding availability of OTC-CGM devices and increasing insurance coverage help improve access.[3][Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]  

Testing Procedures

The steps involved in performing a CBG test with a glucometer are outlined below.[3][15]

1. Perform hand hygiene and assemble all necessary equipment: glucometer, test strips (unexpired and properly stored), lancet device, clean gauze or tissue, and sharps disposal container.[15]
2. Wash and dry the testing site thoroughly. Use warm water to improve blood flow. Alcohol swabs are not routinely required; however, if used, allow the skin to dry completely before lancing to avoid sample dilution or hemolysis.[15]
3. Select and prepare the puncture site. Use the lateral aspect of the distal fingertip of the 2nd, 3rd, or 4th finger, as this minimizes injury to the underlying bone while providing adequate tissue depth for sampling. Avoid the 5th finger, as the tissue may not be deep enough to prevent bone injury. Avoid the thumb and index finger, as these areas are more sensitive than the others.[15][3] When testing on an arm, avoid the ipsilateral side in cases of recent mastectomy or ongoing intravenous infusion. For alternate-site testing (earlobe, forearm, palm), consult the manufacturer’s instructions to confirm device approval for that site.[15]
4. For neonates and infants up to 1 year of age, use the lateral or medial plantar surface of the heel. A heel stick may be more painful and require resampling; consider appropriate pain management strategies.[15]
5. Prepare the lancet device. Set the depth to no more than 2.0 mm to minimize the risk of bone injury.[15] Newer lancing devices produce less pain and greater comfort than older systems, potentially improving adherence to self-monitoring.[16] 
6. Remove the glucose test strip from its container without touching the sensor tip. Insert the test strip into the glucometer; on most devices, this activates the meter automatically.[15]
7. Firmly apply the lancet device to the selected puncture site and release the trigger to pierce the skin.[15]
8. Wipe away the first drop of blood with clean gauze or tissue, as it may contain intracellular or interstitial fluid or be hemolyzed, which can affect the accuracy of the result.[15][17][18] Apply gentle pressure near the puncture site to facilitate blood flow and the formation of the second drop of blood.[15]
9. Collect the second drop by touching it to the test strip's tip. Ensure an adequate sample volume is applied; some modern meters detect insufficient samples and allow additional blood to be applied to the same strip.[16][19] 
10. Place the glucometer on a flat surface and cover the puncture site with clean gauze or tissue. Apply gentle pressure to stop further bleeding.[15]
11. The glucometer normally displays results within seconds. If an error message appears (eg, insufficient sample, low battery, expired strip, or meter time-out), follow the manufacturer’s instructions to troubleshoot and repeat the test if needed.[15][16] 
12. Dispose of the lancet in an appropriate sharps container. Perform hand hygiene and return equipment to the storage container.[15]
13. Record the test result. Integrate BGM data into the individual’s self-management and treatment plan, considering diet, physical activity, and medication use. Healthcare professionals and patients should review and interpret BGM data together to guide adjustments in food intake, physical activity, or pharmacologic therapy to achieve glycemic goals.[8][16]

The ongoing need for and frequency of BGM should be reevaluated at each routine clinical visit to ensure that monitoring remains effective and appropriately tailored to the individual’s treatment regimen and glycemic goals.[8][16]

Results, Reporting, and Critical Findings

Blood glucose is measured in mmol/L (millimoles per liter) or mg/dL (milligrams per deciliter). Normal fasting plasma glucose (FPG) is 3.9 to 5.5 mmol/L (70-99 mg/dL).

Laboratory-Based Blood Glucose Testing

Laboratory-based testing is required for the appropriate diagnosis of diabetes mellitus. The ADA (2026) recognizes 4 diagnostic criteria for diabetes in nonpregnant individuals. Any one of these criteria is sufficient for diagnosis.

• HbA1C 6.5% or higher (48 mmol/mol): The test should be performed in a laboratory using a method that is certified by the National Glycohemoglobin Standardization Program (NGSP) and standardized to the Diabetes Control and Complications Trial (DCCT) assay.[1]
• Fasting plasma glucose 126 mg/dL or higher (7.0 mmol/L): Fasting is defined as no caloric intake for at least 8 hours.[1]
• Two-hour plasma glucose 200 mg/dL or higher (11.1 mmol/L) during a 75 g oral glucose tolerance test: The test should be performed as described by the World Health Organization (WHO), using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.[1]
• Random plasma glucose 200 mg/dL or higher (11.1 mmol/L): This criterion applies to individuals with classic symptoms of hyperglycemia or hyperglycemic crisis.[1]

In the absence of unequivocal hyperglycemia with classic symptoms, diagnosis requires 2 abnormal test results, either from the same sample or from 2 separate samples. If 2 different tests (eg, FPG and A1C) are both above the diagnostic threshold from the same sample, diabetes is confirmed. If the results are discordant, the test above the diagnostic cut point should be repeated, and the diagnosis should be based on the confirmed result.[1]

Currently, insufficient evidence supports the use of CGM for screening or diagnosis of prediabetes or diabetes.[1]

Prediabetes

Prediabetes is defined by the following criteria:[1]

• Impaired fasting glucose: FPG 100 to 125 mg/dL (5.6-6.9 mmol/L). The IDF and WHO define the lower limit of impaired fasting glucose as 110 mg/dL (6.1 mmol/L), whereas the ADA uses a lower threshold of 100 mg/dL (5.6 mmol/L) to better identify individuals at risk.[1]
• Impaired glucose tolerance: Two-hour plasma glucose 140 to 199 mg/dL (7.8-11.0 mmol/L) during a 75 g oral glucose tolerance test (OGTT).[1]
• HbA1C 5.7% to 6.4% (39-47 mmol/mol): The WHO supports the use of HbA1C values of 6.5% or higher for the diagnosis of diabetes but does not currently endorse HbA1C for defining intermediate hyperglycemia.[1] ^{[International Diabetes Federation. IDF Diabetes Atlas, 11th ed. Brussels: International Diabetes Federation; 2025]}

Prediabetes is associated with obesity, particularly abdominal or visceral obesity, dyslipidemia with high triglycerides and/or low high-density lipoprotein cholesterol, and hypertension. The presence of prediabetes should prompt comprehensive screening for cardiovascular risk factors. In people with prediabetes, monitoring for the development of diabetes should occur at least annually, with frequency modified based on individual risk assessment.[1][20]

Oral Glucose Tolerance Test

The OGTT involves collecting a fasting blood sample, administering a 75 g anhydrous glucose load dissolved in water, and collecting a second blood sample at 2 hours. The individual must fast for at least 8 hours before the test. A fasting plasma glucose of 126 mg/dL or higher (7.0 mmol/L) or a 2-hour plasma glucose of 200 mg/dL or higher (11.1 mmol/L) meets the diagnostic criteria for diabetes. Two-hour values of 140 to 199 mg/dL (7.8-11.0 mmol/L) indicate impaired glucose tolerance.[1]

Traditionally, individuals have been advised to consume at least 150 g of carbohydrate daily for 3 days before the test to avoid false-positive results. However, updated evidence suggests that unrestricted carbohydrate intake in the days preceding the test does not significantly affect OGTT results in most clinical scenarios, and this preparatory requirement may not be necessary for all patients.[21]

The 2-hour plasma glucose value during the OGTT diagnoses more individuals with prediabetes and diabetes than FPG or HbA1C alone. Compared with FPG and HbA1C cut points, FPG, 2-hour PG, and HbA1C reflect different aspects of glucose metabolism, and the detection rates of these screening tests vary across populations and individuals.[1]

Glycated Hemoglobin

Glucose molecules attach to hemoglobin in red blood cells to form HbA1c. Because the lifespan of a red blood cell is approximately 120 days under normal physiologic conditions, HbA1c reflects average blood glucose levels over the preceding 2 to 3 months. Normal HbA1c is less than 5.7% (<39 mmol/mol); prediabetes is defined as 5.7% to 6.4% (39-47 mmol/mol); and a value of 6.5% or higher (48 mmol/mol) meets the diagnostic threshold for diabetes mellitus.[1]

The HbA1C test must be performed using a method that is National Glycohemoglobin Standardization Program (NGSP)-certified and standardized to the DCCT assay. Point-of-care HbA1C testing for diabetes screening and diagnosis should be restricted to devices approved for diagnosis by the FDA at Clinical Laboratory Improvement Amendments (CLIA)–certified laboratories that perform testing of moderate complexity or higher by trained personnel.[1]

An initial HbA1C result at or above the diagnostic threshold should be confirmed by repeat testing on a separate day, unless there is unequivocal hyperglycemia with classic symptoms. When there is consistent and substantial discordance between HbA1C and blood glucose values, the possibility of a problem or interference with either test should be evaluated.[1]

Conditions affecting HbA1C accuracy: In conditions associated with an altered relationship between HbA1C and glycemia, such as hemoglobin variants (eg, sickle cell disease, hemoglobin C), pregnancy, glucose-6-phosphate dehydrogenase deficiency, HIV, hemodialysis, recent blood loss or transfusion, erythropoietin therapy, and conditions that alter red blood cell turnover, plasma glucose criteria rather than HbA1C should be used for diagnosis.[1][8] In people with diabetes who have conditions in which the interpretation of HbA1C may be problematic, or when HbA1C cannot be measured (eg, homozygous hemoglobin variants), fructosamine or glycated albumin may serve as useful alternative measures of glycemic status. These serum glycated protein assays reflect glycemia over the preceding 2 to 4 weeks, not 2 to 3 months.[8]

Race and ethnicity should not be considered in determining how HbA1C is used clinically for glycemic monitoring. While there is an emerging understanding of genetic determinants that may modify the association between HbA1C and glucose levels, race and ethnicity are not good proxies for these genetic differences.[8]

Glycemic Goals and Monitoring

While a target HbA1C of less than 7.0% (53 mmol/mol) is commonly recommended for many nonpregnant adults with diabetes, glycemic goals should be individualized using clinical and professional judgment. The ADA (2026) emphasizes shared decision-making when setting glycemic goals, with adjustments based on patient-specific factors including age and life expectancy, duration of diabetes, presence of comorbid conditions, risk of hypoglycemia or other adverse effects, patient preferences and values, and availability of resources and social support.[8]

HbA1C goals now align with CGM-derived metrics to provide a more comprehensive glycemic assessment. For most adults, an HbA1C goal of less than 7.0% aligns with a time in range of 70 to 180 mg/dL (3.9-10.0 mmol/L) with a target above 70%, a time below range of less than 70 mg/dL (<3.9 mmol/L) with a target below 4%, and a time above range of greater than 180 mg/dL (>10.0 mmol/L) with a target below 25%. For older adults with complex or poor health, less stringent HbA1C goals of less than 8.0% correspond to a time in range above 50%, with an emphasis on avoiding symptomatic hypoglycemia. Glycemic status should be assessed at least twice yearly and more frequently (eg, every 3 months) for individuals who are not meeting glycemic goals, have recent treatment changes, or experience frequent or severe hypoglycemia or hyperglycemia.[8]

CGM metrics are particularly useful for people at risk for hypoglycemia and provide information that HbA1C alone cannot, including glycemic variability, real-time glucose levels, and detection of nocturnal or asymptomatic hypoglycemia. For individuals prone to glycemic variability, glycemic status is best evaluated using a combination of BGM or CGM results and HbA1C.[3][8]

Gestational Diabetes Mellitus

Hyperglycemia first detected during pregnancy that does not meet the criteria for diabetes in nonpregnant individuals is classified as gestational diabetes mellitus (GDM). Screening for GDM is performed at 24 to 28 weeks of gestation. 

Recognized Strategies

One-step strategy (IADPSG criteria): A 75 g OGTT is performed after an overnight fast of at least 8 hours. GDM is diagnosed when any 1 of the following plasma glucose values is met or exceeded: fasting 92 mg/dL or higher (5.1 mmol/L), 1-hour 180 mg/dL or higher (10.0 mmol/L), or 2-hour 153 mg/dL or higher (8.5 mmol/L). The ADA recommends the IADPSG diagnostic criteria because these are the only ones based on pregnancy outcomes.[1]

Two-step strategy: Step 1 involves a 50 g glucose load test (nonfasting) with plasma glucose measurement at 1 hour. If the result is 130, 135, or 140 mg/dL or higher (7.2, 7.5, or 7.8 mmol/L, per institutional threshold), Step 2 is performed: a 100 g OGTT (fasting), with glucose measured at fasting and at 1, 2, and 3 hours. Diagnosis is made using the Carpenter-Coustan criteria when at least 2 values are met or exceeded: fasting 95 mg/dL or higher (5.3 mmol/L), 1-hour 180 mg/dL or higher (10.0 mmol/L), 2-hour 155 mg/dL or higher (8.6 mmol/L), 3-hour 140 mg/dL or higher (7.8 mmol/L).[1]

Individuals diagnosed with GDM should receive lifelong screening for prediabetes and type 2 diabetes after delivery. Early detection of hyperglycemia in pregnancy (before 24 weeks) may indicate preexisting undiagnosed type 1 or type 2 diabetes rather than true GDM.[1][International Diabetes Federation. IDF Diabetes Atlas. 2025 Report].

Clinical Note: Capillary versus Venous Glucose Measurements

A clinically significant difference exists between CBG measurements and venous or arterial plasma glucose values obtained in laboratory settings. CBG values tend to be slightly higher than venous values in the postprandial state. Care should be taken when comparing or combining results from point-of-care capillary testing with laboratory venous samples, as discordant values may lead to inappropriate clinical decisions. Healthcare professionals should confirm discrepant capillary glucose results with laboratory-based venous testing, particularly in the hospital setting.[3][11] 

Clinical Significance

BGM is a crucial component of managing patients with diabetes mellitus. Very high or very low blood glucose levels can impair cellular function and may be life-threatening if not managed appropriately. Stress-related hyperglycemia may also occur in patients who have experienced an acute medical or surgical event.[8]

Hyperglycemia

The etiologies of hyperglycemia include, but are not limited to, inadequate insulin administration in patients with type 1 diabetes mellitus; insulin resistance with or without frank type 2 diabetes; stress-related experiences such as critical illness, surgery, or infection; and the dawn phenomenon, which is an early-morning surge of counter-regulatory hormones, including glucagon, cortisol, epinephrine, and growth hormone, typically occurring between 4 AM and 8 AM, that results in a rise in blood glucose levels.[8][5]

Symptoms of hyperglycemia include polyuria (increased and frequent urination), polydipsia (increased thirst), blurred vision, headache, fatigue, and glucosuria. Acute symptoms of hyperglycemia are typically not observed at levels below 14 mmol/L (250 mg/dL).[5]

Episodes of hyperglycemia over an extended period may lead to either diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (HHS). In DKA, insulin deficiency results in lipolysis and hepatic ketogenesis, leading to elevated serum beta-hydroxybutyrate levels and metabolic acidosis. DKA is classified by severity: mild (venous pH >7.25 to <7.30, bicarbonate 15-18 mmol/L, beta-hydroxybutyrate 3.0-6.0 mmol/L), moderate (pH 7.0-7.25, bicarbonate 10 to <15 mmol/L, beta-hydroxybutyrate 3.0-6.0 mmol/L), and severe (pH <7.0, bicarbonate <10 mmol/L, beta-hydroxybutyrate >6.0 mmol/L).[4]

DKA is most commonly associated with type 1 diabetes but may also occur in type 2 diabetes, particularly in the context of severe illness or sodium-glucose cotransporter 2 (SGLT2) inhibitor use. Symptoms may include fruity breath, ketonuria, Kussmaul respiration, tachycardia, nausea, vomiting, abdominal pain, altered mentation, and coma.[5] 

HHS is a rare condition seen most commonly in patients with type 2 diabetes, characterized by profound hyperglycemia (often >33.3 mmol/L or >600 mg/dL), hyperosmolality, and severe dehydration without significant ketoacidosis. Because glucose is hydrophilic, the kidneys produce exceedingly large volumes of urine, resulting in life-threatening dehydration and potential coma. HHS typically develops over days to a week and frequently presents with altered cognition. Both DKA and HHS require emergent management, including intravenous fluid resuscitation, insulin therapy, and electrolyte monitoring. Resolution of DKA is defined as beta-hydroxybutyrate less than 0.6 mmol/L with resolution of acidosis, including a venous pH of 7.3 or higher and a bicarbonate level of 18 mmol/L or higher. Resolution of HHS is considered when the calculated serum osmolality falls below 300 mOsm/kg, urine output exceeds 0.5 mL/kg/h, cognitive status improves, and blood glucose is less than 250 mg/dL (13.9 mmol/L).[5]

Long-term hyperglycemia contributes to oxidative stress and advanced glycation end-product formation, driving both microvascular complications, including diabetic retinopathy, nephropathy, and peripheral neuropathy, and macrovascular complications such as coronary artery disease, cerebrovascular disease, and peripheral arterial disease. Sustained hyperglycemia can also delay wound healing.[9][7][22] 

Hypoglycemia

Symptoms of hypoglycemia are seen when low blood glucose levels deprive the body of essential fuel to sustain life. The ADA classifies hypoglycemia into three levels: Level 1, defined as a measurable glucose concentration less than 70 mg/dL (<3.9 mmol/L) and 54 mg/dL or higher (≥3.0 mmol/L), represents the threshold for adrenergic counter-regulatory responses; Level 2, defined as glucose less than 54 mg/dL (<3.0 mmol/L), is the threshold at which neuroglycopenic symptoms begin to occur and requires immediate action; and Level 3 is a severe event characterized by altered mental and/or physical functioning that requires assistance from another person for recovery, irrespective of glucose level.[8]

Causes of hypoglycemia include, but are not limited to, insulin overdose or dosing errors, inadequate carbohydrate intake in relation to insulin use, and an imbalance between insulin administration, carbohydrate intake, and exercise. Medications such as sulfonylureas are a well-recognized cause of hypoglycemia. Notably, sulfonylureas interact with several commonly used antimicrobials, including fluoroquinolones, clarithromycin, sulfamethoxazole-trimethoprim, metronidazole, and fluconazole, which can markedly increase the effective dose of sulfonylureas, precipitating hypoglycemia.[8]

Important clinical and biological risk factors for hypoglycemia include renal failure (as the kidneys are primarily responsible for metabolizing exogenous insulin and reduced clearance increases hypoglycemia risk), advanced age (≥75 years), cognitive impairment, intensive insulin therapy, history of metabolic surgery (particularly Roux-en-Y gastric bypass), hepatic failure, and polypharmacy. Social and economic risk factors include food insecurity, low-income status, and housing insecurity.[8]

Patients with hypoglycemia may present with shakiness, irritability, confusion, sweating, tachycardia, hunger, blurred vision, lightheadedness, clumsiness, or seizure activity. Impaired awareness of hypoglycemia—a condition in which individuals lose the ability to perceive the typical adrenergic warning symptoms—places patients at significantly elevated risk because they may not recognize the onset of hypoglycemia during everyday activities such as driving or while asleep. Level 3 hypoglycemia may progress to loss of consciousness, seizure, coma, or death.[8]

Emergent treatment to restore normal blood glucose levels is imperative because some organs, notably the brain, are critically dependent on a continuous glucose supply and do not store glucose. Acute, chronic, or recurrent hypoglycemia can result in significant neurological morbidity, including cognitive impairment. Antidiabetic therapy should be reevaluated when blood glucose falls below 3.9 mmol/L (70 mg/dL), and 1 or more episodes of Level 2 or Level 3 hypoglycemia should prompt reevaluation and possible deintensification of the treatment plan.[8][1] 

Patients across the lifespan with diabetes mellitus have varying clinical presentations and underlying clinical pathologies. Patients may not always report the effects of hypoglycemia or hyperglycemia, which should involve monitoring for other signs and symptoms.

Continuous Glucose Monitoring

In addition to CBG testing, CGM has become an increasingly important tool in diabetes management. CGM devices measure interstitial fluid glucose concentrations at regular intervals, typically every 1 to 5 minutes, via a subcutaneously placed sensor, providing trend information on the direction and rate of glucose change that is not available with intermittent point-of-care testing.[3] [Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]

CGM data are used to calculate several clinically important glycemic metrics, including time in range (typically 70-180 mg/dL or 3.9-10.0 mmol/L), time below range, time above range, glucose management indicator, and coefficient of variation, all of which complement HbA1c measurement in assessing glycemic status. Current guidelines recommend assessing glycemic status by HbA1C and/or CGM metrics such as time in range, time above range, and time below range.[8][3] 

Multiple randomized controlled trials have demonstrated that CGM reduces HbA1C levels and episodes of hypoglycemia when participants wear the devices regularly. These benefits have been demonstrated regardless of age, sex, education or income levels, or baseline diabetes characteristics.[3] A recent systematic review with meta-analysis further supports the use of CGM in people with type 2 diabetes, demonstrating benefits in glycemic management, individual experience, healthcare resource utilization, and cost-effectiveness.[3][Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025]  

Clinicians should be aware that interstitial glucose levels may lag behind blood glucose, particularly during periods of rapid glycemic change, with an average delay of 5 to 15 minutes. Point-of-care CBG confirmation remains necessary in certain clinical scenarios, including suspected hypoglycemia and when CGM readings appear erroneous.[3] [Sensors and Actuators Reports. A systematic review of continuous glucose monitoring sensors: principles, core technologies and performance evaluation. Dec 2025] 

Some CGM systems are compatible with insulin-delivery devices and form the basis of automated insulin-delivery systems, which can adjust or suspend insulin delivery based on predicted or detected glucose trends. Automated insulin delivery systems are now the preferred method of insulin delivery for people with type 1 diabetes and are being considered for individuals with type 2 diabetes who are receiving basal insulin and not meeting glycemic goals.[3][12] 

Glycemic Care in the Clinical Setting

For appropriate glycemic control in patients with diabetes mellitus in noncritical care settings, CBG testing is the recommended testing method. Blood glucose testing is recommended before meals and at bedtime for patients who can eat. Patients receiving enteral feeds or who are nil by mouth (nil per OS) should be tested every 4 to 6 hours.[11] 

All hospitalized patients should receive an initial blood glucose assessment, regardless of a history of diabetes mellitus. An HbA1C test should be performed on all patients with diabetes or hyperglycemia (random blood glucose >140 mg/dL or >7.8 mmol/L) at the time of admission if no HbA1C test result is available from the prior 3 months. The initial evaluation should identify the type of diabetes (type 1, type 2, gestational, pancreatogenic, stress hyperglycemia, drug-related, or nutrition-related) when it is known.[11]

Hyperglycemia in hospitalized individuals is defined as any blood glucose level greater than 140 mg/dL (>7.8 mmol/L). Hypoglycemia in the hospital follows the same 3-level classification: Level 1 (54-69 mg/dL or 3.0-3.8 mmol/L), Level 2 (<54 mg/dL or <3.0 mmol/L), and Level 3 (a clinical event requiring assistance). Levels 2 and 3 hypoglycemia require immediate intervention and correction of low blood glucose.[11] 

A hypoglycemia management protocol should be adopted by all health systems, with a plan to identify, treat, and prevent hypoglycemia established for each individual. Hospital episodes of hypoglycemia should be documented in the health record and tracked to inform quality improvement efforts. Insulin is one of the most common medications causing adverse events in hospitalized individuals. Errors in insulin dosing, missed doses, or administration errors occur relatively frequently across prescribing, dispensing, and nursing processes. The use of glucose management protocols, including nurse-initiated treatment protocols, is ideal for managing hypoglycemia in the hospital setting.[11]

In non-ICU settings, CGM has been shown to improve detection of hypoglycemia, particularly nocturnal and asymptomatic episodes, compared with standard point-of-care testing conducted before meals and at bedtime.[10][14] [Volcansek S et al. The evolving role of continuous glucose monitoring in hospital settings: bridging the analytical and clinical needs. Diabetology. 2026;7(1):6.] A scoping review of studies from 2023 to 2025 found that inpatient CGM devices generally show reasonable accuracy, with mean absolute relative differences ranging from 10% to 23%, although several factors, including medications, fluid management, and hemodynamic disturbances, can affect accuracy in hospital settings.[Volcansek S et al. The evolving role of continuous glucose monitoring in hospital settings: bridging the analytical and clinical needs. Diabetology. 2026;7(1):6.] Current guidelines recommend the use of CGM in combination with confirmatory point-of-care BGM for noncritically ill hospitalized patients with insulin-treated diabetes who are at high risk of developing hypoglycemia.

Structured hospital CGM protocols, including patient selection criteria, interprofessional team training, and integration with electronic health records, have been proposed to facilitate implementation.[11][Volcansek S et al. The evolving role of continuous glucose monitoring in hospital settings: bridging the analytical and clinical needs. Diabetology. 2026;7(1):6.] Currently, the FDA approves no CGM devices for inpatient use, and confirmatory point-of-care blood glucose measurements remain recommended for insulin dosing decisions in the hospital.[11] Initiating CGM prior to discharge may facilitate follow-up and help prevent acute diabetes-related complications and readmissions.[11]

Emerging evidence demonstrates that obstructive sleep apnea syndrome significantly affects glycemic variability, and CGM can detect nocturnal hyperglycemic peaks and hypoglycemic episodes that would otherwise go unrecognized by intermittent testing, thereby highlighting the value of continuous monitoring in patients with coexisting sleep-disordered breathing.[23]  

Community and Rehabilitation Setting-Based Care

Patients require education regarding the importance of regulating diet, exercise, and medications to prevent acute or chronic complications resulting from extreme blood glucose fluctuations in conditions such as diabetes mellitus. Diabetes self-management education and support (DSMES) has been shown to improve self-management behaviors, patient satisfaction, and glycemic outcomes and should be integrated into ongoing care.[14]

Patients require specific education to perform CBG testing, including appropriate hand hygiene before testing, calibration of the glucometer when required, correct use of the lancet, obtaining an adequate blood sample, interpreting results, and knowing when and how to report and follow up on results. For patients using CGM, education should cover sensor insertion, alarm settings, interpretation of trend data and glucose metrics, and indications for performing confirmatory CBG testing.[3][14]

Quality Control and Lab Safety

IQC and participation in EQA or proficiency testing are essential components of laboratory practice and healthcare settings where blood glucose and HbA1c testing are performed, whether using point-of-care testing devices or conventional laboratory analyzers.[24][25]  While some point-of-care testing glucose meters are classified as waived devices, many others, including HbA1c analyzers, are nonwaived and must meet stringent requirements, including staff competency, regular IQC, method validation, and documentation to ensure reliable and clinically accurate results.[26]

For HbA1c specifically, the HbA1C test must be performed using a method certified by the NGSP and standardized or traceable to the DCCT reference assay. Point-of-care HbA1C testing for diabetes screening and diagnosis should be restricted to devices approved by the FDA and performed in CLIA–certified laboratories that conduct testing of moderate complexity or higher by trained personnel. CLIA quality standards require documented annual competency assessments and participation in an approved proficiency testing program 3 times per year.[1]

Typically, laboratories employ 2 different levels of IQC to monitor analytical performance and select controls that are relevant to clinically significant medical decision limits, such as hypoglycemia, hyperglycemia, and HbA1c thresholds for diabetes management.[25] Statistical tools should be used to detect trends, shifts, or outliers in IQC data and to verify lot-to-lot consistency of reagents and control materials. If an IQC result fails, corrective and preventive actions must be implemented before patient samples are analyzed on the instrument, regardless of whether the analyzer is a point-of-care testing device, central laboratory analyzer, or HbA1c system.[25]

Clinicians should also be aware of preanalytical and biological factors that can affect the accuracy and interpretation of glucose and HbA1c results. For glucose testing, sample handling and processing time, hemolysis, severe hypertriglyceridemia, and hypotension or critical illness may compromise the accuracy of the results. For HbA1c, conditions that affect hemoglobin concentration or erythrocyte turnover, including hemolytic anemia, glucose-6-phosphate dehydrogenase deficiency, hemoglobin variants (eg, sickle cell trait), recent blood transfusion, use of erythropoietin-stimulating agents, kidney failure, HIV, and pregnancy, can alter the relationship between HbA1C and average glycemia. In such conditions, plasma glucose criteria should be used instead of HbA1C for diagnosis, and alternative approaches to glycemic monitoring, including BGM, CGM, or glycated serum protein assays such as fructosamine, may be required.[1]

Participation in EQA programs is strongly recommended. These programs typically involve sending blind samples periodically to assess laboratory performance, including both blood glucose and HbA1c measurements, and to benchmark results against peer laboratories. Participation in these programs ensures the reliability of results that inform long-term glycemic management and clinical decision-making.[27][28] 

Laboratory safety protocols, including device decontamination, safe handling of blood samples, and adherence to biosafety measures, are mandatory for all glucose and HbA1c testing procedures. These practices minimize the risk of contamination and exposure to infectious agents, ensure safe operation of point-of-care testing devices, conventional analyzers, and HbA1c instruments, and support accurate, reliable, and clinically meaningful monitoring of glycemic status for patient care.[29]

Enhancing Healthcare Team Outcomes

Managing diabetes mellitus to improve patient outcomes requires a coordinated, interprofessional approach that integrates clinical expertise, patient engagement, and evidence-based practice. Current evidence supports the use of structured care models, such as the Chronic Care Model (CCM), which emphasizes proactive, team-based care; self-management support; decision support at the point of care; clinical information systems, including patient registries; community resources; and a quality-oriented health system culture. Randomized controlled trials of CCM-aligned programs have demonstrated significant reductions in HbA1C, with greater improvements observed in interventions incorporating 4 or more CCM elements, as well as improvements in blood pressure and processes of diabetes care. Team-based care interventions specifically have been associated with a mean HbA1C reduction of 0.5%, along with significant improvements in systolic and diastolic blood pressure and low-density lipoprotein cholesterol. These findings underscore that effective glycemic management extends beyond numerical values and requires sound clinical judgment, ethical decision-making, and individualized, patient-centered strategies that address the physiological, psychosocial, and socioeconomic dimensions of diabetes.[30][31] 

A systematic approach to managing altered blood glucose levels depends on active collaboration across an interprofessional team that includes the patient as an informed partner. Individuals with diabetes should receive care from a coordinated team that may include, but is not limited to, diabetes care and education specialists; primary care and subspecialty clinicians, including endocrinologists; nurses, including registered nurses and nurse practitioners; registered dietitian nutritionists; clinical pharmacists; exercise specialists; podiatrists; dentists; behavioral health professionals; laboratory professionals; community health workers; and care coordinators or navigators.

Each discipline contributes distinct expertise to BGM and diabetes management. Physicians and advanced practitioners oversee diagnostic evaluation and therapeutic planning. Nurses perform CBG testing, administer insulin, implement nurse-initiated hypoglycemia and hyperglycemia protocols, and provide bedside education. Pharmacists review medication regimens for agents that may cause hypoglycemia, including sulfonylurea-antimicrobial interactions, and optimize medication safety. Dietitians provide medical nutrition therapy and carbohydrate counting education. Diabetes care and education specialists deliver DSMES and serve as technology champions for CGM and insulin pump systems. Laboratory professionals ensure quality control of glucose and HbA1c testing. Behavioral health professionals address psychosocial barriers to self-management.[14][31] 

Structured interprofessional communication and shared decision-making are essential for cohesive care delivery, patient safety, and quality improvement. The care team should avoid therapeutic inertia—the failure to initiate or intensify therapy when treatment goals are not met—and prioritize timely modification of pharmacologic therapy, behavior-change interventions, technology use, and social or financial support systems. Social determinants of health, including food insecurity, housing instability, low health literacy, and financial constraints, should be routinely assessed and addressed, as these factors directly affect glycemic control and the patient’s ability to perform self-monitoring.

Insulin is one of the most common medications associated with adverse events in hospitalized patients. Therefore, standardized insulin safety protocols, including nurse-initiated treatment algorithms for hypoglycemia prevention and management, are critical. In the context of BGM specifically, the team must ensure coordinated interpretation of glucose data, whether from CBG testing, CGM trend reports, or laboratory HbA1c results, and incorporate these findings into a unified care plan that is communicated across all team members during transitions of care, shift handoffs, and outpatient follow-up.[30][31][32] 

Central to all interprofessional efforts is patient engagement as an active and informed partnership. A communication style that uses person-centered, culturally sensitive, and strength-based language; elicits individual preferences and beliefs; and assesses literacy, numeracy, and potential barriers to care is recommended to optimize health outcomes and health-related quality of life. DSMES should be provided at diagnosis, annually, when complicating factors arise, and during transitions of care. DSMES has been shown to improve self-management behaviors, patient satisfaction, and glycemic outcomes. Health systems should adopt a culture of continuous quality improvement, implement benchmarking programs, and engage interprofessional teams to support sustainable improvements in care processes and health outcomes. Quality improvement methods have been documented to improve diabetes technology uptake, increase screening for psychosocial needs, and reduce inequities in access to diabetes care.[14][30][33]

Review Questions

• Access free multiple choice questions on this topic.
• Comment on this article.

References

1.

American Diabetes Association Professional Practice Committee for Diabetes*. 2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S27-S49. [PMC free article: PMC12690183] [PubMed: 41358893]

2.

GBD 2021 Diabetes Collaborators. Global, regional, and national burden of diabetes from 1990 to 2021, with projections of prevalence to 2050: a systematic analysis for the Global Burden of Disease Study 2021. Lancet. 2023 Jul 15;402(10397):203-234. [PMC free article: PMC10364581] [PubMed: 37356446]

3.

American Diabetes Association Professional Practice Committee for Diabetes*. 7. Diabetes Technology: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S150-S165. [PMC free article: PMC12690173] [PubMed: 41358889]

4.

Irace C, Coluzzi S, Di Cianni G, Forte E, Landi F, Rizzo MR, Sesti G, Succurro E, Consoli A. Continuous glucose monitoring (CGM) in a non-Icu hospital setting: The patient's journey. Nutr Metab Cardiovasc Dis. 2023 Nov;33(11):2107-2118. [PubMed: 37574433]

5.

Umpierrez GE, Davis GM, ElSayed NA, Fadini GP, Galindo RJ, Hirsch IB, Klonoff DC, McCoy RG, Misra S, Gabbay RA, Bannuru RR, Dhatariya KK. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report. Diabetes Care. 2024 Aug 01;47(8):1257-1275. [PMC free article: PMC11272983] [PubMed: 39052901]

6.

American Diabetes Association Professional Practice Committee for Diabetes*. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S183-S215. [PMC free article: PMC12690185] [PubMed: 41358900]

7.

American Diabetes Association Professional Practice Committee for Diabetes*. 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S216-S245. [PMC free article: PMC12690187] [PubMed: 41358899]

8.

American Diabetes Association Professional Practice Committee for Diabetes*. 6. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S132-S149. [PMC free article: PMC12690178] [PubMed: 41358894]

9.

American Diabetes Association Professional Practice Committee for Diabetes*. 12. Retinopathy, Neuropathy, and Foot Care: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S261-S276. [PMC free article: PMC12690177] [PubMed: 41358886]

10.

Pleus S, Baumstark A, Jendrike N, Mende J, Link M, Zschornack E, Haug C, Freckmann G. System accuracy evaluation of 18 CE-marked current-generation blood glucose monitoring systems based on EN ISO 15197:2015. BMJ Open Diabetes Res Care. 2020 Jan;8(1) [PMC free article: PMC7039612] [PubMed: 31958308]

11.

American Diabetes Association Professional Practice Committee for Diabetes*. 16. Diabetes Care in the Hospital: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S339-S355. [PMC free article: PMC12690180] [PubMed: 41358892]

12.

American Diabetes Association Professional Practice Committee for Diabetes*. Summary of Revisions: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(1 Suppl 1):S6-S12. [PMC free article: PMC12690167] [PubMed: 41358896]

13.

Di Molfetta S, Rossi A, Boscari F, Irace C, Laviola L, Bruttomesso D. Criteria for Personalised Choice of a Continuous Glucose Monitoring System: An Expert Opinion. Diabetes Ther. 2024 Nov;15(11):2263-2278. [PMC free article: PMC11467157] [PubMed: 39347900]

14.

American Diabetes Association Professional Practice Committee for Diabetes*. 5. Facilitating Positive Health Behaviors and Well-being to Improve Health Outcomes: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S89-S131. [PMC free article: PMC12690188] [PubMed: 41358898]

15.

Krleza JL, Dorotic A, Grzunov A, Maradin M., Croatian Society of Medical Biochemistry and Laboratory Medicine. Capillary blood sampling: national recommendations on behalf of the Croatian Society of Medical Biochemistry and Laboratory Medicine. Biochem Med (Zagreb). 2015;25(3):335-58. [PMC free article: PMC4622200] [PubMed: 26524965]

16.

Grady M, Lamps G, Shemain A, Cameron H, Murray L. Clinical Evaluation of a New, Lower Pain, One Touch Lancing Device for People With Diabetes: Virtually Pain-Free Testing and Improved Comfort Compared to Current Lancing Systems. J Diabetes Sci Technol. 2021 Jan;15(1):53-59. [PMC free article: PMC7783011] [PubMed: 31311312]

17.

Heenan H, Lunt H, Chan H, Frampton CM. How Much Hemolysis Is Acceptable When Undertaking Deep Lancing for Finger Stick Derived Capillary Plasma Glucose Measurement? J Diabetes Sci Technol. 2017 Jul;11(4):845-846. [PMC free article: PMC5588826] [PubMed: 28627246]

18.

Heenan H, Lunt H, Chan H, Frampton CM. Capillary Samples and Hemolysis: Further Considerations. J Diabetes Sci Technol. 2017 Jul;11(4):847-848. [PMC free article: PMC5588841] [PubMed: 28322064]

19.

Harrison B, Brown D. Accuracy of a blood glucose monitoring system that recognizes insufficient sample blood volume and allows application of more blood to the same test strip. Expert Rev Med Devices. 2020 Jan;17(1):75-82. [PubMed: 31825686]

20.

American Diabetes Association Professional Practice Committee for Diabetes*. 3. Prevention or Delay of Diabetes and Associated Comorbidities: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S50-S60. [PMC free article: PMC12690170] [PubMed: 41358891]

21.

Klein KR, Walker CP, McFerren AL, Huffman H, Frohlich F, Buse JB. Carbohydrate Intake Prior to Oral Glucose Tolerance Testing. J Endocr Soc. 2021 May 01;5(5):bvab049. [PMC free article: PMC8059359] [PubMed: 33928207]

22.

American Diabetes Association Professional Practice Committee for Diabetes*. 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S246-S260. [PMC free article: PMC12690176] [PubMed: 41358881]

23.

Gouveri E, Drakopanagiotakis F, Panou T, Papazoglou D, Steiropoulos P, Papanas N. Continuous Glucose Monitoring Among People with and without Diabetes Mellitus and Sleep Apnoea. Diabetes Ther. 2025 Aug;16(8):1533-1555. [PMC free article: PMC12317927] [PubMed: 40465146]

24.

Lou Y, Shan Z, Chen Q, Kang F. Intra-Laboratory and Inter-Laboratory Variations Analysis for HbA1c Assays in China: Using Internal Quality Control and External Quality Assessment Data. J Clin Lab Anal. 2025 Apr;39(8):e70036. [PMC free article: PMC12019688] [PubMed: 40219668]

25.

Gruber L, Hausch A, Mueller T. Internal Quality Controls in the Medical Laboratory: A Narrative Review of the Basic Principles of an Appropriate Quality Control Plan. Diagnostics (Basel). 2024 Oct 05;14(19) [PMC free article: PMC11475633] [PubMed: 39410627]

26.

Kushner PR, Fonseca V, Nichols JH, Shubrook JH, Miller E, Wright E, DeFilippi C, Vassalotti JA. Clinical Need for Point-of-Care Testing for Diabetes in Clinical and Laboratory Improvement Amendments-Waived Settings. Clin Diabetes. 2025 Spring;43(2):227-239. [PMC free article: PMC12019004] [PubMed: 40290824]

27.

Delatour V, Clouet-Foraison N, Jaisson S, Kaiser P, Gillery P. Trueness assessment of HbA1c routine assays: are processed EQA materials up to the job? Clin Chem Lab Med. 2019 Sep 25;57(10):1623-1631. [PubMed: 31085744]

28.

Buchta C, Marrington R, De la Salle B, Albarède S, Albe X, Badrick T, Berghäll H, Bullock D, Cobbaert CM, Coucke W, Delatour V, Geilenkeuser WJ, Griesmacher A, Henriksen GM, Huggett JF, Juhos I, Kammel M, Luppa PB, Meijer P, Pelanti J, Pezzati P, Sandberg S, Spannagl M, Thelen M, Thomas A, Zeichhardt H, Restelli V, Perrone LA. Behind the scenes of EQA – characteristics, capabilities, benefits and assets of external quality assessment (EQA): Part III – EQA samples. Clin Chem Lab Med. 2025 Apr 28;63(5):868-878. [PubMed: 39753204]

29.

Cornish NE, Anderson NL, Arambula DG, Arduino MJ, Bryan A, Burton NC, Chen B, Dickson BA, Giri JG, Griffith NK, Pentella MA, Salerno RM, Sandhu P, Snyder JW, Tormey CA, Wagar EA, Weirich EG, Campbell S. Clinical Laboratory Biosafety Gaps: Lessons Learned from Past Outbreaks Reveal a Path to a Safer Future. Clin Microbiol Rev. 2021 Jun 16;34(3):e0012618. [PMC free article: PMC8262806] [PubMed: 34105993]

30.

American Diabetes Association Professional Practice Committee for Diabetes*. 1. Improving Care and Promoting Health in Populations: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S13-S26. [PMC free article: PMC12690171] [PubMed: 41358887]

31.

American Diabetes Association Professional Practice Committee for Diabetes*. 4. Comprehensive Medical Evaluation and Assessment of Comorbidities: Standards of Care in Diabetes-2026. Diabetes Care. 2026 Jan 01;49(Supplement_1):S61-S88. [PMC free article: PMC12690184] [PubMed: 41358897]

32.

Montori VM, Ruissen MM, Hargraves IG, Brito JP, Kunneman M. Shared decision-making as a method of care. BMJ Evid Based Med. 2023 Aug;28(4):213-217. [PMC free article: PMC10423463] [PubMed: 36460328]

33.

Nurchis MC, Sessa G, Pascucci D, Sassano M, Lombi L, Damiani G. Interprofessional Collaboration and Diabetes Management in Primary Care: A Systematic Review and Meta-Analysis of Patient-Reported Outcomes. J Pers Med. 2022 Apr 15;12(4) [PMC free article: PMC9029958] [PubMed: 35455759]

Disclosure: Thomas Mathew declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Zubair declares no relevant financial relationships with ineligible companies.