Hyperglycemia

Last updated
Hyperglycemia
Other namesHigh blood sugar, hyperglycemia, hyperglycæmia
Hyperglycemia.png
Artist's depiction of hyperglycemia. White hexagons in the image represent glucose molecules, which are increased in the lower image.
Specialty Endocrinology

Hyperglycemia or hyperglycaemia is a condition where unusually high amount of glucose is present in blood. It is defined as blood glucose level exceeding 6.9 mmol/L (125 mg/dL) after fasting for 8 hours and 10 mmol/L (180 mg/dL) 2 hours after eating. [1] [2]

Contents

Blood glucose level indication

ConditionBlood glucose level rangeMeasure time
Normalbetween 3.9 mmol/L (70 mg/dL) and 5.6 mmol/L (100 mg/dL) [2] Fasting 8 hours
not exceeding 7.8 mmol/L (140 mg/dL) [2] Postprandrial 2 hours
Relatively highbetween 5.6 mmol/L (100 mg/dL) and 6.9 mmol/L (125 mg/dL) [2] Fasting 8 hours
between 7.8 mmol/L (140 mg/dL) and 10 mmol/L (180 mg/dL) [1] Postprandrial 2 hours
Hyperglycemiaabove 6.9 mmol/L (125 mg/dL) [2] Fasting 8 hours
above 10 mmol/L (180 mg/dL) [1] Postprandrial 2 hours

Postprandial hyperglycemic levels as high as 8.6 mmol/L (155 mg/dL) at 1-h are associated with T2DM-related complications, which worsen as the degree of hyperglycemia increases. [3] [4] [5] [6] Patients with diabetes are oriented to avoid exceeding the recommended postprandial threshold of 160 mg/dL (8.89 mmol/L) for optimal glycemic control. [7] [6] [8] Values of blood glucose higher than 160 mg/dL are classified as ‘very high’ hyperglycemia, [9] a condition in which an excessive amount of glucose (glucotoxicity) circulates in the blood plasma. These values are higher than the renal threshold of 10 mmol/L (180 mg/dL) up to which glucose reabsorption is preserved at physiological rates [3] [10] [11] and insulin therapy is not necessary. [12] [13] Blood glucose values higher than the cutoff level of 11.1 mmol/L (200 mg/dL) are used to diagnose T2DM [14] and strongly associated with metabolic disturbances, [15] although symptoms may not start to become noticeable until even higher values such as 13.9–16.7 mmol/L (~250–300  mg/dL). A subject with a consistent fasting blood glucose range between 5.6–7 mmol/L (~100–126 mg/dL) (American Diabetes Association guidelines) is considered slightly hyperglycemic, and above 7 mmol/L (126 mg/dL) is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average, however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time.

Signs and symptoms

The degree of hyperglycemia can change over time depending on the metabolic cause, for example, impaired glucose tolerance or fasting glucose, and it can depend on treatment. [16] Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal and cause pathological and functional changes for significant periods without producing any permanent effects or symptoms. [16] During this asymptomatic period, an abnormality in carbohydrate metabolism can occur, which can be tested by measuring plasma glucose. [16] Chronic hyperglycemia at above normal levels can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic neuropathy may be a result of long-term hyperglycemia. Impairment of growth and susceptibility to certain infections can occur as a result of chronic hyperglycemia. [16]

Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.[ citation needed ]

The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad: [17]

Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response.[ citation needed ]

Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys, which leads to the presence of glucose in the urine. This produces an osmotic diuresis.[ citation needed ]

Signs and symptoms of diabetic ketoacidosis may include:[ citation needed ]

Hyperglycemia causes a decrease in cognitive performance, specifically in processing speed, executive function, and performance. [20] Decreased cognitive performance may cause forgetfulness and concentration loss. [20]

Complications

In untreated hyperglycemia, a condition called ketoacidosis may develop because decreased insulin levels increase the activity of hormone sensitive lipase. [21] The degradation of triacylglycerides by hormone-sensitive lipase produces free fatty acids that are eventually converted to acetyl-coA by beta-oxidation.[ citation needed ]

Ketoacidosis is a life-threatening condition which requires immediate treatment. Symptoms include: shortness of breath, breath that smells fruity (such as pear drops), nausea and vomiting, and very dry mouth. Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure. [22]

Also, a life-threatening consequence of hyperglycemia can be nonketotic hyperosmolar syndrome. [16]

Perioperative hyperglycemia has been associated with immunosuppression, increased infections, osmotic diuresis, delayed wound healing, delayed gastric emptying, sympatho-adrenergic stimulation, and increased mortality. In addition, it reduces skin graft success, exacerbates brain, spinal cord, and renal damage by ischemia, worsens neurologic outcomes in traumatic head injuries, and is associated with postoperative cognitive dysfunction following CABG. [23]

Furthermore, hyperglycemia has been linked to increased susceptibility to a range of infectious diseases. This susceptibility can be attributed to the impairment of the immune system's response, which is often compromised in hyperglycemic conditions. Hyperglycemia also leads to biochemical changes in the body; both of these factors result in increased severity of respiratory infections and vulnerability to pathogens. [24] Hyperglycemic individuals face the most pronounced risk from such types of ailments, including tuberculosis, the flu, and COVID-19. These risks can be compounded even further by the effects of physiological stress.

Importantly, hyperglycemia affects the function of neutrophils, which are white blood cells responsible for responding to infection. In hyperglycemic individuals, the ability for neutrophils to move towards infection sites, ingest bacteria, and kill them are often impaired, leading to reduced effectiveness in combating infections. [25]

Hyperglycemia also creates microbiological changes within the body: hyperglycemia can lead to rapid changes in blood pH and cell viscosity, weakening the cells and making it more conducive for infectious agents to thrive and dampen inflammatory responses. This is because hyperglycemia impacts a few factors such as microenvironment of immune cells, or even bacteria’s supply of energy, adding on stress to the bacterial proliferation metabolism. [24]

The chronic inflammatory state induced by high glucose levels can also lead to dysfunction in various parts of the immune system. For example, advanced glycation end products (AGEs), which are more prevalent in hyperglycemic conditions, can interfere with the normal function of the immune system and contribute to the pathogenesis of infections. [26] AGEs, whose cross-links are permanent will continue to harm the surrounding tissue until the proteins are destroyed. In addition, they can interact with the RAGE receptor to cause oxidative stress, apoptosis, and inflammation.

Due to neutrophil changes, microbiological changes, and chronic inflammation, patients with hyperglycemia are thus more prone to severe respiratory infections. This increased risk is particularly pronounced with pathogens like Mycobacterium tuberculosis (the bacterium responsible for tuberculosis) and the flu. [27] In recent history, hyperglycemic individuals have also responded more severely to the symptoms of COVID-19. Another example is diabetes. Hyperglycemia and risk of severe infectious outcomes can even further be complicated by physiological stress. For instance, elevated blood glucose levels can actively contribute to pathophysiology of this disease, by exacerbating existing inflammation, impairing cellular immune responses, and increasing oxidative stress, which can also lead to more severe infection. In addition, patients with acute hyperglycemia who don’t have a history of diabetes can experience higher rates of mortality and complications.

Causes

Hyperglycemia may be caused by: diabetes, various (non-diabetic) endocrine disorders (insulin resistance and thyroid, adrenal, pancreatic, and pituitary disorders), sepsis and certain infections, intracranial diseases (e.g. encephalitis, brain tumors (especially if near the pituitary gland), brain haemorrhages, and meningitis) (frequently overlooked), convulsions, end-stage terminal disease, prolonged/major surgeries, [28] stress, [29] and excessive eating of carbohydrates. [30]

Endocrine

Chronic, persistent hyperglycaemia is most often a result of diabetes.[ citation needed ] Several hormones act to increase blood glucose levels and may thus cause hyperglycaemia when present in excess, including: cortisol, catecholamines, growth hormone, glucagon, [31] and thyroid hormones. [32] Hyperglycaemia may thus be seen in: Cushing's syndrome, [33] pheochromocytoma, [34] acromegaly, [35] hyperglucagonemia, [36] and hyperthyroidism. [32]

Diabetes mellitus

Chronic hyperglycemia that persists even in fasting states is most commonly caused by diabetes mellitus. In fact, chronic hyperglycemia is the defining characteristic of the disease. Intermittent hyperglycemia may be present in prediabetic states. Acute episodes of hyperglycemia without an obvious cause may indicate developing diabetes or a predisposition to the disorder.[ citation needed ]

In diabetes mellitus, hyperglycemia is usually caused by low insulin levels (diabetes mellitus type 1) and/or by resistance to insulin at the cellular level (diabetes mellitus type 2), depending on the type and state of the disease. [37] Low insulin levels and/or insulin resistance prevent the body from converting glucose into glycogen (a starch-like source of energy stored mostly in the liver), which in turn makes it difficult or impossible to remove excess glucose from the blood. With normal glucose levels, the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20–30 minutes, and so glucose levels must be precisely maintained by the body's internal control mechanisms. When the mechanisms fail in a way that allows glucose to rise to abnormal levels, hyperglycemia is the result.[ citation needed ]

Ketoacidosis may be the first symptom of immune-mediated diabetes, particularly in children and adolescents. Also, patients with immune-mediated diabetes can change from modest fasting hyperglycemia to severe hyperglycemia and even ketoacidosis as a result of stress or an infection. [16]

Insulin resistance

Obesity has been contributing to increased insulin resistance in the global population. Insulin resistance increases hyperglycemia because the body becomes over saturated by glucose. Insulin resistance desensitizes insulin receptors, preventing insulin from lowering blood sugar levels. [38]

The leading cause of hyperglycemia in type 2 diabetes is the failure of insulin to suppress glucose production by glycolysis and gluconeogenesis due to insulin resistance. [39] Insulin normally inhibits glycogenolysis, but fails to do so in a condition of insulin resistance, resulting in increased glucose production. [40] In the liver, Fox06 normally promotes gluconeogenesis in the fasted state, but insulin blocks Fox06 upon feeding. [41] In a condition of insulin resistance insulin fails to block Fox06, resulting in continued gluconeogenesis even upon feeding. [41]

Medications

Certain medications increase the risk of hyperglycemia, including: corticosteroids, octreotide, beta blockers, epinephrine, thiazide diuretics, statins, niacin, pentamidine, protease inhibitors, L-asparaginase, [42] and antipsychotics. [43] The acute administration of stimulants such as amphetamines typically produces hyperglycemia; chronic use, however, produces hypoglycemia.[ citation needed ]

Thiazides are used to treat type 2 diabetes but it also causes severe hyperglycemia. [16]

Stress

A high proportion of patients with an acute stress such as stroke or myocardial infarction may develop hyperglycemia, even in the absence of a diagnosis of diabetes. (Or perhaps stroke or myocardial infarction was caused by hyperglycemia and undiagnosed diabetes.)[ citation needed ] Human and animal studies suggest that this is not benign, and that stress-induced hyperglycemia is associated with a high risk of mortality after both stroke and myocardial infarction. [44] Somatostatinomas and aldosteronoma-induced hypokalemia can cause hyperglycemia but usually disappears after the removal of the tumour. [16]

Stress causes hyperglycaemia via several mechanisms, including through metabolic and hormonal changes, and via increased proinflammatory cytokines that interrupt carbohydrate metabolism, leading to excessive glucose production and reduced uptake in tissues, can cause hyperglycemia. [45]

Hormones such as the growth hormone, glucagon, cortisol and catecholamines, can cause hyperglycemia when they are present in the body in excess amounts. [16]

Diagnosis

Monitoring

It is critical for patients who monitor glucose levels at home to be aware of which units of measurement their glucose meter uses. Glucose levels are measured in either:[ citation needed ]

  1. Millimoles per liter (mmol/L) is the SI standard unit used in most countries around the world.
  2. Milligrams per deciliter (mg/dL) is used in some countries such as the United States, Japan, France, Egypt and Colombia.

Scientific journals are moving towards using mmol/L; some journals now use mmol/L as the primary unit but quote mg/dL in parentheses. [46]

Glucose levels vary before and after meals, and at various times of day; the definition of "normal" varies among medical professionals. In general, the normal range for most people (fasting adults) is about 4 to 6 mmol/L or 80 to 110 mg/dL. (where 4 mmol/L or 80 mg/dL is "optimal".) A subject with a consistent range above 7 mmol/L or 126 mg/dL is generally held to have hyperglycemia, whereas a consistent range below 4 mmol/L or 70 mg/dL is considered hypoglycemic. In fasting adults, blood plasma glucose should not exceed 7 mmol/L or 126 mg/dL. Sustained higher levels of blood sugar cause damage to the blood vessels and to the organs they supply, leading to the complications of diabetes. [47]

Chronic hyperglycemia can be measured via the HbA1c test. The definition of acute hyperglycemia varies by study, with mmol/L levels from 8 to 15 (mg/dL levels from 144 to 270). [48]

Defects in insulin secretion, insulin action, or both, results in hyperglycemia. [16]

Chronic hyperglycemia can be measured by clinical urine tests which can detect sugar in the urine or microalbuminuria which could be a symptom of diabetes. [49]

Group aerobic exercises Aerobic exercise.jpg
Group aerobic exercises

Treatment

Treatment of hyperglycemia requires elimination of the underlying cause, such as diabetes. Acute hyperglycemia can be treated by direct administration of insulin in most cases and may be lessened by the intake of some natural compounds. For example, a single dose of raw cinnamon before a meal containing complex carbohydrates decreases the postprandial hyperglycemia (higher than 140 mg/dL; >7.8 mmol/L) in patients with type II diabetes. [50] Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification. [51]

Replacing white bread by whole wheat bread may help reduce hyperglycemia. Progressively removing bread and reducing carbohydrates may help even more. Whole wheat options.jpg
Replacing white bread by whole wheat bread may help reduce hyperglycemia. Progressively removing bread and reducing carbohydrates may help even more.

In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as metformin, etc.[ citation needed ]

Those with hyperglycaemia can be treated using sulphonylureas or metformin or both. These drugs help by improving glycaemic control. [52] Dipeptidyl peptidase-4 inhibitor alone or in combination with basal insulin can be used as a treatment for hyperglycemia with patients still in hospital. [45]

Hyperglycemia can also be improved through minor lifestyle changes. Increasing aerobic exercise to at least 30 minutes a day causes the body to make better use of accumulated glucose since the glucose is being converted to energy by the muscles. [53] Calorie monitoring, with restriction as necessary, can reduce over-eating, which contributes to hyperglycemia. [54]

Diets higher in healthy unsaturated fats and whole wheat carbohydrates such as the Mediterranean diet can help reduce carbohydrate intake to better control hyperglycemia. [55] Diets such as intermittent fasting and ketogenic diet help reduce calorie consumption which could significantly reduce hyperglycemia.[ citation needed ]

Carbohydrates are the main cause for hyperglycemia. Non-whole-wheat items should be substituted by whole-wheat items. Although fruits can be nutritious, fruit intake should be limited due to high sugar content. [56]

Epidemiology

Environmental factors

Hyperglycemia is lower in higher income groups since there is access to better education, healthcare and resources. Low-middle income groups are more likely to develop hyperglycemia, due in part to a limited access to education and a reduced availability of healthy food options. [57] Living in warmer climates can reduce hyperglycemia due to increased physical activity while people are less active in colder climates. [58]

Population

Hyperglycemia is one of the main symptoms of diabetes and it has substantially affected the population making it an epidemic due to the population's increased calorie consumption. [59] Healthcare providers are trying to work more closely with people allowing them more freedom with interventions that suit their lifestyle. [60] As physical inactivity and calorie consumption increases it makes individuals more susceptible to developing hyperglycemia. [61] Hyperglycemia is caused by type 1 diabetes and non-whites have a higher susceptibility for it. [62]

Etymology

The origin of the term is Greek: prefix ὑπέρ- hyper- "over-", γλυκός glycos "sweet wine, must", αἷμα haima "blood", -ία, -εια -ia suffix for abstract nouns of feminine gender. [63]

See also

Related Research Articles

<span class="mw-page-title-main">Hypoglycemia</span> Decrease in blood sugar

Hypoglycemia, also spelled hypoglycaemia or hypoglycæmia, sometimes called low blood sugar, is a fall in blood sugar to levels below normal, typically below 70 mg/dL (3.9 mmol/L). Whipple's triad is used to properly identify hypoglycemic episodes. It is defined as blood glucose below 70 mg/dL (3.9 mmol/L), symptoms associated with hypoglycemia, and resolution of symptoms when blood sugar returns to normal. Hypoglycemia may result in headache, tiredness, clumsiness, trouble talking, confusion, fast heart rate, sweating, shakiness, nervousness, hunger, loss of consciousness, seizures, or death. Symptoms typically come on quickly.

<span class="mw-page-title-main">Diabetic ketoacidosis</span> Medical condition

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific "fruity" smell. The onset of symptoms is usually rapid. People without a previous diagnosis of diabetes may develop DKA as the first obvious symptom.

<span class="mw-page-title-main">Glucose tolerance test</span> Medical test of how quickly glucose is cleared from the blood

The glucose tolerance test is a medical test in which glucose is given and blood samples taken afterward to determine how quickly it is cleared from the blood. The test is usually used to test for diabetes, insulin resistance, impaired beta cell function, and sometimes reactive hypoglycemia and acromegaly, or rarer disorders of carbohydrate metabolism. In the most commonly performed version of the test, an oral glucose tolerance test (OGTT), a standard dose of glucose is ingested by mouth and blood levels are checked two hours later. Many variations of the GTT have been devised over the years for various purposes, with different standard doses of glucose, different routes of administration, different intervals and durations of sampling, and various substances measured in addition to blood glucose.

<span class="mw-page-title-main">Type 2 diabetes</span> Form of diabetes mellitus

Type 2 diabetes (T2D), formerly known as adult-onset diabetes, is a form of diabetes mellitus that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. Common symptoms include increased thirst, frequent urination, fatigue and unexplained weight loss. Other symptoms include increased hunger, having a sensation of pins and needles, and sores (wounds) that heal slowly. Symptoms often develop slowly. Long-term complications from high blood sugar include heart disease, stroke, diabetic retinopathy, which can result in blindness, kidney failure, and poor blood flow in the lower-limbs, which may lead to amputations. The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon.

<span class="mw-page-title-main">Blood sugar level</span> Concentration of glucose present in the blood (Glycaemia)

The blood sugar level, blood sugar concentration, blood glucose level, or glycemia is the measure of glucose concentrated in the blood. The body tightly regulates blood glucose levels as a part of metabolic homeostasis.

<span class="mw-page-title-main">Gestational diabetes</span> Exercise and Obesity Management During Pregnancy

Gestational diabetes is a condition in which a woman without diabetes develops high blood sugar levels during pregnancy. Gestational diabetes generally results in few symptoms; however, obesity increases the rate of pre-eclampsia, cesarean sections, and embryo macrosomia, as well as gestational diabetes. Babies born to individuals with poorly treated gestational diabetes are at increased risk of macrosomia, of having hypoglycemia after birth, and of jaundice. If untreated, diabetes can also result in stillbirth. Long term, children are at higher risk of being overweight and of developing type 2 diabetes.

Maturity-onset diabetes of the young (MODY) refers to any of several hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production. Along with neonatal diabetes, MODY is a form of the conditions known as monogenic diabetes. While the more common types of diabetes involve more complex combinations of causes involving multiple genes and environmental factors, each forms of MODY are caused by changes to a single gene (monogenic). HNF1A-MODY are the most common forms.

<span class="mw-page-title-main">Hyperinsulinemia</span> Abnormal increase in insulin in the bloodstream relative to glucose

Hyperinsulinemia is a condition in which there are excess levels of insulin circulating in the blood relative to the level of glucose. While it is often mistaken for diabetes or hyperglycaemia, hyperinsulinemia can result from a variety of metabolic diseases and conditions, as well as non-nutritive sugars in the diet. While hyperinsulinemia is often seen in people with early stage type 2 diabetes mellitus, it is not the cause of the condition and is only one symptom of the disease. Type 1 diabetes only occurs when pancreatic beta-cell function is impaired. Hyperinsulinemia can be seen in a variety of conditions including diabetes mellitus type 2, in neonates and in drug-induced hyperinsulinemia. It can also occur in congenital hyperinsulinism, including nesidioblastosis.

Steroid-induced diabetes is characterized as an unusual rise in blood sugar that is linked to the use of glucocorticoids in a patient who may or may not have had diabetes in the past.

Stress hyperglycemia is a medical term referring to transient elevation of the blood glucose due to the stress of illness. It usually resolves spontaneously, but must be distinguished from various forms of diabetes mellitus.

<span class="mw-page-title-main">Type 1 diabetes</span> Form of diabetes mellitus

Type 1 diabetes (T1D), formerly known as juvenile diabetes, is an autoimmune disease that occurs when pancreatic cells are destroyed by the body's immune system. In healthy persons, beta cells produce insulin. Insulin is a hormone required by the body to store and convert blood sugar into energy. T1D results in high blood sugar levels in the body prior to treatment. Common symptoms include frequent urination, increased thirst, increased hunger, weight loss, and other complications. Additional symptoms may include blurry vision, tiredness, and slow wound healing. While some cases take longer, symptoms usually appear within weeks or a few months.

The main goal of diabetes management is to keep blood glucose (BG) levels as normal as possible. If diabetes is not well controlled, further challenges to health may occur. People with diabetes can measure blood sugar by various methods, such as with a BG meter or a continuous glucose monitor, which monitors over several days. Glucose can also be measured by analysis of a routine blood sample. Usually, people are recommended to control diet, exercise, and maintain a healthy weight, although some people may need medications to control their blood sugar levels. Other goals of diabetes management are to prevent or treat complications that can result from the disease itself and from its treatment.

<span class="mw-page-title-main">Diabetes and pregnancy</span> Effects of pre-existing diabetes upon pregnancy

For pregnant women with diabetes, some particular challenges exist for both mother and fetus. If the pregnant woman has diabetes as a pre-existing disorder, it can cause early labor, birth defects, and larger than average infants. Therefore, experts advise diabetics to maintain blood sugar level close to normal range about 3 months before planning for pregnancy.

Hyperosmolar hyperglycemic state (HHS), also known as hyperosmolar non-ketotic state (HONK), is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Symptoms include signs of dehydration, weakness, leg cramps, vision problems, and an altered level of consciousness. Onset is typically over days to weeks. Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.

<span class="mw-page-title-main">Impaired fasting glucose</span> Medical condition

Impaired fasting glucose is a type of prediabetes, in which a person's blood sugar levels during fasting are consistently above the normal range, but below the diagnostic cut-off for a formal diagnosis of diabetes mellitus. Together with impaired glucose tolerance, it is a sign of insulin resistance. In this manner, it is also one of the conditions associated with metabolic syndrome.

Chronic Somogyi rebound is a contested explanation of phenomena of elevated blood sugars experienced by diabetics in the morning. Also called the Somogyi effect and posthypoglycemic hyperglycemia, it is a rebounding high blood sugar that is a response to low blood sugar. When managing the blood glucose level with insulin injections, this effect is counter-intuitive to people who experience high blood sugar in the morning as a result of an overabundance of insulin at night.

<span class="mw-page-title-main">Prediabetes</span> Predisease state of hyperglycemia with high risk for diabetes

Prediabetes is a component of metabolic syndrome and is characterized by elevated blood sugar levels that fall below the threshold to diagnose diabetes mellitus. It usually does not cause symptoms but people with prediabetes often have obesity, dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertension. It is also associated with increased risk for cardiovascular disease (CVD). Prediabetes is more accurately considered an early stage of diabetes as health complications associated with type 2 diabetes often occur before the diagnosis of diabetes.

The dawn phenomenon, sometimes called the dawn effect, is an observed increase in blood sugar (glucose) levels that takes place in the early-morning, often between 2 a.m. and 8 a.m. First described by Schmidt in 1981 as an increase of blood glucose or insulin demand occurring at dawn, this naturally occurring phenomenon is frequently seen among the general population and is clinically relevant for patients with diabetes as it can affect their medical management. In contrast to Chronic Somogyi rebound, the dawn phenomenon is not associated with nocturnal hypoglycemia.

Complications of diabetes are secondary diseases that are a result of elevated blood glucose levels that occur in diabetic patients. These complications can be divided into two types: acute and chronic. Acute complications are complications that develop rapidly and can be exemplified as diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), lactic acidosis (LA), and hypoglycemia. Chronic complications develop over time and are generally classified in two categories: microvascular and macrovascular. Microvascular complications include neuropathy, nephropathy, and retinopathy; while cardiovascular disease, stroke, and peripheral vascular disease are included in the macrovascular complications.

<span class="mw-page-title-main">Diabetes</span> Group of endocrine diseases characterized by high blood sugar levels

Diabetes mellitus, often known simply as diabetes, is a group of common endocrine diseases characterized by sustained high blood sugar levels. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body becoming unresponsive to the hormone's effects. Classic symptoms include polydipsia, polyuria, weight loss, and blurred vision. If left untreated, the disease can lead to various health complications, including disorders of the cardiovascular system, eye, kidney, and nerves. Diabetes accounts for approximately 4.2 million deaths every year, with an estimated 1.5 million caused by either untreated or poorly treated diabetes.

References

  1. 1 2 3 Mouri, MIchelle; Badireddy, Madhu (2024), "Hyperglycemia", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   28613650 , retrieved 2024-12-15
  2. 1 2 3 4 5 "Mean fasting blood glucose". World Healt Organization. Retrieved 2024-12-15.{{cite web}}: CS1 maint: url-status (link)
  3. 1 2 Bergman, Michael; Abdul-Ghani, Muhammad; DeFronzo, Ralph A.; Manco, Melania; Sesti, Giorgio; Fiorentino, Teresa Vanessa; Ceriello, Antonio; Rhee, Mary; Phillips, Lawrence S.; Chung, Stephanie; Cravalho, Celeste; Jagannathan, Ram; Monnier, Louis; Colette, Claude; Owens, David (July 2020). "Review of methods for detecting glycemic disorders". Diabetes Research and Clinical Practice. 165: 108233. doi:10.1016/j.diabres.2020.108233. PMC   7977482 . PMID   32497744.
  4. ↑ Bergman, Michael; Manco, Melania; Sesti, Giorgio; Dankner, Rachel; Pareek, Manan; Jagannathan, Ram; Chetrit, Angela; Abdul-Ghani, Muhammad; Buysschaert, Martin; Olsen, Michael H.; Nilsson, Peter M.; Medina, José Luis; Roth, Jesse; Groop, Leif; del Prato, Stefano (December 2018). "Petition to replace current OGTT criteria for diagnosing prediabetes with the 1-hour post-load plasma glucose ≥ 155 mg/dl (8.6 mmol/L)". Diabetes Research and Clinical Practice. 146: 18–33. doi:10.1016/j.diabres.2018.09.017. PMID   30273707.
  5. ↑ Bergman, Michael (2021-09-07). "The 1-Hour Plasma Glucose: Common Link Across the Glycemic Spectrum". Frontiers in Endocrinology. 12. doi: 10.3389/fendo.2021.752329 . ISSN   1664-2392. PMC   8453142 . PMID   34557166.
  6. 1 2 Chawla, Rajeev; Mukherjee, Jagat Jyoti; Chawla, Manoj; Kanungo, Alok; Shunmugavelu, Meenakshi Sundaram; Das, Ashok Kumar (2021-05-28). "Expert Group Recommendations on the Effective Use of Bolus Insulin in the Management of Type 2 Diabetes Mellitus". Medical Sciences. 9 (2): 38. doi: 10.3390/medsci9020038 . ISSN   2076-3271. PMC   8162981 . PMID   34071359.
  7. ↑ Brand-Miller, Jennie C; Stockmann, Karola; Atkinson, Fiona; Petocz, Peter; Denyer, Gareth (January 2009). "Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1000 foods". The American Journal of Clinical Nutrition. 89 (1): 97–105. doi:10.3945/ajcn.2008.26354. PMID   19056599.
  8. ↑ Alyass, Akram; Almgren, Peter; Akerlund, Mikael; Dushoff, Jonathan; Isomaa, Bo; Nilsson, Peter; Tuomi, Tiinamaija; Lyssenko, Valeriya; Groop, Leif; Meyre, David (January 2015). "Modelling of OGTT curve identifies 1 h plasma glucose level as a strong predictor of incident type 2 diabetes: results from two prospective cohorts". Diabetologia. 58 (1): 87–97. doi:10.1007/s00125-014-3390-x. ISSN   0012-186X. PMID   25292440.
  9. ↑ Biradar, Rajeshwari A.; Singh, Dharmendra P.; Thakur, Harshad; Halli, Shiva S. (July 2020). "Gender differences in the risk factors for high and very high blood glucose levels: A study of Kerala". Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 14 (4): 627–636. doi:10.1016/j.dsx.2020.05.001. PMID   32422447.
  10. ↑ Cui, Shan-Shan; Duan, Li-Jun; Li, Jun-Feng; Qin, Yong-Zhang; Bao, Su-Qing; Jiang, Xia (November 2021). "The Factors Influencing the Renal Glucose Threshold in Patients with Newly Diagnosed Type 2 Diabetes Mellitus". Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 14: 4497–4503. doi: 10.2147/DMSO.S336791 . ISSN   1178-7007. PMC   8590450 . PMID   34785919.
  11. ↑ Hieshima, Kunio; Sugiyama, Seigo; Yoshida, Akira; Kurinami, Noboru; Suzuki, Tomoko; Ijima, Hiroko; Miyamoto, Fumio; Kajiwara, Keizo; Jinnouchi, Katsunori; Jinnouchi, Tomio; Jinnouchi, Hideaki (May 2020). "Elevation of the renal threshold for glucose is associated with insulin resistance and higher glycated hemoglobin levels". Journal of Diabetes Investigation. 11 (3): 617–625. doi:10.1111/jdi.13191. ISSN   2040-1116. PMC   7232275 . PMID   31770476.
  12. ↑ American Diabetes Association Professional Practice Committee (2022-01-01). "6. Glycemic Targets: Standards of Medical Care in Diabetes—2022". Diabetes Care. 45 (Supplement_1): S83–S96. doi:10.2337/dc22-S006. ISSN   0149-5992. PMID   34964868.
  13. ↑ American Diabetes Association (2022-01-01). "Standards of Medical Care in Diabetes—2022 Abridged for Primary Care Providers". Clinical Diabetes. 40 (1): 10–38. doi:10.2337/cd22-as01. ISSN   0891-8929. PMC   8865785 . PMID   35221470.
  14. ↑ Gyberg, Viveca; De Bacquer, Dirk; Kotseva, Kornelia; De Backer, Guy; Schnell, Oliver; Tuomilehto, Jaakko; Wood, David; Rydén, Lars (December 2016). "Time-saving screening for diabetes in patients with coronary artery disease: a report from EUROASPIRE IV". BMJ Open. 6 (12): e013835. doi:10.1136/bmjopen-2016-013835. ISSN   2044-6055. PMC   5168687 . PMID   27932342.
  15. ↑ Selvin, Elizabeth; Rawlings, Andreea; Lutsey, Pamela; Maruthur, Nisa; Pankow, James S.; Steffes, Michael; Coresh, Josef (2016-01-01). "Association of 1,5-Anhydroglucitol With Cardiovascular Disease and Mortality". Diabetes. 65 (1): 201–208. doi:10.2337/db15-0607. ISSN   0012-1797. PMC   4686946 . PMID   26395741.
  16. 1 2 3 4 5 6 7 8 9 10 American Diabetes Association (2014). "Diagnosis and Classification of Diabetes Mellitus". Diabetes Care. 37: S81–S90. doi: 10.2337/dc14-s081 . PMID   24357215.
  17. ↑ James, Norman (30 March 2019). "Hyperglycemia Symptoms". EndocrineWeb. Retrieved 24 December 2022.
  18. ↑ Pais I, Hallschmid M, Jauch-Chara K, et al. (2007). "Mood and cognitive functions during acute euglycaemia and mild hyperglycaemia in type 2 diabetic patients". Exp. Clin. Endocrinol. Diabetes. 115 (1): 42–46. doi:10.1055/s-2007-957348. PMID   17286234.
  19. ↑ Sommerfield AJ, Deary IJ, Frier BM (2004). "Acute hyperglycemia alters mood state and impairs cognitive performance in people with type 2 diabetes". Diabetes Care. 27 (10): 2335–40. doi: 10.2337/diacare.27.10.2335 . PMID   15451897.
  20. 1 2 Geijselaers, Stefan L.C.; Sep, Simone J.S.; Claessens, Danny; Schram, Miranda T.; Van Boxtel, Martin P.J.; Henry, Ronald M.A.; Verhey, Frans R.J.; Kroon, Abraham A.; Dagnelie, Pieter C.; Schalkwijk, Casper G.; Van Der Kallen, Carla J.H.; Biessels, Geert Jan; Stehouwer, Coen D.A. (2017). "The Role of Hyperglycemia, Insulin Resistance, and Blood Pressure in Diabetes-Associated Differences in Cognitive Performance—The Maastricht Study". Diabetes Care. 40 (11): 1537–1547. doi: 10.2337/dc17-0330 . PMID   28842522.
  21. ↑ Kraemer, Fredric B.; Shen, Wen-Jun (2002). "Hormone-sensitive lipase". Journal of Lipid Research. 43 (10): 1585–1594. doi: 10.1194/jlr.R200009-JLR200 . ISSN   0022-2275. PMID   12364542.
  22. ↑ "Chronic hyperglycemia may lead to cardiac damage". Journal of the American College of Cardiology. 2012-02-03. Archived from the original on 2013-12-27. Retrieved 3 February 2012.
  23. ↑ Miller, Miller's Anesthesia, 7th edition, pp. 1716, 2674, 2809.
  24. 1 2 Chávez-Reyes, Jesús; Escárcega-González, Carlos E.; Chavira-Suárez, Erika; León-Buitimea, Angel; Vázquez-León, Priscila; Morones-Ramírez, José R.; Villalón, Carlos M.; Quintanar-Stephano, Andrés; Marichal-Cancino, Bruno A. (2021). "Susceptibility for Some Infectious Diseases in Patients With Diabetes: The Key Role of Glycemia". Frontiers in Public Health. 9. doi: 10.3389/fpubh.2021.559595 . ISSN   2296-2565. PMC   7921169 . PMID   33665182.
  25. ↑ Ngo, Minh Dao; Bartlett, Stacey; Ronacher, Katharina (November 2021). "Diabetes-Associated Susceptibility to Tuberculosis: Contribution of Hyperglycemia vs. Dyslipidemia". Microorganisms. 9 (11): 2282. doi: 10.3390/microorganisms9112282 . ISSN   2076-2607. PMC   8620310 . PMID   34835407.
  26. ↑ CDC (2023-07-31). "Diabetes and Your Immune System". Centers for Disease Control and Prevention. Retrieved 2024-05-06.
  27. ↑ Baccouch, Mahboub (2021-02-17), "A Brief Summary of the Finite Element Method for Differential Equations", Finite Element Methods and Their Applications, IntechOpen, ISBN   978-1-83962-342-4 , retrieved 2024-05-06
  28. ↑ Duncan AE (2012). "Hyperglycemia and Perioperative Glucose Management". Current Pharmaceutical Design. 18 (38): 6195–6203. doi:10.2174/138161212803832236. PMC   3641560 . PMID   22762467.
  29. ↑ "Hyperglycemia in diabetes-Hyperglycemia in diabetes - Symptoms & causes". Mayo Clinic. Retrieved 2024-04-06.
  30. ↑ "Hyperglycemia: Symptoms, Causes, and Treatments". Yale Medicine. Retrieved 2024-04-06.
  31. ↑ Umpierrez, Guillermo E.; Pasquel, Francisco J. (April 2017). "Management of Inpatient Hyperglycemia and Diabetes in Older Adults". Diabetes Care. 40 (4): 509–517. doi:10.2337/dc16-0989. ISSN   0149-5992. PMC   5864102 . PMID   28325798.
  32. 1 2 Hage, Mirella; Zantout, Mira S.; Azar, Sami T. (2011-07-12). "Thyroid Disorders and Diabetes Mellitus". Journal of Thyroid Research. 2011: 439463. doi: 10.4061/2011/439463 . ISSN   2042-0072. PMC   3139205 . PMID   21785689.
  33. ↑ Scaroni, Carla; Zilio, Marialuisa; Foti, Michelangelo; Boscaro, Marco (2017-06-01). "Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management". Endocrine Reviews. 38 (3): 189–219. doi: 10.1210/er.2016-1105 . ISSN   0163-769X. PMID   28368467. S2CID   3985558.
  34. ↑ Mubarik, Ateeq; Aeddula, Narothama R. (2020), "Chromaffin Cell Cancer", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   30570981, archived from the original on 2022-01-26, retrieved 2020-11-22
  35. ↑ Oxford desk reference. Endocrinology. Turner, Helen E., 1967-, Eastell, R. (Richard), Grossman, Ashley (First ed.). Oxford. 2018. ISBN   978-0-19-967283-7. OCLC   1016052167. Archived from the original on 2022-01-26. Retrieved 2020-11-22.{{cite book}}: CS1 maint: location missing publisher (link) CS1 maint: others (link)
  36. ↑ Wewer Albrechtsen, Nicolai J.; Kuhre, Rune E.; Pedersen, Jens; Knop, Filip K.; Holst, Jens J. (November 2016). "The biology of glucagon and the consequences of hyperglucagonemia". Biomarkers in Medicine. 10 (11): 1141–1151. doi: 10.2217/bmm-2016-0090 . ISSN   1752-0371. PMID   27611762.
  37. ↑ "Hyperglycemia in diabetes". Mayo Clinic. Archived from the original on 26 January 2022. Retrieved 22 Sep 2020.
  38. ↑ Kim, J. Y.; Bacha, F.; Tfayli, H.; Michaliszyn, S. F.; Yousuf, S.; Arslanian, S. (2019). "Adipose Tissue Insulin Resistance in Youth on the Spectrum From Normal Weight to Obese and From Normal Glucose Tolerance to Impaired Glucose Tolerance to Type 2 Diabetes". Diabetes Care. 42 (2): 265–272. doi:10.2337/dc18-1178. PMC   6341282 . PMID   30455334.
  39. ↑ Swe MT, Pongchaidecha A, Chatsudthipong V, Chattipakorn N, Lungkaphin A (2019). "Molecular signaling mechanisms of renal gluconeogenesis in nondiabetic and diabetic conditions". Journal of Cellular Physiology . 234 (6): 8134–8151. doi:10.1002/jcp.27598. PMID   30370538. S2CID   53097552.
  40. ↑ Sargsyan A, Herman MA (2019). "Regulation of Glucose Production in the Pathogenesis of Type 2 Diabetes". Current Diabetes Reports . 19 (9): 77. doi:10.1007/s11892-019-1195-5. PMC   6834297 . PMID   31377934.
  41. 1 2 Lee S, Dong HH (2017). "FoxO integration of insulin signaling with glucose and lipid metabolism". Journal of Endocrinology . 233 (2): R67–R79. doi:10.1530/JOE-17-0002. PMC   5480241 . PMID   28213398.
  42. ↑ Cetin M, Yetgin S, Kara A, et al. (1994). "Hyperglycemia, ketoacidosis and other complications of L-asparaginase in children with acute lymphoblastic leukemia". J Med. 25 (3–4): 219–29. PMID   7996065.
  43. ↑ Luna B, Feinglos MN (2001). "Drug-induced hyperglycemia". JAMA. 286 (16): 1945–48. doi:10.1001/jama.286.16.1945. PMID   11667913.
  44. ↑ Capes SE, Hunt D, Malmberg K, Pathak P, Gerstein HC (2001). "Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview". Stroke. 32 (10): 2426–32. doi: 10.1161/hs1001.096194 . PMID   11588337.
  45. 1 2 Umpierrez, Guillermo E.; Pasquel, Francisco J. (2017). "Management of Inpatient Hyperglycemia and Diabetes in Older Adults". Diabetes Care. 40 (4): 509–517. doi:10.2337/dc16-0989. PMC   5864102 . PMID   28325798.
  46. ↑ "diabetes FAQ: general (part 1 of 5)Section - What are mg/dL and mmol/L? How to convert? Glucose? Cholesterol?". www.faqs.org. Archived from the original on 2018-08-28. Retrieved 2007-02-10.
  47. ↑ Total Health Life (2005). "High Blood Sugar". Total Health Institute. Archived from the original on August 17, 2013. Retrieved May 4, 2011.
  48. ↑ Giugliano D, Marfella R, Coppola L, et al. (1997). "Vascular effects of acute hyperglycemia in humans are reversed by L-arginine. Evidence for reduced availability of nitric oxide during hyperglycemia". Circulation. 95 (7): 1783–90. doi:10.1161/01.CIR.95.7.1783. PMID   9107164.
  49. ↑ Florvall, Gösta; Basu, Samar; Helmersson, Johanna; Larsson, Anders (2006). "Hemocue Urine Albumin Point-Of-Care Test Shows Strong Agreement With the Results Obtained With a Large Nephelometer". Diabetes Care. 29 (2): 422–423. doi: 10.2337/diacare.29.02.06.dc05-1080 . PMID   16443900. Archived from the original on 2019-12-06. Retrieved 2019-12-06.
  50. ↑ Moreira, Fernanda Duarte; Reis, Caio Eduardo Gonçalves; Gallassi, Andrea Donatti; Moreira, Daniel Carneiro; Welker, Alexis Fonseca (2024-10-09). Dardari, Dured (ed.). "Suppression of the postprandial hyperglycemia in patients with type 2 diabetes by a raw medicinal herb powder is weakened when consumed in ordinary hard gelatin capsules: A randomized crossover clinical trial". PLOS ONE. 19 (10): e0311501. doi: 10.1371/journal.pone.0311501 . ISSN   1932-6203. PMC   11463819 . PMID   39383145.
  51. ↑ Ron Walls; John J. Ratey; Robert I. Simon (2009). Rosen's Emergency Medicine: Expert Consult Premium Edition – Enhanced Online Features and Print (Rosen's Emergency Medicine: Concepts & Clinical Practice (2v.)). St. Louis: Mosby. ISBN   978-0-323-05472-0.
  52. ↑ Pearson, Ewan R.; Starkey, Bryan J.; Powell, Roy J.; Gribble, Fiona M.; Clark, Penny M.; Hattersley, Andrew T. (2003). "Genetic cause of hyperglycaemia and response to treatment in diabetes". The Lancet. 362 (9392): 1275–1281. doi:10.1016/s0140-6736(03)14571-0. PMID   14575972. S2CID   34914098.
  53. ↑ Aronson, Ronnie; Brown, Ruth E; Li, Aihua; Riddell, Michael C (2019). "Optimal Insulin Correction Factor in Post–High-Intensity Exercise Hyperglycemia in Adults With Type 1 Diabetes: The FIT Study". Diabetes Care. 42 (1): 10–16. doi: 10.2337/dc18-1475 . PMID   30455336. Archived from the original on 2019-12-06. Retrieved 2019-12-06.
  54. ↑ "High Blood sugar". Total health institute. 2005. Archived from the original on 2013-08-17.
  55. ↑ Mattei, Josiemer; Bigornia, Sherman J; Sotos-Prieto, Mercedes; Scott, Tammy; Gao, Xiang; Tucker, Katherine L (2019). "The Mediterranean Diet and 2-Year Change in Cognitive Function by Status of Type 2 Diabetes and Glycemic Control". Diabetes Care. 42 (8): 1372–1379. doi:10.2337/dc19-0130. PMC   6647047 . PMID   31123154.
  56. ↑ "Dietary Guidelines 2015-2020". US Department of Health. 2015. Archived from the original on 2020-01-07. Retrieved 2019-12-06.
  57. ↑ Ma, Ronald CW; Popkin, Barry M (2017). "Intergenerational diabetes and obesity—A cycle to break?". PLOS ONE. 14 (10): e1002415. doi: 10.1371/journal.pmed.1002415 . PMC   5663330 . PMID   29088227.
  58. ↑ Ishii, Hajime; Suzuki, Hodaka; Baba, Tsuneharu; Nakamura, Keiko; Watanabe, Tsuyoshi (2001). "Seasonal Variation of Glycemic Control in Type 2 Diabetic Patients". Diabetes Care. 24 (8): 1503. doi: 10.2337/diacare.24.8.1503 . PMID   11473100. Archived from the original on 2019-12-06. Retrieved 2019-12-06.
  59. ↑ American Diabetes Association (2019). "Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2019" (PDF). Diabetes Care. 42 (Suppl 1): S13–S28. doi: 10.2337/dc19-S002 . PMID   30559228. S2CID   56176183. Archived from the original on 2022-01-26. Retrieved 2019-12-06.
  60. ↑ Inzucchi, Silvio E; Bergenstal, Richard M; Buse, John B; Diamant, Michaela; Ferrannini, Ele; Nauck, Michael; Peters, Anne L; Tsapas, Apostolos; Wender, Richard; Matthews, David R (2012). "Management of Hyperglycemia in Type 2 Diabetes: A Patient-Centered Approach". Diabetes Care. 35 (6): 1364–1370. doi:10.2337/dc12-0413. PMC   3357214 . PMID   22517736.
  61. ↑ Lee IM, Shiroma EJ, Lobelo F, Puska P, Blair SN, Katzmarzyk PT (2012). "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". Lancet. 380 (9838): 219–229. doi:10.1016/S0140-6736(12)61031-9. PMC   3645500 . PMID   22818936.
  62. ↑ Gujral, U. P.; Narayan KMV (2019). "Diabetes in Normal-Weight Individuals: High Susceptibility in Nonwhite Populations". Diabetes Care. 42 (12): 2164–2166. doi: 10.2337/dci19-0046 . PMC   6868465 . PMID   31748211.
  63. ↑ "hyperglycemia", Wiktionary, the free dictionary, 2024-08-19, retrieved 2024-12-15
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.