Hyperglycemia (also spelled hyperglycaemia or hyperglycæmia), is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/l (200 mg/dl), but symptoms may not start to become noticeable until even higher values such as 15–20 mmol/l (~250–300 mg/dl). A subject with a consistent range between ~5.6 and ~7 mmol/l (100–126 mg/dl) (American Diabetes Association guidelines) is considered slightly hyperglycemic, while 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.
|Other names||High blood sugar|
|White hexagons in the image represent glucose molecules, which are increased in the lower image.|
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. 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.  During this asymptomatic period, an abnormality in carbohydrate metabolism can occur which can be tested by measuring plasma glucose.  However, 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 infection can occur as a result of chronic hyperglycemia.
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.
The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad:
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.
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.
Signs and symptoms of diabetic ketoacidosis may include:
Hyperglycemia causes a decrease in cognitive performance, specifically in processing speed, executive function, and performance. Decreased cognitive performance may cause forgetfulness and concentration loss.
In untreated hyperglycemia, a condition called ketoacidosis may develop because decreased insulin levels increase the activity of hormone sensitive lipase. The degradation of triacylglycerides by hormone-sensitive lipase produces free fatty acids that are eventually converted to acetyl-coA by beta-oxidation.
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.
Also, life-threatening consequences of hyperglycemia is nonketotic hyperosmolar syndrome.
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.
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.
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. 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.
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. 
Certain medications increase the risk of hyperglycemia, including corticosteroids, octreotide, beta blockers, epinephrine, thiazide diuretics, statins, niacin, pentamidine, protease inhibitors, L-asparaginase, and antipsychotics. The acute administration of stimulants such as amphetamines typically produces hyperglycemia; chronic use, however, produces hypoglycemia. Some of the newer psychiatric medications, such as Zyprexa (Olanzapine) and Cymbalta (Duloxetine), can also cause significant hyperglycemia.
Thiazides are used to treat type 2 diabetes but it also causes severe hyperglycemia. 
A high proportion of patients suffering 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.) 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.
Somatostatinomas and aldosteronoma-induced hypokalemia can cause hyperglycemia but usually disappears after the removal of the tumour. 
The following conditions can also cause hyperglycemia in the absence of diabetes. 1) Dysfunction of the thyroid, adrenal, and pituitary glands 2) Numerous diseases of the pancreas 3) Severe increases in blood glucose may be seen in sepsis and certain infections 4) Intracranial diseases (frequently overlooked) can also cause hyperglycemia. Encephalitis, brain tumors (especially those located near the pituitary gland), brain bleeds, and meningitis are prime examples. 5) Mild to high blood sugar levels are often seen in convulsions and terminal stages of many diseases. Prolonged, major surgeries can temporarily increase glucose levels. Certain forms of severe stress and physical trauma can increase levels for a brief time as well yet rarely exceeds 6.6 mmol/l (120 mg/dl).
Hormones such as the growth hormone, glucagon, cortisol and catecholamines, can cause hyperglycemia when they are present in the body in excess amounts.  Also, increased proinflammatory cytokines that interrupt carbohydrate metabolism, leading to excessive glucose production and reduced uptake in tissues, can cause hyperglycemia. 
It is critical for patients who monitor glucose levels at home to be aware of which units of measurement their testing kit uses. Glucose levels are measured in either:
Scientific journals are moving towards using mmol/l; some journals now use mmol/l as the primary unit but quote mg/dl in parentheses.
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.
Defects in insulin secretion, insulin action, or both, results in hyperglycemia. 
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. Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification.
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.
Those with hyperglycaemia can be treated using sulphonylureas or metformin or both. These drugs help by improving glycaemic control. Dipeptidyl peptidase 4 inhibitor alone or in combination with basal insulin can be used as a treatment for hyperglycemia with patients still in hospital. 
The blood sugar level, blood sugar concentration, or blood glucose level is the concentration of glucose present in the blood of humans and other animals. Glucose is a simple sugar and approximately 4 grams of glucose are present in the blood of a 70-kilogram (150 lb) human at all times. The body tightly regulates blood glucose levels as a part of metabolic homeostasis. Glucose is stored in skeletal muscle and liver cells in the form of glycogen; in fasted individuals, blood glucose is maintained at a constant level at the expense of glycogen stores in the liver and skeletal muscle.In humans, a blood glucose level of four grams, or about a teaspoon, is critical for normal function in a number of tissues, and the human brain consumes approximately 60% of blood glucose in fasted, sedentary individuals. A persistent elevation in blood glucose leads to glucose toxicity, which contributes to cell dysfunction and the pathology grouped together as complications of diabetes. Glucose can be transported from the intestines or liver to other tissues in the body via the bloodstream. Cellular glucose uptake is primarily regulated by insulin, a hormone produced in the pancreas.Glucose levels are usually lowest in the morning, before the first meal of the day, and rise after meals for an hour or two by a few millimoles.
Blood sugar levels outside the normal range may be an indicator of a medical condition. A persistently high level is referred to as hyperglycemia; low levels are referred to as hypoglycemia. Diabetes mellitus is characterized by persistent hyperglycemia from any of several causes, and is the most prominent disease related to failure of blood sugar regulation. There are different methods of testing and measuring blood sugar levels.
The intake of alcohol causes an initial surge in blood sugar, and later tends to cause levels to fall. Also, certain drugs can increase or decrease glucose levels.Chronic Somogyi rebound
Chronic Somogyi rebound is a contested explanation of phenomena of elevated blood sugars 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.
This theoretical phenomenon was named after Michael Somogyi, a Hungarian-born professor of biochemistry at the Washington University and Jewish Hospital of St. Louis, who prepared the first insulin treatment given to a child with diabetes in the USA in October 1922. Somogyi showed that excessive insulin makes diabetes unstable and first published his findings in 1938.Compare with the dawn phenomenon, which is a morning rise in blood sugar in response to waning insulin and a growth hormone surge (that further antagonizes insulin).Clarke Error Grid
The Clarke Error Grid Analysis (EGA) was developed in 1987 to quantify clinical accuracy of patient estimates of their current blood glucose as compared to the blood glucose value obtained in their meter. It was then used to quantify the clinical accuracy of blood glucose estimates generated by meters as compared to a reference value. A description of the EGA appeared in Diabetes Care in 1987. Eventually, the EGA became accepted as one of the “gold standards” for determining the accuracy of blood glucose meters.
The grid breaks down a scatterplot of a reference glucose meter and an evaluated glucose meter into five regions:
Region A are those values within 20% of the reference sensor,
Region B contains points that are outside of 20% but would not lead to inappropriate treatment,
Region C are those points leading to unnecessary treatment,
Region D are those points indicating a potentially dangerous failure to detect hypoglycemia or hyperglycemia, and
Region E are those points that would confuse treatment of hypoglycemia for hyperglycemia and vice versa.Complications of diabetes mellitus
The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels. Acute complications include hypoglycemia and hyperglycemia, diabetic coma and nonketotic hyperosmolar coma.
Chronic complications occur due to a mix of microangiopathy, macrovascular disease and immune dysfunction in the form of autoimmune disease or poor immune response, most of which are difficult to manage. Microangiopathy can affect all vital organs, kidneys, heart and brain, as well as eyes, nerves, lungs and locally gums and feet. Macrovascular problems can lead to cardiovascular disease including erectile dysfunction. Female infertility may be due to endocrine dysfunction with impaired signalling on a molecular level.
Other health problems compound the chronic complications of diabetes such as smoking, obesity, high blood pressure, elevated cholesterol levels, and lack of regular exercise which are accessible to management as they are modifiable. Non-modifiable risk factors of diabetic complications are type of diabetes, age of onset, and genetic factors, both protective and predisposing have been found.
Complications of diabetes mellitus are acute and chronic. Risk factors for them can be modifiable or not modifiable.
Overall, complications are far less common and less severe in people with well-controlled blood sugar levels. However, (non-modifiable) risk factors such as age at diabetes onset, type of diabetes, gender and genetics play a role. Some genes appear to provide protection against diabetic complications, as seen in a subset of long-term diabetes type 1 survivors without complications.Glucose test
Many types of glucose tests exist and they can be used to estimate blood sugar levels at a given time or, over a longer period of time, to obtain average levels or to see how fast body is able to normalize changed glucose levels. Eating food for example leads to elevated blood sugar levels. In healthy people these levels quickly return to normal via increased cellular glucose uptake which is primarily mediated by increase in blood insulin levels.
Glucose tests can reveal temporary/long-term hyperglycemia or hypoglycemia. These conditions may not have obvious symptoms and can damage organs in the long-term. Abnormally high/low levels, slow return to normal levels from either of these conditions and/or inability to normalize blood sugar levels means that the person being tested probably has some kind of medical condition like type 2 diabetes which is caused by cellular insensitivity to insulin. Glucose tests are thus often used to diagnose such conditions.Glycogen storage disease type 0
Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). Although glycogen synthase deficiency does not result in storage of extra glycogen in the liver, it is often classified as a glycogen storage disease because it is another defect of glycogen storage and can cause similar problems. There are two isoforms (types) of glycogen synthase enzyme; GSY1 in muscle and GSY2 in liver, each with a corresponding form of the disease. Mutations in the liver isoform (GSY2), causes fasting hypoglycemia, high blood ketones, increased free fatty acids and low levels of alanine and lactate. Conversely, feeding in these patients results in hyperglycemia and hyperlactatemia.Hemiballismus
Hemiballismus or hemiballism in its unilateral form is a very rare movement disorder. It is a type of chorea caused in most cases by a decrease in activity of the subthalamic nucleus of the basal ganglia, resulting in the appearance of flailing, ballistic, undesired movements of the limbs. It can also appear rarely due to certain metabolic abnormalities. It is a rare movement disorder, being 500 times rarer than Parkinson's disease. Hemiballismus can cause significant disability. Symptoms can decrease during sleep.Hyperosmolar hyperglycemic state
Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Symptoms include signs of dehydration, weakness, legs 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.The main risk factor is a history of diabetes mellitus type 2. Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1. Triggers include infections, stroke, trauma, certain medications, and heart attacks. Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.Initial treatment generally consists of intravenous fluids to manage dehydration, intravenous insulin in those with significant ketones, low molecular weight heparin to decrease the risk of blood clotting, and antibiotics among those in whom there is concerns of infection. The goal is a slow decline in blood sugar levels. Potassium replacement is often required as the metabolic problems are corrected. Efforts to prevent diabetic foot ulcers are also important. It typically takes a few days for the person to return to baseline.While the exact frequency of the condition is unknown, it is relatively common. Older people are most commonly affected. The risk of death among those affected is about 15%. It was first described in the 1880s.Insulin glulisine
Insulin glulisine is a rapid-acting insulin analogue that differs from human insulin in that the amino acid asparagine at position B3 is replaced by lysine and the lysine in position B29 is replaced by glutamic acid. It was developed by Sanofi-Aventis and is sold under the trade name Apidra. When injected subcutaneously, it appears in the blood earlier than human insulin. When used as a meal time insulin, the dose is to be administered within 15 minutes before or 20 minutes after starting a meal. Intravenous injections may also be used for extreme hyperglycemia, but must be performed under the supervision of a medical professional.MODY 1
MODY 1 is a form of maturity onset diabetes of the young.
MODY 1 is due to a loss-of-function mutation in the HNF4A gene on chromosome 12. This gene codes for HNF4-α protein also known as transcription factor 14 (TCF14). HNF4α controls function of HNF1α (see MODY 3; HNF1A) and perhaps HNF1β (MODY 5) as well. This transcription network plays a role in the early development of the pancreas, liver, and intestines. In the pancreas these genes influence expression of, among others, the genes for insulin, the principal glucose transporter (GLUT2), and several proteins involved in glucose and mitochondrial metabolism.
Although pancreatic beta cells produce adequate insulin in infancy, the capacity for insulin production declines thereafter. Diabetes (persistent hyperglycemia) typically develops by early adult years, but may not appear until later decades. The degree of insulin deficiency is slowly progressive. Many patients with MODY 1 are treated with sulfonylureas for years before insulin is required.
Liver effects are subtle and not clinically significant. Many people with this condition have low levels of triglycerides, lipoprotein(a), apolipoproteins AII and CIII.
Mutations in the alternative promoter of HNF4A are linked to development of type 2 diabetes.MODY 4
MODY 4 is a form of maturity onset diabetes of the young.
MODY 4 arises from mutations of the PDX1 homeobox gene on chromosome 13. Pdx-1 is a transcription factor vital to the development of the embryonic pancreas. Even in adults it continues to play a role in the regulation and expression of genes for insulin, GLUT2, glucokinase, and somatostatin.
MODY 4 is so rare that only a single family has been well-studied. A child born with pancreatic agenesis (absence of the pancreas) was found to be homozygous for Pdx-1 mutations. A number of older relatives who were heterozygous had mild hyperglycemia or diabetes. None were severely insulin-deficient and all were controlled with either diet or oral hypoglycemic agents.Maturity onset diabetes of the young
"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. MODY is often referred to as "monogenic diabetes" to distinguish it from the more common types of diabetes (especially type 1 and type 2), which involve more complex combinations of causes involving multiple genes and environmental factors. MODY 2 and MODY 3 are the most common forms. MODY should not be confused with latent autoimmune diabetes of adults (LADA) — a form of type 1 DM, with slower progression to insulin dependence than child-onset type 1 DM, and which occurs later in life.Miglitol
Miglitol is an oral anti-diabetic drug that acts by inhibiting the ability of the patient to break down complex carbohydrates into glucose. It is primarily used in diabetes mellitus type 2 for establishing greater glycemic control by preventing the digestion of carbohydrates (such as disaccharides, oligosaccharides, and polysaccharides) into monosaccharides which can be absorbed by the body.Miglitol, and other structurally-related iminosugars, inhibit glycoside hydrolase enzymes called alpha-glucosidases. Since miglitol works by preventing digestion of carbohydrates, it lowers the degree of postprandial hyperglycemia. It must be taken at the start of main meals to have maximal effect. Its effect will depend on the amount of non-monosaccharide carbohydrates in a person's diet.
In contrast to acarbose (another alpha-glucosidase inhibitor), miglitol is systemically absorbed; however, it is not metabolized and is excreted by the kidneys.Oxyhyperglycemia
Oxyhyperglycemia is a special type of impaired glucose tolerance characterized by a rapid and transient hyperglycemia (i.e. rise in blood glucose) spike after an oral intake of glucose, the peak of this spike being high enough to cause transient, symptom free glycosuria (i.e. detectable glucose in urine), but this hyperglycemia reverses rapidly and may even go to hypoglycemia in the later phase. This sharp downstroke overshooting towards hypoglycemia distinguishes this pathologic phenomenon from the artificial hyperglycemia inducible by an intravenous bolus dose of a large amount of glucose solution. Early dumping syndrome patients usually have oxyhyperglycemia associated with any meal or OGTT.
The Greek root oxy means "sharp" or "pointy". The OGTT curve in this condition appears sharp and somewhat pointy (at least relative to the other forms of hyperglycemia)- hence this name.
Dorlands dictionary defines oxyhyperglycemia as:
"A condition in which there is slight glycosuria and an Oral Glucose Tolerance curve that rises about 180–200 mg/dL but returns to fasting value 2.5 hrs after ingestion of the glucose."A blood level of approximately 180 mg/dL is the renal glucose threshold below which all glucose is reabsorbed from glomerular filtrate. But at blood concentrations above the renal threshold sugar starts appearing in the urine.
Oxyhyperglycemia, like other forms of Impaired glucose tolerance has also been suggested to be a prediabetic conditionSteroid diabetes
Steroid diabetes is a medical term referring to prolonged hyperglycemia due to glucocorticoid therapy for another medical condition. It is usually, but not always, a transient condition.Stress hyperglycemia
Stress hyperglycemia (also called stress diabetes or diabetes of injury) 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.
It is often discovered when routine blood chemistry measurements in an ill patient reveal an elevated blood glucose. Blood glucose can be assessed either by a bedside ‘fingerstick’ glucose meter or plasma glucose as performed in a laboratory (the latter being more efficacious). A retrospective cohort study by the Mayo Clinic held that bedside glucometry was a reliable estimate of plasma glucose with a mean difference of 7.9 mg/dL, but still may not coincide with every individual. The glucose is typically in the range of 140–300 mg/dl (7.8-16.7 mM) but occasionally can exceed 500 mg/dl (28 mM), especially if amplified by drugs or intravenous glucose. The blood glucose usually returns to normal within hours unless predisposing drugs and intravenous glucose are continued.
Stress hyperglycemia is especially common in patients with hypertonic dehydration and those with elevated catecholamine levels (e.g., after emergency department treatment of acute asthma with epinephrine). Steroid diabetes is a specific and prolonged form of stress hyperglycemia.
People who have experienced stress hyperglycemia during severe illness have a threefold risk of developing diabetes in subsequent years, and it may be appropriate to screen for diabetes in survivors of critical illness.Tipranavir
Tipranavir (TPV), or tipranavir disodium, is a nonpeptidic protease inhibitor (PI) manufactured by Boehringer Ingelheim under the trade name Aptivus AP-tiv-əs. It is administered with ritonavir in combination therapy to treat HIV infection.
Tipranavir has the ability to inhibit the replication of viruses that are resistant to other protease inhibitors and it recommended for patients who are resistant to other treatments. Resistance to tipranavir itself seems to require multiple mutations. Tipranavir was approved by the Food and Drug Administration (FDA) on June 22, 2005, and was approved for pediatric use on June 24, 2008.Tipranavir should only be taken in combination with ritonavir and other antiretroviral drugs, and is not approved for treatment-naïve patients. Like lopinavir and atazanavir, it is very potent and is effective in salvage therapy for patients with drug resistance. However, side effects of tipranavir may be more severe than those of other antiretrovirals. Some side effects include intracranial hemorrhage, hepatitis, hepatic decompensation, hyperglycemia and diabetes mellitus. The drug has also been shown to cause increases in total cholesterol and triglycerides.Aptivus labeling has a black box warning regarding hepatotoxicity and intracranial hemorrhage.VIPoma
A VIPoma or vipoma () is a rare endocrine tumor that overproduces vasoactive intestinal peptide (thus VIP + -oma). The incidence is about 1 per 10,000,000 per year. VIPomas usually (about 90%) originate from the non-β islet cells of the pancreas. They are sometimes associated with multiple endocrine neoplasia type 1. Roughly 50%-75% of VIPomas are malignant, but even when they are benign, they are problematic because they tend to cause a specific syndrome: the massive amounts of VIP cause a syndrome of profound and chronic watery diarrhea and resultant dehydration, hypokalemia, achlorhydria, acidosis, flushing and hypotension (from vasodilation), hypercalcemia, and hyperglycemia. This syndrome is called Verner–Morrison syndrome (VMS), WDHA syndrome (from watery diarrhea–hypokalemia–achlorhydria), or pancreatic cholera syndrome (PCS). The eponym reflects the physicians who first described the syndrome.Voglibose
Voglibose (INN and USAN, trade name Voglib, marketed by Mascot Health Series) is an alpha-glucosidase inhibitor used for lowering post-prandial blood glucose levels in people with diabetes mellitus. Voglibose delays the absorption of glucose thereby reducing the risk of macrovascular complications. Voglibose is a research product of Takeda Pharmaceutical Company, Japan's largest pharmaceutical company. Voglibose was first launched in 1994, under the trade name BASEN, to improve postprandial hyperglycemia in diabetes mellitus.Postprandial hyperglycemia (PPHG) is primarily due to first phase insulin secretion. Alpha glucosidase inhibitors delay glucose absorption at the intestine level and thereby prevent sudden surge of glucose after a meal.
There are three drugs which belong to this class, acarbose, miglitol and voglibose, of which voglibose is the newest.
Abnormal clinical and laboratory findings for blood tests (R70–R79, 790)
|Red blood cells|