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Sulfonylurea derivatives are a class of antidiabetic drugs that are used in the management of diabetes mellitus type 2 ("adult-onset"). They act by increasing insulin release from the beta cells in the pancreas. more...

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Drugs in this class

First generation:

  • Chlorpropamide
  • Tolbutamide
  • Tolazamide

Second generation:

  • Glipizide
  • Gliclazide
  • Glibenclamide
  • Glimepiride
  • Gliquidone

Chemistry

Please see individual members of the class for their chemical structure

All sulfonylureas have a central phenyl ring with two branching chains

Pharmacology

Method of action

Sulfonylureas bind to an ATP-dependent K+ channel on the cell membrane of pancreatic beta cells. This inhibits a tonic, hyperpolarizing outflux of potassium, which causes the electric potential over the membrane to become more positive. This depolarization opens voltage-gated Ca2+ channels. The rise in intracellular calcium leads to increased fusion of insulin granulae with the cell membrane, and therefore increased secretion of (pro)insulin.

There is some evidence that sulfonylureas also sensitize β-cells to glucose, that they limit glucose production in the liver, that they decrease lipolysis (breakdown and release of fatty acids by adipose tissue) and decrease clearance of insulin by the liver.

Pharmacokinetics

Various sulfonylureas have different pharmacokinetics. The choice depends on the propensity of the patient to develop hypoglycemia - long-acting sulfonylureas with active metabolites can induce hypoglycemia. They can, however, help achieve glycemic control when tolerated by the patient. The shorter-acting agents may not control blood sugar levels adequately.

Due to varying half-life, some drugs have to be taken twice (tolbutamide) or three times a day rather than once (glimepiride). The short-acting agents may have to be taken about 30 minutes before the meal, to ascertain maximum efficacy when the food leads to increased blood glucose levels.

Some sulfonylureas are metabolised by liver metabolic enzymes (cytochrome P450) and inducers of this enzyme system (such as the antibiotic rifampicin) can therefore increase the clearance of sulfonylureas. In addition, because some sulfonylureas are bound to plasma proteins, use of drugs that also bind to plasma proteins can release the sulfonylureas from their binding places, leading to increased clearance.

Uses

Sulfonylureas are used almost exclusively in diabetes mellitus type 2. Other types of diabetes generally do not respond to sulfonylurea therapy, or (in diabetes of pregnancy) there are other contraindications.

Although for many years sulfonylureas were the first drugs to be used in new cases of diabetes, in the 1990s it was discovered that obese patients might benefit more from metformin.

Read more at Wikipedia.org


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Managing Diabetes Medically
From Optometric Management, 2/1/04 by Gupta, Deepak

Get up to speed on the disease that causes so many ocular problems.

As primary eyecare providers, we're all familiar with the ocular implications of diabetes mellitus, but how much do you know about the disease itself? Let's take the time to learn a little more about this common endocrine disorder.

Diabetes primer

Experts define diabetes as "a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both." Ultimately, this disease alters the metabolism of carbohydrates, fats and proteins to cause widespread damage throughout the body.

Here's the physiology of the disease: Two hormones (glucagon and insulin), which are respectively secreted by the alpha and beta cells of the islets of Langerhans of the pancreas, regulate blood glucose levels. Insulin enters the blood stream shortly after a person ingests food, particularly those rich in carbohydrates. When the body needs glucose, insulin facilitates its use to meet the body's needs. Any excess glucose converts to glycogen, which is stored in the liver or muscle, or stores as fatty tissue; the net effect of insulin is to lower blood glucose concentration.

Conversely, the alpha cells of the Islet of Langerhans secrete glucagon during fasting states. The overall effect of glucagon is to elevate blood glucose levels by one of three mechanisms:

1. Glycogenolysis (breakdown of stored glycogen in the liver to make glucose)

2. Gluconeogenesis (conversion of non-glucose substrates into glucose)

3. Glucose sparing (a process in which ketones are formed in the liver).

What's your type?

Diabetes falls into one of two categories: type I and type II. These two main clinical patterns are distinct in terms of etiology, pathogenesis, clinical presentation and treatment.

* Type I. Type I diabetes accounts for approximately 10% of all diabetes. Patients who have type I diabetes are typically young, thin and undergo a progressive loss of endogenous insulin leading to hyperglycemia. Professionals used the term "insulin-dependent diabetes" for these patients because of their dependence on insulin administration for survival. The peak incidence is between 10 and 13 years of age.

Physicians often diagnose these patients after they experience an abrupt onset of symptoms. The classic triad of symptoms includes the three Ps:

1. polydipsia (increased thirst)

2. polyphagia (increased hunger)

3. polyuria (increased urination).

These patients are prone to ketoacidosis, a life-threatening complication that results from severe insulin deficiency and can result in diabetic coma and death.

* Type II. Type II diabetes is the more common form, accounting for 90% of the total disease population. Two major pathogenetic mechanisms are operative in type II diabetes: impaired islet_-cell function (impaired insulin secretion) and impaired insulin action (insulin resistance or decreased insulin sensitivity). Insulin resistance may be defined as being present whenever normal concentrations of insulin elicit a less-than-normal biologic response. When this patient eats a meal, some insulin secretion still occurs, but at reduced levels.

Patients who have type II diabetes usually aren't dependent on insulin to prevent ketosis or maintenance of life (thus it was called non-insulin-dependent diabetes), but insulin is commonly needed to maintain reasonable blood glucose concentrations.

Type II diabetes typically occurs in people who are older than 40 years, are obese and/or have a family history of diabetes. Unlike type I diabetes, in which the symptoms are pronounced, the onset of type II diabetes is gradual. Doctors often diagnose type II diabetes in asymptomatic patients during routine physical examinations when their laboratory work shows elevated blood glucose levels.

Diagnosing diabetes

Physicians make a definitive diagnosis of diabetes based on any one of the following criteria:

* Elevated plasma glucose (greater than 200 mg/dL or 11.2 mmol/L) along with the classic signs and symptoms of diabetes in addition to unexplained weight loss (type I) or obesity (type II).

* A fasting plasma glucose (FPG) value of 126 mg/dL (7.0 mmol/L) or greater on at least two separate tests.

* Oral glucose tolerance test values at two hours and at least one other sampling during the exam greater than 200 mg/dL.

FPG is the most common test. The physician performs this after the patient fasts for at least eight hours, usually in the morning before a patient has breakfast. In this test, the patient ingests a 75 g glucose load dissolved in water and the doctor checks his blood glucose levels after two hours.

Meet the dangers

The chronic complications of diabetes include accelerated vascular dis ease, neurologic deficits, and other organ-specific degenerative processes. The vascular disease consists of both microangiopathy and macroangiopathy.

* Microangiopathy. A disease of the capillaries specifically associated with diabetes. It's characterized by thickening of capillary basement membranes and manifests clinically mostly in the retina and kidney.

* Macroangiopathy. An accelerated form of atherosclerotic disease of the arteries that usually manifests clinically in the coronary arteries, cerebral arteries and peripheral vessels of the lower extremities.

Make the treatment specific

Each variation of the disorder has its own approaches to treatment.

* Treating type I diabetes. Because patients who have type I diabetes suffer from relative or absolute loss of insulin, these patients require insulin injections. Insulin therapy regimens vary greatly among patients based on their clinical condition, their meal times, exercise schedule and waking/sleeping patterns.

Clinicians generally use one of three therapeutic approaches to insulin therapy:

1. Conventional therapy. This involves one or two daily injections of intermediate-acting insulin alone or in conjunction with rapid-acting insulin.

2. Multiple subcutaneous injections. This technique requires a rapid-acting insulin before each meal and either intermediate or long-acting insulin at bedtime. The advantage is tighter glycémie control than conventional therapy.

3. Continuous subcutaneous insulin infusion. This involves a battery-powered insulin pump to inject insulin into the abdominal wall. A basal rate of insulin infusion occurs throughout the day with additional amounts delivered before each meal. The patient usually checks her glucose level before eating and programs the insulin pump accordingly.

The continuous subcutaneous insulin infusion method provides the tightest glucose control, but also the greatest risk of inducing hypoglycemia (when the blood glucose drops below 70 mg/dL). For more information on insulin, see "Insulin 101," on page 70.

* Treating type II diabetes. Although many patients use medications and even insulin, the cornerstone of therapy for type II diabetes is proper nutrition, weight loss and exercise. Patients must attain and maintain ideal body weight, reduce intake of fats, increase intake of high-fiber carbohydrates (e.g., bran, beans, fruits and vegetables), reduce intake of refined sugars and salt and restrict alcohol consumption.

Also, five different oral drug classes are available for the management of type II diabetes.

1. Sulfonylureas. This includes tolbutamide (Orinase), tolazamide (Tolinase), acetohexamide (Dymelor), chlorpropamide (Diabinese) glyburide (Diabeta), Micronase, Glynase), glipizide (Glucotrol, Glucotrol XL) and glimepiride (Amaryl). Sulfonylureas work by binding to receptors on the pancreatic b-cell, causing a cascade of reactions leading to insulin secretion.

2. Meglinitides. The mechanism of action of the two metiglinides, repaglinide (Prandin) and nateglinide (Starlix), is similar to the Sulfonylureas stimulation of pancreatic insulin release. The difference is that meglinitides have a shorter half-life, which results in brief stimulation of insulin release. Patients take these medications at each meal to decrease postprandial blood glucose.

3. Biguanides. Metformin lowers blood glucose primarily by inhibiting hepatic glucose production and secondarily by enhancing peripheral muscle glucose uptake. It also helps to combat insulin resistance, which may help decrease the risk of cardiovascular disease.

4. a-Glucosidase inhibitors, a-Glucosidase enzymes, which are found in the small intestinal epithelium, break down complex starches into oligo- and monosaccharides and glucose, which are more easily absorbed. The medications, acarbose (Precose) and miglitol (Glycet), inhibit these enzymes that delay carbohydrate absorption. This decreases the postprandial glucose elevation, but has little or no effect on fasting glucose levels.

5. Thiazolidinediones. These work by increasing insulin sensitivity and by increasing glucose use in peripheral tissues, mainly in muscle and fat. Experts don't completely understand their novel mechanism of action, but thiazolidinediones may help suppress glucose synthesis in the liver.

Because these five drug classes work by different mechanisms, many patients are on two or three combinations.

Last but not least

As with any other disease, patient participation is vital in the long-term management of diabetes. Give patients detailed education about nutrition, exercise and the importance of controlling blood glucose levels.

BY DEEPAK GUPTA, O.D., F.A.A.O.

Stamford, Conn.

Dr. Gupta

practices full-scope primary care optometry at Stamford Ophthalmology. You can reach him at deegup4919@hotmail.com.

Copyright Boucher Communications, Inc. Feb 2004
Provided by ProQuest Information and Learning Company. All rights Reserved

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