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Antidiabetic agents

Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels, which result from defects in insulin secretion, or action, or both. Diabetes mellitus, commonly referred to as diabetes, means "sweet urine." Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine, hence the term sweet urine. Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas to normalize the glucose level. In patients with diabetes mellitus, the absence or insufficient production of insulin causes hyperglycemia. Diabetes mellitus is a chronic medical condition, meaning it can last a lifetime.
Over time, diabetes mellitus can lead to blindness, kidney failure, and nerve damage. Diabetes mellitus is also an important factor in accelerating the hardening and narrowing of the arteries (atherosclerosis), leading to strokes, coronary heart diseases, and other blood vessel diseases. Diabetes mellitus affects 15 million people (about 8% of the population) in the United States. In addition, an estimated 12 million people in the United States have diabetes and don't even know it. From an economic perspective, the total annual economic cost of diabetes in 1997 was estimated to be 98 billion dollars in the United States. The per capita cost resulting from diabetes in 1997 amounted to $10,071, while to health care costs for people without diabetes incurred a per capita cost of $2,699. During this same year, 13.9 million days of hospital stay were attributed to diabetes, while 30.3 million physician office visits were diabetes related. Remember, these numbers reflect only the population in the United States. Globally, the statistics are staggering.
HUMALOG (Antidiabetic agents)


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(3 ml) 100 IU/ml, 3,5 mg/ml 5 amp.
USD 0.00

MILGAMMA

Substance (drage): 250 mcg cyancobalaminum, 50 mg benfotiaminum.
Substance (injection): 1 mg cyancobalaminum, 100 mg pyridoxinum chloratim, 100 mg thiaminium chloratum, 20 mg lidocainium chloratum / 2 ml
Substance (capsules): 250 mcg cyancobalaminum, 40 mg benfotiaminum, 90 mg pyridoxinium chloratum

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mg
50 drage
USD 39.00
mg
100 drage
USD 74.00
mg
500 drage
USD 297.00
2 ml
10 amp
USD 26.00
2 ml
30 amp
USD 79.00
mg
20 caps
USD 0.00
mg
50 caps
USD 37.00
mg
100 caps
USD 76.00
mg
500 caps
USD 297.00
METFORMIN (glucophage)
Brand name: Adimet
Manufacturer: Merckle GmbH

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850 mg
120 tab
USD 34.00
850 mg
240 tab
USD 34.00

Antihyperglycemic agent
Metformin is used to treat a type of diabetes mellitus (sugar diabetes) called type 2 diabetes. With this type of diabetes, insulin produced by the pancreas is not able to get sugar into the cells of the body where it can work properly. Using metformin will help to lower blood sugar when it is too high and help restore the way you use food to make energy.
Metformin does not help patients who have insulin-dependent or type 1 diabetes because they cannot produce insulin from their pancreas gland. Their blood glucose is best controlled by insulin injections.

 

PRECOSE (GLUCOBAY) (Acarbose)
Manufacturer: Bayer Corporation

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50 mg
120 tab
USD 35.00
100 mg
120 tab
USD 48.00
AMARYL
Substance: Glimeperide
Manufacturer: Sanofi-Aventis
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1 mg
30 tab
USD 19.00
2 mg
30 tab
USD 29.00
4 mg
30 tab
USD 53.00
AMARYL - GENERIC (generic - what is it?)
Substance: Glimeperide
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1 mg
100 tab
USD 0.00
2 mg
100 tab
USD 0.00
4 mg
100 tab
USD 0.00
AVANDIA
Substance: Rosiglitazone
Manufacturer: GlaxoSmithKline
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4 mg
28 tab
USD 79.00
4 mg
56 tab
USD 154.00
8 mg
28 tab
USD 169.00
AVANDIA - GENERIC (generic - what is it?)
Substance: Rosiglitazone
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4 mg
100 tab
USD 75.00
8 mg
100 tab
USD 144.00
What are the different types of diabetes mellitus?
There are two major types of diabetes mellitus, called type 1 and type 2. Type 1 diabetes mellitus was also called insulin dependent diabetes mellitus (IDDM), or juvenile onset diabetes mellitus. In type 1 diabetes mellitus, the pancreas undergoes an autoimmune attack by the body itself, and is rendered incapable of making insulin. Abnormal antibodies have been found in patients with type 1 diabetes. Antibodies are proteins in the blood that are part of the body's immune system. The patient with type 1 diabetes must rely on insulin medication for survival.
In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies that are directed against and cause damage to patients' own body tissues. It is believed that the tendency to develop these abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood. (Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. These antibodies can be measured, and may help determine which individuals are at risk for developing type 1 diabetes. At present, the American Diabetes Association does not recommend general screening, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age, however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Only approximately 10% of the patients with diabetes mellitus have type 1 diabetes and the remaining 90% have type 2 diabetes mellitus.
Type 2 diabetes mellitus was also referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells) these larger quantities of insulin are produced as an attempt to get these cells to recognize that insulin is present. In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective, and occur late in response to increased glucose levels. Finally, the liver in these patients continues to produce glucose despite elevated glucose levels.
While it is said that type 2 diabetes mellitus occurs mostly in individuals over 30 years old and the incidence increases with age, we are seeing an alarming number patients with type 2 diabetes who are barely in their teen years. Most of these cases are a direct result of poor eating habits, higher body weight, and lack of exercise. While there is a strong genetic component to developing this form of diabetes, there are other risk factors - the most significant of which is obesity. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes, and this holds true in children as well as adults. It is estimated that the chance to develop diabetes doubles for every 20% increase over desirable body weight and for each decade after 40 years of age regardless of weight. The prevalence of diabetes in persons 65 to 74 years of age is nearly 20%. Type 2 diabetes is more common in certain ethnic groups. Compared with a 6% prevalence in Caucasians, the prevalence in African Americans and Asian Americans is estimated to be 10%, in Hispanics 15%, and in certain Native American tribes 20% to 50%. Finally, diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy (gestational diabetes - see below). Type 2 diabetes is often associated with a strong familial, probably genetic predisposition. This is less common in the autoimmune form of type 1 diabetes.
Diabetes mellitus can occur temporarily during pregnancy. Significant hormonal changes during pregnancy can lead to blood sugar elevation in genetically predisposed individuals. Blood sugar elevation during pregnancy is called gestational diabetes. Gestational diabetes usually resolves once the baby is born. However, 25-50% of women with gestational diabetes will eventually develop diabetes mellitus later in life, especially in those who require insulin during pregnancy and those who are overweight. Patients with gestational diabetes are usually asked to undergo an oral glucose tolerance test about 6 weeks after giving birth to determine if their diabetes has persisted beyond the pregnancy.
"Secondary" diabetes mellitus refers to elevated blood sugar levels from another medical condition. Secondary diabetes mellitus also develops when the pancreatic tissue responsible for the production of insulin is absent because it is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas. Diabetes can also result from other hormonal disturbances, such as excessive growth hormone production (acromegaly) and Cushing's syndrome. In acromegaly, a pituitary gland tumor at the base of the brain causes excessive production of growth hormone, leading to hyperglycemia. In Cushing's syndrome, the adrenal glands produce an excess of cortisol, which promotes blood sugar elevation. In addition, certain medications may worsen diabetes control, or "unmask" latent diabetes. This is seen most commonly when steroid medications (such as prednisone) are taken.
Research articles on Antidiabetic agents
Gut. 2005 Apr;54(4):533-9.
Diabetes increases the risk of hepatocellular carcinoma in the United States: a population based case control study.
Davila JA, Morgan RO, Shaib Y, McGlynn KA, El-Serag HB.
Houston Veterans Affairs Medical Center, 2002 Holcombe Blvd. (152), Houston, TX 77030, USA. hasheme@bcm.tmc.edu.

BACKGROUND: Diabetes has been associated with an increased risk of hepatocellular carcinoma (HCC) in studies of referred patients. This is the first population based case control study in the USA to examine this association while adjusting for other major risk factors related to HCC. METHODS: We used the Surveillance Epidemiology and End-Results Program (SEER)-Medicare linked database to identify patients aged 65 years and older diagnosed with HCC and randomly selected non-cancer controls between 1994 and 1999. Only cases and controls with continuous Medicare enrolment for three years prior to the index date were examined. Inpatient and outpatient claims files were searched for diagnostic codes indicative of diabetes, hepatitis C virus (HCV), hepatitis B virus (HBV), alcoholic liver disease, and haemochromatosis. HCC patients without these conditions were categorised as idiopathic. Unadjusted and adjusted odds ratios were calculated in logistic regression analyses. RESULTS: We identified 2061 HCC patients and 6183 non-cancer controls. Compared with non-cancer controls, patients with HCC were male (66% v 36%) and non-White (34% v 18%). The proportion of HCC patients with diabetes (43%) was significantly greater than non-cancer controls (19%). In multiple logistic regression analyses that adjusted for demographics features and other HCC risk factors (HCV, HBV, alcoholic liver disease, and haemochromatosis), diabetes was associated with a threefold increase in the risk of HCC. In a subset of patients without these major risk factors, the adjusted odds ratio for diabetes declined but remained significant (adjusted odds ratio 2.87 (95% confidence interval 2.49-3.30)). A significant positive interaction between HCV and diabetes was detected (p<0.0001). Similar findings persisted in analyses restricted to diabetes recorded between two and three years prior to HCC diagnosis. CONCLUSIONS: Diabetes is associated with a 2-3-fold increase in the risk of HCC, regardless of the presence of other major HCC risk factors. Findings from this population based study suggest that diabetes is an independent risk factor for HCC.

Ann N Y Acad Sci. 2004 Dec;1031:204-13.
Oxidative stress and antioxidant treatment in diabetes.
Scott JA, King GL.
Research Division, Joslin Diabetes Center, Harvard Medical School, One Joslin Place, Boston, MA 02215. george.king@joslin.harvard.edu.

The many studies on oxidative stress, antioxidant treatment, and diabetic complications have shown that oxidative stress is increased and may accelerate the development of complications through the metabolism of excessive glucose and free fatty acids in diabetic and insulin-resistant states. However, the contribution of oxidative stress to diabetic complications may be tissue-specific, especially for microvascular disease that occurs only in diabetic patients but not in individuals with insulin resistance without diabetes, even though both groups suffer from oxidative stress. Although antioxidant treatments can show benefits in animal models of diabetes, negative evidence from large clinical trials suggests that new and more powerful antioxidants need to be studied to demonstrate whether antioxidants can be effective in treating complications. Furthermore, it appears that oxidative stress is only one factor contributing to diabetic complications; thus, antioxidant treatment would most likely be more effective if it were coupled with other treatments for diabetic complications.

J Assoc Physicians India. 2004 Jun;52:459-63.
Use of glimepiride and insulin sensitizers in the treatment of type 2 diabetes--a study in Indians.
Ramachandran A, Snehalatha C, Salini J, Vijay V.
Diabetes Research Centre and M.V. Hospital for Diabetes WHO Collaborating Centre for Research, Education and Training in Diabetes Royapuram, Chennai.

AIM: Short-term efficacy of glimepiride, metformin and pioglitazone in newly diagnosed type 2 diabetes was compared with a group treated with diet and exercise. Effects on insulin secretion and sensitivity were also assessed. METHODS: New type 2 diabetic subjects, aged 30-60 years with BMI < 30 kg/m2 were selected. Subjects having glycosylated haemoglobin (HbA1c) of < 8.5% were advised diet and exercise (control group). Others having HbA1c > or = 8.5 to 11.0% were randomized to receive glimepiride (group 2), metformin (group 3) and pioglitazone (group 4). At the final review between 12-14 weeks, changes in plasma glucose, HbA1c, lipid profile, HOMA insulin resistance (HOMA-IR), beta cell function (HOMA-BF) and insulinogenic index (delta I/G) were measured. Comparisons were made using appropriate statistical analyses. RESULTS: Seventy-seven of the 97 subjects randomized equally into four groups, were available for review. Glycaemic parameters improved in all groups. Mean cholesterol decreased significantly in groups treated with metformin and pioglitazone. HDL-cholesterol increased with pioglitazone. Insulin resistance decreased significantly with metformin and pioglitazone, beta cell fuhction also showed improvement CONCLUSIONS: Glycaemic control was seen in all study groups, the improvement was better in drug treated groups than in the control group. Glimepiride improved insulin secretion including the early phase secretion and reduced plasma triglycerides. Metformin and pioglitazone had beneficial effects on lipid levels, improved insulin sensitivity and improved insulin secretion also.

Clin Podiatr Med Surg. 2003 Oct;20(4):635-53
Diabetes mellitus and pharmacological therapy.
Bernene J, Zgonis T, Jolly GP.
Department of Medicine, New Britain General Hospital, New Britain, CT 06052, USA.

Diabetes mellitus can be a devastating lifelong disease if not treated appropriately. The physician and the patient should be aware of both extremes involved with DM: hyperglycemia and hypoglycemia. Patient education and preventive care are perhaps more important in this disease than many others. A multidisciplinary approach involving the patient, physician, and diabetic educator is best to assure a better quality of life. Enormous advances in the treatment of diabetes have occurred over the past decade and even greater ones can be expected in the future. New drugs, insulin delivery devices, and noninvasive glucose monitoring machines have the potential to normalize blood sugar levels and return diabetics to a near normal lifespan without complications.

 

Postgrad Med. 2003 May;Spec No:35-44.
Beneficial effects resulting from thiazolidinediones for treatment of type 2 diabetes mellitus.
Bell DS.
University of Alabama at Birmingham, School of Medicine, Department of Medicine, Birmingham, USA.

Because new drugs continue to be developed, physicians treating patients with type 2 diabetes have a wide range of agents from which to choose. The newest class, the thiazolidinediones (TZDs), should be a mainstay of treatment for most patients with type 2 diabetes, because these agents reduce insulin resistance as well as improve glycemic control. Patients with the insulin resistance syndrome are at increased risk for developing cardiovascular disease. However, decreasing insulin resistance with TZD use may reduce the incidence of adverse cardiovascular outcomes. TZDs also may reduce cardiovascular events by acting directly on vascular smooth muscle cells and by helping patients maintain normal hemoglobin levels, without the risk of hypoglycemia. Furthermore, prolonged glycemic control is expected with TZDs because of their effects on beta-cell rejuvenation, a function unique to this class. TZDs can be used safely in renally impaired patients with diabetes, and hepatotoxicity has not been a problem with second-generation TZDs, making these agents both safe and effective in the treatment of type 2 diabetes.

 

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