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Antidiabetic agents |
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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. |
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HUMALOG (Antidiabetic agents)
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Dosage |
Packing |
Price |
Pay now |
(3 ml) 100 IU/ml, 3,5 mg/ml 5 amp. |
USD 0.00 |
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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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Dosage
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mg
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50 drage
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USD 39.00
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mg
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100 drage
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USD 74.00
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mg
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500 drage
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USD 297.00
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2 ml
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10 amp
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USD 26.00
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2 ml
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30 amp
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USD 79.00
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mg
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20 caps
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USD 0.00
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mg
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50 caps
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USD 37.00
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mg
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100 caps
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USD 76.00
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mg
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500 caps
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USD 297.00
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METFORMIN (glucophage)
Brand name: Adimet
Manufacturer: Merckle GmbH
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Dosage
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850 mg
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120 tab
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USD 34.00
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850 mg
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240 tab
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USD 34.00
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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.
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PRECOSE (GLUCOBAY) (Acarbose)
Manufacturer: Bayer Corporation
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Dosage |
Packing |
Price |
Pay now |
50 mg |
120 tab |
USD 35.00 |
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100 mg |
120 tab |
USD 48.00 |
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AMARYL
Substance: Glimeperide
Manufacturer: Sanofi-Aventis
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Dosage |
Packing |
Price |
Pay now |
1 mg |
30 tab |
USD 19.00 |
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2 mg |
30 tab |
USD 29.00 |
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4 mg |
30 tab |
USD 53.00 |
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Dosage |
Packing |
Price |
Pay now |
1 mg |
100 tab |
USD 0.00 |
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2 mg |
100 tab |
USD 0.00 |
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4 mg |
100 tab |
USD 0.00 |
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AVANDIA
Substance: Rosiglitazone
Manufacturer: GlaxoSmithKline
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Dosage |
Packing |
Price |
Pay now |
4 mg |
28 tab |
USD 79.00 |
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4 mg |
56 tab |
USD 154.00 |
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8 mg |
28 tab |
USD 169.00 |
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Dosage |
Packing |
Price |
Pay now |
4 mg |
100 tab |
USD 75.00 |
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8 mg |
100 tab |
USD 144.00 |
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What are the different
types of diabetes mellitus? |
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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. |
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Research articles
on Antidiabetic agents |
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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.
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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.
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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.
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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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