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REFRESH THIS PAGE EVERY TIME YOU OPEN IT...IT'S
UPDATED CURRENTLY!!
Click on the Image to see my German .
IN THIS PAGE YOU CAN TAKE A LOOK ON MY RESEAECH THAT I PERFORMED ON METFORMIN.
Diabetes
Mellitus is a chronical metabolic syndrome characterised by hyperglycaemia,
resulting from impaired insulin secretion or effectiveness, glucoseurea, and
other metabolic disturbances. Clinically Diabetes Mellitus is classified as:
1)
Insulin Dependent Diabetes Mellitus (IDDM)
2)
Non – Insulin Dependent Diabetes Mellitus (NIDDM)
3)
Tropical Diabetes Mellitus
4)
Gestation Diabetes Mellitus.
IDDM
or type I Diabetes Mellitus is represented by about 10 to 15% of all cases of
Diabetes Mellitus, and clinically characterised by hyperglycaemia and risks of
diabetic ketoacidosis. Genetic predisposition is revealed in changed occupation
of amino acids in a
and b
chains which constitute the allele Dq.This allele belongs to locus D on the
short arm of 6th chromosome. This results in formation of antibodies
directed for selective destruction of insulin secreting b-
cells. Clinical manifestation is revealed when 80% of
b
- cells are destructed. Its treatment requires chronic insulin injections.
NIDDM
or type II Diabetes Mellitus is characterised clinically by hyperglycaemia but
it’s not associated with diabetic ketoacidosis; some patients may require
insulin to control symptomatic degrees of hyperglycaemia, which may lead to
nonketotic hyperglycaemic hyperosmolar coma. The pathogenic picture starts from
precipitating factors, such as over eating and hypodynamia that results in
obesity. Consequently, deformation
of insulin – receptors on the cell membrane of insulin – dependent cells (adipocytes,
hepatocytes, myocytes) prevents insulin from identifying these receptors. As a
result, insulin accumulates in blood; that is, HYPERINSULINEMIA.(Scheme 1)
SCHEME1
Non
– ketotic Hyperglycaemic - Hyperosmolar Coma is a syndrome characterised by
impaired consciousness accompanied by seizures, extreme dehydration, and extreme
hyperglycaemia that is not accompanied by ketoacidosis. It’s a complication of
NIDDM, and has mortality >50%. It develops after a period of symptomatic
hyperglycaemia in which fluid intake is inadequate to prevent extreme
dehydration from hyperglycaemia – induced osmotic diuresis. It can be induced
by giving drugs that impair glucose tolerance and increase fluid loss (glucocorticoids,
phenytoin, immunosuppresive drugs, diuretics); and may result after hemodialysis,
tube feeding, giving large intravenous glucose loads.
DIAGNOSTIC
criteria for fasting hyperglycaemia is a plasma glucose level ³
140 mg/dl. Periodical determination of glycosylated haemoglobin (HbA1c)
estimates plasma glucose during the preceding three months. Urine analysis are
done to reveal glucose urea, and other changes if complications
has proceeded.
TREATMENT
of Diabetes Mellitus can be
achieved through one of the following categories
1)
Diet
2)
Oral Hypoglycaemic Agents
3)
Insulin therapy
Our
concern in the field of treatment is focused on the group of
BIGUANIDES, oral hypoglycemic agents, more specifically on Metformin.
H
H2N
- C – N – C – N (CH3)2
Metformin
Investigation
were done in the department of Endocrinology in Kursk State Medical University
in December 1999 under the direction of the Head of department, Larisa A.
Zhukova, associate professor and member of European Association Study
Diabetes (EASD), metabolic dieticians of diabetic center, and undergraduate
students. Investigations were carried on twenty patients with moderate degree of
non- – insulin dependent Diabetes Mellitus (NIDDM).
Half
of the patients were considered as a control – group, and they didn’t take
Siaphor as a medication. The second half were given Siaphor 850 in dosage 1700
mg/day. The aim of the
investigation was to reveal the influence of
Siaphor on the level of lactate in patients of Diabetes Mellitus type II.
Patients
selected for investigations, all suffered of Diabetes Mellitus for more than
five years (including the control group). There were fourteen
female patients and six male patients. Their age ranged between 50-65
years old. They all were treated with Maninil –5 of a dose 10 mg/day. After
appearance of Diabetic complications, they were treated by insulin of a dose
relative to the ideal body weight. Insulin injections were twice a day one in
the morning and one the evening. Each injection contains proportion of short and
intermediate acting insulin. Anamnesis of selected patients were similar in
having diabetic complications such as angiopathy, retinopathy (first stage), slight forms of peripheral
neuropathy.
The
criteria of selecting the patients for the course of Siaphor took into
consideration the contraindication factors of prescribing Siaphor. Patients with
acute complications of diabetes (ketoacidosis) were excluded; as well as
patients with kidney diseases, cardiovascular diseases, and liver diseases.
As
a conclusion, it was revealed that lactic acidosis in patients with NIDDM is not
a result of Siaphor – treatment, instead, it’s a result of other subsequent
illnesses accompanying the pathogenesis of Diabetes Mellitus.( Scheme2 )
SCHEME2:LEVEL OF LACTATE
The results of the other analysis shows significant decrease in the levels of fasting glucose level and post-prandial levels. The level of cholesterol was considered before the starting of course, since it needs more time to cause recognizable changes in the level of cholesterol in plasma (scheme 3).
SCHEME3:GLUCOSE
LEVEL
In
the light of the effectiveness of treatment of Diabetes Mellitus, statistical
analysis of levels of blood glucose before and after intake of Siaphor (scheme
3), shows significant effectiveness of Siaphor in the lowering of fasting
glucose level and post-prandial level. Since the goal of research was to show
the relationship between Metformin and lactic acidosis; effectiveness of drug on lowering the level
of cholesterol was not demanded, for it takes longer time.
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