RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE, KARNATAKA
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,
BANGALORE, KARNATAKA
SYNOPSIS
OF
DISSERTATION
" STUDY OF LIPID PROFILE IN
TYPE 2 DIABETES MELLITUS
IN A.I.M.S , RURAL SETUP-
A COMPARATIVE STUDY"
Submitted by
Dr. MITHUN SOMAIAH C.S. M.B.B.S
POST GRADUATE
GENERAL MEDICINE (M.D)
Under the guidance of
Dr. SHASHIKANTHA M.B.B.S M.D
PROFESSOR
DEPARTMENT OF GENERAL MEDICINE
DEPARTMENT OF GENERAL MEDICINE
ADICHUNCHANAGIRI INSTITUTE OF MEDICAL SCIENCES,
B.G.NAGARA-571448
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION
1
NAME OF THE CANDIDATE
AND ADDRESS
(in block letters)
Dr. MITHUN SOMAIAH C.S.
P.G (GENERAL MEDICINE)
ADICHUNCHUNAGIRI INSTITUTE OF
MEDICAL SCIENCES.B.G NAGARA,
MANDYA DISTRICT -571448
2.
NAME OF THE INSTITUTION
ADICHUNCHANAGIRI INSTITUTE OF
MEDICAL SCIENCES, B.G.NAGARA.
3.
COURSE OF STUDY AND SUBJECT
M.D. ( GENERAL MEDICINE)
4.
DATE OF ADMISSION TO COURSE
24th May, 2010
5.
TITLE OF THE TOPIC
" STUDY OF LIPID PROFILE IN
TYPE 2 DM IN A.I.M.S RURAL SETUP-
A COMPARATIVE STUDY”
6.
BRIEF RESUME OF INTENDED WORK
6.1 NEED FOR THE STUDY
6.2 REVIEW OF LITERATURE
6.3 OBJECTIVES OF THE STUDY
APPENDIX-I
APPENDIX-IA
APPENDIX-IB
APPENDIX-IC
7
MATERIALS AND METHODS
7.1 SOURCE OF DATA
7.2 METHOD OF COLLECTION OF DATA : (INCLUDING SAMPLING PROCEDURE IF ANY)
7.3 DOES THE STUDY REQUIRE ANY INVESTIGATION OR INTERVENTIONS TO BE CONDUCTED ON PATIENTS OR OTHER ANIMALS, IF SO PLEASE DESCRIBE BRIEFLY.
7.4 HAS ETHICAL CLEARENCE BEEN OBTAINED FROM YOUR INSTITUTION IN CASE OF 7.3
APPENDIX-II
APPENDIX-IIA
APPENDIX-IIB
YES
APPENDIX-IIC
YES
8.
LIST OF REFERENCES
APPENDIX – III
9.
SIGNATURE OF THE CANDIDATE
10.
REMARKS OF THE GUIDE
WITH THE RISING NUMBER OF DIABETICS IN INDIA, THE FOLLOW UP OF LIPID PROFILE HAS CERTAINLY EMERGED AS AN IMPORTANT PROGNOSTICATION TOOL TO ASSESS CARDIOVASCULAR RISK FACTORS IN THESE PATIENTS SO AS TO REDUCE MOBIDITY AND MORTALITY IN THEM. HENCE THE STUDY WILL GIVE US AN INSIGHT INTO RISK STRATIFICATION WHICH CAN BE CORELATED WITH THE ALTERATIONS IN LIPID PROFILE
11
NAME AND DESIGNATION
(in Block Letters)
11.1 GUIDE
Dr. SHASHIKANTHA . M.B.B.S, M.D
PROFESSOR,
DEPARTMENT OF GENERAL MEDICINE
AIMS, B.G. NAGARA-571448
11.2 SIGNATURE OF THE GUIDE
11.3 CO-GUIDE (IF ANY)
-
11.4 SIGNATURE
-
11.5 HEAD OF DEPARTMENT
Dr JAGANNATHA. K M.B.B.S,M.D
PROFESSOR and HOD
DEPARTMENT OF GENERAL MEDICINE
AIMS, B.G. Nagara-571448
11.6 SIGNATURE
12
12.1 REMARKS OF THE CHAIRMAN
AND PRINCIPAL
12.2 SIGNATURE
APPENDIX-I
6 . BRIEF RESUME OF THE INTENDED WORK:
APPENDIX –I A
6.1. NEED FOR THE STUDY:
Diabetes as a metabolic disorder is rising at an alarming rate all over the world and has
been a reason for concern due to the complications associated with it . With India having
the highest number of diabetic patients in the world, the sugar disease is posing an
enormous health problem in the country. Calling India the diabetes capital of the
world, the International Journal of Diabetes in Developing Countries says that there
is alarming rise in prevalence.
The International Diabetes Federation estimates that the number of diabetic
patients in India more than doubled from 19 million in 1995 to 40.9 million in 2007.
It is projected to increase to 69.9 million by 2025. Currently, up to 11 per cent
of India’s urban population and 3 per cent of rural population above the age of 15
have diabetes. Diabetes affects all people in the society, not just those who live with
it. The World Health Organization estimates that mortality from diabetes and heart
disease cost India about $210 billion every year and is expected to increase to $335
billion in the next ten years. These estimates are based on lost productivity, resulting
primarily from premature death.
Various studies have shown that the high incidence of diabetes in India is
mainly because of sedentary lifestyle, lack of physical activity, obesity, stress and
consumption of diets rich in fat, sugar and calories.
Dyslipidemia is commonly seen in diabetes. Type 2 diabetes mellitus is one of
the most common secondary cause of hyperlipidemia.The relationship between
hyperlipidemia and vascular complication of diabetes has long been of interest
because both tend to occur with greater frequency in type 2 diabetes mellitus. Insulin
resistance and obesity combine to cause dyslipidemia.and hyperglycemia and
hyperlipidemia has additive cardiovascular risk.. Diabetes,particularly type 2 diabetics
have higher lipid levels than non-diabetics and those patients with poor diabetic
control exaggerate this11.
.
There are several reasons for this association. Firstly, insulin plays an important role in
the regulation of intermediary lipid metabolism (Nikkila, E.A, 1974) and fluctuations in the
degree of diabetic control thus produce a variable effect on plasma lipoprotein metabolism.
Secondly, many non-insulin dependent diabetic patients are obese, and obesity leads to the
development of hyperlipidemia(Bierman, E.L1968). Thirdly ,although diabetes and
hyperlipidemia represent different genetic disorders, each of these disorders is common in the
population and the two disorders may co-exist by chance in thesame individual (Brunzell, J.D 1975).
Hence identification, critical evaluation, follow up of serum lipid profile in type 2
diabetes mellitus continue to be important and help in the prognostication of
cardiovascular risk.
APPENDIX –I B
6.2 REVIEW OF LITERATURE
HISTORY AND REVIEW OF LITERATURE
Diabetes mellitus is a group of metabolic diseases in which a person has high blood
sugar, either because the body does not produce enough insulin, or because cells do not
respond to the insulin that is produced resulting in polyuria( frequent urination), polydipsia
(increased thirst) and polyphagia( increased hunger).
The term diabetes was coined by Aretaeus of Cappadocia. It was derived from the
Greek verb, itself formed from the prefix dia-, "across, apart," and the verb bainein, "to walk,
stand." The verb diabeinein meant "to stride, walk, or stand with legs asunder"; hence, its
derivative diabētēs meant "one that straddles," or specifically "a compass, siphon." The sense
"siphon" gave rise to the use of diabētēs as the name for a disease involving the discharge of
excessive amounts of urine. Diabetes is first recorded in English, in the form diabete, in a
medical text written around 1425. In 1675, Thomas Willis added the word mellitus, from the
Latin meaning "honey", a reference to the sweet taste of the urine. This sweet taste had been
noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians. In 1776,
Matthew Dobson confirmed that the sweet taste was because of an excess of a kind of sugar in
the urine and blood of people with diabetes.
Sushruta (6th century BCE) identified diabetes and classified it as Medhumeha. He
further identified it with obesity and sedentary lifestyle, advising exercises to help "cure" it.
The ancient Indians tested for diabetes by observing whether ants were attracted to a person's
urine, and called the ailment "sweet urine disease" (Madhumeha). The Chinese, Japanese and
Korean words for diabetes are based on the same ideographs which mean "sugar urine
disease".
Medicine first recognized the existence of abnormal fatty content of the
circulating blood through the milky appearance observed during the days when blood
letting was widely practiced. The term lipemia was formulated by Babington in the 18th
century, when he showed that fats were responsible for giving this milky appearance
to the serum.The presence of lactescent serum with diabetes was first noted by Mariet
in 1799 and in 1958 by Thannhauser.S.J.
Owing to lack of research facilities no further advance was made till the
beginning of the 20th century. The deficiency in knowledge was made evident in 1903
when Fischer reviewed the subject. He listed all the conditions where doctors had
earlier observed milky appearance of blood. These included apoplexy, peritonitis,
malaria, jaundice, leprosy, etc. He finally retained diabetes and alcoholic lipaemia as
being genuine. In the years that followed data accumulated about hyperlipemia
accompanying diabetes. Man and Peters (1935) found that triglyceride was the
primary lipid to be elevated. Harries et al (1952) found elevations of serum lipid levels
in diabetic acidosis.
More recently, Chaturvedi et al1(2001) found elevation in triglyceride rich VLDL
to be a common abnormality. In a study of Lowy A.D et al (1957) found a significant
increase in the incidence of hyperlipidemia in association with poor diabetic control.
In a study of the significance of blood lipid alterations in diabetes mellitus,
Mazzone,T et al (2000) 2 measured plasma triglyceride and cholesterol levels in a
large series of diabetic and non-diabetic subjects of all ages. Their results showed that
plasma triglycerides increase with age in diabetics but not in nondiabetics, while
cholesterol levels increase with age in both groups.
Bagdade et.al. (1967) 3 studied five patients with chronic symptomatic diabetes
and minimal ketoacidosis who had marked hyperlipidemia and concluded that diabetic
lipemia can be considered to be a reversible form of dietary fat induced lipemia
secondary to chronic insulin deficiency.
Nikkila EA and Hormila P (1978) 4, concluded that the average serum lipid and
lipoprotein pattern of insulin treated chronic diabetic patients was not_more
atherogenic than non-diabetic subjects of similar age and sex. On the contrary the
increase in HDLc levels which they found, should make them less liable to develop
coronary heart disease. Thus they felt that the increased incidence of cardiovascular
disease in type II diabetes must be accounted for by some other factors.
Chance et.al. (1969)5 studied serum lipids and lipoproteins in 135 diabetic
children prior to treatment and found elevated serum total lipids in 64% of the patients
and elevated cholesterol in 43%. Abnormal lipoprotein patterns were found in 77%, the
commonest anomaly being increase in pre P-lipoprotein.
Strisower E H et al (1958)6 found significant increase in serum cholesterol, LDL
and VLDL values in poorly controlled insulin treated diabetics, which returned to
normal on achieving rigid control
Dewind et. al. (1952) carried out studies in patients with advanced diabetic
atherosclerosis and found no obvious correlation between any of the lipid fractions
although the mean serum cholesterol values were significantly higher in diabetics than
in non-diabetic elderly controls.
Hokanson JE, et al (1996) 7 stated that plasma triglyceride is an independent
risk factor for the development of cardiovascular disease.
Sharma D et.al. (1970)8 studied serum lipid profile in type 2I diabetic patients
below 40 years of age and found significant elevations in the level of serum
cholesterol, phospholipids, esterified fatty acids and triglyceride as compared to a
control group.
In the study of Barr et al (1951) HDL concentrations were Strikingly reduced
in some atherosclerotic diabetic patients. In a recent Study of HDLc in diabetics by
P.K.Bijlani et.al. (1983), it was found that the HDLc values in diabetics and subjects
with impaired glucose tolerance were significantly lower than normal controls. Females
in all groups had higher HDLc than males. Higher HDLc values were also observed in
diabetics on insulin therapy and with better glycemic control.
V.J. Retnam et al (1983) 9 reported hyperlipoproteinemia in a study of 152
adult diabetics on treatment. They found that 20 out of 70 controlled patients and 48
of 82 uncontrolled patients had hyperlipoproteinemia.
Over the past years there has been increasing awareness on the part of the
physicians and general population of the potential benefits of detecting and treating
hypercholesterolemia. This is particularly important in diabetics for two reasons:
1.There already is an increased risk of premature coronary heart disease
In patients with diabetes independent of raised plasma cholesterol levels.
2.Alterations in plasma lipoprotein metabolism are common in diabetes
as they tend to exaggerate any pre-existing tendencies towards elevated lipid levels.
The new recommendations by the National Cholesterol Education Program
have provided guidelines for practicing physicians in treatment of
hypercholesterolemia. These guidelines can be easily applied to patients with diabetes
and optimal. care of diabetic patients require that these recommendations be followed.
However it is also important to understand the effect of diabetes on lipoprotein
metabolism,because in many cases it may be more appropriate to make a change in
diabetic treatment rather than treat the hyperlipidemia.
DYSLIPIDEMIA AND DIABETES
Dyslipidemia is a relatively common problem in patients with poorly
controlled diabetes mellitus. It has been estimated that the frequency of elevated
plasma lipid levels in diabetic patients is between 20 and 90 %. (Billimoria, J.D 1976,
Chance.G.W 1969, Chase. H.P 1976) 5 . Diabetes,particularly type 2 diabetics have
higher lipid levels than non-diabetics and those patients with poor diabetic control
exaggerate this. There are several reasons for this association.
Firstly, insulin plays an important role in the regulation of intermediary lipid
metabolism (Nikkila, E.A, 1974) and fluctuations in the degree of diabetic control thus
produce a variable effect on plasma lipoprotein metabolism.
Secondly, many non-insulin dependent diabetic patients are obese, and obesity
leads to the development of hyperlipidemia(Bierman, E.L1968). Third,although
diabetes and hyperlipidemia represent different genetic disorders, each of these
disorders is common in the population and the two disorders may co-exist by chance
in the same individual (Brunzell, J.D 1975).
TYPE 2 DIABETES AND ITS EFFECT ON LIPID PROFILE
The most common abnormality in type-2 diabetes is hypertriglyceridemia
caused by increase in VLDL. The effect of type-2 diabetes on TG is moderate and
increases in plasma TO >500 mg/dl is caused by the coexistence of a genetic form of
hypertriglyceridmeia aggravated by the hyperglycemia.
Type-2 diabetes causes both overproduction and impaired clearance of
VLDL triglyceride. The mechanism of overproduction of VLDL - TG most likely is
because of increased flow of glucose and free fatty acids to the liver. The removal
defect is caused by impaired lipoprotein lipase activity, but is minimal except in poorly
controlled type-2 diabetes. VLDL overproduction and lipoprotein lipase levels can be
controlled with normalization of glucose levels .
There is also increased production of VLDL apoprotein -B which may be
related to obesity.
Plasma LDLc in type-2 diabetes is increased because of decreased
clearance of LDL.In some individuals with type-2 diabetes, LDL production is low
because of impaired conversion of VLDL to LDL. These patients have normal LDL
levels but increased levels of VLDL.
HDLc in type-2 diabetes is consistently low, especially HDL2. Studies have
shown that an inverse relation between HDLc and arterial disease is present. They
increase with diabetic treatment, but often remain low. The mechanism appears to be
both increased catabolism and reduced production,the former being related to
increased hepatic lipase activity. Insulin is more effective than sulphonylureas in
raising HDLc levels.
HYPERLIPIDEMIC SYNDROMES ASSOCIATED WITH DIABETES
& CHYLOMICRONEMIA SYNDROME IN DIABETES
Diabetic lipemia is a rare but well recognized manifestation of uncontrolled
diabetes. It is characterized by the development of gross lipemia caused by
accumulation of chylomicrons and VLDL in patients with chronic hyperglycemia.
Usually patients develop eruptive xanthomas, lipemia retinalis, chronic abdominal pain
or pancreatitis. The lipemia corrects with insulin treatment and is thought to be caused
by decreased lipoprotein lipase activity secondary to insulin deficiency.
In many individuals with type-2 diabetes, insulin treatment ameliorates the
severe hypertriglyceridemia but does not return plasma lipid values to normal; these
individuals often have hypertriglyceridemic relatives, suggesting the coexistence of a
familial form of hypertriglyceridemia. For this group of patients the term
"chylomicronemia syndrome" 10 is used, which describes development of
hypertriglyceridemia resulting from the interaction of genetic and secondary forms of
hyperlipidemia.
Studies of triglyceride metabolism in patients with type-2 diabetes and
hypertriglyceridemia show both overproduction and impaired clearance of VLDL and
triglycerides. Both improve with treatment, but do not necessarily return to normal.
These patients appear to have abnormality of lipoprotein metabolism, which is
aggravated by poorly controlled diabetes. They require lipid-lowering therapy along
with treatment for diabetes.
PRIMARY DIABETES AND SECONDARY HYPERLIPIDEMIA
This is frequently seen during poor diabetic control and is characterized by mild
to moderate hyperlipidemia. Most of these patients rarely develop increases in TG
>500mg\dl and often only mild to moderate hypercholesterolemia, both of which return
to normal levels after treatment with insulin or oral hypoglycemic drugs.
Occasionally patients develop secondary hypercholesterolemia alone, even with
good diabetic control because of carbohydrate restricted and high fat diet which was
prescribed earlier change in diet to more prudent fat or low cholesterol approach often
controls this secondary hyperchoIesterolemia (American Diabetes Association). 11 This
group of patients represents a primary from of diabetes and a secondary form of
hyperlipidemia due to either poor diabetic control,primarily affecting the triglycerides or
high fat diet.
PRIMARY HYPERLIPIDEMIA AND SECONDARY GLUCOSE INTOLERANCE
An increased incidence of abnormal glucose tolerance has been reported in
individuals with various primary forms of hyperlipidemia (Glueck, C.J1969).
One reason for this maybe that obesity is common in patients with_primary form of
hyperlipidemia and this may also result in glucose intolerance (Bierman, E.L1968).
A second reason may be related to the fact that insulin resistance is often observed in
patients with endogenous onset of hypertriglyceridemia (Steiner.G 1981, Olefsky, J.M
1974)12 and this may increase the likelihood of developing glucose intolerance and/or
overt diabetes.
The clinical significance of this association is that treatment of hyperlipidemia
frequently results in amelioration of glucose intolerance. Thus primary emphasis in the
treatment of this group of patients should be directed towards treatment of
hyperlipidemia and they do not require specific treatment for diabetes.
PRIMARY DIABETES MELLITUS AND PRIMARY HYPERLIPIDEMIA
The association of primary forms of diabetes mellitus and hyperlipidemia is
greater than would be expected by chance alone. Brunzell et al (1975) studied the
frequency of diabetes in adults, first degree relatives of patients with familial forms of
hypertriglyceridemia. In the families with both familial hypertriglyceridemia and
diabetes, diabetes occurred with equal frequency in normolipemic and hyperlipemic
relatives.
Similar findings were found in families of individuals with only
hypertriglyceridemia, but in them the overall frequency of diabetes in the relatives
were much lower. These findings suggested diabetes is frequently associated with
hypertriglyceridemia. Genetic hypertriglyceridemia does not carry an increased risk of
diabetes. Thus diabetes and genetic forms of hypertriglyceridemia appear to be
independent entities which may happen to coexist by chance in the same individllal.
These investigators further evaluated diabetic patients with either familial forms
or sporadic forms of hypertriglyceridemia with regard to their response to diabetic
treatment. They observed that the triglyceride levels before treatment were much
higher in patients with a coexistent familial form of hypertriglyceridemia compared to
those with sporadic forms.
CLINICAL FEATURES
The most common hyperlipidemia in diabetes is hypertriglyceridemia which is
characterized by increased VLDL-TG.
Fasting plasma triglyceride is in the range of 200 -800 mg/dl. The plasma is
opalescent on inspection if Tg concentration is more than 300 mg%.
At times there is associated fasting chylomicronemia, usually increasing fasting
plasma TG to more than 1000mg%. The plasma becomes more opalescent with a
layer of chylomicrons floating on the top of the plasma.
The clinical signs and symptoms of hypertriglyceridemia are as follows:
Signs:
Eruptive xanthomas
Hepatosplenomegaly
Hyperuricemia
Sjogren-like syndrome
Symptoms:
• Abdominal pain (mostly due to pancreatitis )
• Arthralgia
• Peripheral neuropathy
Although these manifestations are said to occur with increased VLDL alone,
they are ordinarily seen with chylomicronemia.
The characteristic skin lesions are eruptive xanthomas which are small, firm,
non-tender papules with a yellow tip on an erythematous base, erupting over a
period of several weeks. When hypertriglyceridemia is severe and diabetes is in poor
control, they are usually seen on the buttocks and extensor surface of the
extremeties.They rarely involve the face and resolve in months if hypertriglyceridemia
is controlled.
Xanthelasma is a distinctive type of xanthoma that occurs on eyelids. They
begin as small yellow macules that thicken to form oval foamy plaques.
Lipemia retinalis is blanching of retinal arteries and veins.
Treatment of diabetic dyslipidemia in adults is as follows:
LDLc lowering
· First choice-HMG CoA reductase inhibitors
· Second choice- Bile-acid binding resin
VLDLc lowering
- Behavorial changes such as weight loss, increased physical activity and smoking cessation.
- Nicotinic acid or fibrates
Triglyceride lowering
· Glycemic control first prioirty
· Fibric acid derivatives (gemfibrozil, fenofibrate)
Statins
COMBINED HYPERLIPIDEMIA-
FIRST CHOICE
· Improved glycemic control plus high dose statins
SECOND CHOICE
· Improved glycemic control plus statins, fibric acid derivative
THIRD CHOICE
· Improved glycemic control plus statins, nicotinic acid
· Improved glycemic control plus resin plus fibric acid derivative
· Estrogen should be the first line of therapy in post menopausal women with high cholestrol levels.Estrogens decrease LDLc levels and raise HDLc levels,but also increase triglyceride levels
APPENDIX –IC
6.3 AIMS AND OBJECTIVES OF STUDY:
TO STUDY THE LIPID PROFILE IN PATIENTS OF
TYPE-2 DIABETES MELLITUS IN A.I.M.S , RURAL SETUP
AS A CASE-CONTROL STUDY.
APPENDIX-II
7.0 MATERIALS AND METHODS
APPENDIX-II A
7.1 SOURCE OF DATA
Study Design : A COMPARATIVE study
Study Period
: 24 months (November 2010 to November 2012)
Source of Data:
The subjects for the study are selected from patients who were admitted to
Sri .Adichunchanagiri Research centre and Hospital, B.G.Nagar, Nagamangla taluk, Mandya
attached to the Sri.Adichunchanagiri institute of medical sciences,B.G.Nagara, Mandya.
APPENDIX- II B
7.2 METHOD OF COLLECTION OF DATA
SAMPLE SIZE : TOTAL: 100
CASE: 50
CONTROL: 50
INCLUSION CRITERIA:
1) Patients with Type 2 diabetes mellitus
2) Duration of Diabetes more than 4 years.
.
EXCLUSION CRITERIA
1) Type -2 diabetes patients with concomittant diseases or condition effecting the lipid levels liken hypothyrodism, on lipostatic drugs, thiazides etc.
2) Type-1 DM patients
METHODOLOGY:
- A detailed history, careful physical examination,
- Routine Blood & Urine examination.
- Biochemical analysis for Fasting blood sugar, post prandial blood sugar.
- Fasting lipid profile
Serum Triglycerides
Total Cholesterol
HDLc , LDLc, VLDLc
APPENDIX – II C 7.3 Does the study require any investigation or intervention to be conducted on the patients or animals , if so please describe briefly
YES
Investigation :
Blood sampling and preparation of serum.
The blood samples will be drawn in the fasting state. The venepuncture will be done
in the cubital fossa. Torniquet shall be used but will be released just before sampling to
avoid artificial increase in the concentration of serum lipids. About 10 ml of blood will be
drawn using perfectly dry and sterile syringes and the blood shall be transferred to dried
glass vials.
Serum has to be seperated within 2 hrs of collection to prevent artifical changes in
concentration of HDL. The blood has to be centrifuged at 5000 rpm for 10 minutes. The
supernatant clean serum will then be pipetted out using dry piston pipettes with
disposable tips and stored in dry thin walled vials . The samples shall be analysed
the same day. Care shall be taken to exclude the haemolysed serum.
Laboratory procedure:
1.Estimation of Total cholesterol
Method - CHOD - DAP method
Principle - Enzymatic estimation
2.Estimation of Total Triglycerides
Method: GPO - DAP method
3.Estimation of HDL cholesterol
Principle: Enzymatic estimation
APPENDIX-II D
PROFORMA APPLICATION FOR ETHICS COMMITTEE APPROVAL
SECTION A
A
Title of the study
“STUDY OF LIPID PROFILE IN
TYPE-2 DM IN A.I.M.S, RURAL SETUP- A COMPARATIVE STUDY”
B
Principle investigator
(Name and Designation)
Dr. MITHUN SOMAIAH
P.G. (GENERAL MEDICINE),
ADICHUNCHUNAGIRI INSTITUTE OF
MEDICAL SCIENCES.B.G NAGARA,
MANDYA DISTRICT -571448
C
Co-investigator
(Name and Designation)
Dr.SHASHIKANTHA.
Professor
Department of GENERAL MEDICINE
AIMS, B.G. Nagara-571448
D
Name of the Collaborating
Department/Institutions
DEPT OF BIOCHEMISTRY
e
Whether permission has been obtained from the heads of the collaborating departments & Institution
YES
Section – B
Summary of the Project
APPENDIX – I
Section – C
Objectives of the study
APPENDIX – I
Section – D
Methodology
APPENDIX – II
A
Where the proposed study will be undertaken
DEPARTMENT OF GENERAL MEDICINE.,
S.A.H. & R.C., B.G.NAGARA
B
Duration of the Project
24 MONTHS
C
Nature of the subjects:
Does the study involve adult patients?
Does the study involve Children?
Does the study involve normal volunteers?
Does the study involve Psychiatric patients?
Does the study involve pregnant women?
YES
NO
NO
NO
NO
D
If the study involves health volunteers
I. Will they be institute students?
II. Will they be institute employees?
III. Will they be Paid?
IV. If they are to be paid, how much per session?
NO
NO
NO
NO
E
Is the study a part of multi central trial?
NO
F
If yes, who is the coordinator?
(Name and Designation)
Has the trail been approved by the ethics Committee of the other centers?
If the study involves the use of drugs please indicate whether.
I. The drug is marketed in India for the indication in which it will be used in the study.
II. The drug is marketed in India but not for the indication in which it will be used in the study
III. The drug is only used for experimental use in humans.
IV. Clearance of the drugs controller of India has been obtained for:
· Use of the drug in healthy volunteers
· Use of the drug in-patients for a new indication.
· Phase one and two clinical trials
· Experimental use in-patients and healthy volunteers.
NA
NA
-
NA
NA
NA
NA
NA
G
How do you propose to obtain the drug to be used in the study?
· Gift from a drug company
· Hospital supplies
· Patients will be asked to purchase
· Other sources (Explain)
NA
H
Funding (If any) for the project please state
· None
· Amount
· Source
· To whom payable
NO
I
Does any agency have a vested interest in the out come of the Project?
NO
J
Will data relating to subjects /controls be stored in a computer?
NO
K
Will the data analysis be done by
· The researcher?
· The funding agent
YES
NO
L
Will technical / nursing help be required form the staff of hospital.
If yes, will it interfere with their duties?
Will you recruit other staff for the duration of the study?
If Yes give details of
I. Designation
II. Qualification
III. Number
IV. Duration of Employment
NO
NO
NO
NA
M
Will informed consent be taken? If yes
Will it be written informed consent:
Will it be oral consent? Will it be taken from the subject themselves?
Will it be from the legal guardian? If no, give reason:
YES, INFORMED CONSENT WILL BE TAKEN FROM THE SUBJECT THEMSELVES
N
Describe design, Methodology and techniques
APPENDIX II
Ethical clearance has been accorded.
Chairman,
P.G Training Cum-Research Institute,
A.I.M.S., B.G.Nagara.
Date :
PS : NA – Not Applicable
APPENDIX-III
8. LIST OF REFERENCES
1. Chaturvedi, N., John H. Fuller and Marja- Ritta Taskinen 2001:
"Differing associations of lipid and lipoprotein disturbances with the macrovascular and micro vascular complications of type 2 diabetes". Diabetes Care, 24(12): 2071-2076.
2. Mazzone, T., 2000: "Current concepts and controversies in the pathogenesis,prevention nd of the macrovascular treatment complications of diabetes. J Lab. Clin. Med., 135: 437-443.
3 Bagdade, J.D., et al 1967:"Diabetic lipemia. A form of acquired fat induced lipemia". N. Engl. J Med.,276: 427-433.
4. Nikkila, E.A. and Hormila, P., 1978: "Serum lipids and lipoproteins in insulin-treated diabetes.Demonstration ofincreased HDL concentrations". Diabetes, 27: 1078-1086.
5. CHANCE GW,; ALBUTT EC,; EDKINS SM . Serum lipids and lipoproteins in untreated diabetics. Lancet. 1969;1:1126-8. MedlineWeb of Science. 4. BILLIMORIA JD,; ISAACS AJ, ... CHASE HP,; GLASGLOW AM d. 1976;130:1113-7 www.annals.org/content/95/4/426.refs
6. Blood Lipids and Human Atherosclerosis
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10. Brunzell, J.D., et al 1982:"Chylomicronemia syndrome". Med. Clin. .North Am., 66: 455-468.
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12. JM Olefsky, JW Farquhar… - The American Journal of …, 1974 - ElsevierWe have previously proposed a sequential hypothesis to help explain the genesis of endogenous hypertriglyceridemia in man. This scheme states that insulin resistance → hyperinsulinemia→ increased very low density lipoprotein (VLDL)-triglyceride (TG) production rate
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ABBREVIATIONS
TG -Triglyceride
TC -Total Cholesterol
VLDLc -Very Low Density Lipoprotein Cholesterol
HDLc -High Density Lipoprotein Cholesterol
LDLc -Low Density Lipoprotein Cholesterol
CAD -Coronary Artery Disease
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