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

JOHN W. GOFMAN M.D., PH.D.1; HARDIN B. JONES PH.D.1; FRANK T. LINDGREN B.S.1; THOMAS P. LYON M.D.1; HAROLD A. ELLIOTT B.S.1; BEVERLY STRISOWER B.S.1; , Ultracentrifugal Laboratory Group1 ..From the Donner Laboratory, Division of Medical Physics and the Radiation Laboratory, University of California, Berkeley 4, California.

7. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies by John E. Hokanson

8. Sharma (1970) and Jain (1980) observed increase in the levels of serum total lipids,in type 2 DM .... Sharma D, Bansal BC, Prakash C. Serum lipid studies in thin insulin dependent diabetics ... Ganda OP, Hayes EJ, Soledner Js, et al. www.rssdi.org/1995_jan-mar/original_article3.pdf

9. Nerurkar SV, Retnam VJ, Taskar SP, Bhandarkar SD. Lipid composition of plasma lipoproteins in treated diabetics. J Postgrad Med 1983;29:201

Nerurkar SV, Retnam VJ, Taskar SP, Bhandarkar SD. Lipid composition of plasma lipoproteins in treated diabetics. J Postgrad Med [serial online] 1983 [cited 2010 Nov 15];29:201. Available from: http://www.jpgmonline.com/text.asp?1983/29/4/201/5511

10. Brunzell, J.D., et al 1982:"Chylomicronemia syndrome". Med. Clin. .North Am., 66: 455-468.

11.. American Diabetes Association 1987 :"Nutritional recommendations and for individuals with diabetes mellitus". Diabetes Care, 10:126-132

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

NEWER ARTICLES

1. IMPACT OF DURATION OF TYPE 2 DIABETES

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This cross-sectional study was conducted at Khyber Medical College Peshawar from

February 2009 to July 2009

Riffat Sultana, Department of Physiology, Khyber Medical College, Peshawar, Pakistan.

2. A Study on Lipid Profile Levels of Diabetics and Non-

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Division of Biochemistry, Allahabad Agricultural

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3. Vascular Structural and Functional Changes in Type 2 Diabetes Mellitus

Evidence for the Roles of Abnormal Myogenic Responsiveness and Dyslipidemia

Ian Schofield, MRCP; Rayaz Malik, PhD, MRCP; Ashley Izzard, PhD; Clare Austin, PhD; Anthony Heagerty, MD, FRCP From the Cardiovascular Research Group, Department of Medicine, Manchester Royal Infirmary, Manchester, UK

4. Alterations in high-density lipoprotein metabolism and reverse cholesterol transport in insulin resistance and type 2 diabetes mellitus: role of lipolytic enzymes, lecithin:cholesterol acyltransferase and lipid transfeR proteins.(S. E. Borggreve,†, R. De Vries,†, R. P. F. Dullaar)

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5. Lipids and Lipoproteins in Patients With Type 2 Diabetes

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Maryse Guérin; Wilfried Le Goff; Taous S. Lassel; Arie Van Tol; George Steiner; M. John Chapman, Erasmus University, Rotterdam, Netherlands (A.V.T.); and the Toronto Hospital, Toronto, Ontario, Canada (G.S.). )

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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