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Diabetes is one of the leading causes of morbidity and mortality due to its macrovascular
and microvascular complications. The incidence of DM in our country is 2-3% and is bound to increase in future years. It is said that for every one diabetic there are 4 undiagnosed diabetics. Keeping all these points in mind it is necessary to plan prevention of diabetes.
Primary prevention of non-insulin dependent diabetes mellitus
- High risk group in whom prevention is contemplated are :-
- Those with strong family history of diabetes.
- Gestational diabetes
- Migrants of ethnic population who are predisposed to diabetes
- Women with multiple pregnancies, those given birth to large babies and bad
obstetrical history in the past.
- Metabolic syndromes cr syndrome - X patients who have obesity, hypertension,
hyperlipidemia and impaired GTT.
- Patients with central obesity Patients with impaired GTT
Following interventions can be done
- Weight reduction in obesity to ideal weight by
Diet control
- Reduction in calories and carbohydrates specially
- monosaccharieds
- Reduction in fat consumption specially saturated fats.
- Use of complex carbohydrates
- Use of unsaturated fats
- Increased use of dietary fibers
- Not to consume alcohol
Exercises - Inculcate the habit of regular exercises mainly aerobic (dynamic or isometric)
and ask the patient to do so for 30-45 minutes at ieast five days a week with the aim to increase maximum heart rate to ideal (220 - age) for 15 minute period.
Anorectic agents - Role of anorectic agents is disputable. Fenfluramine has been tried
successfully but there are clinical reports saying that prolonged use for more than 3 months may produce primary pulmonary hypertension. Hence better avoid the drug.
- Role of behaviour modification in weight reduction is well known.
- Regulation of lipid profile Reduce cholesterol in diet
- Use of cholesterol lowering drugs like Cholestyramine, Lovastatin, Pravastatin and
Probucol
- Use of cholesterol and tri-glyceride lowering drugs like Nicotinic acid, Clofibrate,
Gemfibrozil, Gugulipid and Fish oils.
- Lifestyle modification.
- Regular surveillance of status of metabolic profile and cardiovascular status.
- Counteract insulin resistance hy using Troglitazone.
- Avoidance of diabetogenic drugs like steroids and others.
- Moderation of alcohol intake.
- Marriage Counselling
- Change in hamburger - cola culture.
- Use of antioxidants.
Primary prevention of insulin dependent diabetes mellitus
There are now reliable techniques to monitor the pancreatic inflammatory process & on-
going Beta cytopathic effect, with increasingly accurate methods for predicting disease in susceptible individuals. Some of these markers that can predict the development of autoimmune type of IDDM are listed below :
- Genetic markers - Among monozygotic twins there is a concordance value of 30-50%
for IDDM. The major genetic markers associated with development of IDDM is the
possession of HLA Allelle DR3 and DR4. It has been shown that HLA-DQB is protective
against IDDM.
- Islet cell antibodies (ICA) - Antibody directed against the cytoplasm of islet cells are
found at the time of diagnosis of IDDM. They tend to disappear after few weeks to few
months. 75% of individuals with ICA titre more than 20JDF units (Juvenille Diabetes
Foundation Unit) progresses to IDDM within 8 years. ICA is of 2 types
- Those detected by conventional immunoflourescence (IF-ICA) ICA positive patients
who are at high risk are
- ICA 20 JDF units
- Age 10 years
- First degree relative of IDDM
- Membership in a family of twins
- ICA persistently positive for 6 months
- Insulin Auto Antibodies (IAA) - 30 - 40% of IDDM children having circulating IAA are
likely to develop IDDM.
- Pro-Insulin Levels - It has been found that fasting Pro-Insulin concentrations are
raised in siblings, parents and children of IDDM patients. Pro-Insulin levels are
increased in those with ICA positive subjects, indicating minor beta cell damage.
- In IDDM and first degree relatives circulating addition molecules (C-ICAMA, CL-
Selectine) are elevated. This probably reflects on- going immune process.
- Anti-Glutamic Acid decarboxylase (Anti-GAD) - This was found to be the best
maker in a study for early detection of IDDM and young NIDDM. By measurement of
Anti-GAD by Radio immunoprecipitation assay in 15% women with newly diagnosed
Diabetes Mellitus, it was observed that 82% of IDDM, 36% NIDDM and 5% of GDM
have Anti-GAD positivity in pre-diabetic state.
- IVGTT - Early deficient response can assess final islet cell mass.
- Combination of Test
- ICA 20 JDF units. +
- IAA positive. +
- Deficient early phase response to IVGTT. +
- Minimal elevation of FBG
- In these patients there is more than 50% chance of development of IDDM in 3 years.
- Cell mediated dysfunction
- Prolilferative response of peripheral blood lymphocytes to GAD 65.
T Lymphocytes with Gama Delta T cell receptor. Anti - viral antibodies.
Interventions
If limited amount of Beta cell mass is destroyed at the time of diagnosis and immuno
intervention adopted earlier, more frequent and longer clinical remissions can be achieved and will prolong the honeymoon phase of disease.
(1) Jmmunosuppresants
- Azathioprim - When given with steroids in a dose of 1-3 mg/Kg body weight for 10 days
after short course of methyl predinosolone 30-mg on alternate days for 4 doses and then tapered over 10 weeks, this combination increases serum mean plasma-C peptide level and reduced mean Insulin doses.
- Cyclosporin - A - In controlled trails of 10 week treatment with doses based on organ
transplantation protocols, rate of non-insulin remission was 24%. In others partial remission was achieved. In high doses may damage pancreatic Beta cell mass.
- Cyclophosphamide
- FK-506 - Powerful immunosuppressent is under trial but it is nephro toxic.
(2) Immunotoxins
Monoclonal antibodies Anti-CD5 antibodies Anti IL-2 receptor antibodies Anti-viral
vaccines
(3) Immunomodulators
- Nicotinamide - Low levels of superoxide desmutase are found in islets in prediabetic
and early diabetes. This makes the patient vulnerable to damage by free oxygen radicals. This acts as a free radical scavenger, Nicotinamide 25 mg/ 10kg body weight was given which improved insulin secretion. It may efficiently prevent IDDM if given in early stages.
- Vaccination with BCG - BCG vaccine has been used in newly diagnosed IDDM in a
pilot study and clinical remission was achieved in 65% patients compared to 7% in control, (clinical remission was defined as FBS 150, 2 hour PPBS 200 mg and exogenous insulin requirement less than 0.2 unit/kg/day for more than 4 weeks). No adverse effects were reported. It protects residual Beta cell mass.
(4) Immunotoleranee Induction
- Intensive Insulin Therapy - It acts by inducing "Beta cell rest" that is exogenous insulin
may place Beta cells in a resting condition in which they secrete less insulin and all cellular products that could act as autoantigens, are inhibited. Beta cells are less antigenic for autore-active lymphocytes.
- Oral Insulin Therapy - This type of therapy induces blocking antibodies and may induce
T cell tolerance.
- Glutamic Acid decarboxylase
(5) Other Measures
- Role of cassava in tropical chronic pancreatitis leading to fibro calcific pancreatic
diabetes is well known and dietary deficiency of sulphur containing amino acids methionine & cystine could hamper detoxification of cyanide to thicyanate and leads to high levels of free cyanide in cassava eaters, leading to beta cell damage. Prevention of this type of DM can be done by not eating cassava.
- There is an association of bottle feeding and IDDM. It is hypothesized that molecular
mimicry between islet antigen P69 and Bovine serum albumin in cow's milk may occur and leading to IDDM. Hence avoid cow's milk in infancy.
- Infants weighing 2.5 kg and below at birth will develop IGT at age 64 years in 56%, while
children who are less than 8 kg at age 6 years develop 17% IGT. During fetal stage due to maternal malnutrition there is deficiency of sulphur containing aminoacids, which is useful in islet cell proliferation. Hence maternal nutrition should be proper so that small-for-date babies are not born and incidence of diabetes mellitus can be reduced.
Secondary prevention of diabetes mellitus
Once diabetes mellitus has been diagnosed it should be adequately treated so that long
term complications are either prevented or delayed and the aims of treatment are:
To maintain euglycemia or good glycemic control To maintain ideal body weight To
maintain sense of well being
Interventions are :
- Educate the patient regarding self care i.e.
- Adherence to diet & drug regimen
- Examination of urine
- Blood glucose monitoring
- Self administration of
- Insulin Abstinence from alcohol
- Maintenance of optimum weight
- Recognition of symptoms of hypoglycemia
- Periodic check up for target organ damage
- Glycosylated Hb estimations at 6 monthly intervals.
- Hypertension
- Salt restriction
- Use of thiazide diuretics judiciously
- Avoid smoking
- Diabetes Mellitus Nephropathy
- Prevent & Treat UTI.
- Reduce protein intake to 0.8 gm/kbw
- Reduce Salt intake
- Avoid use of contrast medias & nephrotoxic drugs like aminoglycosides.
- Early detection of microalbuminuria
- Use of ACE inhibitors in early diabetes mellitus nephropathy
- Stop ACE inhibitors if macroalbuminuria develops or creatinine & potassium goes up.
- Diabetes mellitus retinopathy
- Control hypertension
- Avoid vigorous exercises
- Avoid hypoglycemia
- Use of laser photocoagulation
- Diabetes mellitus with peripheral vascular disease
- Avoid smoking
- Control of lipid profile
- Use of alpha blockers
- Foot care –
- Ask not to walk barefooted
- Use proper fitting shoes
- Avoid sharp instruments to cut nails, corns and callosities
- Avoid very hot or electric heaters to prevent burns in DM with neuropathy
- Early treatment of foot infections
- Use of aldose reductase in neuropathy.
- Coronary artery disease with DM
- Routine ECG to pick up silent infarct or IHD cases.
- Left ventricular dysfunction may be first manifested as exertional dyspnoea or
paroxysmal nocturnal dyspnoea.
- Identify poor risk groups by getting LVEF by Echocardiography. Factors predisposing to
LVF are:
- Occult CAD
- Primary myocardial disease due to microangiopathic lesions
- Volume overload due to ongoing nephropathy
- High salt intake
- Poor LVEF (Left Ventricular Ejection Fraction)
- Identifying such cases and adding ACE inhibitors to therapy will be of immense help
because it will help in controlling LV dysfunction itself, microalbuminuria and
nephropathy and also hypertension induced by either microangiopathic complications or
due to nephropathy.
REFERENCES
1. Ashok Kumar Das, Early detection and immune therapy of IDDM 1DDM Special
Issue, JAPI, Supplement I 1995, Page 42-45.
2. Paolopozzilli, intervention Therapy for Type IDDM. Diabetes reviews international,
Vol. 4, No. 2, April 1995.
3. Andrewmuir, Desmond A. Schatz and Noel K. Maclaren. The Pathogenesis prediction
and prevention of IDDM, Endocrinology & Metabolism Clinics of North America, Vol.
21, No. 2, June 1992.
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