ONSET OF JUVENILE

DIABETES MELLITUS

BY
DR.AMIT.D.
INTRODUCTION
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 Definition of JDM

• Juvenile onset of diabetes condition is

characterized by severe insulinopenia
&dependence on exogeneous insulin to
prevent ketosis to preserve life,

• DM is a syndrome of disturbed energy

homeostasis resulting in abnormal metabolism
of carbohydrate,protein & fat.
• In children it is found due to destruction of
beta cells of the pancreatic islets.

• DM in childhood affects Growth, puberty&

psychological well-being.
 PREVALENCE
• In India type –1 DM Incidence is 10/1 lakh

• The peak incidence is seen at :

5yrs of age
10-12yrs of age
ETIOLOGY
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• Genetic

• Inheritance from the parents

• Infections(environmental factors)
 GENETIC FACTORS
The• EPIDEMIOLOGY
major susceptibility loci are the Human
leucocyte antigen(HLA) class II gene& Insulin gene.

The gene for HLA system is located on chromosome

no 6.

HLA-DR3&DR4 associated with greater risk of

DM1.Where HLA-DR2 Confers protection.
 Inheritence from Parents
• If only father is Type 1DM 7%of children
can acquire Type 1 DM.

• If only mother is involved 2% of children

can get affected.
INFECTIONS(environmental factors)
 Viral infection.eg.,coxackie etc,cong rubella

 Environmental factors like Early weaning to cows

milk ,Toxins like Nitrosamines & Stress.

 Environmental factors may induce autoimmunity

by molecular mimicry or directly stimulating
cytokine production.
 Pathogenesis of Auto immune
destruction
• Studies has shown that identical twins of proband
have only 30-50% of developing type I
DM.suggesting equal & major role for post natal
(environmental) factors.
• DM1 is frequently associated with conditions of
known auto immune etiology like Hashimoto
thyroidits,Pernicious anemia &Addison disease.
• 30-40% of patients of DM1 in India have islets
cell antibodies.
• Abnormalities in ‘T’Lymphocytes sets off a series
of responses including cytokine production
resulting in beta cell destruction.
 Pathophysiology
• Insulin mainly acts on 3 tissues,viz., Liver, Muscle
& Adipose tissue.

• LIVER-glucose uptake, glycogen synthesis,

lypogenesis & stops gluconeogenesis.

• MUSCLE-glucose uptake ,oxidation & glycogen

synthesis.

• ADIPOSE TISSUE-glucose uptake & lipid

synthesis.
 Thus in Dibetes mellitus hyper
glycemia results due to
• Glycogenolysis.

• Lipolysis.

• Absence glucose uptake.

CLINICAL
FEATURES
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EARLY ONSET

• Polyuria

• Polydypsia

• Polyphagia

• Wt loss & weakness

LATE ONSET(Indication of ketoacidosis))

• Vomitting

• Abdominal pain

• Deep & rapid respiration(kussmaul)

• Fruity odor of acetone in breath

 Rare /Less common features
• Enuresis

• Skin sepsis

• Fungal(candida) & other infection

• Ketoacidosis may cause an abdominal
surgical emergency

• Severe acidosis is accompanied by

decreasing consciousness & hypotension

• The presence of fever is an important clue

to infection
LABORATORY
FINDINGS
• Glycosuria

• Hyperglycaemia( FBS>126mg%, RBS>200mg/dl )

• Ketonemia & Ketonuria

• Lecocytosis may be present without infection

• Hyper triglyceremia
 COMPLICATIONS

Acute Chronic Intermediate

Hypoglycemia - Retinopathy - Cataract
Ketoacidosis - Neuropathy -Growth reta-

Sec infection -Nephropathy rdation

Wt loss -Delayed sexual
maturation
 DIFFERENTIAL DIAGNOSIS
• Accidental findings of glycosuria should be
differentiated from

- Renal glycosuria
- Fanconi syndrome
 TYPE1 TYPE2
Rapid onset Insidious & slow onset

Seen <30yrs Seen >30yrs

Only 10% family H/O Strong family H/O

In 25-30% both twins Both twins affected

affected
Anti islet cell antibody Less incidence (<5%)
found(>80%)
Insulin required for Un commonly insulin
treatment required
MANAGEMENT
PRINCIPLES
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 AIMED AT

• To ensure proper growth & development

• To prevent immediate & long term complication

• To control the symptom of diabetes at the

earliest
MY VIEWS
• Etiology & clinical features of Sahaja prameha
matches with modern explanation.
• Acc to Ayurveda ,Pathology of Sahajameha has
to be explored.
• The Role of Infection(environmental factors) in
the manifestation is to be discussed in terms of
Ayurveda.
• As Such Balaprameha & its detailed explanation
is not found in Kas. Sam & other classics.
CONCLUSION
• Sahaja prameha can be considered as JDM

• Onset of JDM at the max <30yrs

• Complete manifestation of disease occurs

within 2-5yrs

• Genetic factors & Environmental factors

takes equal share in onset of disease

• JDM affects Growth, puberty &

psychological well being .
THANK YOU