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cardiovascular disease (CVD) risk factors, after optimal glycemic control
and MNT. Lipid profile should be monitored yearly thereafter. However,
the treatment recommendations for hypertriglyceridemia in children and
adolescents with T1DM are not defined. The treatment strategies for dys-
lipidemia in children and adolescents with T1DM are summarized in the
table given below.Age LDL-C Therapy
2–10 years >100 mg/dl MNT
>10 years 100–130 mg/dl MNT
130–160 mg/dl with ≥ 1
CVD risk factorMNT + statin>160 mg/dl MNT + statin- When to screen for microvascular complications in patients with T1DM?
The children and adolescents with T1DM of ≥5 years of duration should
undergo annual screening for albuminuria by estimation of albumin to cre-
atinine ratio (ACR) in a random spot urine sample. The presence of an ele-
vated ACR >30 mg/g should be reconfirmed with repeat testing twice within
6 months duration (three samples). Treatment with ACE inhibitors or ARBs
should be considered if two out of three tests are abnormal. Annual screen-
ing for retinopathy is recommended by dilated fundus examination in chil-
dren and adolescents with T1DM who have duration of diabetes ≥3 years
and either older than 10 years or entered into puberty (whichever is earlier).
Annual comprehensive foot examination is recommended at the onset of
puberty or at age ≥ 10 years, whichever is earlier, once the duration of diabe-
tes is ≥5 years.- When should a child of 9 years of age with T1DM of 5 years of duration with no
pubertal development be screened for diabetic retinopathy?
Annual screening for diabetic retinopathy is recommended at the onset of
puberty or at age ≥10 years, whichever is earlier, once the duration of diabetes
is ≥3 years. The index child has duration of diabetes of 5 years but does not
have any pubertal sign; therefore, he should be screened at the age of 10 years.- What is the effect of puberty on diabetic retinopathy?
Onset and progression of puberty is associated with development and wors-
ening of diabetic retinopathy. The postulated mechanisms include peripuber-
tal GH–IGF1 surge, rising level of gonadal steroids, and alterations in sex
hormone- binding globulin (SHBG). GH–IGF1 surge is associated with del-
eterious effect on vessel wall, which include vascular cell proliferation and12 Diabetes in the Young