1. To know at what age,
the lipid profile showed any variation in the high risk children, 100
children were initially divided into three age groups of 5-9 years,
10-14 years and > 14 years. The number of children in the age group
of > 14 years was only 11. Mean HDL-C was significantly higher in
the risk group of 5-9 years and 10-14 years than controls. But HDL-C
level became lower in the risk group of > 14 years than controls
although insignificantly. But on reviewer’s suggestions, the age
groups of 10-14 years and > 14 years were clubbed together. The new
data so obtained showed that the mean HDL-C was significantly higher
in the high risk children of both the age grops now formed i.e. 5-9
years and 10-15 yeras. Thus, this new data did not highlight the
earlier observation regarding fall of HDL-C level at the age of >
14 years. That is why a special reference has been made about these 11
children to show that at this age the mean HDL-C started falling. So
its protective effect observed below this age group may not be
operative now thus predisposing these children of > 14 years of age
to the risk of getting these diseases at quite a younger age.
2. Serum cholesterol/HDL-C
ratio in the present study as shown in the Table I varied from 2.53 to
2.66 but is wrongly printed as 2.53-2.80 in the Discussion Section. So
it should be read as 2.53-2.66.
3. This study was
undertaken on 100 children of diseased parents along with controls.
The lipid profile of diseased parents and their high risk children
turned out to have a direct correlation as far as LDL-C and serum
cholesterol fractions were concerned. Serum triglycerides did not show
any significant difference whereas mean HDL-C of high risk children
showed an interestingly different trend as already mentioned. It is
well known fact that these diseases have multifactorial etiology but
this study was not intended to explore all these factors individually.
Drop out rate in present study was nil because it was one time on the
spot cross sectional study.
4. The lipid profile of
these high risk children showed a significant correlation with their
diseased parents even when none of these parents had serum cholesterol
level > 240 mg/dL as reported by American Academy of Pediatrics. It
means lipid profile of the children must be done as it may be
disturbed even when the parental serum cholesterol is lower than the
cut off level of 240 mg/dL which is a western figure.
5. It is mentioned in
the ‘Subjects and Methods’ section that only those diseased
parents (either fathers or mothers) were selected that suffered from
only one of the diseases (i.e. IHD, HT or DM) for more than 5 years.
It is also mentioned that the 100 children selected for the study (not
the parents) were divided into 4 groups of 25 each with parental
history of IHD, HT, DM and a control group. When the number of
children in a particular group of children (and not the parents) was
25, that group was considered complete. Same data is shown in the
Table I where lipid profile of father and mother means lipid profile
of diseased fathers and mothers. Sample size of 25 in Table I means
number of children in each group with parental history of IHD, HT, DM
and controls is 25. It does not mean number of parents is 25 as
mentioned already in selection of parents. Thus observations of Table
I and selection of cases coincide well with each other.
