Clinical_Rounds_in_Endocrinology_Volume_II_-_Pediatric_Endocrinology

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angiogenesis. Gonadal steroids, testosterone, lead to rise in blood pressure,
worsening of dyslipidemia, and increase in vascular cell adhesion molecule
1 (VCAM1) and intercellular adhesion molecule 1 (ICAM1). Estrogen also
increases the expression of vascular endothelial growth factor (VEGF) and
thereby promotes angiogenesis. Decline in SHBG during peripubertal period
in boys results in increase in free testosterone which further worsens diabetic
retinopathy.


  1. Why is there worsening of diabetic retinopathy after intensive insulin therapy?


Intensive insulin therapy is associated with initial worsening of diabetic reti-
nopathy followed by slow progression of the disease. The initial worsening of
diabetic retinopathy after initiation of intensive insulin therapy has been
attributed to increased breakdown of blood–retinal barrier (consequent to
upregulation of VEGF and HIF 1α), retinal ischemia due to loss of glucose-
mediated vasodilatation, and increased neovascularisation as a result of ele-
vated IGF1 consequent to hyperinsulinemia. Further, increased IGF1 induces
VEGF expression which also contributes to angiogenesis. Therefore, periodic
fundus examination should be performed after initiation of intensive insulin
therapy.


  1. What is limited joint mobility?


Limited joint mobility is a manifestation of long-standing uncontrolled severe
hyperglycemia and is seen in patients with both T1DM and T2DM. Clinically,
it is appreciated by either “prayer sign” or “table sign.” This occurs as a result
of abnormal cross-linking of collagen fibers due to accumulation of advanced
glycosylation end products. Limited joint mobility correlates with diabetic
microvascular complications particularly diabetic retinopathy (Fig. 12.2).

Fig 12.2 Limited joint
mobility in a patient with
type 1 diabetes illustrated
as “prayer sign”


12 Diabetes in the Young

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