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bolic abnormalities but also decreases hepatic steatosis. However, due to non-
availability of recombinant leptin and expenses incurred, insulin remains the
mainstay of therapy for the management of hyperglycemia. Metformin and pio-
glitazone have been shown to be partially effective in improving metabolic
abnormalities; however, their effect on redistribution of peripheral body fat
may be detrimental. In addition, the use of fibrates is indicated for the manage-
ment of hypertriglyceridemia. Statins have also been used to improve cardio-
vascular outcome through their pleiotropic effects.
- What is insulin therapy-related lipodystrophy?
Insulin therapy-related lipodystrophy includes hypertrophy or atrophy of
adipose tissue at injection site. Lipohypertrophy is more common than
lipoatrophy and occurs with all insulin preparations including analogues.
However, lipoatrophy was common with the use of animal-derived insulin
and is rare with recombinant human insulin. Lipohypertrophy is a result of
activation of local lipoprotein lipase (lipogenesis) by insulin, whereas
lipoatrophy occurs as a result of release of cytokines (TNF-α) at local site
in response to type III hypersensitivity reaction (Arthus reaction, as insulin
acts as a hapten). Insulin therapy- related lipodystrophy leads to variability
in absorption of insulin and consequently worsening of glycemic control.
Therefore, the injection site should be examined periodically in patients
who are receiving insulin. Management of insulin lipohypertrophy includes
change in the site of insulin administration and, rarely, surgical excision.
Lipoatrophy responds to change in injection site and sometimes to admin-
istration of dexamethasone along with insulin at the site of atrophy
(Fig. 12.7).
ab
Fig 12.7 (a) Lipoatrophy and lipohypertrophy in a patient on insulin therapy, (b) lipohypertrophy
in another patient with T1DM
12 Diabetes in the Young