Congenital segmental lymphedema in tuberous sclerosis complex with associated subependymal giant cell astrocytomas treated with Mammalian target of rapamycin inhibitors

J Child Neurol. 2014 Sep;29(9):NP54-7. doi: 10.1177/0883073813499969. Epub 2013 Sep 20.

Abstract

Tuberous sclerosis complex is a genetic, multisystemic disorder characterized by circumscribed benign lesions (hamartomas) in several organs, including brain. This is the result of defects in the TSC1 and/or TSC2 tumor suppressor genes, encoding the hamartin-tuberin complex that inhibits the mammalian target of rapamycin pathway. Specific inhibitors of this pathway have been shown to reduce the volume of subependymal giant cell astrocytomas associated with tuberous sclerosis. Congenital lymphedema is rarely seen in association with tuberous sclerosis, with only a few reported cases. Although this association can be coincidental, the dysgenetic lymphatic system can represent a hamartia as a consequence of gene mutation. We describe a child with congenital lymphedema in tuberous sclerosis and associated subependymal giant cell astrocytoma who experienced lymphangitis under treatment with mammalian target of rapamycin inhibitors. Because our patient did not show worsening of lymphedema, congenital lymphedema does not seem to be a contraindication for this therapy.

Keywords: congenital lymphedema; mammalian target of rapamycin inhibitors; tuberous sclerosis complex.

Publication types

  • Case Reports

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Arm / pathology
  • Astrocytoma / complications
  • Astrocytoma / drug therapy*
  • Astrocytoma / pathology
  • Brain / pathology
  • Brain Neoplasms / complications
  • Brain Neoplasms / drug therapy*
  • Brain Neoplasms / pathology
  • Child, Preschool
  • Female
  • Humans
  • Lymphedema / complications*
  • Lymphedema / congenital*
  • Lymphedema / drug therapy
  • Lymphedema / pathology
  • Magnetic Resonance Imaging
  • TOR Serine-Threonine Kinases / antagonists & inhibitors*
  • TOR Serine-Threonine Kinases / metabolism
  • Tuberous Sclerosis / complications*
  • Tuberous Sclerosis / pathology

Substances

  • Antineoplastic Agents
  • MTOR protein, human
  • TOR Serine-Threonine Kinases