Novel Mutations in SH2D1A Gene in X-linked Lymphoproliferative Syndrome, Diagnosed After B-Cell Non-Hodgkin Lymphoma

J Pediatr Hematol Oncol. 2017 May;39(4):e203-e206. doi: 10.1097/MPH.0000000000000815.

Abstract

Background: X-linked lymphoproliferative disease type I (XLP I) is caused by mutations in the SH2D1A gene and characterized mainly by hypogammaglobulinemia and abnormal response to Epstein-Barr virus with a high predisposition to B-cell non-Hodgkin lymphoma development.

Observations: In this article, we describe the experience of 2 centers in Belarus and in Russia that follow 3 male patients who were diagnosed with XLP I after lymphoma development and treatment. Three novel mutations c.51G>C (p.E17D), c.192G>T (p.W64C), and c.53insA (p.K18KfsX67) were found in 3 males patients with XLP I. Two of them did not have any signs of immunodeficiency before B-cell non-Hodgkin lymphoma development.

Conclusions: We propose SH2D1A mutational screening be considered in male patients with or without hypogammaglobulinemia who received rituximab treatment for lymphoma and did not recover immunoglobulin G in a year after B-depleting therapy.

Publication types

  • Case Reports
  • Multicenter Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Agammaglobulinemia
  • Child
  • Humans
  • Immunoglobulin G / blood
  • Lymphoma, Non-Hodgkin / complications*
  • Lymphoma, Non-Hodgkin / drug therapy
  • Lymphoproliferative Disorders / complications*
  • Lymphoproliferative Disorders / diagnosis
  • Lymphoproliferative Disorders / genetics*
  • Male
  • Mutation
  • Rituximab / therapeutic use
  • Signaling Lymphocytic Activation Molecule Associated Protein / genetics*

Substances

  • Immunoglobulin G
  • SH2D1A protein, human
  • Signaling Lymphocytic Activation Molecule Associated Protein
  • Rituximab