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Indian Pediatr 2015;52: 347-348 |
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Grave’s Disease Following Aplastic Anemia:
Predisposition or Coincidence?
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Wei Zhang and *Zonghong Shao
Department of Hematology, General Hospital of Tianjin
Medical University, Tianjin, China.
Email: *[email protected]
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A 3-year-old boy, whose mother had Grave’s disease for 9 years, was
diagnosed with severe aplastic anaemia in October, 2010. Bone marrow
aspiration showed hypoplasia. and bone marrow cytogenetic studies were
normal. He was diagnosed to be having severe aplastic anemia and was
treated with immunosuppressive therapy of anti-thymocyte globulin at 5
mg/kg/d intravenously for 5 days, prednisone 1 mg/kg/d orally for 1
month and cyclosporine A 3 mg/kg/d orally. Because of neutropenia,
recombinant Human granulocyte colony-stimulating factor therapy was
initiated. Erythrocyte and thrombocyte infusions were also given
moderately because of low blood counts. Four months after
immunosuppressive therapy, cyclosporin was continued orally. The blood
work-up was normal after 6 months of immunoceppressive therapy .
On follow-up, the parents informed us that the
patient had a voracious appetite but had poor weight-gain, and
palpitations and excessive sweating. Grave’s disease was confirmed by a
low TSH, elevated total thyroxine (T4), triodothyronine (T3), free
triodothyronine (FT3) and free thyroxine (FT4). Thyroid-associated
antibodies TRAb(+), ATG(+) and ANTI-TPO(-) were present. Thyroid
ultrasound showed bilateral diffuse thyroid lesions. The patient was put
on 0.5 mg/kg/d of prednisone and methimazole, which successfully
improved the thyroid function later on.
Severe aplastic anemia has now been identified as a
kind of bone marrow failure caused by T lymphocyte hyper-function, which
induces the apoptosis of hematopoietic cells by excessive secretion of
Th1 lymphokines such as IL-2 and interferon-gamma (IFN- g)
[1]. Grave’s disease involving the thyroid gland is typically
characterized by the presence of circulating auto-antibodies that bind
to and stimulate the thyroid hormone receptor, resulting in
hyperthyroidism and goiter. It is postulated that the failure of
T-suppressor cells allows expression of T-helper cells, sensitized to
the TSH antigen, which interact with B cells. These cells differentiate
into plasma cells, which produce thyrotropin receptor-stimulating
antibody. Thus, both aplastic anemia and Grave’s disease appear to have
altered T-cell function.
A previous report details the appearance of Grave’s
disease after cyclosporine was discontinued for several months. As GD is
also considered an autoimmune disorder with abnormal T lymphocytes, it
is interesting to speculate that cyclosporine CSA was keeping the
disease under control by immune modulation. Grave’s disease is not
commonly seen in pediatric patients, less so in boys, and the
association with severe aplastic anemia in a child has not been
frequently described. Our patient’s mother had Grave’s diseases for 9
years and was put on propylthiouracil treatment, but neonatal Grave’s
disease is rare, and it is probable that Grave’s disease may be
hereditary [3].
We propose that both diseases might be related in the
autoimmune pathology under certain genetic backgrounds, which needs to
be further studied.
References
1. Young NS, Scheinberg P, Calado RT. Aplastic anemia.
Curr Opin Hematol. 2008; 15:162-8.
2. Kumar M, Goldman J. Severe aplastic anaemia and
Grave’s disease in a paediatric patient. Br J Haematol. 2002;118:327-9.
3. Levy-Shraga Y, Tamir-Hostovsky L, Boyko V, Lerner-Geva L,
Pinhas-Hamiel O. Follow up of newborns of mothers with Graves’ disease.
Thyroid. 2014; 24:1032-9.
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