8 3 6 Editorial correspondence The Journal of Pediatrics May 1992

reduction fails to control monoclonal LPD in these patients, a suit- ably "aggressive" regimen, such as the GRAB protocol, should be used.

Jon Pritchard, FRCP Consultant Paediatric Oncologist

Department of Haematology and Oncology Ayad Atra, MRCP

Clinical Research Fellow/Senior Registrar Department of Haematology and Oncology

Hospitals for Sick Children Great Ormond Street

London WC1N 3JH, England

We thank Dr. Rosemary Radley-Smith for referring the patient to us.

R E F E R E N C E

1. A1-Attar A, Pritchard J, A1-Saleem T, A1-Naimi M, Alash N, Atra A. Intensive chemotherapy for non-localised Burkitt's lymphoma. Arch Dis Child 1986;61:1013-9.

Reply To the Editor."

The comments of Drs. Pritchard and Atra in response to our ar- ticle are not at odds with our conclusions. However, a few comments

require a response. Three children received chemotherapy in our series; a Table II

footnote points out that of the three patients who received chemo- therapy, one received it so late in the course that efficacy could not be evaluated. Of the two remaining patients, both went into clin- ical remission. The second patient had a relatively prolonged remission before his relapse. The patient described in the letter by Pritchard and Atra would have met our criteria for initiating che- motherapy. As noted in the second to the final paragraph of our ar- ticle, "intervention in the patients with a lymphomatous presenta- tion, if disease progresses without immunosuppressive therapy, should conform to current approaches to the management of dis- seminated Burkitt lymphoma, including immunomodulation, che- motherapy, or bone marrow transplantation." Drs. Pritchard and Atra properly selected their patients for chemotherapy. However, their comments, meant to avoid what they view as a misleading implication of our article, should not mislead the reader in the op- posite direction. We are, in fact, concerned that the further immu- nosuppression occurring with chemotherapy could lead to an adverse outcome for those patients with lymphoproliferative dis- ease who are still immune responsive (i.e., those whose disease po- tentially could regress when normal cytotoxic T-ceU function is al- lowed to occur). We believe that it is important that the patient to be given chemotherapy be appropriately selected, as was Pritchard and Atra's patient, from the group of patients with lymphoprolif- erative disease. These are patients with monoclonal monomorphic disease whose tumor progresses in the absence of immunosuppres- sion. Monoclonal monomorphic disease that progresses despite elimination of immune suppression should be viewed as a lym- phoma and treated as such. We remain interested in the outcome of Pritchard and Atra's patient because, as noted, a brief remission in one patient and a prolonged remission in another was obtainable

with chemotherapy in our series. However, both patients ultimately had a relapse.

Finally, in the last paragraph of our article we raised the concern that the use of the new immunosuppressive agent FK506 would likely have the same complication of lymphoproliferative disease as did cyclosporine. Since the publication of that article, we have seen a number of patients who have had various presentations of lym- phoproliferative disease and whose immunosuppressive therapy was with FK506 and steroids only.

J. Jeffrey Malatack, MD Associate Professor of Pediatrics Children's Hospital of Pittsburgh

University of Pittsburgh Pittsburgh, PA 15213-2583

Thyroid dysfunction after cranial irradiation

To the Editor: One mechanism of thyroid dysfunction caused by cranial irradi-

ation not considered by Ogilvy-Stuart et al. 1 is secretion of immu- noreactive but biologically hypoactive thyroid-stimulating hor- mone. 2 This might be mistaken for mild primary hypothyroidism

or "compensated hypothyroidism" and attributed to direct thyroid damage. A simple way of attempting to detect this condition is to look for the absence of a rise in the triiodothyronine level at the end of a thyrotropin releasing hormone test, but definitive evidence could be obtained by testing thyrotropin for bioactivity or receptor binding. 2

Lyman A. Page, MD Director, Waterbury Regional

Department of Pediatrics Professor of Pediatrics

University of Connecticut School of Medicine Waterbury, CT 06721

R E F E R E N C E S

1. Ogilvy-Stuart AL, Shalet SM, Gattamaneni HR. Thyroid function after treatment of brain tumors in children. J PEon- ATe 1991;119:733-7.

2. Beck-Peccoz P, Amr S, Menzezes-Ferreira MM, et al. De- creased receptor binding of biologically inactive thyrotropin in central hypothyroidism. N Engl J Med 1985;312:1085-7.

Reply

To the Editor." We completely agree with the suggestion that one explanation

for thyroid dysfunction after cranial irradiation might be secretion of immunoreactive but biologically inactive thyroid-stimulating hormone. As far back as 1977 we made the very same suggestion I but did not actively pursue this line of research. We note, however, that Lee et al. 2 recently described central hypothalamic hypothy- roidism with thyroid-stimulating hormone of decreased bioactivity