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Reply to Vazquez and Castano

turbance. First, in this particular report, as is many cases of LCH, the patient suffers from diabetes insipidus, secondary to hypothalamic-hypophyseal damage. The majority of these cases also present with decreased growth hormone levels and thyroid axis deficiency. In these cases, including the patient described here, multihormonal involvement and data from imaging techniques as well as biopsy of the pituitary stalk could indicate a central origin of the biochemical hypothyroidism (2). Also, there are previous cases where central hypothyroidism with normal or elevated TSH concentrations and an exaggerated and retarded response to TRH is caused by hypothalamic pathology. It has been shown that these patients secrete a TSH with reduced biological activity bothin vivo and in vitro, which can be reverted to normal with exogenous TRH treatment (3). Additionally, in this case, there is no biopsy confirmation for thyroid involvement and the reduced size of the gland is in discordance with most of the published cases of children or teenagers with thyroid disease, the majority of which are males who present with goitre (4). In view of these considerations, we believe that in the absence of any morphological evidence of thyroid infiltration by Langerhans cells, the cause of high levels of TSH may be compatible with an hypothalamic origin.