Search

In preparation for whole body radioactive iodine scanning, recombinant human TSH (rhTSH) is usually administered as 0.9-mg i.m. injections on 2 consecutive days without regard to age, body size, or other comorbid conditions.Our objective was to determine whether the usual adult rhTSH dosing regimen would result in excessive elevations of serum TSH in children and teenagers with thyroid cancer. DESIGN/SETTING/PATIENTS/INTERVENTIONS: A retrospective review identified 53 children and teenagers with thyroid cancer who underwent whole body radioactive iodine (RAI) scanning over a 12-yr period at two major medical centers (34 after thyroid hormone withdrawal and 19 after rhTSH treatment).The dynamic time course of changes in serum TSH after rhTSH administration and/or hypothyroid withdrawal was examined. Peak TSH levels were correlated with age, weight, and body surface area.The mean serum TSH at the time of RAI administration was similar in patients undergoing hypothyroid preparation (188 +/- 118 mIU/liter; range, 110-452 mIU/liter) and those treated with rhTSH (134 +/- 75 mIU/liter; range, 32-290 mIU/liter; P = 0.07). Serial determinations after rhTSH injections revealed a mean serum TSH of 268 +/- 76 mU/liter (range, 87-628) at 6 h and 130 +/- 58 mU/liter (range, 67-250) at 24 h after the initial injection, and 361 +/- 78 mU/liter (range 161-524) at 6 h and 134 +/- 44 mU/liter (range, 32-290) at 24 h after the second injection.The mean TSH levels achieved in children after rhTSH injections are remarkably similar to values previously reported in adults despite marked differences in clinical characteristics between children and adults. These data suggest that dose adjustments are not generally required in children and teenagers undergoing rhTSH stimulation for RAI scanning or serum-stimulated thyroglobulin determinations.

Serum thyroid hormones, serum thyroxine-binding proteins and serum thyroid hormone fractions have been measured in children with congenital heart disease before and after open cardiac surgery. Twenty prepubertal patients, mean (+/- SD) age 3.6 +/- 3.7 yr, were studied before, immediately after, and 24 and 48 h after surgery. A control group of 6 normal prepubertal children was also studied in basal conditions. Serum TSH was normal in all samples collected. Significantly low mean levels of serum TBG (261 +/- 57 vs 456 +/- 71 nmol/L in normals), serum TBPA (2692 +/- 1119 vs 5999 +/- 2226 nmol/L), serum TBG-bound T4, serum TBPA-bound T4, serum TT3, serum TBG-bound T3 and free T3 were found before cardiac surgery in the patients. While serum binding proteins did not change after surgery, significant decrements in serum TT4, serum TBG-bound T4, serum TT3, serum TBG-bound T3, serum albumin-bound T3 and free T3 were observed after surgery. Free T4 and albumin-bound T4 remained normal. Our study shows that many features of nonthyroidal illness were present in our patients before surgery. In this context, the stress of surgery induced further alterations in several parameters of thyroid metabolism. It is concluded that the changes occurring in this model of chronic, as well as acute, nonthyroidal illness reflect adaptative changes, rather than altered thyroid function, as shown by normal serum free T4, serum albumin-bound T4 and serum TSH.

The specific thyroid hormone transporter, MCT8, located on the X chromosome, has led to the identification a novel syndrome. The objective is to relate phenotype with several tissue-specific thyroid functions. A 1-year-old boy, who had severe psychological damage and low serum T4, had received l-T4 for 3 months. At admission, body length was normal but weight was low. Off therapy, serum TSH was mildly elevated, serum T4 and free T4 were low, and serum T3 and free T3 were high. Direct sequencing of the MCT8 gene revealed a single nucleotide change that resulted in a novel nonsense mutation at codon 261 (Q261X) in exon 3. Since serum T3 was high, peripheral markers of hyperthyroidism were looked for. Bone age was advanced, despite the presence of malnutrition and low T4. Serum SHBG, a marker of thyroid hormone action in liver, was markedly elevated. Markers of skeletal muscle catabolism, ammonemia and lactic acid, were found to be elevated. The phenotype of MCT 8 mutation might be explained by differences in the entry of thyroid hormones into different cells. In the presence of an inactive MCT8 transporter, the high blood T3 levels might not be enough to prevent brain damage early in life, while they seem to be able to induce a postnatal state of peripheral hyperthyroidism in other tissues, such as liver, bone and skeletal muscle.

Background: Congenital isolated thyrotropin (TSH) deficiency is an unusual condition characterized by low levels of thyroid hormones and TSH, usually presenting early typical signs of severe hypothyroidism. Five different β-TSH mutations have been described so far. While 4 of them affect only consanguineous families, a frameshift mutation in exon 3 (C105fs114X) has been found also in nonconsanguineous families. Objective: The aim of the present study was to characterize β-TSH mutations in Argentinean patients with congenital central hypothyroidism (CCH) and to emphasize the importance of early biochemical and molecular diagnosis of this disorder. Patients and Methods: We investigated 8 Argentinean children (3 boys, 5 girls) from 7 unrelated families with CCH based upon low levels of T4 and T3, and low basal and stimulated TSH levels. Mutation characterizations for the β-TSH gene were performed by PCR amplification followed by sequence and restriction enzyme analysis with SnaBI in the patients, 9 parents and in 100 newborn children. Results: All patients presented the same homozygous mutation in exon 3 of the β-TSH gene (C105fs114X), the 9 studied parents were heterozygous for the same mutation and 1 carrier was found in the 100 studied newborns. Conclusion: Our findings show that the C105fs114X mutation is prevalent in our population and may constitute a hot spot at codon 105 in the β-TSH gene. Since this mutation is easily demonstrable by a SnaBI digestion in DNA amplified from dried blood spots, its investigation would be indicated in patients in our milieu with clinical and biochemical features of CCH, allowing early L-thyroxine (LT4) replacement and genetic counseling of the family.

RET proto-oncogene mutation results in a dominant autosomic inherited syndrome (MEN 2) presenting three distinct subtypes: MEN 2A, MEN 2B, and familial medullary thyroid carcinoma (FMTC). Detection of RET proto-oncogene mutation is a predictor before clinical or biochemical evidence of the disease is present and leads to preventive thyroid removal since there is no effective treatment for metastases. The aim of the present study was to characterize mutations in the RET proto-oncogene in affected patients and to identify potential carriers in their families. Two families with FMTC (5 and 6 members), 4 with MEN 2A (5, 5, 4 and 3 members) and 2 with MEN 2B (5 and 1 members), were studied. DNA was obtained from blood samples in all patients and from thyroid or from pheonochromocytoma tissues in patients submitted to surgery. PCR amplification was performed using specific primers for exons 10, 11 and 16, followed by direct sequencing. Mutations at codon 634 in exon 11 were found in 16 subjects with FMTC and MEN 2A: TGC --CGC (cysteine to arginine) in 9 cases, TGC --TAC (cysteine to tyrosine) in 3, and TGC --TTC (cysteine to phenilalanine) in 4. A unique mutation of codon 918 in exon 16, ATG --ACG (methionine to threonine), was found in both MEN 2B affected patients. The mutations detected in DNA from peripheral blood were the same as those present in DNA extracted from tumor material. RET mutations were detected in all affected patients, confirming the diagnosis, and in 10 members of their families. In five of the carriers total thyroidectomy was performed. Anatomopathological study showed C-cells hyperplasia or in-situ microcarcinoma in two children (9 and 12 y) with no clinical signs of diseases and medullary thyroid carcinoma in three adults, who were previously unaware of the presence of thyroid nodules. The early detection of RET mutation followed by total thyroidectomy may prevent the development of the disease, specially in affected families, and avoid the fatal outcome of delayed medullary thyroid carcinoma diagnosis.

Tumor oncotypes, initial symptoms and endocrine disturbances before and/or 1 month after surgery were studied in 66 patients with prepubertal and pubertal ages having suprasellar or pineal intracranial tumors. Neoplasms found in patients of prepubertal age were: 15 craniopharyngiomas (CRA), 24 neuroepithelial-cell-derived tumors (NEC), 5 germ cell tumors (GERM) and 4 other lesions (OTHER). In patients of pubertal age, there were 7 CRA, 7 pituitary tumors (PIT), 2 NEC, 1 GERM and 1 OTHER. Approximately 90% of patients had visual abnormalities as one of the initial signs and symptoms, while 59% had increased intracranial pressure. Short stature was observed in only 10% of patients. Before surgery, somatotropic function was found to be deficient (by 2 pharmacological tests) in 90-100% of patients with CRA, PIT or GERM and in 40% of patients with NEC. Overt hypothyroidism was found in 5-25% of CRA, NEC or GERM but in 40% of PIT. Abnormal TSH responses to TRH were observed in 64% of CRA and in 29% of NEC. Low basal serum cortisol was found in 21 or 6% of patients with CRA or NEC, but in 100 or 60% of patients with PIT or GERM, respectively. Diabetes insipidus was diagnosed in 13.6% of all patients. Surgery produced few additional disturbances in endocrine function, except for the incidence of diabetes insipidus which was doubled. Gonadotropic deficiency was found in most patients of pubertal age with CRA and PIT. They were readily differentiated by the high prolactin or growth hormone (GH) levels of the latter.(ABSTRACT TRUNCATED AT 250 WORDS)

Early Diagnosis of Multiple Endocrine Neoplasia Type 2 by Detection of Mutated Ret Proto-Oncogen Carriers

Juvenile Hyperthyroidism (JH): Long Term Treatment with Low Doses of Methimazole (MMI). When Should it be Stopped?

Influence of Iodinated Disinfectants (Id) on Tsh Values in A Screening for Congenital Hypothyroidism (Ch) in A Neonatal Intensive Care Unit (Nicu) Population. 18

Intracranial Tumors (It) of the Midline in Pediatrics. Incidence of Cellular Types and of Precocious Puberty

Short(St) and Long Term (Lt) Thyroid (T) Dysfunction After Treatment in Patients With Hodgkin's Disease (H) With Different Agressive Scores

PAPILLARY THYROID CARCINOMA (Ca) IN CHILDREN AND ADOLESCENTS: DIFFERENCES IN AGGRESIVENESS AND NEW STRATEGY OF FOLLOW UP

FNABT was done in patients with ATD (Chronic Lymphocytic Thyroiditis= CLT and Graves'Disease= GD), and processed according to the mothod of Hayry at al., applied to follow up transplanted organs. Citospin samples were stained with May Grunewald-Giemsa, and HLA-DR, CD25, CD4, CD8, CD3, CD11 and surface immunoglobulines were detected by immunofluorescence. In transplanted kidneys, a corrected increment (inflamatory INDEX) (CI)3,5 indicates immunological activation. We analized thyroid samples, obtaining the CI, and the phenotype of infiltrating cells. 56 FNABT were perfomed on 43 pts. (CLT n=23 and GD n=20), followed up from 1 y. to 4,5y. They were divided in 2 gr., according to their thyroid status. Gr.I:CLT n=29 and Gr.II:GD n=27. Results: (%±SD). Gr.I: CI: 6.3±0.97; B-cells: 33.9±10.5; T-cellS: 61.2±11.4; CD4:63.1±6.2; CD 8:34.4±6.6. CD4/CD8 ratio: 1.9±0.5 HLA-DR expression was found on 56.6±18.8% of the follicular cells and CD25 was expressed in 27/29 pts. Gr.II:CI 4.2±1.3(Gr.I vs II = p

The influence of infiltrating lymphocytic immunophenotype (Part I) and cytological findings on samples obtained by fine needle aspiration biopsy (FNABT) were correlated with the presence (+) and titers of circulating thyroid antibodies (Ab) in 43 patients with autoimmune thyroid disease (chronic Lymphocitic Thyroiditis= CLT, n=23 and Graves Disease= GD, n=20). Ab (Antimicrosomal= MiAb and Antithyroglobulin= TgAb)were determined by hemagglutination. CLT:Cytology: 23/23 pts had CLT MiAb+: 17/23 (74%); Titers:Range 1/400 - 1/25.600. TgAb+: 5/23(22%)Titers:range 1/100 -1/600. GD: Cytology: 7/20 pts were CLT, 12/20 were normal and 1/20 adenomatous goiter (AB). Antibodies were determined in 18/20: MiaAb+: 15/18 (83%) Titers: range 1/400 - 1/409.600; TgAb+:10/18 (55%) Titers: range 1/100 to 1/6400. 6/7 pts with CLT cytology had MiAb+ and 4/7 TgAb+. 9/11 pts (10 with normal cytology and 1 A. Goiter) had MiAb ranged 1/400 - 1/102.400 and in 6/11 had TgAb ranged 1/100-1/6400. Less serological expression were seen in CLT (were) the prevalence of intrathyroid T-Cells and other sings of cellular aggression (Part I) would suggest mainly a cellular immune reaction. 2) Higher titers of both Ab were found in GD, Together with the prevalence of B lymphocytes among the infiltrating cells (Part I) would sustain mainly a humoral mechanism of autoimmunity. 3) Normal cytology in GD along with high titers of Ab would suggest antigen presentation in lymphoid organs (ei.nodes) but not within the thyroid itself. Thyroid gland would be a “passive captive” of specific events of the whole immune system, as Volpe has suggested.

In a previous work we pointed out the high correlation among the presence of antithyroid antibodies (AB), thyroid function alteration and clinical symptoms in children with insulin dependent diabetes mellitus (DMID). In the actual study, the chronic lymphocitic thyroiditis (CLT), antithyroid AC and alteration function in patients with DMID was evaluated. From a total of 228 pts, in 78 (age 11.6 + 4.3), basal TSH and/or post TRH, T4, T3 by RIE and microsomal antifraction (MiAF) antithyroid AC and antithyroglobulin (ATg) haemoglutination was done. CLT presence (Fisher's criteria) was determined in 20 pts (25%): 16 girls, 4 boys; 11,6 years + 3.43, 90% (18/20) of which presented thyroid function alteration with high basal TSH X 7.39 + 3.49 uUml (p of 25 uUml). 85% of the patients presented clinical symptoms; goiter was detected in 65%. CLT prevalence was significatively greater in the first four years of the diabetes evolution. The frequency of MiAF positive titles was 15.4% of the diabetic and 50% of CLT patients. Due to the high prevalence, 25%, we conclude that thyroid function study, AC dosage and clinical exam must be included in all the children with DMID, specially in the first four years after the onset of the disease.

Pituitary function was evaluated in 25 patients with intracraneal Tumors (T). Basal thyroid function (T4, T3 and TSH) was altered in 1/22 patients before (Pre) and in 3/19 within the first month after surgery (Post). TRH-TSH was abnormal in 7/14 Pre and in 9/18 Post. Basal prolactin (PRL) was high in 4/14 Pre and in 4/15 Post (2 patients had prolactinoma) while TRH-PRL was high in 3/12 Pre and in 2/15 Post. Serum somatotropin response to a stimuli was < 10ng/ml in 8/14 patients Pre and in 13/15 Post and < 5ng/ml in 5/14 patients Pre and in 7/15 Post. In pubertal patients gonadotrophic function was deficient in 4/7 Pre and 2/3 Post. In prepubertal patients (n= 8-9), the LH-RH test was normal. Basal cortisol was low in 1/14 Pre and 2/11 Post; in another 2 patients symptoms of adrenal insufficiency were observed Post. Diabates insipidus was diagnosed in 3/25 patients Pre and in 10/25 Post being transient in 4 of the latter. B-hCG was high in 2/7 cases, both with germ cell T. A high Pre incidence of somatotrophic, thyrotrophic and pubertal gonadotrophic deficiency was found. PRL was high in prolactinomas and it was moderately increased in only 2 other patients. Surgical morbidity was low, except for the somatotrophic function.

Top of pageAbstract Non-thyroidal illness was evaluated in 9 children, chronological age 3.88±3.16 y (+SD), before (B), immediately after (I), and 24 and 48 hs after cardiac surgery. Serum levels of T-binding globulin (TBG), and T4-binding prealbumin (TBPA), albumin (ALB), Total T4 and T3 (TT4, TT3), Albound T4 and T3 (ALB-b T4 and T3), free T4 and T3 (by calculation according to the law of mass action) were determined. ALB-b T4 was also measured experimentally in undiluted serum, using labelled T4. Serum TGB and TBPA were significantly lower in B, I, 24 and 48 hs (TBPA only) (261±17.05, 272±70.17, 259±65.47, 374±103, and 3013±625, 2870±493, 3373±1443, 2309±398 nmol/l respectively) than in controls (c)(456±71 and 5999±2226, respectively, p

Thirteen children with medulloblastoma, were studied after 2 to 62 months off radiotherapy and chemotherapy with methotrexate and BCNU. Ages at time of study ranged from 2.3 to 15.7 years. Eleven patients, followed for a mean of 22 months, showed a significant decrease of height score, whereas nine patients had deficient growth hormone (GH) response to provocative tests. Clinical pubertal progression was normal in all patients, and three of five girls with advanced pubertal development had menarche. No evidences of gonadotropin disturbances were found in five patients whereas seven had raised basal folliclestimulating hormone (FSH) level or FSH response to luteinizing hormone-releasing hormone (LH-RH). Abnormalities in thyrotrophin (TSH) secretion were found in 9 of 13 patients. This study shows that poor growth and GH deficiency were frequent in our patients. The high frequency of thyroid disturbances observed point out the need of evaluating thyroid function for adequate replacement therapy. Perhaps modification of adjuvant chemotherapy in the future can diminish drug-induced gonadal damage. Cancer 59:801-806, 1987.

Radiotherapy to the neck and/or polychemotherapy late effects on the thyroid were investigated in 51 patients (34 males and 17 females) with Hodgkin's disease. Except for two untreated, recently diagnosed patients, all were studied after 1 to 105 months (median, 27.5 months) of completion of polychemotherapy. Age ranged from 6.2 to 36.6 years (median, 13.6 years). Patients were divided according to treatment into four groups: (A) patients treated with CVPP (cyclophosphamide, vinblastine, procarbazine, and prednisone); (B) 22 patients treated with CVPP plus radiotherapy (median radiation dose to the thyroid, 3000 cGy); (C) seven patients with ACOP/BVP (adriamycin, cyclophosphamide, vincristine, prednisone, bleomycin, vinblastine, procarbazine); and (D) seven patients treated with different polychemotherapy protocols, four of whom also received radiotherapy. Elevated basal and/or post-TRH, -TSH levels were found in the following: Group A: two of 12 patients (17%); Group B: 11 of 22 (50%); Group C: four of seven (57%); and Group D: two of seven (28%). Positive antimicrosomal thyroid antibody titers (AM Ab) were found in the following: Group A: three of 12 patients (25%); Group B: six of 21 (28%), Group C: two of seven (28%); and Group D: one of six (17%). Of 46 patients studied, 12 (26%) had positive AM Ab; 37 of 46 patients were younger than 20 years of age, 11 (30%) of whom had positive AM Ab versus 4% in the normal population (P less than 0.001). Two recently diagnosed, untreated patients had either high TSH response to TRH or positive AM Ab. In conclusion, higher frequency of thyroid dysfunction was observed in patients receiving radiotherapy (50% versus 27%). Prevalence of positive AM Ab, apparently unrelated to therapy, was higher in young patients than in the normal population. A predisposition to autoimmune thyroid disease seems to be present in these patients, but it is not possible to discern how lymphoma and thyroiditis are interrelated.

The TSH response to TRH was studied in 42 children with hypopituitarism. Basal TSH was similar to the control group except in seven patients who had elevated values (Group A). These children also had an altered TSH response to TRH but normal increments in T 4 , T 3 , and 131 I thyroid uptake after administration of bTSH. Three different patterns of TSH responses to TRH were observed in patients with normal basal TSH: delayed and exaggerated response (Group B, n=15), deficient response (Group C, n=4), and normal response (Group D, n=16). Some patients of groups A, B, and C with blunted basal growth velocity had an improved growth rate with T 4 therapy. However, a better response was observed when hGH and T 4 were administered simultaneously. The following conclusions were drawn: (1) high immunoreactive TSH in the presence of a thyroid gland responding normally to TSH suggests a dissociation between the biologic and immunologic activity of serum TSH; (2) an exaggerated and delayed response to TRH was frequently found in secondary hypothyroidism and suggests hypothalamic TRH deficiency; (3) an impaired TSH response to TRH is less frequent and suggests a pituitary abnormality; (4) patients with a normal response to TRH probably have normal hypothalamic-pituitary thyroid axis. The TRH test is useful in the diagnosis of hypothalamic-pituitary thyroid abnormalities and helps to unmask thyroid dysfunction. A number of such patients with stunted growth benefit from thyroid therapy.

Thirteen children with medulloblastoma, were studied after 2 to 62 months off radiotherapy and chemotherapy with methotrexate and BCNU. Ages at time of study ranged from 2.3 to 15.7 years. Eleven patients, followed for a mean of 22 months, showed a significant decrease of height score, whereas nine patients had deficient growth hormone (GH) response to provocative tests. Clinical pubertal progression was normal in all patients, and three of five girls with advanced pubertal development had menarche. No evidences of gonadotropin disturbances were found in five patients whereas seven had raised basal follicle-stimulating hormone (FSH) level or FSH response to luteinizing hormone-releasing hormone (LH-RH). Abnormalities in thyrotrophin (TSH) secretion were found in 9 of 13 patients. This study shows that poor growth and GH deficiency were frequent in our patients. The high frequency of thyroid disturbances observed point out the need of evaluating thyroid function for adequate replacement therapy. Perhaps modification of adjuvant chemotherapy in the future can diminish drug-induced gonadal damage.

SUMMARY A diagnosis of chronic lymphocytic thyroiditis (CLT) was made in forty-two children and adolescents according to Fisher's criteria. The age of the group ranged between 4±3 and 18±5 years. On the basis of serum TSH, T4 and RAI uptake, three groups of patients were distinguished at the time of diagnosis: 1, euthyroid group (n= 3) with normal TSH and T4; 2, hypothyroid group (n= 36) with high values of TSH, where three subgroups were distinguished: (a) compensated hypothyroidism (n= 14) with normal T4, (b) overt hypothy-roidism with high or normal RAI uptake and low T4 (n= 19), (c) overt hypothyroidism with low RAI uptake and low T4 (n= 3); 3, Hyperthyroid group (n= 3) with high T4. In CLT, variability is a feature not only of the initial presentation, but also of the subsequent evolution of the disease. Sixteen patients were followed for periods between 4 months and 6 years. Thyroid function did not change in six. Six patients with compensated or overt hypothyroidism improved, four became euthyroid with normal basal TSH and T4 values, however, all three tested had an exaggerated response to TRH. Three patients who were initially hyperthyroid progressed to a state of compensated hypothyroidism. One patient with overt hypothyroidism on presentation developed hyperthyroidism after 15 months and became hypothyroid once more 8 months later. The variable clinical course of CLT is characteristic of immunological disturbances.

Preferential conversion to rT3, an inert metabolite of T4, has been proposed as a homeostatic mechanism for thyroid hormone inactivation in several physiopathological situations (1,2).

Retarded effects of the radiotherapy to the neck and/or polychemoterapy on the thyroid were investigated in 66 patients (P), 47 with Hodgdn's disease (HD) and 19 with rcn-Hodgkin's lymphoma (NHL). Two, recently diagnosed, untreated P, were also studied. Age ranged from 6.2 to 52 years (median 13.5). Patients were divided in 3 groups: a-) 29 P treated with chemo and radiotherapy (radiation dose to the thyroid ranged from 300 to 6300r, median 3000); b-) 37 P with chemotherapy and c-) 2 P without treatment. Group a: 16 P (55%) showed an elevated basal and/or post TRH, TSH value; 7 (25%) of 28 P studied had positive antimicrosomal thyroid antibody titers (AM Ab); diagnosis of papillary carcinoma was made in 1 P. Prevalence of high TSH level was 33% within 2 years of radiotherapy and 66% after 61 months. Group b: 11 (30%) of 36 P showed elevated TSH levels; 9 (27%) of 33 P had positive AM Ab. Group c: 1 P with HD had goiter, elevated TSH levels and negative AM Ab. Sixteen (26%) of 61 P studied post-treatment had positive AM Ab. Higher frequency of high TSH levels was observed in P receiving radiotherapy (56 vs 30%). With longer intervals free of treatment, the prevalence increased. Prevalence of positive AM Ab was higher in our P than in our normal population (26 vs 4.4%). A genetic predisposition to autoimmune thyroid disease cannot be ruled out and the influence of treatment is difficult to assess.

At present no Laboratory test is available to predict the evolution of J H (Graves'disease). A follow ip to 2 to 14 y. was carried up in 59 patients aged 2 4/12 to 17 y. old (X ± SD: 9.4 ± 3.9). They all received antithyroid drugs as initial treatment. Thirty six patients followed for 3 to 14 y., could be reevaluated with T4, T3 and TSH and/or TRH after treatment in at least 2 ocassions: at short-term (ST: 1-2 y. post onset of treatment) and at long-term (LT:more than 3 y.; X ± 6.23 ± 3.3). Twenty three patients (64%) remained hyperthyroid (Hper) between ST and LT and 9(25%) hypo or euthyroid (Hpo/Eu) between ST and LT; only 4 (11%) changed from Hper at ST to Hpo/Eu at LT. Thus, 89% did not modify their thyroid function between ST and LT. The period of the evolution from Hper to Hpo/Eu showed two distinct populations, one with a X ± SD of 17.3 ± 3.8 months and another with X ± SD of 9.4 ± 2.5 y. It is concluded that evaluation of thyroid function at ST is useful to predict their status at LT since 90% of patients showed no variations. Since patients who changed thyroid fuction from Hper to Hpo/Eu at ST did it in X 17.3 months it is advisable to wait up to this time to select another therapeutic options. If Hper persists the possibility of I 131 administration should be considered to avoid the excessively long treatment required by the unrelenting course of this disease.

At present, no laboratory test is available to predict the evolution of Graves' disease. A follow up of 1 to 14 y. in 59 patients aged 2 4/12 to 17 y. old (±SD: 9.4±3.9) is presented. They all received antithyroid drugs as initial treatment, 7 were treated with 131I for intolerance or social problems. Thirty six patients followed for 3 to 14 y., could be reevaluated with T4, T3 and TSH and/or TRH after treatment in at least 2 occasions, at short term (ST: 1-2 y. post onset of treatment) and at long term (LT: more than 3 y.; : 6.2±3.3). According to thyroid status at ST and LT respectively 3 groups were found: I) hyperthyroidism (Hper) and Hper n=23, 64%; II) Hper and hypo or euthyroidism (Hpo/Eu) n=4, 11%; III)Hpo/Eu and Hpo/Eu n=9, 25%. No patient changed from Hpo to Hper. Eighty nine percent of patients did not modify their thyroid function between ST and LT. The influence of age at admission on persistence of Hper 3 y. later was also studied. Fourteen out of 16 patients (87.5%) less than 8 y. were still Hper while only 14 out of 24 (58.3%) were Hper after 8 y. old. It is concluded that evaluation of thyroid function at ST is useful to predict thyroid status at LT since 90% of patients showed no variations. Patients developing Graves' disease before the age of 8 y. have a high chance of remaining Hper 3 y. later. If Hper persits at ST evaluation, the possibility of 131I adminstration should be considered to avoid the excessively long treatment required by the unrelenting course of this disease.