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L Baldet

Publications and source records attributed to L Baldet.

At least 19 recordsLinked to original sources
PubMed1992

Thyroid hormone generalized resistance.

The syndromes of thyroid hormone resistance may affect overall or only some tissues. The generalized resistance is an inherited disease which involves a familial eumetabolic or hypometabolic goiter, increased free thyroid hormones with normal or elevated plasma TSH levels; children may present mental retardation, deafness, short stature and delayed bone age. The disease is frequently misdiagnosed. In vivo and in vitro tests may be used to assess the diagnosis. The defect of increment of sex hormone-binding globulin after administration of T3 may be useful in the demonstration of the disease. Therapy uses high T4 or T3 doses in hypometabolic patients. The generalized thyroid hormone resistance could be linked to abnormalities at the T3 receptor and c-erb A gene level, as a consequence of different point mutations or deletions involving the hormone-binding domain.

Drug Resistance↗
PubMed1992

[Endemic goiter in the La Kara region (Togo). Analysis of etiologic factors].

Among 6,035 people living in 3 villages from the area of La Kara (Togo), 984 randomized subjects were investigated to evaluate goiter prevalence and related etiologic factors. Creatinine and thiocyanates (SCN-) were measured in urine, thyroid hormones and TSH in plasma. Iodine was evaluated in urine, water, salt, soil, millet and sorgho. The amount of cassava was evaluated in food. Mean goiter prevalence was 32%, reaching to 45.9% in one village; urinary iodine remained in a low range (27.2 +/- 2.18 micrograms/g creatinine in adults, 34.3 +/- 6.7 in children--m +/- SEM) independently of the presence of endemic goiter. Urinary SCN- was increased. Low iodine values were found in food, salt, soil and water which contained few mineral elements except flour which was increased in the samples collected in one of the 3 villages. Cretinism was absent, T4, T3, TSH remained in a normal range. This study confirms a high prevalence of endemic goiter in the area of La Kara with iodine deficiency, leading to an urgent iodine supplementation.

Goiter, Endemic↗
PubMed1979

The TRG Test. Which is the best index of TSH release?.

Prolonged (two hours) TRH tests were performed on 29 controls and 182 thyrotoxicosis patients of varying thyroid status after treatment with radioiodine. The object was to find which of the simple measurements of TSH from the TRH test most faithfully reflected the total amount of TSH (TTSH) released in response to the TRH. The simple indices compared were the absolute levels of TSH (ATSH) achieved at intervals during the test, and the increments in TSH (delta TSH) recorded at the same points in time. TTSH was measured by planimetry of the area beneath the response curve. Patients were classified as normo-responders, hyper-responders or hypo-responders according to normal limits for TTSH deduced from the controls. When each simple index of TSH response was substituted in turn for TTSH, the overall frequency of misclassification was considerably greater for ATSH than for delta TSH. This was largely due to the wide variability of passive or basal TSH secretion, which seriously confused the distinction between normally-responsive and hypo-responsive patients when ATSH was used. The delta TSH measured at 30 minutes gave the best overall results in terms of least classification error and closest correlation with TTSH.

Adult↗
PubMed1978

[Hyperthyroidism].

Explore the source record for details and available documents.

Graves Disease↗
PubMed1978

[Chronologic study of free T3 and T4, of responses to TRH and of the suppression test during treatment of Basedow's disease].

32 patients with Graves' Disease were investigated before treatment, during ATD therapy and after recovery with a normal T3 suppression test. Before treatment, TRH response was negative with elevated values of plasma TT4, AFT4, TT3 and AFT3. The 3d, 6 - 9 and 12-18 months and after recovery, several patients remained unresponders to TRH despite normal AFT4 and AFT3 in serum. In an opposite way some patients were responders, 1 month after ATD withdrawal, at the 6-9 month, with elevated values of AFT4 or AFT3. The discrepancy between TRH response and T3 suppression test is pointed out after recovery. The unresponsiveness of TSH to TRH unexplained by serum AFT4 or AFT3 may be due to : 1) a decrease in pituitary TSH stores. 2) an unknown factor inhibiting TSH release during Graves' disease 3) an hypersensitivity of thyreotrop cells to T3.

Graves Disease↗
PubMed1978

[Interference of T4 in different serum T3 radioimmunologic determination kits].

The cross reactivity of T3 antibodies for T4 was studied with five T3 RIA kits. T4 used was provided from T4 RIA Kits (Abbot Beckman, Corning). The results are shown on the table indicating the concentration of T3 or T4 required to displace 50% of the T3 125 from anti T3. The cross reactivity for T4 of T3 antibodies from Lepetit and Phadebas was the same and was smaller than cross reactivity with the other laboratories. In clinical practice serum T4 levels of hypo and euthyroid subjects are not so high to false T3 determination. In hyperthyroid subjects the diagnosis cannot be influenced by this cross reactivity. However, the study of the kinetic and monodeiodination of T4 into T3 may be wrong when T4/T3 ratio increases.

Cross Reactions↗
PubMed1977

Short and long term effects of radioiodine and antithyroid drugs on T4 binding proteins, free T4 and T3, during Graves' disease therapy.

Ninety five patients with Graves' disease were studied before and at three months intervals after antithyroid drugs (ATD) (31 cases) or radioiodine (64 cases) therapy until recovery. Before treatment, the T4 maxima binding capacity of TBPA was significantly decreased 253.5 +/- 11.4 mug/100 ml)(mean + se) (control values: 287 +/- 10.4 mug/100 ml) (alpha = 0.04), especially in 53.7% of patients (m = 177 +/- 8 mug/100 ml). The mean of TBG (m = 20.7 +/- 0.9 mug/100 ml) was not different from euthyroid subjects (m = 19.7 +/- 1.7 mug/100 ml) except in 51.2% of patients who had a low TBG (m = 14.3 +/- 1.1 mug/100 ml). An inverse linear correlation was found between TBG-DFT4 (alpha = 0.05) and DF T 3 (alpha = 0.002), TBPA-log DF T4 (alpha = 0.05) but not between TBG and TBPA. The physiological relationship between DFT3, DFT4, TT3, TBG and TBPA was studied in vitro; after adding increased quantities of T4 to a pool of sera collected from eu, hypo or hyperthyroid patients, DFT4, DFT3, FT3 index increased in linear positive relationship with TT4 concentrations, the kinetic of this phenomena was inversely correlated with T4 maximal binding capacity of TBG or TBPA for T4. Addition of T3 to the same sera did not show any effect on the previous parameters. DFT3 depended on the level of T4 in serum more than T3 concentration and was in inverse relationship with the maximal binding capacity of TBG. This data might explain the paradoxal normal or slightly increased values of DFT3 found in T3 thyrotoxicosis. In patients treated with ATD or radioiodine, TBPA but not TBG increased significantly on year after. However, in subjects with an initial very low TGB or TBPA, this phenomenon occurred on the third month after radioiodine or ATD. During the same period, DF T4 and DF T3 were inversely correlated to TBG and TBPA. In conclusion, important changes in T4 binding proteins and free fractions of thyroid hormones were observed in Graves' disease but were corrected by antithyroid therapy. All these data were in good agreement with the normalisation of thyroid function.

Adolescent↗
PubMedDate not supplied

[Study of the HL-A system in Basedow's disease (author's transl)].

HL-A typing has been carried out in 100 caucasians with Graves' disease and compared with 270 healthy controls. 25 HL-A antigens were characterized using a lymphocytotoxicity microtechnique. Analysis of the results reveals an increased incidence of HL-A8 antigen (35% in patients as compared to 16,3% in controls), with a high degree of statistical significance: p=0.0002 and corrected p X 25) = 0.005. We did not observe a clearcut correlation between the presence of HL-A8 and different characteristics of the disease: sex, age of onset, familial history, exophtalmia, goiter, severity. The knowledge of the relationships between the HL-A8 gene and several auto-immune diseases is a strong argument in favor of the auto-immune nature of Graves' disease. The association between HL-A8 and Graves' disease could be explained by a close linkage between the second HL-A locus and one or several Ir-IgG loci occupied in predisposed individuals by predisposing alleles. In these subjects, an antigenic contact with an exogenous etiological agent would induce a pathological immune response, with production of thyroid stimulating IgG.

Graves Disease↗
PubMedDate not supplied

[HLA B8 and Graves' disease (author's transl)].

HLA typing has been carried out in 100 caucasions with Graves' disease and compared with 270 healthy controls. 25 HL-A antigens were characterized using a lymphocytotoxicity micro-technique. Analysis of the results reveals an increased incidence of HLA-B8 antigen (35% in patients as compared to 16.3% in controls) with a high degree of statistical significance: p = 0.0002 and corrected p (X 25) = 0.005. We did not observe a clear-cut correlation between the presence of HLA-B8 and different characteristics of the disease: sex, age of onset, familial history, exophtalmia, goiter, severity. The knowledge of the relationships between the HLA B8 gene and several auto-immune diseases is a strong argument in favor of the auto-immune nature of Graves' disease. The association between HLA B8 and Graves' disease could be explained by a close linkage between the second HLA locus and one or several Ir-IrG loci, occupied in predisposed individuals by "predisposing" alleles. In these subjects, an antigenic contact with an exogenous etiological agent would induce a pathological immune response, with production of thyroid stimulating IgG.

Adult↗
PubMedDate not supplied

[Proceedings: Kinetics and disposal rate of triiodothyronine in patients with atuonomous hot nodular goiter, with or without thyrotoxicosis (author's transl)].

Eight female patients are studied, four of them without hyperthyroidism. The following were measured before and after surgery = hormonal iodine by column, serum concentrations of T T3, AF T3, TSH, total T3 distribution space, T3 pool size T3 fractional turnover rate. T T3 is measured in the serum of peripheral venous blood, nodular venous blood and of jugular venous blood of the opposite side of the adenoma. Before surgery, the mean of T T3 in patients with hyperthyroidism is increased in serum obtained from brachial and not nodule venous blood. Are also increased AF T3 and T3 production rate. In patients without hyperthyroidism, T T3, AF T3 are increased in two subjects only, but T3 production rate is rised among three of them. After surgery the previous values are not different with normal values. These data are in good agreement with the hypothesis that, in patients without thyrotoxicosis, there is an increase in T3 production from not nodular goiter. There phenomena may explain unresponsiveness to TRH test and inactivity of normal thyroid. Absence of hyperthyroidism may be due to a lack of sensitivity of peripheral tissues to the increase of T3.

Female↗