Nicolau Lima

Prognostic value of serial serum thyroglobulin determinations after total thyroidectomy for differentiated thyroid cancer

Serial weekly serum samples (for 3 weeks) were obtained from 42 patients with differentiated thyroid cancer (DTC, papillary no.=35, follicular no.=6, Hürthle cell no.=1) for serum thyroid hormone, TSH and TG before and after total thyroidectomy. Serum specimens were also obtained one month after radioiodine (131I) therapy followed by suppressive dose of L-thyroxine (L-T4, 2.5 μg/kg). The patients were subdivided into four groups: group I: the DTC was confined to a single solid nodule (no.=12); group II: thyroid malignancy invaded local cervical structures but there were no lymph node metastases (no.=8); group III: DTC with lymph node metastases (no.=6); and group IV: DTC with distant metastases (no.=16). In all group I patients serum TG remained undetectable in spite of elevated serum TSH levels at the 3rd week post-surgery (PS). Only one of group II patients had a detectable serum TG value of 5.2 ng/ml (3rd week PS). By contrast, 37.5% of group III patients had detectable serum TG levels, ranging from 3.4 to 16.8 ng/ml (3rd week PS). Lymph node metastases were detected in 5 of these patients by whole body scan (WBS) and removed surgically in 3. As expected, group IV patients had elevated serum TG values ranging 33.0–958.0 ng/ml and distant metastases were confirmed in all of them by WBS. From the calculations through univariate logistic regression comparing TG concentrations at the 3rd week PS from groups I and II vs groups III and IV, we obtained a cut-off value of 2.3 ng/ml with the following efficacy features: sensitivity= 74.5%; specificity=95%; positive predictive value=92.3%; negative predictive value= 65.5%; and accuracy=73.8%. After 131I and L-T4 suppressive therapy, only 5 out of 36 patients of groups I, II and III had detectable serum TG levels (3.1–7.0 ng/ml) whereas serum TG was detectable in all group IV patients (ranging 2.5–8.6 ng/ml). We concluded that serum TG concentrations above 2.3 ng/ml at the 3rd week PS could be suggestive of lymph node or distant metastases in patients with DTC. Patients with serum TG above this limit could be considered at risk for metastatic disease and higher doses of diagnostic iodine-131 (131I) may be indicated for actinic ablation.

Natural course of iodine-induced thyrotoxicosis (Jodbasedow) in endemic goiter area: A 5 year follow-up

In the Balsas region of North Brazil (85% prevalence of goiter), 1876 goitrous subjects (1663 with goiter grade I and II and 103 with grade III multinodular goiter) were treated with 1 ml of iodized oil im (I-oil). From the population with grade III goiter we were able to follow-up for 5 yr 13 euthyroid goitrous patients (group 1 ) and 8 goitrous individuals (group 2) who developed iodine-induced thyrotoxicosis (NT, 0.42% of the total population or 7.76% of the multinodular goiter subjects). The two groups were matched for age and goiter size, and had no significant differences in the baseline levels of thyroid hormone concentration, T3/T4 ratio or mean serum TSH. However, group 2 had a higher concentration of serum Tg, and 48 h after challenge with 10 U of bovine TSH (bTSH) had a significantly higher absolute release of T3 and Tg than group 1. In 4 patients IIT was transitory and resolved by 12 months. Four other subjects, however, maintained a mild clinical form of IIT that only normalized at 50 months. Only one patient needed treatment with methylmercaptoimidazol. There was no evidence of autoantibodies (TSH-receptor inhibiting antibody, anti-Tg or anti-microsomal antibodies) against thyroid antigens in group 2 patients. All subjects, including those with thyrotoxicosis, showed a remarkable shrinkage of the goiter by 60 months which was reflected by a significantly lower absolute response of T3 and Tg after bTSH. We conclude that IIT induced by I-oil is a rare complication of I-oil prophylaxis in a general goitrous population, is more common in patients with multinodular goiters and has a transient form and a persistent form that tends to resolve spontaneously by 60 months.

The effect of hypocaloric diet with and without d-fenfluramine treatment on growth hormone release after growth hormone-releasing factor stimulation in patients with android obesity☆

Basal and stimulated growth hormone (GH) secretions are impaired in obesity, and partial restoration of the GH response to various stimuli is observed after weight loss. The aim of the present study was to investigate whether D-fenfluramine, a serotoninergic agent, would increase the GH response to growth hormone-releasing factor (GRF) as compared with placebo in obese android patients. The subjects were 17 patients with android obesity (four men and 13 women) aged 21 to 58 years with a body mass index (BMI) ranging from 32.0 to 52.2 kg/m2 and an abdominal-gluteal ratio greater than 1.0. The following four GRF (1-44) tests were performed: T-30 (control), T0 (after 30 days of a hypocaloric diet), T1 (after 30 days of either placebo or D-fenfluramine 15 mg twice daily), and T2 (after 30 additional days of placebo or D-fenfluramine). The hypocaloric diet was maintained during the T1 and T2 periods. At each test, the serum GH response to GRF was measured at frequent intervals, and the peak GH response and the GH area under the curve were calculated. Serum insulin concentrations were also assayed before GRF stimulation, and the insulin to GH ratio was obtained. The D-fenfluramine-treated group had a mean +/- SEM GH peak level after GRF significantly higher at T1 (43.3 +/- 8.2 micrograms/L) and T2 (50.9 +/- 9.2 micrograms/L) compared with the placebo group. Likewise, the mean integrated areas of GH response were significantly higher for the D-fenfluramine-treated group as compared with the placebo group at both T1 and T2 of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Thyroid atrophy in myxedematous endemic cretinism: possible role for growth-blocking immunoglobulins.

We have examined the ability of IgGs obtained from 8 endemic cretins to inhibit TSH-stimulated thyroid cell growth in culture. Clinical and laboratory evidence for hypothyroidism was present in six subjects; the two remaining patients had borderline low serum T4, normal T3 and exaggerated TSH response to TRH. In six patients 2 mg IgG exhibited an inhibitory effect in the cellular growth expressed by a diminished incorporation of 3H-thymidine into the DNA of TSH-stimulated FRTL-5 cells (range: 26-87% inhibition). Seven patients presented clinically with thyroid atrophy of relatively small thyroid enlargements for the degree of chronic iodine deficiency that was present in the area. The remaining subject had a large multinodular goiter and IgG purified from this patient had no inhibitory effect in the FRTL-5 cellular growth. A direct relationship was noted between the degree of thyroid growth inhibition (%) and the basal serum TSH concentration. We conclude that the presence of thyroid growth inhibiting immunoglobulin may be related to the absence of thyroid growth or even thyroid atrophy in endemic cretins.

A função gonadal do homem obeso

In obese men, sex hormone-binding globulin (SHBG) as well as total testosterone (TT) levels are decreased. Data concerning serum free testosterone (FT) levels in obese men are discordant. FT levels are decreased in only some morbidly obese men consistent with an impairment of the feedback regulatory mechanism. It has been suggested that a functional decrease of LH pulse amplitude and serum LH levels are reflected in their hypoandrogenism. We have studied two groups of obese men (Group 1: BMI £ 35kg/m2 and Group 2: BMI ³ 35.1kg/m2) before and after six months of a low calorie diet (1200kcal/day), Every patient received a therapeutic prescription of dexfenfluramine (15mg b.i.d.) that was maintained for six months. Plasma insulin levels, serum total testosterone, free testosterone and LH concentrations were obtained before and after weight loss. Moderately obese men (BMI = 32.3 ± 1.9kg/m2) presented significantly decreased TT levels (390 ± 120ng/dL) as well as FT (mean ± SD: 16.0 ± 4.8pg/mL) as compared with normal controls. Serum LH concentrations (4.5 ± 2.9mlU/mL) were normal. Insulin levels were elevated in all patients (46,3 ± 30.1 mU/mL). After weight-loss there was a significant (p < 0.01) increase in TT, FT and LH levels whereas insulin concentrations significantly decreased, In massively obese men (BMI = 43.0 ± 6.7kg/m2) TT (320 ± 110ng/dL), FT (11.0 ± 2.1pg/mL) and LH (3.1 ± 1.3mlU/mL) were decreased and significantly lower as compared with the previous group and normal controls. As expected, after weight loss as expected, TT, FT and LH levels increased significantly while insulin concentrations decreased. We concluded that FT levels are dependent on the degree of obesity, massively obese men (BMI ³ 35.1kg/m2) being considered as candidates for consistently low FT levels.