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Background. Chronic autoimmune thyroiditis (CAT) frequently alters thyroid vascularization, likely as a result of the autoimmune process. Objective. To evaluate the effects of low-level laser therapy (LLLT) on the thyroid vascularization of patients with hypothyroidism induced by CAT using color Doppler ultrasound parameters. Methods. In this randomized clinical trial, 43 patients who underwent levothyroxine replacement for CAT-induced hypothyroidism were randomly assigned to receive either 10 sessions of LLLT (L group, n = 23) or 10 sessions of a placebo treatment (P group, n = 20). Color Doppler ultrasounds were performed before and 30 days after interventions. To verify the vascularity of the thyroid parenchyma, power Doppler was performed. The systolic peak velocity (SPV) and resistance index (RI) in the superior (STA) and inferior thyroid arteries (ITAs) were measured by pulsed Doppler. Results. The frequency of normal vascularization of the thyroid lobes observed in the postintervention power Doppler examination was significantly higher in the L than in the P group (P = 0.023). The pulsed Doppler examination revealed an increase in the SPV of the ITA in the L group compared with the P group (P = 0.016). No significant differences in the SPV of the STA and in the RI were found between the groups. Conclusion. These results suggest that LLLT can ameliorate thyroid parenchyma vascularization and increase the SPV of the ITA of patients with hypothyroidism caused by CAT. [ABSTRACT FROM AUTHOR]

The article presents a study which evaluated thyroid volume, ultrasonographic abnormalities and urinary iodine excretion (UIE) in schoolchildren living in an iodine-sufficient area in southern Brazil. It explains that high levels of iodine may induce autoimmune thyroiditis, hypothyroidism, goiter and hyperthyroidism mostly in the elderly. Results of the tests show high levels of UIE and abnormalities detected including hemiagenesis, nodules, cysts and hypoechogenicity which have all been linked to excessive iodine intake.

OBJECTIVE Postpartum thyroid dysfunction (PPTD) is an autoimmune disorder characterized by the development of transient hyperthyroidism and, more frequently, hypothyroidism (or both) during the first six months of the puerperal period. A variable incidence has been reported in part because of differences in the number of women studied, the frequency of thyroid assessment postpartum, diagnostic criteria and methodology. The aim of this study was to evaluate thyroid function, ultrasound images and titre of autoantibodies against thyroid antigens in a cohort of pregnant women who met the criteria of ‘normal’ thyroid gland structure on clinical examination and imaging and normal thyroid function tests without a significantly positive anti-thyroid peroxidase (TPO) antibody titre (i.e. < 100 U/ml) in the first trimester. DESIGN AND PATIENTS Eight hundred nulliparous or multiparous (one to seven previous pregnancies) pregnant women (age 26.1 ± 4.8 years, mean ± SD), were submitted to clinical, laboratory and ultrasonographic examination in the first trimester of pregnancy. Among these forty-six patients were excluded because of thyroid dysfunction, ultrasound structural abnormalities or a positive anti-TPO antibody titre (> 100 U/ml). A total number of 754 women were available for further studies in the postpartum period. A relatively large number of these patients (386) were lost for follow-up either before or after delivery. MEASUREMENTS A cohort of 368 puerperal women was followed up regularly at 3, 6, 12 and 24 months after delivery, with periodic thyroid function tests, random urine iodine measurements, assays for serum autoantibodies against thyroid antigens and imaging by ultrasound. RESULTS The provisional diagnosis of PPTD was established in 78 out of 368 who had positive anti-TPO levels and ultrasonographic thyroid structural changes. Twenty-nine of these patients had a transient rise of anti-TPO autoantibodies characterizing an... [ABSTRACT FROM AUTHOR]

Objective: To evaluate the prevalence of chronic autoimmune thyroiditis (CAT) and iodine-induced hypothyroidism, hyperthyroidism (overt and subclinical), and goiter in a population exposed to excessive iodine intake for 5 years (table salt iodine concentrations: 40-100 mg/kg salt). Design This was a population-based, cross-sectional study with 1085 participants randomly selected from a metropolitan area in São Paulo, Brazil, and conducted during the first semester of 2004., Methods: Thyroid ultrasound examination was performed in all participants and samples of urine and blood were collected from each subject. Serum levels of thyroid-stimulating hormone, free thyroxine, and anti-thyroid peroxidase (TPO) antibodies, urinary iodine concentration, thyroid volume, and thyroid echogenicity were evaluated. We also analyzed table salt iodine concentrations., Results: At the time the study was conducted, table salt iodine concentrations were within the new official limits (20-60 mg/kg salt). Nevertheless, in 45.6% of the participants, urinary iodine excretion was excessive (above 300 microg/l) and, in 14.1%, it was higher than 400 microg/l. The prevalence of CAT (including atrophic thyroiditis) was 16.9% (183/1085), women were more affected than men (21.5 vs 9.1% respectively, P=0.02). Hypothyroidism was detected in 8.0% (87/1085) of the population with CAT. Hyperthyroidism was diagnosed in 3.3% of the individuals (36/1085) and goiter was identified in 3.1% (34/1085)., Conclusions: Five years of excessive iodine intake by the Brazilian population may have increased the prevalence of CAT and hypothyroidism in subjects genetically predisposed to thyroid autoimmune diseases. Appropriate screening for early detection of thyroid dysfunction may be considered during excessive nutritional iodine intake.

Background: Thyroglobulin (Tg) is a large glycoprotein that is intimately involved in the biosynthesis of thyroxine and triiodothyronine. At least 38 mutations have been described in the Tg gene that are associated with varying degrees of hypothyroidism. We studied the Tg gene in four related subjects with congenital hypothyroidism., Summary: We found a novel compound heterozygous constellation (IVS30 + 1G>T/A2215D) in a brother and sister and one previously described related mutation (IVS30+1G>T) in their two sibling second degree cousins. The brother with the IVS30 + 1G>T/A2215D mutation and the two siblings with the IVS30+1G>T mutation had fetal or neonatal goiter and all had hypothyroidism., Conclusions: This study further confirms the association of the IVS30+G>T mutation of the Tg gene with hypothyroidism. Computer analysis predicts that the A2215D mutation, first reported here, should cause structural instability of Tg but when present as a compound heterozygous mutation with IVS30+G>T/A its effect is unclear but is likely to be influenced by iodine intake.

Purpose: To evaluate the prevalence of chronic autoimmune thyroiditis in 2 urban areas of metropolitan São Paulo (Brazil): Polo Area neighboring a large petrochemical complex and São Bernardo Campo Area (control area)., Subjects and Methods: Subjects were randomly included from the adult population (20 to 70 years of age) of both genders (women 80%, men 20%) who voluntarily agreed to participate. From the Polo Area, in the vicinity of a large petrochemical industrial complex, 409 subjects were included; from the control area (São Bernardo Campo Area) 420 individuals were included. All subjects were clinically examined, and a detailed record of past thyroid illness and medications was obtained. Ultrasonographic studies were performed using a portable GE Medical Systems apparatus. Blood samples were obtained for free T4, serum TSH, and serum anti-thyroid peroxidase autoantibodies. Urine specimens were collected in Monovette syringes for assaying iodine content. Salt samples were collected at households, and the iodine content was measured., Results: Chronic autoimmune thyroiditis was diagnosed both echographically (marked hypoechogenicity) and immunologically (presence of autoantibodies against thyroid peroxidase). In the Polo Area, 15.6% of the examined population had chronic autoimmune thyroiditis, and in the control area (São Bernardo Campo Area), 19.5% of the population had evidence of chronic autoimmune thyroiditis (P > 0.057, not significant). The prevalence of hypothyroidism was 4.9% in the Polo Area and 8.3% in the São Bernardo Campo Area (P = 0.0461 significant). Taking the 2 populations together, 6.6% had hypothyroidism (about one third of these patients were on L-T4 treatment). The mean thyroid volume was 11.2 mL. Domestic salt had a normal concentration of iodine (35.5 + 6.61 mg/kg). Urinary excretion of iodine was above 300 microg Iodine/L in 58.5% of the total population., Conclusion: The high iodine intake (above 300 microg Iodine/L of urine) that was present from 1998 through 2005 may be related to a higher prevalence of chronic autoimmune thyroiditis in both areas that were studied. There was no apparent or documented relationship of chronic autoimmune thyroiditis prevalence to the proximity to the petrochemical complex.

The thyroid gland promotes its adaptation to iodine deficiency inducing an increase in the iodine uptake followed by a substantial increase in the thyroid gland mass (goiter). Simultaneously, there is a preferential T3 secretion by the follicular cell and a persistently elevated serum TSH. Laboratory tests, isotopic methods and imaging are routinely used to verify the altered thyroid pathophysiology. In certain populations the presence of goitrogenic natural substances, present in the locally consumed staple food, were found and may add to the pathogenic process. Endemic cretinism is usually present when the iodine deficiency is quite low and may present with the neurologic or myxedematous sub-types, frequently associated with deafmutism. In Brazil, the prevalence of iodine-deficiency disorders has been evaluated, periodically, with schoolchildren examined for goiter. Universal salt iodination was implemented in Brazil in the early fifties but recently the system was considered effective for the supply of iodine to the Brazilian population.