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Elevated anti-Gal antibody activity may have a physiopathological growth-stimulating
role in endemic goiter as proposed by Knobel and collaborators
(from Sào Paulo, Brazil). Anti-Gal is a human polyclonal antibody
that constitutes approximately 1% of the circulating IgG and interacts
specifically with the mammalian carbohydrate a-galactosyl epitope. Anti-Gal
titers were found to be markedly elevated in Graves' disease patients but
not normal subjects. Binding of anti-Gal to epitopes aberrantly expressed
on human thyrocytes in endemic goiter is likely to contribute to the pathogenesis
of this disease. Serum was obtained from 36 grade III-IV (WHO) goitrous
patients (group 1), 20 goitrous patients grade I-II living in a chronic
iodine-deficient area of Brazil (Grao Mogol, MG) (group 2) and 55 normal
controls (group 3). Anti- Gal was evaluated by ELISA in comparison with
a radioimmunological method. Serum anti-Gal antibodies (ELISA) were more
elevated in both goitrous groups (group 1, mean ± SD OD = 2,200
±2,100 U; group 2, mean ± SD OD = 1,220 ± 990 U) than
group 3 (mean ± SD OD = 45 ± 44 U). The antibody activity
as measured by the radioimmunological assay was also more elevated in group
1 (21.2 ± 9%) and group 2 (18.6 ± 9.9 %) than normal controls
(3.1 ± 2.7 %). The authors concluded that the anti-Gal activity
in patients with endemic goiter is higher than in healthy individuals and
is likely to contribute to the pathogenesis of this disease. More specifically
anti-Gal Ab have been demonstrated to interact with the TSH receptor followed
by a stimulation of intracellular cAMP. This could lead to further growth
of the iodine deficient goiter.
Urinary excretion of iodine was assayed in Brazilian school children, randomly selected during the 1995 national survey of Iodine Deficiency Disorders (IDD), reported Esteves and co-authors (Sào Paulo, Brazil). They analyzed 16,803 casual urine samples by a semi-automated method developed by ICCIDD with minor modifications from their laboratory; by this method, urine samples, controls and iodate standards are first oxidized with 1M ammonium persulfate and then urinary iodine is measured by the iodide catalysis of the redox reaction between Ceric (Ce+4) and Arsenic (As+3), being the iodine concentration proportional to its catalytic activity. The final part of the reaction is then transferred to microplates which were read automatically at 405 nm. Using casual urine samples, ICCIDD classifies the severity of the iodine deficiency as severe when the median of the urinary iodide is less than 2 µg/dL and normal when above 10 µg/dL. Of the 401 studied counties, the group found 4 moderately deficient (Almas, Arraias and Parana in the State of Tocantins and Cocos in the State of Bahia, with medians of 3.3, 3.4, 2.6 and 4.4 µg/dL, respectively) and 116 mildly deficient. The majority of these counties are in regions of sedimentary basins (rivers Tocantins, Araguaia, Sào Francisco, Paraná) or recently populated. It is concluded that, despite universal salt iodination, there are still some areas with persistent IDD in Brazil. |
