The predominant form of non-toxic goiter in Greece is now autoimmune thyroiditis.
(17/1350)
Endemic non-toxic goiter (NTG) in Greece has been attributed primarily to iodine deficiency. Thirty years ago about 60% of the prepubertal boys and girls examined in endemic goiter regions presented with NTG and among them thyroid autoimmunity was rarely detected. Although iodine supplementation has corrected this deficiency during the past 30 years, new cases of NTG still appear. To evaluate the prevalence and type of NTG and the effect of iodine supplementation on them in Greece at present, we performed two cross-sectional clinical studies and a retrospective pathology one: (i) thyroid gland volume and urinary iodine excretion (UIE) were assessed in a representative sample of 1213 schoolchildren from previously endemic and non-endemic regions; (ii) serum thyroxine, tri-iodothyronine, TSH, thyroid autoantibodies (AAB) (anti-thyroid peroxidase and anti-thyroglobulin antibodies) and UIE (in 60 patients) were measured in 300 consecutive patients with NTG from Athens and Heraklion; and (iii) we compared the prevalence of autoimmunity among fine needle aspiration smears of benign thyroid pathologies performed by the same pathologist between 1985 and 1986 (975 cases) and between 1994 and 1995 (2702 cases). We found that 12. 5% of the schoolchildren examined in regions with a previous history of endemic goiter had NTG, whereas this percentage was only 1.7% in areas without such a history. In Athens (61.6%) and Heraklion (58. 5%) a substantial number of NTG patients were AAB positive and biochemically hypothyroid. UIE in Athens did not differ between patients with autoimmune goiter (ATG) and simple goiter. The prevalence of autoimmune stigmata in pathology smears has increased from 5.94% (years 1985-1986) to 13.91% (years 1994-1995) (P<0.05). We conclude that: (i) the persistence of endemic goiter in regional foci despite iodine deficiency correction suggests a possible role for a naturally occurring goitrogen; (ii) ATG is the predominant form of NTG in Greece nowadays; and (iii) the five-fold decrease in the prevalence of NTG during the past 30 years followed by the increase of ATG may support the relative character of the latter. (+info)
Urinary iodine and thyroid antibodies in Okinawa, Yamagata, Hyogo, and Nagano, Japan: the differences in iodine intake do not affect thyroid antibody positivity.
(18/1350)
Excess iodine intake may affect the development of Hashimoto's thyroiditis. Kelp consumption is very high in Okinawa. We expected a high prevalence of Hashimoto's thyroiditis in Okinawa. We studied urinary iodine excretion and the positivities of anti-thyroglobulin antibodies (TGAb) and anti-thyroid peroxidase antibodies (TPOAb) in the residents of Nishihara in Okinawa, Yamagata in Yamagata, Kobe in Hyogo, and Hotaka in Nagano, Japan. TGAb and/or TPOAb were positive in 142 (13.7%) of 1039 subjects in Nishihara, in 16 (16.0%) of 100 subjects in Yamagata, in 31 (13.4%) of 232 subjects in Kobe, and in 35 (13.9%) of 252 subjects in Hotaka; TGAb and/or TPOAb positivity was about the same in these 4 areas. One tenth of the subjects with positive TGAb and/or TPOAb had hypothyroidism; the frequencies of hypothyroidism in those with positive TGAb and/or TPOAb were about the same in Nishihara, Yamagata, Kobe, and Hotaka. The iodine concentration in samples of morning urine correlated well with the 24-h urine iodine excretion. The urinary iodine excretion was 1.5 mg/day in Nishihara. There were no differences between Nishihara and Yamagata in the urinary iodine concentration, but the urinary iodine concentrations in Kobe and Hotaka were less than those in Nishihara or Yamagata. The amounts of iodine excretion in Kobe and Hotaka were moderate, and less than those in Nishihara or Yamagata. The amounts of iodine intake in Kobe and Hotaka were less than those in Nishihara or Yamagata, but TGAb and/or TPOAb positivity was about the same in Nishihara, Yamagata, Kobe, and Hotaka. The differences in dietary iodine intake do not affect TGAb and/or TPOAb positivity. (+info)
Oral iodine supplementation does not reduce neutralizing antibody responses to oral poliovirus vaccine.
(19/1350)
Iodine deficiency is a major cause of impaired mental development, goitre, and cretinism in many parts of the world. Because existing immunization programmes can be used to deliver oral iodized oil (OIO) to infants at risk, it was important to know whether OIO could adversely affect the antibody response to vaccines, such as trivalent oral poliovirus vaccine (OPV). A randomized, double-blind, placebo-controlled clinical trial was conducted in Subang, West Java, Indonesia, in which 617 eight-week-old infants received either OIO or a placebo (poppy-seed oil) during a routine visit for their first dose of OPV as part of the Expanded Programme on Immunization (EPI). The infants received two boosters of OPV at 4-week intervals after the first dose, and were followed up when 6 months old. Neutralizing antibody titres to poliovirus serotypes 1, 2, and 3 were compared in serum samples that were taken from 478 of these infants just before the first dose of OPV and at 6 months. It was found that oral iodized oil did not reduce the antibody responses to any of the three serotypes of OPV. These results indicate that oral iodine may safely be delivered to infants at the same time as oral poliovirus vaccine according to current EPI immunization schedules. (+info)
Thyroid nodules, thyroid function and dietary iodine in the Marshall islands.
(20/1350)
BACKGROUND: Thyroid nodules have been found to be common in the population of the Marshall Islands. This has been attributed to potential exposure of radioiodines from the nuclear weapons tests on Bikini and Eniwetok between 1946 and 1958. METHODS: In order to get a full picture of thyroid pathology in the Marshallese population potentially exposed to radioactive fallout we performed a large thyroid screening programme using palpation, high resolution ultrasound and fine needle biopsies of palpable nodules. In addition, various parameters of thyroid function (free T3, free T4, thyroid stimulating hormone [TSH]) and anti-thyroid antibodies were examined in large proportions of the total population at risk. Since dietary iodine deficiency is an established risk factor for thyroid nodules, iodine concentration in urine samples of 362 adults and 119 children was measured as well as the iodine content of selected staple food products. RESULTS: The expected high prevalence of thyroid nodules was confirmed. There was no indication of an increased rate of impaired thyroid function in the Marshallese population. A moderate degree of iodine deficiency was found which may be responsible for some of the increased prevalence of thyroid nodules in the Marshallese population. CONCLUSIONS: Studies on the relationship between exposure to radioiodines and thyroid nodules need to take dietary iodine deficiency into account in the interpretation of findings. (+info)
China moves to tackle iodine deficiency.(21/1350)
(+info)
Linking iodine with autoimmune thyroiditis.
(22/1350)
A great deal of circumstantial evidence has linked iodine with the rising incidence of autoimmune thyroiditis in the United States. In our investigations, we have shown directly that T cells from humans with chronic lymphocytic thyroiditis proliferate in the presence of iodinated but not in the presence of noniodinated human thyroglobulin. Moreover, the proliferative response is restored when the thyroglobulin is iodinated artificially in vitro. Using a panel of monoclonal antibodies, we found evidence that the presence of iodine induces a number of stereochemical changes in the conformation of the molecule, resulting in the loss of some antigenic determinants and the appearance of others. One prominent determinant was associated with the iodine-containing amino acid thyroxine. Both the number and position of the iodine substituents determine the precise specificity of this epitope. A new model for the study of the role of iodine in inducing thyroid autoimmunity has become available in the form of the nonobese diabetic (NOD)-H2(h4) mouse. This animal develops autoimmune thyroiditis spontaneously but in relatively low prevalence. However, if iodine is added to the drinking water, the prevalence and severity of the thyroid lesions increase markedly. The immune response is specific for thyroglobulin, both in terms of the antibody response and T-cell proliferation. In fact, the appearance of lesions can be predicted by the presence of thyroglobulin-specific IgG2b antibody. The disease, moreover, can be transferred adoptively, using spleen cells from iodine-fed donors treated in vitro with iodinated thyroglobulin. The effects of iodine feeding are greater in conventional animals compared with those maintained under specific pathogen-free conditions. Based on T-cell proliferation, it appears that the NOD-H2(h4) strain of mice has innately a greater response to murine thyroglobulin than do other mouse strains and that the proliferation is increased even more by feeding iodine. We suggest, therefore, that the presence of iodine increases the autoantigenic potency of thyroglobulin, a major pathogenic antigen in the induction of autoimmune thyroiditis. This animal model provides a unique opportunity for investigating in detail the mechanisms by which an environmental agent can trigger a pathogenic autoimmune response in a susceptible host. (+info)
Repair of chronic peritoneal dialysis catheter.
(23/1350)
BACKGROUND: Damage to the peritoneal dialysis catheter may be due to wear from long-term use, exposure to antibacterial agents (strong oxidants), and accidental injury from sharp objects. Repair of such catheter, if not associated with subsequent complications, would extend catheter life and reduce costs and patient inconvenience related to catheter replacement. OBJECTIVE AND DESIGN: Retrospective analysis of seven peritoneal catheters repaired 11 times over a 15-year period by splicing the old catheter with an extension tube using the Peri-Patch Repair Kit (Quinton Instrument Co., Bothwell, WA, U.S.A.). RESULTS: The life of these seven catheters was extended by a mean of 26 months (range 1-87 months), without increasing infection rates after splicing. The peritonitis rate after catheter splicing was 0.40 per year, not higher than the overall rate (0.76 per year) in our center during the same time period. Exit-site infections occurred in 6 patients after catheter splicing. Only one infection was related to trauma during the procedure and resulted in chronic exit infection; the catheter was eventually removed. In this patient, damage to the catheter was less than 1.5 cm from the exit site. CONCLUSIONS AND RECOMMENDATIONS: Splicing of the damaged peritoneal catheter, if properly done, is a safe procedure and can significantly prolong catheter life. We recommend that measures to prevent catheter damage, such as avoiding the use of scissors and other sharp objects, should be emphasized during the initial patient education and training. Alcohol and iodine should not be used on silicone rubber catheters. We suggest that the patient should report catheter damage immediately and come to the clinic within a few hours for catheter splicing (if possible) and prophylactic antibiotic to prevent peritonitis. Finally, we recommend that repair of the catheter should not be attempted if the breakage is less than 2 cm from the exit site, unless done as an emergency procedure if immediate catheter replacement cannot be performed. (+info)
Immunohistochemical analysis of Na+/I- symporter distribution in human extra-thyroidal tissues.
(24/1350)
131Iodine concentration has been described in several extra-thyroidal tissues. Recent evidence has shown that iodine uptake is achieved by the recently cloned human Na(+)/I(-) symporter (hNIS) gene. However, conflicting results were observed in the expression of hNIS transcripts in extra-thyroidal tissues. In order to document further the distribution of hNIS, we investigated its expression using an immunohistochemical method, based on a polyclonal antibody raised against a synthetic peptide. Various extra-thyroidal tissues were examined, particularly from the digestive tract. Our results confirm that the salivary glands and the stomach express hNIS protein significantly. In contrast, hNIS was undetectable in the colon but the rectal mucosa, which has never been examined, exhibited positive immunohistochemical staining. Other digestive tissues, including the oesophagus, small intestine and appendix, were negative. Weak staining was observed in the mammary gland, indicating that hNIS is expressed in this tissue. The pancreas, skin, ovaries, spleen and kidney showed no positive immunostaining. (+info)