Iodine induced lymphocytic thyroiditis in the BB/W rat: early and late immune phenomena.

The effect of iodine excess on thyroid function and on the immunological sequence of events leading to lymphocytic thyroiditis (LT) was studied in the NB subline of BB/W rats to determine the mechanisms by which the level of iodine intake influences the development of LT in this animal model. Iodine supplemented water (500 micrograms/l, Group 1 or 500 mg/l, Group 2) or non-iodine supplemented tap water (Group 3) was given to breeding pairs and their offspring ad libitum. A Wistar rat group, also given tap water (Group 4) served as controls. To determine the immunological sequence of events, the phenotypic nature of the infiltrating thyroid lymphocytes was examined by specific immunoperoxidase staining in BB/W and Wistar rats at 6, 9, 12, and 15 weeks. Antigen-presenting cells and class II (Ia) antigen expression on thyrocytes were also examined. The first immunological event apparent in the iodine-treated BB/W rats was a sharp increase in the number of Ia positive dendritic cells at 9 weeks compared with control BB/W and Wistar rats. In the iodine excess groups dendritic cells were associated with scattered areas of lymphocytic infiltration, comprising predominantly T helper cells (W3/25). T suppressor cells (OX 8) and IL-2 receptor positive activated T-cells (OX 39) were both present in small numbers. B-cells (OX 12) were absent. In addition, thyrocytes did not exhibit Ia antigen expression. By contrast, lymphocytic infiltration was not found at 9 weeks in control BB/W rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Supplementary iodine fails to reverse hypothyroidism in adolescents and adults with endemic cretinism.

The efficacy of supplemental iodine in correcting hypothyroidism in adults and older children with endemic myxedematous cretinism is not known. To investigate this issue we administered im iodized oil (1.5 mL) to 28 hypothyroid endemic cretins (TSH, greater than 5 mIU/L) from western China, aged 14-52 yr (mean = 29 SD = 11 yr). Clinical examination, intelligence testing (Hiskey Nebraska Test of Learning Aptitude and the Griffiths Mental Development Scales), and thyroid function tests were performed before and 6 months after iodine supplementation. We found that signs of thyroid hormone deficiency, dwarfism, and delayed sexual maturity persisted after iodine supplementation. Further, mental disability and other clinical features of neurological damage were not altered by treatment. The mean serum concentration of total T4 before treatment was 75 nmol/L (SD = 40) and fell after iodized oil administration to 56 nmol/L (SD = 29; P less than 0.001). Mean serum levels of TSH before and after iodine showed a paradoxical fall [85 mIU/L (SD = 102) and 46 mIU/L (SD = 46), respectively]. Serum TSH levels decreased into the normal range (less than 5 mIU/L) in only 1 of 28 patients (4%). We conclude that iodine supplementation does not reverse thyroid hormone deficiency or its sequelae in adolescents and adults with endemic myxedematous cretinism. Iodized oil in this age group of patients with endemic cretinism does not appear to be beneficial and should be used with caution.

Endemic goitre and iodine deficiency disorders--aetiology, epidemiology and treatment.

Disorders caused by iodine deficiency continue to be a major health problem in many underdeveloped areas of the world. The most significant is the impaired mental and physical development which occurs as a result of iodine deprivation early in life. Individuals in affected communities show a spectrum of abnormalities which can be attributed to two interacting pathological processes. Fetal hypothyroidism in the first and early second trimester predominantly affects the developing nervous system causing deaf-mutism and mental retardation. If hypothyroidism occurs in the early postnatal period the main abnormalities are growth stunting and related somatic abnormalities. Subclinical deficits of intellectual and motor development may also be found in apparently normal individuals living in affected areas. Although dietary iodine deficiency is clearly the major aetiological factor in both endemic goitre and cretinism, cofactors such as goitrogens, other trace element deficiencies and immunological mechanisms may greatly modify the expression of these disorders. Iodine supplementation programmes form the basis of the public health strategy in combatting these disorders. Where the iodization of foodstuffs is not feasible, an alternative is the use of iodine containing oil which can be given orally or intramuscularly to provide a long-lasting supply of iodine.

Endemic goitre in Sarawak, Malaysia: I. Somatic growth and aetiology.

A comparative epidemiological and anthropometric survey was conducted among Ibans, the largest indigenous ethnic group in Sarawak, in three regions where the endemicity of goitre exhibited marked differences , to assess the effect of endemic goitre on somatic growth. In the Ai river region the prevalence of goitre was 99.5%; 35% having grade 3 goitres, 55% grade 2 goitres and 9.5% grade 1 goitres. At Rubu the prevalence of endemic goitre was 74%; 3% having grade 3 goitre, 16% grade 2 goitre and 55% grade 1 goitre. In the Bajong region relatively few people were detected with goitre and most of these had migrated from other regions. Neurological cretinism was estimated at 3.6% in the severely goitrous Ai river population but was not detected in the other regions. Anthropometric data obtained from the three adult populations did not reveal any statistically significant differences in the following parameters: weight, height, weight/height ratio, height/sitting height ratios, head circumference, scapular skinfold thickness and left mid arm muscle circumference. The haemoglobin, serum total protein and serum albumin concentrations were similar in the three populations. It is concluded that endemic goitre occurs with a frequency of close to 100% in certain Iban populations which represents one of the highest incidences of endemic goitre in the world. Neurological cretinism is common in this population. Our observations suggest that body proportions and somatic growth do not vary among similar ethnic populations exhibiting greatly different endemicity of goitre. Although no iodine balance studies were performed, assessment of diets suggested that iodine deficiency is a significant contributory factor in the development of endemic goitre in Sarawak. Urgent attention to iodine supplementation is indicated to prevent the development of endemic goitre and neurological cretinism.