ABSTRACT
Studies were performed to assess the role of combined selenium and iodine deficiency in the etiology of endemic myxedematous cretinism in a population in Zaire. One effect of selenium deficiency may be to lower glutathione peroxidase activity in the thyroid gland, thus allowing hydrogen peroxide produced during thyroid hormone synthesis to be cytotoxic. In selenium-and-iodine-deficient humans, selenium supplementation may aggravate hypothyroidism by stimulating thyroxin metabolism by the selenoenzyme type I iodothyronine 5'-deiodinase. Selenium supplementation is thus not indicated without iodine or thyroid hormone supplementation in cases of combined selenium and iodine deficiencies.
Subject(s)
Congenital Hypothyroidism/etiology , Iodine/administration & dosage , Iodine/deficiency , Selenium/deficiency , Thyroxine/deficiency , Adolescent , Adult , Child , Child, Preschool , Democratic Republic of the Congo , Glutathione Peroxidase/blood , Humans , Infant , Selenium/adverse effects , Selenium/therapeutic use , Thyroxine/bloodABSTRACT
Severe goiter, cretinism, and the other iodine deficiency disorders (IDD) have their main cause in the lack of availability of iodine from the soil linked to a severe limitation of food exchanges. Apart from the degrees of severity of the iodine deficiency, the frequencies and symptomatologies of cretinism and the other IDD are influenced by other goitrogenic factors and trace elements. Thiocyanate overload originating from consumption of poorly detoxified cassava is such that this goitrogenic factor aggravates a relative or a severe iodine deficiency. Very recently, a severe selenium deficiency has also been associated with IDD in the human population, whereas in animals, it has been proven to play a role in thyroid function either through a thyroidal or extrathyroidal mechanism. The former involves oxidative damages mediated by free radicals, whereas the latter implies an inhibition of the deiodinase responsible for the utilization of T4 into T3. One concludes that: 1. Goiter has a multifactorial origin; 2. IDD are an important public health problem; and 3. IDD are a good model to study the effects of other trace elements whose actions in many human metabolisms have been somewhat underestimated.
Subject(s)
Deficiency Diseases/etiology , Goiter, Endemic/etiology , Iodine/deficiency , Trace Elements/deficiency , Adolescent , Child , Congenital Hypothyroidism/epidemiology , Congenital Hypothyroidism/etiology , Congenital Hypothyroidism/metabolism , Deficiency Diseases/epidemiology , Deficiency Diseases/metabolism , Democratic Republic of the Congo/epidemiology , Europe/epidemiology , Female , Goiter, Endemic/epidemiology , Goiter, Endemic/metabolism , Humans , Infant, Newborn , Male , Pregnancy , Pregnancy Complications/epidemiology , Pregnancy Complications/etiology , Pregnancy Complications/metabolism , Prospective Studies , Public Health , Selenium/deficiency , Thiocyanates/poisoningABSTRACT
Selenium status was determined in an endemic-goiter area and in a control area of Zaire. Compared with the reference values of a noniodine-deficient area, serum selenium in subjects living in the core of the northern Zaire endemic-goiter belt (Karawa villages) was seven times lower in 52 school-children and similarly low in 23 cretins; erythrocyte glutathione peroxidase (RBC-GPX) was five times lower in schoolchildren and still two times lower in cretins (P = 0.004). In a less severely iodine-deficient city of the same endemia (Businga), selenium status was moderately altered. RBC-GPX activity was linearly associated with serum selenium concentration up to a value of 1140 nmol/L and leveled off at approximately 15 U/g Hb at greater selenium concentration. At Karawa villages, selenium supplementation normalized both the serum selenium and the RBC-GPX. This combined iodine and selenium deficiency could be associated with the elevated frequency of endemic myxedematous cretinism in Central Africa.
