Einfluß einer Selen-Substitution auf den Verlauf einer Autoimmunthyreoiditis
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vor 21 Jahren
Selenium Supplementation in Patients with Autoimmue Thyroiditis
Decreases Thyroid Peroxidase Antibodies Concentrations ROLAND
GÄRTNER, BARBARA C. H. GASNIER, JOHANNES W. DIETRICH, BJARNE KREBS,
AND MATTHIAS W. A. ANGSTWURM Departement of Endocrinology,
Medizinische Klinik Innenstadt, University of Munich, D-80336
Munich, Germany In areas with severe selenium deficiency there is a
higher incidence of thyroiditis due to a decreased activity of
selenium-dependent glutathione peroxidase activity within thyroid
cells. Selenium-dependent enzymes also have several modifying
effects on the immune system. Therefore, even mild selenium
deficiency may contribute to the developpement and maintenance of
autoimmune thyroid dideases. We performed a blinded,
placebo-controlled, prospective study in female patients (n = 70;
mean age, 47.5 + 0.7 yr) with autoimmune thyroiditis and thyroid
peroxidase antibodies (TPOAb) and/or Tg antibodies (TgAb) above 350
IU/ml. The primary end point of the study was the change of TPOAb
concentrations. Secondary end points were changes in TgAb, TSH, and
free thyroid hormone levels as well as ultrasound pattern of the
thyroid and quality of life estimation. Patients were randomized
into 2 age- and antibody (TPOAb)-matched groups; 36 patients
received 200 µg (2.53 µmol) sodium selenite/d, orally, for 3
months, and 34 patients recieved placebo. All patients were
substituted with L-T4 to maintain TSH within the normal range.
TPOAb, TgAb, TSH, and free thyroid hormones were determined by
commercial assays. The echogenicity of the thyroid was monitored
with high resolution ultrasound. The mean TPOAb concentration
decreased significantly to 63.6% (P = 0.013) in the selenium group
vs. 88% (P = 0.95) in the placebo group. A subgroup analysis of
those patients with TPOAb greater than 1200 IU/ml revealed a mean
40% reduction in the selenium-treated patients compared to a 10%
increase in TPOAb in the placebo group. TgAb concentrations were
lower in the placebo group at the beginning af the study and
significantly further decreased (P = 0.018), but were unchanged in
the selenium group. Nine patients in the selenium-treated group had
completely normalized antibody concentrations, in contrast to two
patients in the placebo group (by x2 test, P = 0.01). Ultrasound of
the thyroid showed normalized echogenicity in these patients. The
mean TSH, free T4, and free T3 levels were unchanged in both
groups. We conclude that selenium substitution may improve the
inflammatory activity in patients with autoimmune thyroiditis,
especilally in those with high activity. Whether this effect is
specific for autoimmune thyroiditis or may also be effective in
other endocrine autoimmune diseases has yet to be investigated. (J
Clin Endocrinol Metab 87: 1687-1691, 2002)
Decreases Thyroid Peroxidase Antibodies Concentrations ROLAND
GÄRTNER, BARBARA C. H. GASNIER, JOHANNES W. DIETRICH, BJARNE KREBS,
AND MATTHIAS W. A. ANGSTWURM Departement of Endocrinology,
Medizinische Klinik Innenstadt, University of Munich, D-80336
Munich, Germany In areas with severe selenium deficiency there is a
higher incidence of thyroiditis due to a decreased activity of
selenium-dependent glutathione peroxidase activity within thyroid
cells. Selenium-dependent enzymes also have several modifying
effects on the immune system. Therefore, even mild selenium
deficiency may contribute to the developpement and maintenance of
autoimmune thyroid dideases. We performed a blinded,
placebo-controlled, prospective study in female patients (n = 70;
mean age, 47.5 + 0.7 yr) with autoimmune thyroiditis and thyroid
peroxidase antibodies (TPOAb) and/or Tg antibodies (TgAb) above 350
IU/ml. The primary end point of the study was the change of TPOAb
concentrations. Secondary end points were changes in TgAb, TSH, and
free thyroid hormone levels as well as ultrasound pattern of the
thyroid and quality of life estimation. Patients were randomized
into 2 age- and antibody (TPOAb)-matched groups; 36 patients
received 200 µg (2.53 µmol) sodium selenite/d, orally, for 3
months, and 34 patients recieved placebo. All patients were
substituted with L-T4 to maintain TSH within the normal range.
TPOAb, TgAb, TSH, and free thyroid hormones were determined by
commercial assays. The echogenicity of the thyroid was monitored
with high resolution ultrasound. The mean TPOAb concentration
decreased significantly to 63.6% (P = 0.013) in the selenium group
vs. 88% (P = 0.95) in the placebo group. A subgroup analysis of
those patients with TPOAb greater than 1200 IU/ml revealed a mean
40% reduction in the selenium-treated patients compared to a 10%
increase in TPOAb in the placebo group. TgAb concentrations were
lower in the placebo group at the beginning af the study and
significantly further decreased (P = 0.018), but were unchanged in
the selenium group. Nine patients in the selenium-treated group had
completely normalized antibody concentrations, in contrast to two
patients in the placebo group (by x2 test, P = 0.01). Ultrasound of
the thyroid showed normalized echogenicity in these patients. The
mean TSH, free T4, and free T3 levels were unchanged in both
groups. We conclude that selenium substitution may improve the
inflammatory activity in patients with autoimmune thyroiditis,
especilally in those with high activity. Whether this effect is
specific for autoimmune thyroiditis or may also be effective in
other endocrine autoimmune diseases has yet to be investigated. (J
Clin Endocrinol Metab 87: 1687-1691, 2002)
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