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(Continued from Introduction)
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Scand J Gastroenterol. 1998 Oct;33(10):1057-61.
Selenium depletion in patients with gastrointestinal diseases: are there
any predictive factors?
Rannem T, Ladefoged K, Hylander E, Hegnhoj J, Staun M.
Dept. of Medical Gastroenterology CA, Rigshospitalet, Copenhagen, Denmark.
BACKGROUND: Patients with intestinal disease are at risk of developing
selenium deficiency due to impaired intestinal absorption. The aim of the
present study was to evaluate selenium status and to identify predictive
factors of selenium depletion in patients with gastrointestinal disease.
METHODS: The concentration of selenium and the activity of glutathione
peroxidase in plasma and erythrocytes were measured by fluorometry and by
spectrophotometry. Eighty-six patients with Crohn's disease, 40 patients
with ulcerative colitis, and 39 patients with various other
gastrointestinal diseases were studied. Twenty-seven patients (16%)
received home parenteral nutrition. Stool mass, faecal fat, and vitamin B12
absorption were analysed in 100 patients. RESULTS: The plasma selenium
concentration was decreased in 85% of the patients receiving supplementary
parenteral nutrition and in 20% of the patients receiving oral nutrition,
among them in 26% of the patients with Crohn's disease. Almost all patients
with ulcerative colitis had normal selenium levels. A statistically
significant correlation was found between plasma selenium and vitamin B12
absorption, stool mass, faecal fat excretion, body mass index, P-albumin, P-
zinc, and the length of the remaining small bowel. Stepwise regression
analyses showed that the strongest predictors of selenium deficiency were
stool mass, vitamin B12 absorption, and the length of the small-bowel
resection. CONCLUSION: Selenium deficiency is common in patients with
severe gastrointestinal disorders. The deficiency is mainly related to
malabsorption, and a low selenium level was almost invariably present in
patients who needed parenteral supplementation due to gut failure.
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Thyroid. 2002 Oct;12(10):867-78.
The impact of iron and selenium deficiencies on iodine and thyroid
metabolism: biochemistry and relevance to public health.
Zimmermann MB, Kohrle J.
Laboratory for Human Nutrition, Swiss Federal Institute of Technology,
Zurich, Switzerland. [log in to unmask]
Several minerals and trace elements are essential for normal thyroid
hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting
deficiencies of these elements can impair thyroid function. Iron deficiency
impairs thyroid hormone synthesis by reducing activity of heme-dependent
thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation
improves the efficacy of iodine supplementation. Combined selenium and
iodine deficiency leads to myxedematous cretinism. The normal thyroid gland
retains high selenium concentrations even under conditions of inadequate
selenium supply and expresses many of the known selenocysteine-containing
proteins. Among these selenoproteins are the glutathione peroxidase,
deiodinase, and thioredoxine reductase families of enzymes. Adequate
selenium nutrition supports efficient thyroid hormone synthesis and
metabolism and protects the thyroid gland from damage by excessive iodide
exposure. In regions of combined severe iodine and selenium deficiency,
normalization of iodine supply is mandatory before initiation of selenium
supplementation in order to prevent hypothyroidism. Selenium deficiency and
disturbed thyroid hormone economy may develop under conditions of special
dietary regimens such as long-term total parenteral nutrition,
phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced
nutrition in children, elderly people, or sick patients.
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Med Hypotheses. 2001 Oct;57(4):480-3.
Role of thyroid hormones in the effects of selenium on mood, behavior, and
cognitive function.
Sher L.
Changes in thyroid function may affect mood, behavior, and cognitive
function. Selenium is required for appropriate thyroid hormone synthesis,
activation, and metabolism. Selenium status influences thyroid function.
Selenium status also affects psychological condition and cognitive
function. The author suggests that the effects of selenium status on mood,
behavior, and cognition may be partly mediated by changes induced by
selenium deficiency or selenium supplementation in thyroid function.
Selenium deficiency decreases immunocompetence and promotes viral
infections. The author proposes that patients who have a combination of
depression, hypothyroidism, and increased susceptibility to viral
infections, could reasonably be assessed for selenium deficiency,
especially if they live in an area where the soil is low in selenium.
Copyright 2001 Harcourt Publishers Ltd.
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Biol Trace Elem Res. 2000 Dec;77(3):199-208.
Selenium deficiency and hypothyroidism: a new etiology in the differential
diagnosis of hypothyroidism in children.
Pizzulli A, Ranjbar A.
Three female children presented with different clinical symptoms that could
be related to impaired thyroid function. They underwent an accurate
pediatric-endocrinologic diagnosis. Laboratory tests revealed no
pathological findings, except latent hypothyroidism and selenium
deficiency. Hypothyroidism was diagnosed by elevated basal TSH and by a
pathological i.v.-TRH-stimulation test. After treating the children with
sodium selenite orally for 4 wk, their metabolism had returned to normal
and we saw a marked improvement of all clinical symptoms. For the first
time, we have been able to describe hypothyroidism caused exclusively by
selenium deficiency, the pathophysiology of which may be expressed as a
malfunction of human 5'-deiodinases.
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J Pediatr Gastroenterol Nutr. 2003 Jul;37(1):63-6.
Autoimmune thyroid disease and celiac disease in children.
Ansaldi N, Palmas T, Corrias A, Barbato M, D'Altiglia MR, Campanozzi A,
Baldassarre M, Rea F, Pluvio R, Bonamico M, Lazzari R, Corrao G.
Azienda Ospedaliera O.I.R.M.-S.ANNA, III Divisione Universitaria di
Pediatria, Servizio di Gastroenterologia, Universita di Torino, Italy.
[log in to unmask]
BACKGROUND: Celiac disease (CD) may be associated with other immunologic
disorders in adults and children. Previous studies linking CD and
autoimmune thyroid disease in children have included very few patients with
limited biochemical and immunologic screening tests. The aim of this
multicenter study was to establish the prevalence of autoimmune thyroid
involvement in a large series of pediatric patients with CD. METHODS: Five
hundred seventy-three consecutive pediatric patients were enrolled from
clinics in Torino, Bologna, Foggia, Rome (two clinics), Naples, and Bari.
Three hundred forty-three patients with CD were studied, 230 girls and 113
boys (median age, 8.5 years). Two hundred fifty-six of the patients with CD
(median age, 9 years) had been following a gluten-free diet for 3 months to
16 years; 87 patients were untreated (median age, 6.2 years). The diagnosis
of CD was made using the European Society for Paediatric Gastroenterology,
Hepatology and Nutrition (ESPGHAN) criteria. A control group of 230
subjects (median age, 8.3 years) was enrolled. Serum free triiodothyronine,
free thyroxine, and thyroid-stimulating hormone (TSH), antithyroperoxidase,
antithyroglobulin, anti-TSH receptor antibodies, and thyroid echographic
pattern were considered. RESULTS: Autoimmune thyroid disease was found in
90 of 343 (26.2%) patients with CD (62 on a gluten-free diet) and in 20
(10%) of the control subjects (P = 0.001). Fifty-four (15.7%) patients with
CD and autoimmune markers had normal thyroid function (euthyroidism) as did
12 (6.0%) of the control subjects; hypothyroidism was observed in 28 (8.1%)
patients with CD and in 7 (3.5%) of the control subjects. Hyperthyroidism
was diagnosed in four patients with CD and in none of the control subjects
with autoimmune markers. An abnormal echographic pattern was seen in 37
patients with CD (16.8%) and only in 1 (1.6%) of the control subjects (P =
0.002). CONCLUSIONS: The high frequency of autoimmune thyroid disease found
among patients with CD, even those on a gluten-free diet, may justify a
thyroid status assessment at diagnosis and at follow-up evaluation of
children with CD.
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Physiol Res. 2003;52(1):79-88.
IgA and IgG antigliadin, IgA anti-tissue transglutaminase and
antiendomysial antibodies in patients with autoimmune thyroid diseases and
their relationship to thyroidal replacement therapy.
Jiskra J, Limanova Z, Vanickova Z, Kocna P.
Third Medical Department, First Medical Faculty, Charles University,
Prague, Czech Republic. [log in to unmask]
Celiac disease is a chronic illness of the small bowel caused by gliadin
intolerance in genetically predisposed subjects. The aim of this study was
to investigate serum levels of IgA and IgG antigliadin antibodies, IgA
antiendomysial antibodies, and IgA anti-tissue transglutaminase antibodies
in 169 patients with autoimmune thyroid diseases, i.e. chronic thyroiditis
and Graves' disease. Antiendomysial antibodies were positive in 2 out of
169 persons (1.18%), IgA antigliadin antibodies in 15.98%, IgG antigliadin
antibodies in 51.48%, and IgA anti-tissue transglutaminase in 14.79%. The
prevalence of positivity was higher compared to the 1312 control blood
donors described in our previous study (Vancikova et al. 2002) (p<0.05).
Patients with chronic thyroiditis treated with a high replacement dosage of
levothyroxin (125-200 microg daily) had higher serum levels of IgA
antigliadin antibodies in comparison with patients treated with a lower
dosage (50-100 microg daily) (medians: 13.00 vs. 19.69, p=0.033). We found
a negative correlation of IgA anti-tissue transglutaminase antibodies and
total calcium serum levels (r = -0.480, p=0.0236, n=22). We can conclude
that in persons with autoimmune thyropathy there is a high prevalence of
positive antigliadin, anti-tissue transglutaminase and antiendomysial
antibodies. Latent celiac disease may lead to impaired resorption of
therapeutically administered levothyroxine, calcium, or other substances.
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(Continued in Part 2)
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