• Journal of Nutrition and Health
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• v.30 no.10
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• pp.1195-1202
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• 1997

Iodine-rich seaweed soup has been traditionally supplied to postpartum women in Korea. This dietary habit might introduce over-intake of iodine above the recommended requirements, and might provoke postpartum thyroid dysfunction. Although the response to excess iodine intake is highly variable, goiter, hyperthyroidism, hypothyroidism, and thyroiditis could follow the daily intake of 1,500$\mu\textrm{g}$ of iodine. A few studies are available concerning iodine toxicity in Korea. The purpose of this study was to investigate the relationships between the dietary intake of iodine and thyroid function change as well as the incidence of postpartum thyroiditis. One hundred and thirty-seven postpartum women who had experienced normal deliveries were studied. Dietary intake of iodine and excretion concentration of iodine in breast milk and maternal urine were measured . Serum T$_3$, T$_4$, TSH, anti-thyroglobulin antibody, and anti-microsomal antibody were anlayzed 1 week before delivery and 1, 6, 12, and24 weeks after delivery. Iodine intake was analyzed by one-to-one interviews using 24-hr recall and a food frequncy questionnaire. The result showed that the intake of dietary iodine before delivery and 1 and24 weeks after delivery were 483$\mu\textrm{g}$/day, 3367$\mu\textrm{g}$/day, and 1069$\mu\textrm{g}$/day, respectively. The concentration of iodine in urine at the first week after delivery was 63$\mu\textrm{g}$/dL, and 23.9$\mu\textrm{g}$/dL in breast milk . The levels of serum T$_3$ and T$_4$ before delivery were 2.01ng/mL and 11.49$\mu\textrm{g}$U/dL, respectively, showing that the levels were gradually dropping to normal values after delivery. Positive serum anti-thyroglobulin antibody and anti-microsomal antibody appeared in 3 cases. After a 24 week follow-up period , 6 women(10.3%) experienced cases of postpartum thyroiditis, 5 of which were cases of hyperthyroidism and one of which was a case of hypothyroidism. These figures of postpartum thyroiditis are similar to those of other countries.

• Tuberculosis and Respiratory Diseases
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• v.62 no.5
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• pp.417-420
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• 2007

Sarcoidosis is a multisystemic granulomatous disease with an of unknown etiology, involving bilateral hilar lymphadenopathy, pulmonary, skin and eye lesions. However, involvement of the endocrine system in sarcoidosis is quite rare, and the coexistence of both diseases is extremely unusual. We describe a 60-year-old woman presenting with sarcoidosis and Graves' disease. She was admitted for evaluation of dry cough, dyspnea, palpitation and general weakness. Both thyroid glands were enlarged diffusely. The thyroid function tests showed suppressed serum thyrotropin and an increased thyroid hormone level. The levels of the TSH receptor antibody, anti-thyroglobulin antibody and anti-microsomal antibody were higher than normal. The radionuclide scan($^{131}I$) showed increased iodine uptake. The chest X-ray revealed pulmonary hilar enlargement and high resolution CT showed both hilar lymph nodes enlargement and tiny parenchymal nodules. The transbronchial lung biopsy showed a noncaseating granuloma without necrosis. We report this case of pulmonary sarcoidosis plus Graves' disease with a review of the relevant literatures.

• Archives of Pharmacal Research
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• v.15 no.1
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• pp.78-86
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• 1992

The induction of hepatic cytochromes P450 and metabolic effects have been examined in male and female Sprague-Dawley rats following treatment with either phenobarbital or 3-methylcholanthrene. Hepatic cytochrome P450 levels were higher in males than in females by ~40%. Treatment of male and female rats with phenobarbital or 3-methylcholanthrene resulted in an ~1.6 and 2-fold increase, respectively, in heptic microsomal cytochrome P450 levels in both sexes, relative to untreated animals. Immunoblot analyses were performed to compare sex-related changes in P450 levels. Hepatic P45IIB1 levels in males were greater than those in females following phenobarbital treatment. 3-Methylcholanthrene-induced male hepatic microsomes exhibited greater levels of P450 females failed to exhibit a band. Mab PCN 2-13-1 against P-45-IIIA recognized an intense in uninduced microsomes from female rats. The levels of P450IIIA in males were increased 2 to 3-fold following treatment with phenobarbital, while the increase of IIIA levels in females by phenobarbital was minimal, as monitored by immunoblot analysis. Solid phase radiommunoassay using monoclonal antibodies supported the results of immunoblot analysis. Phenobarbital treatment caused a 6.5-fold increase in the monoclonal iantibody binding to IIBI in males, whereas treatment of females with phenobarbital resulted of IA levels by 3-methylcholanthrene was also greater in females than in males (10-vs. 8-fold) although the levels of induced IA were comparable inboth sexes, as assessed by radiommunoassay. Radioimmunoassay also showed that hepatic IIEI level was 1.5-fold higher in males than in females and that either phenobarbital or 3-methylcholanthrene treatment caused 80% to 40% decrease in IIEL levels, relative to control, in both sexes. Sex-related metabolic activities were examined in hepatic microsomes. Hexobarbital hydroxylase activity was 2-to 3-fold higher in uninduced microsomes from males than that from females. This hydroxylase activity was increased 2-and 3-fold in males and females, respectively, following phenobarbital treatment, as compared to controls. Addition females produced 64% and 84% inhibition of hexobarbital oxidation, respectively. Aryl hydrocarbon hydroxylase activity was increased -12 and 26-fold in males and females respectively. Following phenobarbital treatment, as compared to controls. Addition of anti-P450IIB1 antibody to phenobarbital-induced hepatic microsomes from males and females produced 64% and 84% inhibition of hexobarbital oxidation, respectively. Aryl hydrocarbon hydroxylase activity was increased -12 and 26 fold in males and females, respectively, following 3-methylcholanthrene treatment relative to controls. The anti-P-450IA antibody inhibitable rate of aryl hydrocarbon hydroxylase activity was comparable in both sexes following 3-methylcholanthrene treatment relative to controls. The anti-P450LA antibody inhibitable rate of aryl hydrocarbon hydroxylase activity was comparable in both sexes following 3-methylcholanthrene treatment (-70%). These results demonstrate that levels of hepatic P450IIB1 or P450IA are greater in male than in female for untreated, phenobarbital-or-3-methylcholanthrene treated rats. In addition, the relative for untreated phenobarbital-or 3-methylcholanthrene treated rats. In addition, the relative increase of phenobarbital-or 3-methylcholanthrene treated rats. In addition, the relative increase of phenobarbital-or 3-methylcholanthrene treated rats. In addition, the relative increase of P450IIB1 or IA phenobarbital or 3-methylcholanthrene is more significant in females.

• Journal of Yeungnam Medical Science
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• v.5 no.1
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• pp.173-179
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• 1988

Since 1931, sporadic reports have appeared noting an apparent association between hyperthyroidism and idiopathic thrombocytopenic purpura. Recent various studies suggested that these two diseases may share a similar immunologic background, but the the exact mechanism is still a matter of speculation. This 22-year old female patient visisted this hospital because of general weakness and purpura of legs for 2 months. The laboratory findings were compatible with Graves' disease associated with idiopathic thrombocytopenic purpura. The palatclet count was 16000/$mm^3$, hemoglobulin was 10.9g/dl and MCV was 60.1tL. T3 was 490.53ng/dL, T4 was 24ug/dL and free T4 was 5.66ng/dL. Antiplatelet antibody and anti-microsomal antibody were positive. The bone marrow findings were compatible with tron deficiency anemia and idiopathic thrombocytopenic purpura. The thyroid biopsy showed adenomatous goiter. She was administered with propyl thiouracil, Beta-blocker, iron and prednisolon. On the 10th hospital day, platelet count was 184000/$mm^3$, hemoglobulin was 12.0gm/dL and MCV was 67.5fL. On the 20th hospital day, T4 was 10.35ug/dL and free T4 was 2.30ng/dL. Therefore she was discharged and followed up.

• The Korean Journal of Pharmacology
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• v.31 no.2
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• pp.241-250
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• 1995

Protein B23 is one of the major nucleolar phosphoproteins associated with pre-ribosomal particles, and is localized in the granular region of the nucleolus. Recent studies suggest that protein B23 shuttles between nucleus and cytoplasm and also interacts with HIV Rev. These findings indicate that protein B23 is important in nucleocytoplasmic relationship and viral replication. However, the exact function of protein B23 is not clear yet. In acute nucleolar hypertrophy of rat liver, treated with thioacetamide, there was observed an increase of not only protein B23 but also B23-like protein p45 when anti-B23 monoclonal antibody (MAb) was used for identification. On the basis of the large B23 specific epitope structure composed of 68 amino acids, a hypothesis was formulated to examine that p45 is the pre-B23 resulting from excessive production of B23. In an attempt to investigate the precursor of B23, we analyzed the subcellular fractions and microsomal subfractions. Subsequently, we analyzed the finger printings of B23-like proteins using the tryptic peptide mapping. The results are summarized: 1) Using B23 MAb, we observed the presence of B23-like proteins in nucleolar fraction, nucleoplasmic fraction and microsomal fraction. 2) In the further microsomal subfractionation, we could partially purify B23-like protein in 2M layer of sucrose gradient. 3) When ion exchange chromatography was employed, there were protein species 80kDa(p80), 65kDa(p65) and 60kDa(p60). 4) Based on the tryptic map analysis of $^{125}I$ labeled proteins, the similarity between B23 and p80 was found only in 9 out of 14(B23) and 21(p80) peptides, and difference was found in the remaining peptides. p80 and p60 had 18 common peptides, and all the peptides of p60 were similar to those of p80. From these results, it is proposed that p45 is an abnormal metabolite resulting from carcinogenesis by thioacetamide, and it is not the precursor of B23. In addition, we suggest that p80 may be a precursor of p45.