scholarly journals Cause of Hypothyroidism in Post Iniversal Salt Iodization era in Nepal

2019 ◽  
Vol 3 (1) ◽  
pp. 10-15
Author(s):  
Sunil Pokharel

Introduction: Iodine deficiency remains the most common cause of hypothyroidism worldwide, but in areas of iodine sufficiency autoimmune disease (Hashimoto’s thyroiditis) is most common. After implementation of Universal Salt Iodization (USI) to control Iodine Deficiency Disorder(IDD), Nepal is heading towards iodine sufficiency but the prevalence of clinical and subclinical hypothyroidism is still high. So this study was done to find out either chronic autoimmune thyroiditis is the cause of clinical hypothyroidism in post universal salt iodization era of Nepal by measuring Anti-TPO antibody. Method: Newly diagnosed patients with Clinical or Sub clinical hypothyroidism by thyroid function test were included in this study. Anti-TPO antibody was measured by Elisa method, Anti-TPO >34 was considered positive. All the data’s were analyzed using SPSS software. Result: In this study 1000 patients were included, male to female ratio was 5:1. 270 patients had clinical hypothyroidism among which 230(85.1%) patients had Anti-TPO antibody positive. Among 730 patients with subclinical hypothyroidism only 220(30.1%) patients had antibody positive. Our result showed that TPO antibody was positive in clinical hypothyroidism compared to subclinical hypothyroidism with statistical significance (p<0.001). Our result also showed that clinical hypothyroidism had higher TPO value (mean 225.14) compared to subclinical hypothyroidism (74.34) with statistical significance p<0.001. Conclusion: The cause of hypothyroidism in present day Nepal is chronic autoimmune thyroiditis (Hashimoto’s thyroiditis). As we are moving from iodine deficiency status to iodine adequate or iodine excess status there might be an increased burden of thyroid disorders in Nepal due to the increased prevalence of autoimmune thyroiditis.

1998 ◽  
pp. 23-28 ◽  
Author(s):  
W Reinhardt ◽  
M Luster ◽  
KH Rudorff ◽  
C Heckmann ◽  
S Petrasch ◽  
...  

OBJECTIVE: Several studies have suggested that iodine may influence thyroid hormone status, and perhaps antibody production, in patients with autoimmune thyroid disease. To date, studies have been carried out using large amounts of iodine. Therefore, we evaluated the effect of small doses of iodine on thyroid function and thyroid antibody levels in euthyroid patients with Hashimoto's thyroiditis who were living in an area of mild dietary iodine deficiency. METHODS: Forty patients who tested positive for anti-thyroid (TPO) antibodies or with a moderate to severe hypoechogenic pattern on ultrasound received 250 microg potassium iodide daily for 4 months (range 2-13 months). An additional 43 patients positive for TPO antibodies or with hypoechogenicity on ultrasound served as a control group. All patients were TBII negative. RESULTS: Seven patients in the iodine-treated group developed subclinical hypothyroidism and one patient became hypothyroid. Three of the seven who were subclinically hypothyroid became euthyroid again when iodine treatment was stopped. One patient developed hyperthyroidism with a concomitant increase in TBII titre to 17 U/l, but after iodine withdrawal this patient became euthyroid again. Only one patient in the control group developed subclinical hypothyroidism during the same time period. All nine patients who developed thyroid dysfunction had reduced echogenicity on ultrasound. Four of the eight patients who developed subclinical hypothyroidism had TSH concentrations greater than 3 mU/l. In 32 patients in the iodine-treated group and 42 in the control group, no significant changes in thyroid function, antibody titres or thyroid volume were observed. CONCLUSIONS: Small amounts of supplementary iodine (250 microg) cause slight but significant changes in thyroid hormone function in predisposed individuals.


2021 ◽  
Vol 10 (6) ◽  
pp. 277-285
Author(s):  
Olga Koczorowska-Talarczyk ◽  
◽  
Katarzyna Kordus ◽  

The thyroid is an odd endocrine gland located in the neck. Hashimoto’s thyroiditis is a diseases of the gland which often leads to changes in skin and its appendages. The aim of this study was to investigate the relationship between hormonal disorders due to chronic autoimmune thyroiditis and skin, hair and nails conditions. This article presents the results and conclusions of a survey conducted in a group women suffering from Hashimoto’s thyroiditis, diagnosed for at least a year. The conclusions from the questionnaire showed that Hashimoto’s disease adversely affects skin, hair and nails.


2008 ◽  
Vol 19 (7) ◽  
pp. 1336-1339 ◽  
Author(s):  
M. Troch ◽  
S. Woehrer ◽  
B. Streubel ◽  
M. Weissel ◽  
M. Hoffmann ◽  
...  

2020 ◽  
Vol 47 (2) ◽  
pp. 34-37
Author(s):  
S. Dermendzhiev ◽  
A. Dzhambov ◽  
T. Dermendzhiev

AbstractWe present a case of a 29-year-old Bulgarian woman with autoimmune thyroiditis and recurrent angioedema. The patient presented with a one-year-long history of recurrent angioedema and Hashimoto’s thyroiditis. Physical examination showed oedema surrounded by erythema on the forearms, and erythematous, itchy plaques spreading over her face, neck, chest, abdomen, and extremities. Blood tests showed elevated total immunoglobulin E (IgE). The patient had been diagnosed with Hashimoto’s thyroiditis and hypothyroidism. She had been taking levothyroxine 50 μg/d, resulting in a good hormonal control; however, her anti-thyroid peroxidase (anti-TPO) antibodies were high. She was started on methylprednisolone and antihistamines. In three weeks, we observed a good therapeutic response to the treatment and the lesions remitted. IgE dropped within normal range. Levels of anti-TPO antibodies were persistently high. In conclusion, patients with angioedema should be tested for thyroid autoimmunity. Further delve into the pathogenesis of angioedema in them is warranted in order to explore the possibility of an underlying atopy in those not responding to the standard treatment with levothyroxine.


Author(s):  
Siti Nurul Hapsari ◽  
Sidarti Soehita

Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient areas of the world. This condition, however, can sometimes show hyperthyroidism. A 39-year-old femalewas admitted to hospital due to shortness of breath and tremor four hours before hospitalization. There were nausea, chestpain, cold chills, and palpitation. She was diagnosed with Hashimoto's thyroiditis and routinely received tyrosol,propranolol, and dexamethasone. Physical examination showed cervical mass, afebrile, blood pressure of 130/70 mmHg,pulse rate of 110 beats/minute and respiratory rate of 20 breaths/minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count of 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory testswere performed, abnormal results were as follows: FT4 level of 2.96 ng/dL (increased), TSH level of 0.003 µIU/mL(decreased), anti-TPO (antithyroid microsomal antibody) level of 306 IU/ml (increased), and IgE level of 213.6 IU/mL(increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis,CEA and Ca 125 were within normal limits. Thyroid ultrasound was performed and showed a benign lesion. Fine needleaspiration biopsy showed lymphocytic Hashimoto's thyroiditis. Echocardiography showed hyperthyroid heart disease. Dueto an increase of anti-TPO and FT4 levels, a decrease of TSH levels and lymphocytic thyroiditis from FNAB, this patient wasdiagnosed with a hyperthyroid phase of Hashimoto's thyroiditis. Thyroid function tests and thyroid antibody tests must bemonitored to distinguish between the hyperthyroid and hypothyroid phase of Hashimoto thyroiditis.


1991 ◽  
Vol 125 (5) ◽  
pp. 502-509 ◽  
Author(s):  
Hiroyuki Ohashi ◽  
Tadamasa Okugawa ◽  
Mitsuyasu Itoh

Abstract. To investigate the relationships between lymphocyte subsets and thyroid function, peripheral blood lymphocytes were analysed with cell surface antigens of activated (HLA-DR+) T, helper T (CD4+2H4−, CD4+4B4+) and suppressor-inducer T (CD4+2H4+, CD4+4B4−) cells subsets in 56 patients with Graves' disease, 16 patients with Hashimoto's thyroiditis, 7 patients with typical subacute thyroiditis and 2 patients with the thyrotoxic phase of autoimmune thyroiditis. Both patients with Graves' disease and Hashimoto's thyroiditis had increased percentages of HLA-DR+T (Ia+CD3+) cells as well as HLA-DR+ helper-inducer T (Ia+CD4+) cells, which seemed to be independent of treatments. The percentage of HLA-DR+ suppressor-cytotoxic T (Ia+CD8+) cells was increased in euthyroid or hypothyroid patients with Graves' disease following treatment, but was normal in hyperthyroid patients. The percentages of Ia+CD4+ cells and Ia+CD8+ were also increased in patients with thyrotoxic phases of subacute thyroiditis and autoimmune thyroiditis, whereas these abnormal values normalized in the remission phase. These findings suggest that an increase in Ia+CD4+ cells characteristically occurs during immune system activation in patients with hyperthyroid Graves' disease, Hashimoto's thyroiditis and the thyrotoxic phase of subacute thyroiditis, whereas the activated CD8+ cells in Graves' disease are induced by antithyroidal therapy.


1994 ◽  
Vol 141 (2) ◽  
pp. 309-315 ◽  
Author(s):  
R Paschke ◽  
F Schuppert ◽  
M Taton ◽  
T Velu

Abstract Cytokines are thought to mediate the initiation and perpetuation of autoimmune thyroiditis. However, this concept is mainly based on in vitro findings and to date only interleukin (IL)-6 and interferon-γ (IFN-γ) have been detected in Graves' disease in vivo. The cytokine pattern produced by T-helper (Th) cells has important regulatory effects on the nature of the immune response. We therefore determined these cytokine mRNAs in Graves' disease and Hashimoto's thyroiditis. RNA was extracted by cesium chloride gradient centrifugation from the thyroid tissue of 12 patients undergoing thyroid resection for Graves' disease and from two patients being treated for Hashimoto's thyroiditis. Two patients with parathyroid adenomas and one patient with a goiter were used as controls. RNA was also extracted from normal human thyroid epithelial cells in primary culture. The cDNAs were prepared by reverse transcription and amplified for IL-2, -4, -5, -6 and -10 and IFN-γ by polymerase chain reaction. All the cytokine mRNAs were detected in the Hashimoto's thyroid glands in large quantities. Six of the 12 Graves' disease thyroid glands showed, when compared with controls, an increased accumulation of transcripts for: IFN-γ, IL-2, -4 and -10 or IL-2, -4 and IFN-γ or IL-2 and IFN-γ or IFN-γ alone, each in one case or IL-2 alone in two cases. These cytokine profiles were not representative of a Th1 or Th2 phenotype. Increased amounts of cytokine mRNA in thyroid glands from Graves' disease patients were mostly associated with high microsomal antibody titres and/or prominent intrathyroidal lymphocytic infiltration. IL-6 and/or IL-10 mRNAs were detectable in all Graves' disease thyroid glands and in control thyroid tissue. IL-10 mRNA was not detectable in normal human thyroid epithelial cells in primary culture. Graves' disease and Hashimoto's thyroiditis clearly differ with respect to the number of positive intrathyroidal cytokine mRNAs and their levels. The different cytokine patterns in Graves' disease and in Hashimoto's thyroiditis could reflect the clinical spectrum of autoimmune thyroiditis which is characterized by thyroid tissue destruction and/or thyroid autoantibody production. These data suggest that the course of autoimmune thyroiditis is regulated by the interplay of several cytokines. Journal of Endocrinology (1994) 141, 309–315


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