Hyperthyroidism due to excess iodine

TWO TYPES: Hyperthyroidism may develop in around 10% of patients in excess iodine. It may reveal an undetected pretoxic thyroid disease (type I) or have been induced by excess iodine in previously normal thyroid gland or in an euthyroid goiter (type II). IODINE EXCESSE REVEALING THYROTOXICOSIS: In the former situation, symptoms appear shortly after the iodine load, thyroid scintigraphy shows significant uptake and therapy includes discontinuation of iodine excess, antithyroid drugs, potassium perchlorate and, if necessary, thyroidectomy or a therapeutic dose of iodide 131. IODINE-INDUCED THYROTOXICOSIS: In the latter situation (type II) hyperthyroidism may occur several years after the initiation of iodine excess, scintigraphy shows very low or no uptake, spontaneous remission is observed within six months, despite the persistence of iodine excess, and treatment is based on corticosteroids.     

Adaptation of thyroid function to excess iodine

NORMALLY: The production of thyroid hormones is normally stable, despite iodine supplies that may vary widely and even on sudden excess iodine. The metabolism of iodine is characterised by adapted thyroid uptake, the requirements varying on the age and physiological status of the individual (pregnancy, breastfeeding) and by insufficient supplies in several areas in France. IN THE CASE OF EXCESS: The mechanisms that permit the thyroid to adapt to a sudden or chronic excess of iodine are immature in the newborn and sometimes deficient in adults, and may lead to iodine-induced dysthyroidism. Thanks to the recent progress made in thyroid physiology, these mechanisms are now better known. PATHOLOGICAL IMPACT: Iodine-induced hyperthyroidisms in a healthy or pathological thyroid are frequent. They are predominantly related to amiodarone. Iodine-related hypothyroidism frequently appears in cases of pre-existing thyroid diseases (asymptomatic autoimmune thyroiditis, for example). They are frequent in the newborn, notably in the premature. The iodine prophylaxis organised in Poland following the Tchernobyl accident led to very few pathological consequences in adults or children.     

碘过剩对甲状腺的病理生理效应

目的　探讨碘过剩与甲状腺疾病的关系。方法　观察不同浓度的高碘对大鼠甲状腺的影响 ,以及对人类甲状腺滤泡上皮细胞的作用。结果　实验动物组均出现弥漫性胶质性甲状腺肿 ,随着投碘量的增加 ,甲状腺绝对与相对重量与正常对照组比均见明显增加 (P <0 .0 0 5 ) ;不典型增生区域增多 ;甲状腺滤泡上皮高度降低 ,甲状腺滤泡腔面积扩大 ,核仁组成区嗜银蛋白 (AgNOR )计数增加 ,与正常对照组比较均有明显差异 (均P <0 .0 0 1)。培养的人甲状腺滤泡上皮细胞在碘浓度 0 .75 μg/ml中 6 %～ 2 5 %的细胞出现变形 ,线粒体、粗面内织网及绒毛增多 ;碘浓度 3.75 μg/ml时 ,30 %～ 40 %细胞表现为线粒体肿胀 ,粗面内织网扩张 ;碘浓度 18.75 μg/ml时 90 %细胞溶解 ,可见层状小体。 结论　过量摄碘与甲状腺机能亢进症 ,甲状腺机能减退症 ,甲状腺炎及甲状腺癌等疾病的发生可能有密切关系。     

Effect of excess iodine on thyroid and liver lysosomal enzymes

The lysosomal enzymes, cathepsin D and β-glucuronidase, were measured in subcellular fractions of rat thyroid and liver tissue after the rats were subjected to 3 days of excess iodine administration. Excess iodine resulted in a statistically significant reduction in the activity of both of these thyroid tissue lysosomal enzymes, as well as a redistribution of enzyme activity. The latency of isolated intact lysosomes from excess iodine-treated rats was also compared to that of lysosomes from untreated rats and those administered pharmacological doses of methylprednisolone. Lysosomal stabilization occurred in the methylprednisolone-treated rats, but not in those which received excess iodine. In addition, excess iodine was found to be organ specific in that it did not significantly change liver lysosomal enzyme activity or stabilize isolated liver lysosomes. Our data support the hypothesis that excess iodine may decrease thyroglobulin hydrolysis by reducing available lysosomal proteolytic enzymes. Iodine does not function by the mechanism of lysosomal membrane stabilization.     

Hypothyroidism and resistance to human recombinant erythropoietin

Sir, Many possible causes of resistance to human recombinant erythropoietin(rh-EPO) have been reported in patients with renal failure [1].However, some factors remain controversial. We     

Hyponatremia due to excess natriuresis

Nine cases with hyponatremia were precisely examined during the past 2 years. Seven of them showed normal plasma volume, serum aldosterone and pituitary function, although ADH was detected. Therefore, those seven cases were diagnosed without dilutional hyponatremia due to SIADH (a syndrome of inappropriate secretion of antidiuretic hormone). The mechanism of hyponatremia of such a type has not been yet explained definitely, but it may be referring to excess natriuresis. Only each one case of hyponatremia due to hypopituitarism and dilutional hyponatremia due to SIADH was verified in this series. SIADH showing high plasma volume value was thought to be rare. Differential diagnosis between SIADH and hyponatremia due to excess natriuresis is essential and simple. Non-invasive plasma volume measurement using RISA is significantly useful for it. For the hyponatremia due to excess natriuresis, water restriction is not necessary, but digestive supply of NaCl is needed.     

Hypothyroidism After Hemithyroidectomy

Background

The risk of hypothyroidism after hemithyroidectomy is variable, and most estimates come from single institutional studies. The purpose of the present study was to determine the incidence of hypothyroidism at the population level, and to evaluate predictive factors for hypothyroidism after hemithyroidectomy.

Methods

This retrospective study identified euthyroid patients who underwent hemithyroidectomy between 2000 and 2010 for benign disease in Kaiser Permanente Southern California regional hospitals. The incidence of hypothyroidism [thyroid stimulating hormone (TSH) levels >4 μIU/ml] was analyzed. The independent effect of age-quartile, gender, race, thyroiditis, and preoperative TSH level on the development of hypothyroidism was evaluated.

Results

Of 1,240 euthyroid patients identified, 417 (34 %) developed hypothyroidism, and 314 (25 % of total group) needed levothyroxine. Hypothyroidism was more common in age-quartile 2 (32 %), age-quartile 3 (37 %), and age-quartile 4 (42 %) than in age-quartile 1 (25 %) [adjusted odds ratio (OR) = 1.87; 95 % confidence interval (CI) 1.27–2.76, p = 0.002; age-quartile 4 compared to age-quartile 1]. Hypothyroidism was more frequent with increasing preoperative TSH levels 36, 72, and 92 % in patients with TSH levels of 1.0–2, 2.01–3, and 3.01–4 μIU/ml, respectively, compared to 17 % in those with TSH levels <1 μIU/ml [adjusted OR = 45.1; 95 % CI 13.5–151, p < 0.0001; 3.01–4 μIU/ml compared to <1 μIU/ml]. Thyroiditis was also an independent predictor of hypothyroidism.

Conclusions

About one third of euthyroid patients who undergo hemithyroidectomy develop hypothyroidism. The most significant predictor is the preoperative TSH level, with an approximate doubling of risk for each 1 unit of TSH increase over 1 μIU/ml. Our categorical scale is simple and allows for easy recall when counseling patients preoperatively.     

Hypothyroidism following partial thyroidectomy

OBJECTIVE: To compare rates of hypothyroidism following three types of partial thyroidectomy for multinodular goiter. STUDY DESIGN AND METHODS: All cases of partial thyroidectomies (hemi-, near-total, or subtotal) carried out at one Israeli and one Russian medical center (1990-2006) were retrospectively studied to determine the incidence of hypothyroidism after each procedure. RESULTS: There were 881 near-total, 1538 subtotal, and 1051 hemithyroidectomies (total 3470). Postoperative follow-up was 2 to 15 years. Twenty-eight percent of the hemithyroidectomy patients suffered permanent hypothyroidism compared to 100% of the near-total and 87% of the subtotal patients. Forty-six percent of the hemithyroidectomy patients suffered temporary hypothyroidism compared to 100% of the near-total and 93% of the subtotal patients. CONCLUSION: Subtotal and near-total thyroidectomies produced a rate of hypothyroidism close to that of total thyroidectomy compared to 28% after hemithyroidectomy. SIGNIFICANCE: Partial thyroidectomies provide no decisive advantage over total thyroidectomies in terms of subsequent requirements of supplemental hormone therapy.     

Hypothyroidism abolishes the hyperdynamic phase and increases susceptibility to sepsis

To evaluate the role of thyroid hormones in sepsis, 250-400 g rats were surgically thyroidectomized and 2-6 weeks later sepsis was produced by cecal ligation and puncture (CLP). In normal rats, total body O2 consumption (VO2) increased by 12.8% (P less than 0.05) in early sepsis (6 hr after CLP) and decreased slightly in late sepsis (16 hr after CLP). In hypothyroid (HT) rats, VO2 was depressed by 19.8% (P less than 0.05) in early sepsis and further decreased to 46.7% (P less than 0.001) of preoperative levels in late sepsis. Hepatic blood flow increased in early sepsis in normal rats but was unchanged in HT rats. The normal hyperglycemic response to early sepsis was also absent in HT rats. The respiratory control ratio (RCR) of isolated mitochondria with succinate was not increased in HT rats in early sepsis. In late sepsis, hypothyroid animals showed further decreases in VO2 and mitochondrial RCR, and, in contrast to normal rats, showed no change in blood glucose levels. Survival (5 days) following late sepsis in normal, HT, and HT rats given daily ip injections of thyroxine (30 micrograms/kg) were 65.2% (15/23), 30% (6/20) (P less than 0.025), and 77.1% (14/18), respectively. Thus, absence of thyroid hormone abolishes the hyperdynamic phase of sepsis and significantly increases mortality in sepsis, and thyroxine replacement following thyroidectomy prevents the increased mortality from sepsis.     

Mineralocorticoid excess secondary to adrenal cortical carcinoma

Adrenal cortical carcinoma may present solely with a syndrome of mineralocorticoid excess. Primary aldosteronism, resulting from adrenal carcinoma, is unusual and has only been reported rarely. A review of the literature revealed 19 cases with marked hypertension and hypokalemia, resulting from mineralocorticoid excess produced by adrenal cortical carcinoma. We report an additional case that supports the hypothesis that adrenal carcinoma may mimic hyperaldosteronism. Extensive assay of adrenal function will demonstrate the presence of biologically inactive steroids, suggesting the presence of adrenal cortical carcinoma.     

Hypothyroidism in association with systemic amyloidosis

Background. Systemic amyloidosis leads to functional compromise of various organs through infiltration of these tissues by amyloid protein. The majority of affected patients develop infiltration of the thyroid gland; yet thyroid dysfunction rarely occurs. Methods and Results. Described herein is a case of hypothyroidism occurring in a patient with amyloid goiter. An alternative explanation for her hypothyroidism could not be determined by histologic or serologic evaluation. Hormonal assays were consistent with progressive hypothyroidism in spite of oral and, finally, parenteral replacement therapy. A review of the literature describes other cases of thyroid dysfunction reported in patients with systemic amyloidosis. Conclusions. This case illustrates how amyloid infiltration may be a cause of hypothyroidism in patients with systemic amyloidosis. Therefore, all patients who develop a goiter, including those with systemic amyloidosis, must be screened for thyroid dysfunction. When a physician diagnoses the patient with hypothyroidism, that physician must be aware of potential pitfalls in the administration of thyroxine replacement as outlined below.