Genetic and non-iodine-related factors in the aetiology of nodular goitre.

Genetic and a large number of environmental non-iodine-related factors play a role in the cause of nodular goitre. Most evidence for the influence of genetic and environmental factors in the cause of goitre is from cross-sectional, population-based studies. Only a few studies have included prospective data on risk factors for nodular goitre, although few prospective data are available on the effect of iodine and tobacco smoking on goitre development. Goitre is not one single phenotype. Many epidemiological studies do not distinguish diffuse from nodular goitre, as the investigated parameter is often thyroid volume or frequency with increased thyroid volume. Moreover, information on the presence and effect of gene-environment, gene-gene, and environment-environment effect modifications is limited. Thus, firm conclusions about the relative contributions and causality of the investigated risk factors should be made with caution. Smoking seems to be an established risk factor for nodular goitre, possibly with effect modification from iodine intake, as the risk associated with smoking is smaller or absent in areas with sufficient iodine intake. The use of oral contraceptives might have protective effects against goitre, and childbirth is an increased risk factor for goitre in areas with non-optimal iodine intake. Insulin resistance is a recently investigated risk factor, and the risk of goitre may be reversible with metformin treatment. Iodine remains the major environmental risk factor for nodular goitre.

Overview of thyroid physiology: an essential for understanding familial euthyroid multinodular goiter.

Nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. Familial forms of goiter in areas not known to feature iodine deficiency are much less common. However, not all individuals in the same iodine deficiency region develop goiter and iodine supplementation does not prevent goiter development in all treated individuals. The etiology of euthyroid goiter is still incompletely understood. It is assumed that the development of goiter depends on various interactions between genetic and environmental factors. We present an overview on the thyroid physiology, which is important for a better understanding of Familial Euthyroid Multinodular Goiter.

Cribriform-morular variant of papillary thyroid carcinoma: characteristic histologic feature of adenomatous polyposis. A case report.

We report the case of a 24-year-old woman with familial adenomatous polyposis and diagnosed with cribriform-morular variant of papillary thyroid carcinoma. Neck ultrasound and computed tomography identified multiple nodules in the thyroid gland and neck lymph nodes. The cytological analysis was compatible with the diagnosis of papillary cancer of the thyroid. Total thyroidectomy with lymph node dissection was performed. The histological analysis established the diagnosis of cribriform-morular variant of papillary thyroid carcinoma. Despite preoperative findings suggesting an aggressive form of thyroid cancer with lymph node involvement, the final diagnosis was a variant of papillary thyroid carcinoma often associated with familial adenomatous polyposis and known to have a good prognosis.

[Study on the effects of increased iodized salt intake on the incidence of thyroid diseases].

OBJECTIVE: To study the annual incidence of thyroid diseases before and after the increase of iodized salt intake. METHOD: A total of 26,010 persons were examined from mid August to the end of December in 1999. RESULTS: 1. Three hundred and ten patients of thyroid diseases were identified from 1990 to July 1999. One hundred and eighty-three patients were diagnosed after iodine supplementation. 2. The constitution of thyroid diseases had changed significantly regarding the increase of hyperthyroidism, simple goiter and thyroid nodule. 3. Fifty-five patients with hyperthyroidism including 39 patients (70.91%) receiving iodine supplementation were diagnosed. The average annual incidence of hyperthyroidism after iodine supplementation was 36.87 per 100,000, a three-time increase as compared with that before iodine supplementation. The incidence of hyperthyroidism began to show a significant rise in 1996. The year with highest annual incidence was 1997, remaining at high level after supplying iodized salt. Since then the annual relative risk for hyperthyroidism had been increasing. CONCLUSION: The number of patients with thyroid diseases showed a significant increase after mass iodine supplement. At the same time, the spectrum of thyroid diseases had also changed. Iodized salt intake and the incidence of hyperthyroidism showed a significant correlation. However, the typical model of the change of disease patterns incidence needs further study.

Serum selenium levels in multinodular goitre.

Serum selenium levels were measured in 22 patients with a multinodular goitre and compared to 15 normal controls using atomic absorption spectrophotometry. The serum selenium was significantly low in these patients (patients' mean = 9.6 +/- 1.24 mcg/l, versus control mean = 11.7 +/- 1.64 mcg/l and P < 0.005). Serum T4 and T3 were within the normal range in all patients and controls. Their levels correlated positively, though weakly, with the serum selenium levels (r = 0.4 and 0.36, respectively). The control selenium levels in this study were lower than the reported figures from some European countries, but they were close to those from other studies in Egypt. It seems that Egypt is a low selenium area. A wide-scale epidemiological study is recommended, together with the examination of the possible preventive role of selenium supplementation in areas of endemic goitre.