Format

Send to

Choose Destination
See comment in PubMed Commons below
Schweiz Med Wochenschr. 1995 Jul 22;125(29):1379-87.

[Goiter: from epiphenomenon of iodine deficiency to benign tumor. A 30-year long guided story].

[Article in German]

Author information

  • 1Medizinischen Universit√§tsklinik Bern.

Abstract

Thirty years ago, iodine deficiency was highly prevalent in Switzerland and, consequently, few people doubted that shortage of this element fully accounted for the very high incidence of nodular goiters. Most research efforts were aimed at unraveling the mechanisms that allowed the thyroid to maintain adequate hormone production - at the expense of goiter formation - despite insufficient iodine supply. In 1982 iodine deficiency was eradicated in this country, a remarkable achievement of preventive medicine. Although the incidence of goiter dramatically decreased thereafter, this thyroid disease has remained and still is a common problem. Only now has it become clear that factors other than or in addition to iodine shortage must be operative in goitrogenesis and that classical features, such as the tremendous functional and morphological heterogeneity of goitrous tissue, and, in particular, the growth of nodules, must result from causes and mechanisms that are common to the pathological growth of other tissues too. Subsequently, the thyroid has become a rewarding source of information about cellular and - more recently - molecular events that accompany and might possibly cause pathological growth. Today, thyroid nodules are considered to be true monoclonal and polyclonal tumors. Hence, we no longer wonder why eradication of iodine shortage cannot totally prevent or reverse goiter growth. - While modern molecular biology unravels - at an amazing pace - the mechanisms that cause heterogeneity between individuals of a single species, goitrogenesis offers a unique opportunity to go one step beyond, which is the inborn and acquired heterogeneity between the individual cells of the same tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID:
7676226
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center