Goiter Growth

Goiters result from focal follicular cell hyperplasia at one or multiple sites within the thyroid gland. Iodine deficiency works synergistically with other causes of goiter but does not appear to change the basic mechanisms of goitrogenesis. There is a positive correlation between the total DNA content of the goiter and goiter weight. The increased amount of interstitial tissue and colloid formation usually contributes little to the total goiter growth. An intrinsically abnormal growth pattern of some thyroid cells is usually the driving force behind goiter growth. Heterogeneous subpopulations of thyrocytes proliferate at different rates. Both extrathy-roidal and intrathyroidal growth factors modulate goiter formation. Under physiologic in vivo conditions, TSH is the most important stimulator of thyroid growth and function. A decrease in iodine intake leads to decreased synthesis and

FIGURE 4-1. Frontal (A) and side (B) views of a 45-year-old man with long-standing multinodular goiter in an endemic area.

FIGURE 4-1. Frontal (A) and side (B) views of a 45-year-old man with long-standing multinodular goiter in an endemic area.

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