For the differentiation of benign from malignant thyroidal disease, ultrasound displays anatomic but not histologic features. Other visualization techniques can be used including isotope scanning (radioiodine, 99m technetium, 241 americium fluorescence, 131 cesium, 67 gallium, 75 selenomethionine, 201 thallium, 32 phosphorus, 99m Tc-bleomycin, 197 mercury, 133 xenon), thermography, x-ray techniques (plain films, computed tomographic scan, xeroradiography, chest x-ray barium swallow, lymphography, angiography), and thyroid hormone suppression. Needle biopsy can be done by core biopsy (Vim-Silverman and drill biopsy), large needle biopsy for histologic processing and fine needle aspiration for cytologic interpretation. The latter is the safest, most reliable, and most cost-effective technique currently available to differentiate between benign and malignant thyroidal disease and has great promise for the future.

No abstract

The approach to the management of the thyroid nodule remains controversial. Confusion exists because virtually any thyroidal disease can present as a clinically solitary nodule which means there is no uniformity regarding natural history, incidence, prevalence, epidemiology, and pathophysiology.. The variety of definitions of thyroid nodules and thyroid carcinoma and the different modes of study selection and individual bias add to the confusion. Diagnostic approaches have not yielded a completely reliable technique to differentiate benign from malignant thyroidal disease. A history of neck irradiation of cervical lymphadenopathy significantly increases the chance of thyroid malignancy, but other parameters of the history or physical examination as well as blood tests are unreliable. Ultrasound displays anatomic but not histologic features. X-ray techniques (plain films, computed tomographic scans, xeroradiography, chest x-ray, barium swallow, lymphography, and angiography) have been used to visualize thyroid nodules, with some techniques proving more useful than others.

Acromegaloidism is a syndrome characterized by features of acromegaly without biochemical evidence of excessive GH or somatomedin production. We searched for a growth factor in the serum of patients with this syndrome. Growth-promoting activity was measured by determining the stimulatory effect of whole and fractionated serum on colony formation by human erythroid progenitors in vitro. Sera from five subjects with acromegaloidism gave a mean (+/- SEM) stimulated colony growth of 211 +/- 4.0 colonies, in contrast to normal sera which yielded a mean colony growth of 100 +/- 11.0 (n = 9; P less than 0.001). When serum was chromatographed on a Sephadex G-200 column, the maximal stimulation of colony growth was found in the fractions coinciding with the descending slope of the second protein peak. Based on gel filtration chromatography, the estimated molecular weight was 70,000 daltons. Epidermal growth factor, nerve growth factor, fibroblast growth factor, and platelet-derived growth factor resulted in no substantial stimulation of colony growth under the conditions used. Although the erythroid progenitor cells of a Laron dwarf were unresponsive to 200 ng/ml human GH, they were clearly stimulated by serum from a patient with acromegaloidism. The present study describes the presence of a heretofore unidentified growth factor in the serum of subjects with acromegaloidism. This factor also stimulated the erythroid precursor cells of a Laron dwarf whose cells were unresponsive to GH. The physiological role of this growth factor in normal man as well as its pathogenic role in subjects with acromegaloidism remain to be established.

No abstract