In a previous report (1) the disappearance curves of 181-11Abeled L-thyroxine and L-triiodothyronine were described in euthyroid subjects. The radioactive compounds were injected intravenously, and the radioactivity of the plasma or se- terminations. were carried out2 (4, 5). The BEI was done to avoid interference from inorganic iodine previously administered in the three instances where this had occurred. The two determinations were used interchangeably in the calculations of "organic iodine" figures; PBI ordinarily exceeds BEI by approximately 0.6,ug. per cent in the absence of inorganic iodine (5). Calculations T-he injection of radiothyroxine was followed by a relatively rapid initial fall in radioactivity of the plasma (Figure 1). This was attributed to diffusion of the tracer out of the vascular compartment as it was distributed throughout the body's extrathyroidal organic iodine (EOI) pool. After two days the plasma radioactivity declined more gradually, resulting in a straight line when plotted seniilogarithmically. This slow exponential com-

No abstract

No abstract

No abstract

No abstract

Grossly evident black pigmentation of the thyroid has been observed in a number of patients, most of whom have a history of chronic ingestion of minocycline. In the majority of reported cases, no thyroid dysfunction or lesion has been noted, although rare instances of papillary carcinoma have been described. We describe a patient with a history of chronic minocycline ingestion, who presented with a neck mass of recent onset. Histologic examination of the thyroid revealed diffuse pigment deposition, typical for that seen in association with minocycline ingestion. Also present was a 3.2-cm follicular neoplasm with capsular and vascular permeation, consistent with minimally invasive follicular thyroid carcinoma. This represents the first report of follicular carcinoma associated with minocycline-induced black thyroid (MIBT).

1. Folic acid, when administered alone, did not prevent the development or progression of subacute combined degeneration in 12 of 22 patients receiving this agent for from twelve to twenty-five months. 2. One patient with total gastrectomy and a macrocytic anemia developed subacute combined degeneration after five months of folic acid therapy. 3. Neurologic disease did not develop in 6 pernicious anemia patients treated with folic acid and liver extract for three and one-half to thirty-nine months. 4. In 10 pernicious anemia patients with good nutrition, neurologic relapses did not progress when liver extract or vitamin B12 therapy was instituted, even though folic acid therapy was continued. In 2 patients with abnormal nutrition and complicating organic abnormalities, nervous system disease progressed after institution of liver extract therapy. 5. Our observations are best explained by the theory that the hematologic and neurologic manifestations of pernicious anemia and other macrocytic anemias associated with gastro-intestinal tract pathology and inadequate nutrition are due to a deficiency of more than one substance. The administration of folic acid may improve the hematologic status but induce a deficiency of another substance or substances, e.g., vitamin B12, which are essential for the maintenance of a normal blood picture and the integrity of the central nervous system. This deficiency will eventually result in the development of a suboptimal blood picture or subacute combined degeneration of the spinal cord, or both. 6. The hematologic status of patients with pernicious anemia is not maintained in a more satisfactory state by supplementation of liver extract or vitamin B12 therapy with folic acid. 7. Folic acid therapy did not produce neurologic disease in patients with iron deficiency anemia who had free gastric hydrochloric acid in their gastric secretions and presumably sufficient intrinsic factor. It did not influence response to ferrous sulfate therapy. 8. Patients with sprue, nutritional macrocytic anemia and other macrocytic anemias associated with gastro-intestinal tract pathology who are treated with folic acid should also be given supplemental liver extract or vitamin B12 to insure against the development of nervous system disease.

No abstract