Persistent Binding of Tc-99m Pertechnetate to Erythrocytes in a Patient Receiving Multiple Pharmaceuticals
Authors: JOHN A. VENTO, LARRY S. SWING, RICHARD P. SPENCER
Journal: Clinical Nuclear Medicine (2000)

In a 50-year-old man, an attempt to visualize the thyroid using intravenous Tc-99m pertechnetate produced a blood-pool scan. The same finding was noted when the study was tried again 7 days later. The thyroid was functional, as shown by accumulation of I-123 sodium iodide. The patient was taking a “polypharmacy” of medications, which may have facilitated binding of Tc-99m pertechnetate to erythrocytes. FIGURE 1Fig. 1: A 50-year-old man with a long history of ethanol addiction was evaluated because of a low thyroid-stimulating hormone level and a thyroxine value in the high normal range. The thyroid evaluation had been prompted by a history of use of lithium carbonate for a bipolar psychiatric disorder. Thyroid imaging was attempted after intravenous administration of 10 mCi (37 MBq) Tc-99m pertechnetate (left). The image resembled a blood-pool scan, and the thyroid was not identified. The study was repeated 7 days later (also with 10 mCi Tc-99m pertechnetate). Again, an image resembling a blood-pool scan was observed (right).FIGURE 2Fig. 2: To determine if the thyroid gland was present, the patient was subsequently given 0.32 mCi I-123 sodium iodide orally. The thyroid was visualized, with little background activity. Thus we have a case with Tc-99m pertechnetate binding to endogenous erythrocytes after intravenous administration. The thyroid was able to concentrate I-123 sodium iodide, suggesting that the gland was functional. Uptake values were 5% at 4 hours and 11% at 24 hours. Direct binding of Tc-99m pertechnetate to erythrocytes in vivo may be related to the many drugs the patient was taking. The list of prescribed medications (although we cannot be certain of compliance) included atenolol (a beta-1 blocker), carbamazepine (an anticonvulsant), cellulose fiber, disulfiram (to treat alcoholism), fluoxetine hydrochloride (an antidepressant), lorazepam (an antianxiety and antidepressant), lubricant eye drops, multivitamins, olanzapine (an antipsychotic), ranitidine (an H-2 antagonist), acetaminophen (for pain), epinephrine autoinject, guanifensin/d-methorphan (an expectorant, suppressant), hydrocortisone cream, and oral magnesium/aluminum hydroxides with simethicone (an antigas agent). The many and varied medications taken by this patient may have had sufficient lipophilicity to mediate entry of Tc-99m pertechnetate into erythrocytes. In addition, metallic ions or other components may have adsorbed to the erythrocytes, providing a point of adherence for the Tc-99m pertechnetate ion. Callahan and Rabito (1) have described the role of band-3 protein in the transport of Tc-99m pertechnetate into erythrocytes. The “polypharmacy” of our patient might have affected this transport mechanism. Multiple other medications and food materials have been reported to alter the erythrocyte membrane or internal structure. Among these is ethanol (our patient was taking an antiethanolic medication) (2). In sickle cells (Hb SS), potassium transport is altered by fluoride and by okadaic acid (3). Captopril has been reported to alter erythrocyte lipids and glutathione in diabetes (4). The drug 5-fluorouracil can induce erythrocyte membrane defects and a change in rheologic status (5). In terms of food-produced changes, dietary fish oils have been noted to inhibit erythrocyte sodium–potassium exchange (6), whereas tea polyphenols appear to be protective against erythrocyte oxidative damage (7). Dipyridamole induces shape alterations in erythrocyte (8), and Adriamycin (Adria Laboratories, Columbus, OH) has been shown to bind to erythrocyte channels (9). At this point, we do not know which of the patient’s many medications induced pertechnetate binding to erythrocytes. The topic however, provides insight into radionuclide-erythrocyte interactions.