Treatment with radioactive iodine ((131)I) may be necessary for thyroid cancer or for hyperthyroidism in patients with end-stage renal disease who require hemodialysis. Because (131)I is cleared mainly by the kidneys in patients with normal renal function, many issues arise in patients who require (131)I treatment but who are on hemodialysis. This paper presents a case report of a patient on dialysis who required treatment with (131)I for thyroid cancer. We describe a mathematical model, which suggests that the treatment dose of (131)I for a patient with thyroid cancer on hemodialysis would be approximately 13%-28% of a typical empiric dose of (131)I for a patient with normal renal function. Also, we present a comprehensive review and discussion of the literature on patients who are receiving hemodialysis who were treated with (131)I for either thyroid cancer or hyperthyroidism. Using a multidisciplinary approach and special precautions, (131)I therapy can be administered safely and effectively for patients with thyroid cancer or hyperthyroidism who are receiving hemodialysis.

The steroid hormones are synthesized in the adrenal cortex, the gonads, and the placenta; are all derived from cholesterol and many are of clinical importance. Steroid hormones are synthesized in the mitochondria and smooth endoplasmic reticulum. Because they are lipophilic, they cannot be stored in vesicles from which they would diffuse easily and are therefore synthesized when needed as precursors. Upon stimulation of the parent cell, steroid hormone precursors are converted to active hormones and diffuse out of the parent cell by simple diffusion as their intracellular concentration rises.Because all steroid hormones are derived from cholesterol, they are not soluble in plasma and other body fluids. As a result, steroids are bound to transport proteins that increase their half-life and insure ubiquitous distribution. The protein-bound steroids are in equilibrium with a small fraction of free steroids, which are 'active.' Steroids can act quickly, by binding to cell surface receptors, or slowly, by binding to cytoplasmic or nucleic receptors and ultimately activate gene transcription.The adrenal glands are composed of the adrenal medulla and the adrenal cortex. The adrenal cortex is divided into three major anatomic zones: the zona glomerulosa, which produces aldosterone; and the zonae fasciculata and reticularis, which together produce cortisol and adrenal androgens. The medulla synthesizes catecholamines. More than 30 steroids are produced in the adrenal cortex; they can be divided into three functional categories: mineralocorticoids, glucocorticoids, and androgens.The steroids that are made almost exclusively in the adrenal glands are cortisol, 11-deoxycortisol, aldosterone, corticosterone, and 11-deoxycorti-costerone. Most other steroid hormones, including the estrogens, are made by the adrenal glands and the gonads [ MineralocorticoidsThe mineralocorticoids are formed in the zona glomerulosa. The main function of the mineralocorticoids is to promote tubular reabsorption of sodium and secretion of potassium and hydrogen ions at the collecting tubule, distal tubule, and collecting ducts [2]. When sodium is reabsorbed, water is absorbed simultaneously. The absorption of sodium and water increases fluid volume and arterial pressure.Aldosterone is the most potent mineralocorticoid and accounts for about 90% of the total mineralocorticoid activity. Mineralocorticoid potency in descending order is: aldosterone, 11-deoxycorticosterone, 18-oxocortisol, corticosterone, and cortisol [1]. Although cortisol has mainly glucocorticoid activity, it also has some mineralocorticoid activity. Cortisol has 1/400 of the potency of aldosterone, but its concentration is about 80 times greater than that of aldosterone [4]. The adrenal production of cortisol is approximately 25 mg/day and that of aldosterone is 100μg/day. Corticosterone has mainly glucocorticoid activity and some mineralocorticoid activity.Aldosterone secretion is regulated primarily by the renin-angiotensin system; it also is stimulated by increased serum potas...

Hypothesis-A cortisol response to adrenocorticotropin injection is the standard test for diagnosing adrenal insufficiency. Multiple steroid hormones can now be accurately measured by tandem mass spectrometry in a single sample. The study objective was to determine whether a steroid profile, created by simultaneous measurement of ten steroid hormones by tandem mass spectrometry, would help determine the cause of adrenal insufficiency.Design-A ten-steroid profile was measured by tandem mass spectrometry during the performance of a standard high dose cortrosyn stimulation test. The steroids were measured at baseline, and 30 and 60 minutes following synthetic adrenocorticotropin injection. Adrenal insufficiency was defined as a peak cortisol level of less than 20 μg/dL. Testing was conducted in the General Clinical Research Center of a University Medical Center. Normal volunteers, patients suspected of having adrenal insufficiency, and patients with known adrenal insufficiency participated.Results-Our results showed that adrenal insufficiency of any cause was adequately diagnosed using the response of 11-deoxycortisol, dehydroepiandrosterone, or these analytes combined in a two-steroid profile. A three-steroid profile yielded a test with 100% accuracy for discriminating primary adrenal insufficiency from normal status. Primary adrenal insufficiency was well separated from secondary adrenal insufficiency using only a single aldosterone value. 11-deoxycortisol, dehydroepiandrosterone, and a two-steroid profile each provided fair discrimination between secondary adrenal insufficiency and normal status.Conclusions-We conclude that stimulated levels of aldosterone, 11-deoxycortisol, dehydroepiandrosterone, and a two-or three-steroid profile provided additional discrimination between states of adrenal sufficiency and insufficiency. It is proposed that a steroid profile measuring

Objective To determine whether the time of day at which corticotropin stimulation testing is performed influences the steroid concentrations observed in persons with normal adrenal function. Methods In this retrospective, secondary analysis, participants with normal adrenal function were studied to determine whether the time of corticotropin stimulation testing influenced results. Participants consisted of 2 groups: healthy volunteers who were not suspected of having adrenal insufficiency and patients being tested for adrenal insufficiency as part of their standard of care who were subsequently shown to have normal adrenal function on the basis of a peak cortisol value of at least 20 μg/dL. A high-dose corticotropin stimulation test was performed in all participants. Baseline, peak, and delta steroid concentrations were documented after corticotropin injection. Steroid concentrations were measured by tandem mass spectrometry. Multivariate analyses adjusted for patient age, sex, and baseline steroid concentrations. Results With progression through the day for the time of testing, the baseline cortisol concentration decreased, while the peak and delta cortisol concentration increased (P values: <.001, .007, .007, respectively). For 11-deoxycortisol, the baseline decreased, while peak and delta values increased with later testing (P values: .017, .012, .02, respectively). Peak aldosterone concentrations increased according to their baseline values (P<.001), but were unaffected by time. Peak and delta dehydroepiandrosterone concentrations increased with time (P = .015 and .021, respectively). Referring to the various criteria for adequate steroid responses to corticotropin available in the literature, the time-related differences in this small group of patients were insufficient to draw different conclusions about results of testing. Conclusions Cortisol, 11-deoxycortisol, and dehydroepiandrosterone values were most influenced by testing times. In patients with borderline adrenal function who are tested at different times of the day, the modest differences we observed may be sufficient to affect conclusions about whether adrenal insufficiency is present.