Paper chromatography prior to cortisol RIA allows for accurate use of the dexamethasone suppression test in chronic renal failure.

The assessment of the hypothalamic-pituitary-adrenal axis in patients with chronic renal failure (CRF) on hemodialysis is often hampered by abnormal responses to the standard 1-mg dexamethasone suppression test. Various mechanisms have been proposed to explain this lack of suppressibility. The present study was designed to look into the mechanisms possible for these findings in patients with CRF. We studied 6 patients with CRF on hemodialysis and 5 healthy subjects utilizing the 1-mg dexamethasone suppression test as well as the 50-mg hydrocortisone suppression test. Samples were assayed for dexamethasone, adrenocorticotropic hormone, corticosterone, and cortisol by both direct radioimmunoassay (RIA) and RIA after paper chromatography. Utilizing the direct cortisol RIA, 4 of 6 patients with CRF exhibited blunted dexamethasone suppression, while all 6 patients showed normal suppressibility after dexamethasone when cortisol was measured after paper chromatography. In contrast, all controls showed normal suppressibility regardless of the cortisol assay procedure used. The hydrocortisone suppression test was unreliable in the setting of CRF. Mean dexamethasone levels were similar in both groups. Plasma adrenocorticotropic hormone levels were significantly higher in the CRF patients, possibly indicative of an underlying hypothalamic-pituitary-adrenal axis abnormality. Abnormalities in dexamethasone suppression testing in patients with CRF may be explained by the overestimation of cortisol levels by direct RIA rather than by alteration of dexamethasone absorption or metabolism. Measurement of cortisol after paper chromatography is superior to direct RIA of cortisol in patients with CRF.

Immunoreactive thyroglobulin in sera and saliva of patients with various thyroid disorders: role of autoantibodies.

The present study was designed to assess the transfer of thyroglobulin (Tg) and anti-Tg antibodies (TgAb) to saliva in subjects with positive TgAb in their sera. Group I consisted of normal euthyroid control subjects (n = 10). Group II were patients with various thyroid disorders and no TgAb in their sera (n = 6). Group III were patients with thyroid disorders and TgAb in their sera (n = 31). The mean serum Tg level (+/- SE) and mean TgAb level [mean % binding +/- SE (range)] were as follows: Group I, Tg: 22.0 ng/ml +/- 1.64 (n = 10); TgAb 1.91% +/- 0.34 (range 0.6% to 4%). Group II, Tg: 119.8 ng/ml +/- 28.0 (n = 6) TgAb 1.59% +/- 0.34 (0.64% to 2.7%). Group III Tg 167.9 ng/ml +/- 41.0 (n = 31) TgAb 23.2% +/- 3.87 (4.2% to 67.5%). The mean salivary Tg level (SaTg) and mean TgAb binding (% +/- SE range) in saliva were as follows: Group I SaTg 2.07 ng/ml +/- 0.39 (n = 10) SaTgAb 1.13% +/- 0.38 (0% to 3.1). Group II SaTg 3.41 ng/ml +/- 0.67 (n = 6), SaTgAb 0.55% +/- 0.29 (0-1.9%). Group III SaTg 5.22 ng/ml +/- 0.96 (n = 31), SaTgAb 3.1% +/- 1.58 (0 to 47.7%). Salivary TgAb were only present in 4 out of 31 cases of Group III. Mean serum Tg in group IV-A was 75.01 ng/ml +/- 52.1 (n = 11). Mean serum TgAb in group IV-A was 1.94% +/- 0.31 (n = 11).(ABSTRACT TRUNCATED AT 250 WORDS)