11/12. Reverse T3 does not reliably differentiate hypothyroid sick syndrome from euthyroid sick syndrome. To assess the efficacy of reverse T3 in differentiating between the hypothyroid and euthyroid state in the setting of illness, all reverse T3 determinations obtained over a 4-year period in a University teaching hospital were analyzed in the context of concurrent thyroid function tests, bilirubin, albumin, creatinine, subsequent treatment, and follow-up. Based on T4 (or free T4 index) and TSH, the thyroidal state of the patient and the appropriateness of the reverse T3 determination were assigned. A total of 262 reverse T3 determinations were made in 246 patients. There is an inverse linear relationship between the log TSH and the reverse T3. patients with hypothyroidism plus illness may have a normal reverse T3 and patients with euthyroidism may have a low reverse T3. Reverse T3 is linearly related to bilirubin up to a bilirubin of approximately 171 microM (10 mg/dL). Sixty percent of the reverse T3 determinations were obtained for seemingly inappropriate indications. In association with a low free T4 index/T4, an unmeasurable reverse T3 did not lead to institution of thyroid hormone treatment in over 52% of cases. Although reverse T3 may be elevated in the setting of nonthyroidal illness, it is not reliable in distinguishing between the hypothyroid sick patient and the euthyroid sick patient. This is probably because of drug and disease effects on thyroid hormone metabolism as well as the presence of sufficient T4 substrate for conversion to reverse T3 in many hypothyroid sick patients. ( info) |
12/12. Transiently decreased sialylation of thyrotropin (TSH) in a patient with the euthyroid sick syndrome. A 60-year old woman was admitted to the medical intensive care unit with respiratory distress and worsening renal function, and was found to have bilateral renal artery occlusion. Aggressive nutrition per nasogastric tube was begun on day 8 of her illness, and she eventually recovered after bilateral renal artery bypass surgery, which was performed on day 15. She developed the euthyroid sick syndrome. Levels of serum TSH, T3, and T4 fell during the first few days of her illness, then all trended to normal levels by day 28. The TSH level declined from 1.6 microU/mL on day 2 to 0.2 microU/mL on day 5, then rose to 4.5 microU/mL on day 10, and was 3.8 microU/mL on day 14. The ratios of free T4/TSH, a crude measure of the bioactivity of TSH, were 1.4, 8.0, 0.16, 0.32, and 1.14 on days 2, 5, 10, 14 and 28, respectively. TSH was immunoaffinity concentrated from serum collected on four dates. The TSH oligosaccharides were enzymatically released, treated with or without neuraminidase, labeled with a fluorescent probe, and analyzed by gel electrophoresis. The TSH oligosaccharides were found to be transiently less sialylated on day 13 as compared to days 2, 4, and 24. Three gel bands representing poorly sialylated oligosaccharides represented a mean of 20.6% of TSH oligosaccharides on days 2, 4, and 24, but represented 33.7% of TSH oligosaccharides on day 13. This is the first report of altered TSH oligosaccharide sialylation in the euthyroid sick syndrome. If confirmed by studies of additional patients, altered TSH sialylation may, in part, explain the altered TSH bioactivity that has been described in the euthyroid sick syndrome. ( info) |