| Huber et al., Basel, Switzerland, investigated the effects of T4 substitution in 63 women (mean age 57 years) with subclinical hypothyroidism with regard to clinical scores and lipid profile, which were measured at baseline and 6 and 12 months after initiation of therapy. This prospective study was double blind in that 32/63 subjects received a placebo. During T4 treatment, TSH levels returned to normal and clinical scores of hypothyroidism improved (p < 0.05), cholesterol levels decreased from a mean value of 6.3 to 6.0 (p < 0.05) and LDL-cholesterol decreased from a mean value of 4.0 to 3.7 (p < 0.05). HDL levels remained unchanged. Basal parameters did not differ between T4 treated and placebo treated patients and no changes in parameters occurred during placebo treatment. (Comment: It becomes more and more evident that not only in subclinical hyperthyroidism but also in subclinical hypothyroidism treatment is beneficial. In this study not only risk factors for atherosclerosis decreased, but patients also improved clinically. I would suggest that the term subclinical (both for hyper- and hypothyroidism) is a misnomer in the sense that scrutinized clinical evaluation will find abnormalities even when T4 and T3 levels are normal in these situations. Maybe the term "minimal" hypo- or hyperthyroidism is more appropriate in patients with abnormal TSH but normal serum thyroid hormone concentrations.) Ward et al., Campinas, SP, Brazil, found that of 632 subjects (434 females) over 60 years who were referred for thyroid function analysis, in 153/632 (24%) of cases subclinical hypothyroidism was detected. Depression was diagnosed in 32/153 patients, which is significantly higher than in 5% of controls. (Comment: This is again a report indicating that "subclinical" hypothyroidism does not exist, i.e. that clinical symptoms are present when looked for.) Benvenga et al., Messina, Italy, measured early morning basal and TRH stimulated TSH (peak value and area under the curve) in 35 patients with circulating thyroid antibodies and a FT4 = the normal mean and a serum TSH = 1.5 mU/L. Tests were done in early morning (EM) between 7 and 8.30 am and at late morning (LM) between 9 and 11.30 am. A TSH > 4.2 mU/L occurred in 73% at EM vs. 29% at LM. In 19/35 patients all tests were completed (group A). In 16/35 patients not all parameters were available at the time of the report. In group A, mean basal AM and LM TSH were 5.3 and 3.7 mU/L (p < 0.02) and in group B, 5.3 vs. 4.0 (p < 0.01). Serum TSH after TRH was only complete in group A and was at EM > LM at time points 15 minutes, 30 minutes, and 60 minutes in 47%, 68%, and 74% respectively. The area under the curve at EM was significantly higher (p < 0.01) vs LM. Peak values of TSH were also frequently higher at EM as at LM. The authors recommend early sampling of both TSH and TSH after TRH. They furthermore stress the importance of measuring the area under the TSH curve after TRH. ( Comment: The crucial point here is of course if reference values were separately collected both for EM and LM.) |
