Serum thyroxine (T4) and triiodothyronine (T3) concentration and binding were measured in 34 clinically euthyroid patients hospitalized for a wide variety of nonthyroidal diseases. Despite clinical euthyroidism, serum T3 was in the hypothyroid range (less than 90 ng/100 ml) in 24 of the 34 patients, and the mean serum T3 of this group, 78.4 +/- 38.3 (SD), was significantly decreased from that of control, 134.0 +/- 29.3 ng/200 ml. Mean serum T4 levels were essentially the same in both groups, 7.3 +/- 2.0 for sick patients and 7.2 +/- 1.0 mug/100 ml for the controls. Plasma binding of both T4 and T3 was decreased in the patient group to 69.9 and 78% of control values, respectively. In accord with previous studies, the mean free T4 index, proportional to free T4 concentration, was significantly increased to 10.0 +/- 4.1 in the patient group (control, 7.6 +/- 1.3). However, the mean free T3 index of the patient group, 92.9 +/- 38.4 remained decreased from that of control, 138.9 +/- 34.4. Of the 24 patients with decreased serum T3 (less than 90 ng/100 ml), low T3 levels could be attributed to decreased plasma binding in 8; in 5, serum T3 was within the normal range for their advanced age. Mean TSH was greater in the patient group 2.6 +/- 1.9, than in the controls, 1.9 +/- 1.1 muU/ml. Moreover, the TSH response to administered TRH was moderately exaggerated in 7 patients with low free T3 index compared to 7 patients with normal free T3 index. Although significant statistically, neither the basal nor TRH induced TSH levels were in the range generally found in primary hypothyroidism. The data suggest that the high incidence of low serum T3 (70%) and free T3 index (32%) in nonthyroidal disease may be related to the catabolic state that accompanies illness rather than to specific disease entities. At the present time, the use of serum T3 or free T3 measurements for the diagnosis of hypothyroidism does not appear justified in patients with nonthyroidal disease.

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SUMMARY1. Growing male domestic fowl of an egg-laying strain were fed ad libitum and injected intraperitoneally with melatonin or intramuscularly with triiodothyronine (T3) to study the effects on sleep, food intake, blood glucose, e.e.g., oxygen consumption and carbon dioxide production.2. Melatonin caused a dose-related depression of food intake with sleep and aphagia lasting for 21 hr following 8 mg, drowsiness and greatly reduced intake following 4 and 2 mg and a slight reduction in food intake after 1 mg.3. T3 injection was followed by increased feeding within the range 50-200 jug. The higher dose (200 jug) completely prevented the effects of 10 mg melatonin injected simultaneously.4. Melatonin (10 mg) depressed plasma glucose levels whereas T3 (200 ,sg) elevated blood glucose.5. Either darkness or melatonin (10 mg) caused an increase in amplitude and a decrease in frequency of the e.e.g. 6. Birds fasted for 3 hr before injection showed significantly lower oxygen consumption and carbon dioxide production when given melatonin (10 mg); T3 had no effect within the 4 hr period after injection and did not modify the effects of melatonin.7. It is postulated that the rapid effects of melatonin and T3 which were observed result from direct effects of these hormones on the central nervous system.

Background: In some patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (coronavirus disease 2019 [COVID-19]), an uncontrolled release of inflammatory cytokines is characteristic. COVID-19 and adult-onset Still’s disease (AOSD) have been included by some authors in the “hyperferritinemic syndromes.” Another hyperinflammatory syndrome (with variable features of Kawasaki disease) called multisystem inflammatory syndrome (MIS) has been described in patients who have had SARS-CoV-2 infection. Case Presentation: We present a previously healthy patient who developed hyperinflammatory reaction compatible with MIS; the clinical presentation is additionally compatible with AOSD, complicated with a mild myocarditis. The patient had a positive SARS-CoV-2 serology (immunoglobulins G and immunoglobulins M ), but multiple reverse transcription-polymerase chain reaction (RT-PCR) testing for SARS-CoV-2 on nasopharyngeal swab were negative or indeterminate, so we considered that it is possible that an asymptomatic SARS-CoV-2 infection could have been the trigger for Still’s disease. 24 hours after starting methylprednisolone treatment, the fever was resolved and symptoms improved over the next few days, with persistent arthralgias. Conclusion: Asymptomatic SARS-CoV-2 infection could trigger MIS with AOSD-like features.