1291 of radioiodine in the neck. In 25 the uptake was totally suppressed during therapy when the response to T.R.H. was absent, but in 7 there was still a definitely localised, though slight, uptake (about 1% of the dose). In these cases the small residual thyroid probably contained normal tissue only. Our findings suggest that the level of thyroid hormones in the blood is not a reliable indication of suppression of T.S.H. secretion. The response to T.R.H., however, did give useful information about pituitary suppression, as Bosnardo et aI.8 and Hoffman et al.9 have found. Hoffman et al. used not only basal T.S.H. but also the absence of secretion peaks during the day as evidence of good suppression. However, 4 out of 26 patients lacking the circadian random peaks still responded to T.R.H. A total suppression of the response was achieved by increasing the dose of thyroxine by 20 p.g a day. However, we found that even when there was no response to T.R.H. the thyroid neck remnant uptake was not totally suppressed but could be suppressed in 1 patient by increasing the thyroxine dose by 50 .g a day. In most patients, however, there is no neck uptake to be used as a guideline. However, absence of response to T.R.H. does not necessarily mean total suppression T.S.H. secretion;

after

of acromegaly by hypophysectomy a significant of proportion patients remain euthyroid despite lack of response to T.R.H.1O The dose of thyroxine required for total suppression of the T.R.H. response was 218±44 .g which is equal to that reported by Hoffman et al.9 in their carcinoma patients (220±49 g). The dose of thyroid hormone should be at least as great as that resulting in suppression as judged by the T.R.H. response, and an increase from that level by 20-50 g per day might be recommended. The final daily thyroxine dose would then be 220-250 p.g, which is close to that considered by Oddie et al.’ to suppress thyroidal uptake of radioiodine totally.

HLOOIPRESSURE AND NUMBER OF HYPERTENSIVES IN MEN WITH NORMAL AND IMPAIRED HEARING (NOISE TRAUMA TYPE)

be estimated by recording hearing defects, even if the years of noise exposure are taken into account. Hearing might be impaired because the noise has not been felt annoying enough to prompt the use of ear protectors. Furthermore selection mechanisms may be operating when industrial workers are recruited. Prospective investigations are required. HANS HEDSTRAND Departments of Audiology, BÖRJE DRETTNER and Internal Medicine, Otolaryngology INGMAR KLOCKHOFF University Hospital, ALF SVEDBERG Uppsala, Sweden

treatment

Endocrine Research Laboratory, University of Helsinki,

B.-A. LAMBERG M. RANTANEN P. SAARINEN

SF-00101 Helsinki 10, Finland, and 3rd Department of Medicine, University Hospital, Helsinki

SUPPRESSOR T CELL FUNCTION IN DIABETES MELLITUS

SiR,-Autoaggression against pancreatic cells has been described in patients with diabetes mellitus.’ Based on the hypothesis that a loss of immune regulatory suppressor T cells could be important in the development of these autoaggressive reactions, we examined suppressor T cell function in nine children with insulin-dependent diabetes mellitus. Suppressor cell activity was determined by assessing the effect of concanaSUPPRESSOR T CELL FUNCTION IN DIABETES MELLITUS

NOISE AND BLOOD-PRESSURE

SiR,-Jonsson and Hansson’ suggested that repeated and exposure to industrial noise may be a contributing rise in blood-pressure. This report was based on a of 118 out of 196 male industrial workers showing sigstudy nificantly higher systolic and diastolic pressures as well as having more individuals with hypertension among those with noise-

prolonged

factor

to a

induced auditory impairment. In a study of cardiovascular risk factors among men aged 49-50 tone audiometry was done.2 Of 2202 participants 393 fulfilled the criteria of noise-induced hearing-loss set by Jonsson and Hansson (≥65 dB at 3000, 4000, or 6000 Hz), dB at whereas 376 men had normal-tone audiograms (