J. Endocrinol. invest. 11: 231, 1988 The influence of diabetes mellitus on thyrotropin response to thyrotropin-releasing hormone in untreated acromegalic patients C. Shigemasa*, K. Abe**, S. Taniguchi*, Y. Mitani*, Y. Ueta*, T. Adachi*, K. Urabe*, T. Tanaka*, A. Yoshida*, T. Hori***, and H. Mashiba* *The First Department of Internal Medicine and ***Division of Neurosurgery, Institute of Neurological Sciences, Tottori University School of Medicine, and **Department of Nursing, Tottori University College of Medical Care Technology, 36-1 Nishimachi, Yonago 683, Japan ABSTRACT. Impairment of thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been documented in patients with uncontrolled diabetes mellitus (OM). In acromegalic patients, however, there have been no data regarding TSH secretion studied taking the existence of OM into consideration. Therefore, we investigated the TSH response to TRH [expressed as TSH increment (b TSH)] in 14 untreated acromegalic patients, who did not show the suprasellar extension of adenoma, divided into two groups on the basis of either presence or absence of uncontrolled OM, and in 28 normal subjects. The mean max b TSH was significantly reduced (p < 0.02) in acromegalic patients despite similar mean serum T4 and free T4 index (FT41) levels. Furthermore, the mean basal and max bTSH in 7 patients with OM (FBS, 120-300 mg/dl; HbA1, 8.8-1S.2%) were significantly lower than those in 7 patients without OM (p<O.OS and p<0.02, respectively) despite similar the mean serum T3, T 4, FT 41, growth hormone (GH) and prolactin (PRL) levels and sellar volume. In 4 patients with OM the TSH response to TRH 6-8 weeks after insulin therapy, when their HbA1 levels were normal, increased compared to that before insulin therapy. The mean max b TSH after selective adenomectomy in 8 patients (3 in OM group and S in non-OM group), whose fasting basal GH fell to less than S ng/ml, was almost identical to that in normal subjects. In conclusion, the present study suggests that the abnormal- ity in TSH secretion in acromegalic patients may be increased by the existence of uncontrolled OM. INTRODUCTION It has been reported that the thyrotropin (TSH) re- sponse to thyrotropin-releasing hormone (TRH) is fre- quently impaired in acromegaly (1-6), and suggeste.d that this decreased TSH response may result from pressure on the normal pituitary gland by a pituitary adenoma or the direct or indirect effect of growth hor- mone (GH) excess. Acromegaly is frequently asso- ciated with diabetes mellitus (OM) and/ or hyperprolac- tinemia. Several previous reports have described the decreased TSH response to TRH in patients with type I OM (7 -9) and type II OM (10). In acromegalic patients, however, there have been no data regarding TSH se- cretion studied taking the existence of OM into consid- eration. On the other hand, the abnormal TSH response to TRH has also been observed in patients with pro lac- Key-words. Acromegaly, diabetes mellitus, basal thyrotropin level, thyrotropin response, thyrotropin-releasing hormone. Correspondence: Chiaki Shigemasa, MD .. The First Department of Internal Medi- Cine, Tottori University School of Medicine, 36-1 Nishimachi, Yonago 683, Japan. Received July 24. 1987; accepted November 19. 1987. 231 tinoma (11, 12). In this study, in order to investigate . whether the existence of uncontrolled OM influences the TSH secretion in acromegalic patients, the differ- ence between the TSH response to TRH in untreated acromegalic patients with OM and without OM was evaluated, taking the serum concentrations in PRL and thyroid hormones and the sellar volume into consider- ation. MATERIALS AND METHODS Fourteen untreated acromegalic patients (6 men and 8 women), aged from 25 to 66 yr, were studied (Table 1). The diagnosis of acromegaly was made by the combi- nation of the presence of clinical signs and symptoms due to the increased GH secretion with the elevated fasting serum GH levels, ranged from 12 to 120 ng/ml, which could not be inhibited by oral glucose. Duration of symptoms ranged from 3 to 12 yL In these patients no medication that might increase serum PRL level was taken and the existence of primary hypothyroidism was excluded. Their serum antithyroglobulin and anti- microsome antibodies by hemagglutination method (Thyroid test and Microsome test, respectively; Fuji-