CO-EXISTENT PRIMARY HYPOTHYROIDISM AND ISOLATED ACTH DEFICIENCY

1976 ◽  
Vol 82 (2) ◽  
pp. 467-474 ◽  
Author(s):  
T. Yamamoto ◽  
T. Ogihara ◽  
K. Miyai ◽  
Y. Kumahara ◽  
Y. Hirata
Keyword(s):  
Growth Hormone ◽  
Elevated Serum ◽  
Pituitary Hormones ◽  
Primary Hypothyroidism ◽  
Simultaneous Occurrence ◽  
Plasma Acth ◽  
Acth Deficiency ◽  
Thyrotrophic Hormone ◽  
Serum Thyroid Hormones

ABSTRACT A 52 year old man is described in whom the simultaneous occurrence of isolated adrenocorticotrophin (ACTH) deficiency and primary hypothyroidism was documented by the determination of six anterior pituitary hormones by specific radioimmunoassays after suitable stimulations. The urinary 17-hydroxycorticosteroids excretion was persistently reduced and was increased by repeated ACTH injections. The low basal metabolic rate, reduced serum thyroid hormones and elevated serum thyrotrophic hormone were consistent with primary hypothyroidism. After resumption of euthyroidism, secretory reserves of growth hormone and ACTH were assessed. The growth hormone response to insulin-induced hypoglycaemia was normal. No rise in plasma cortisol and ACTH was observed following insulin-induced hypoglycaemia. Plasma ACTH was not augmented by iv infusion of metyrapone. The pathogenesis of two co-existent endocrine deficiencies was discussed.

Isolated ACTH deficiency accompanied by 'primary hypothyroidism' and hyperprolactinaemia

1983 ◽  
Vol 104 (4) ◽  
pp. 397-401 ◽  
Author(s):  
Tadayoshi Yoshida ◽  
Tetsuya Arai ◽  
Jinpei Sugano ◽  
Hiroshi Yarita ◽  
Hideo Yanagisawa
Keyword(s):  
Pituitary Gland ◽  
Primary Hypothyroidism ◽  
Hormonal Changes ◽  
Plasma Acth ◽  
Isolated Acth Deficiency ◽  
Acth Deficiency ◽  
Corticotrophin Releasing Factor ◽  
Lysine Vasopressin ◽  
Before And After

Abstract. A 55 year old man with isolated ACTH deficiency is reported. The lesion would appear to be located in the pituitary gland since plasma ACTH and cortisol did not respond to lysine vasopressin and corticotrophin releasing factor (CRF). A fall in T4, a rise in basal values of TSH, prolactin (Prl), LH and FSH, excessive responses of TSH and Prl to TRH, and hyperreactive responses of LH and FSH to LRH were observed. These hormonal changes were examined before and after administration of cortisol. The abnormality in these hormones might be caused by deficiency of long-term glucocorticoid.

scholarly journals A Case of Transient ACTH Deficiency Associated with Polymyalgia Rheumatica

2010 ◽  
Vol 1 ◽  
pp. JCM.S6215
Author(s):  
Hitoo Nishi ◽  
Yuichi Nishi ◽  
Masato Yagita ◽  
Yoshiko Tamaru ◽  
Sadayuki Matsumoto ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Polymyalgia Rheumatica ◽  
Serum Cortisol ◽  
Final Diagnosis ◽  
Pituitary Hormones ◽  
Sudden Onset ◽  
Plasma Acth ◽  
Acth Deficiency ◽  
Normal Increase ◽  
Short Time

We report a case of 79-year-old man, who was diagnosed to have transient ACTH deficiency associated with polymyalgia rheumatica (PMR). The patient presented with sudden onset bilateral shoulder pain, which was gradually aggravated. Plasma ACTH was undetectable, and both serum cortisol and urinary 17-OHCS were very low. Other pituitary hormones were normal, suggesting that hypothalamo-pituitary-adrenal (HPA) axis is selectively damaged. However, within several weeks, plasma ACTH returned to normal, and showed a normal increase response to corticotropin-releasing hormone stimulation test. These results indicated that ACTH deficiency was only transient. After hydrocortisone (10 mg/day) was administered, his symptoms became suddenly improved. Based on those results and clinical course, ie, elevated erythrocyte sedimentation rate, negative rheumatoid factor and the typical symptoms, which showed improvement to glulcocorticoid therapy, the final diagnosis was PMR, which was associated with transient ACTH deficiency. This is the first report of a case of PMR, in which the HPA axis was examined in its very acute phase. It was demonstrated that the case was associated with the transient adrenocortical hypofunction, which was recovered during a short time. It is therefore possible that PMR may show a different responsiveness of HPA axis depending on its phases.

Timing of growth hormone injections and reproduction in gilts

1991 ◽  
Vol 71 (3) ◽  
pp. 717-723 ◽  
Author(s):  
J. Gilbertson ◽  
R. N. Kirkwood ◽  
P. A. Thacker
Keyword(s):  
Growth Hormone ◽  
Ovarian Function ◽  
Elevated Serum ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Ovulation Rate ◽  
Serum Concentrations ◽  
Lh Pulsatility ◽  
And Control

Sixty-eight Yorkshire × Landrace gilts were selected at 85 kg body weight (BW) and exposed to a mature boar for 20 min d−1 to detect puberty. At the onset of puberty, gilts were allocated to receive daily intramuscular injections of porcine growth hormone (pGH, 90 μg kg−1 BW) from either 14 to 17 d (GH17, n = 22) or from 14 to 22 d (GH22 n = 22) after puberty, inclusively. A third group of gilts served as controls (n = 24) and received vehicle buffer. A single blood sample was obtained from each gilt on days 14, 17 and 20. Also, four gilts from each pGH treatment and eight control gilts were sampled at 15-min intervals for 8 h on day 16. Gilts were slaughtered 30 d after puberty at which time their ovaries were recovered for the determination of ovulation rate. Injection of pGH resulted in elevated serum concentrations of triiodothyronine, insulin and glucose (P < 0.01). There was no significant (P > 0.1) treatment effect on mean serum concentrations of LH or FSH. However, pGH treatment tended (P = 0.1) to increase LH pulse frequency and to decrease (P = 0.01) LH pulse amplitude. The incidence of a second estrus was reduced (P < 0.01) in GH22 compared to control gilts, with GH17 being intermediate (72.7 vs. 90.9 vs. 100% for GH22, GH17 and control gilts, respectively). Ovulation rate was not affected by pGH treatment (15.1 vs. 14.3 vs 14 0 for GH22, GH17 and control gilts, respectively). The present data confirm an adverse effect of pGH on ovarian function and suggest that an altered LH pulsatility may be involved. Key words: Gilts, growth hormone, estrus, endocrinology

STIMULATION OF LONGITUDINAL BONE GROWTH BY HYPOPHYSEAL HORMONES IN THE HYPOPHYSECTOMIZED RAT

1977 ◽  
Vol 84 (3) ◽  
pp. 485-496 ◽  
Author(s):  
K.-G. Thorngren ◽  
L. I. Hansson
Keyword(s):  
Growth Hormone ◽  
Bone Growth ◽  
Growth Stimulation ◽  
Pituitary Hormones ◽  
Pituitary Hormone ◽  
Longitudinal Bone Growth ◽  
Thyrotrophic Hormone ◽  
Hypophysectomized Rats ◽  
Higher Doses ◽  
Effective Growth

ABSTRACT The stimulating effect of different pituitary hormones on longitudinal bone growth was determined with tetracycline as intravital marker in hypophysectomized rats. Growth hormone was found to be the most effective growth stimulating pituitary hormone. At considerably higher doses, thyrotrophic hormone (TSH) and prolactin also showed growth stimulating activity. TSH exerts its effect via the production of thyroxine, whereas the growth stimulation by prolactin seems to be a direct effect of this hormone, similar to the effect of growth hormone. The LH, FSH, ACTH, MSH, vasopressin and oxytocin preparations did not stimulate longitudinal bone growth.

SERUM THYROTROPHIN AND THE RESPONSE TO THYROTROPHIN RELEASING HORMONE IN SYMPTOMLESS AUTOIMMUNE THYROIDITIS AND IN BORDERLINE AND OVERT HYPOTHYROIDISM

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg
Keyword(s):  
Autoimmune Thyroiditis ◽  
Elevated Serum ◽  
Mean Value ◽  
Primary Hypothyroidism ◽  
Overt Hypothyroidism ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Mean ◽  
The Individual ◽  
Serum Tsh

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.

Counterregulation of insulin-induced hypoglycaemia in primary hypothyroidism

1986 ◽  
Vol 111 (4) ◽  
pp. 516-521
Author(s):  
Nina Clausen ◽  
Per-Eric Lins ◽  
Ulf Adamson ◽  
Bertil Hamberger ◽  
Suad Efendić
Keyword(s):  
Growth Hormone ◽  
Insulin Infusion ◽  
Primary Hypothyroidism ◽  
Constant Rate Infusion ◽  
Counterregulatory Hormones ◽  
Insulin Metabolism ◽  
Hormonal Responses ◽  
Glucose Levels ◽  
Constant Rate ◽  
Rate Infusion

Abstract. Hypothyroidism has been alleged to modulate insulin action and influence the secretion of growth hormone and catecholamines. We recently investigated the influence of hypothyroidism on glucose counterregulatory capacity and the hormonal responses to insulin-induced hypoglycaemia in 6 patients with primary hypothyroidism (age 32–52 years, TSH-values 66–200 mU/l). Hypoglycaemia was induced in the hypothyroid state and again when the subjects were euthyroid. After an overnight fast a constant rate infusion of insulin (2.4 U/h) was given for 4 h. Glucose was measured every 15 min and insulin, C-peptide, glucagon, epinephrine, norepinephrine, growth hormone and cortisol every 30 min for 5 h. During insulin infusion somewhat higher concentrations of the hormone were obtained in the hypothyroid state and simultaneously glucose levels were 0.5 mmol/l lower. As expected, basal norepinephrine levels were higher in hypothyroidism. However, no increase in circulating norepinephrine during hypoglycaemia was registered in the two experiments. The responses of counterregulatory hormones showed an enhanced response of cortisol, similar responses of growth hormone and epinephrine while the glucagon response was paradoxically impaired. Our findings suggest that hypothyroidism alters insulin metabolism, and that the glucagon response to hypoglycaemia is impaired in this condition.

DETERMINATION OF AFTER-RIPENING PERIOD AND HORMONAL RESPONSE OF OROBANCHE SOLMSII C.D. CLARKE SEEDS

1970 ◽  
Vol 11 (1) ◽  
Author(s):  
A. Bista ◽  
G. B. Khattri ◽  
B. D. Acharya ◽  
S. C. Srivastava
Keyword(s):  
Growth Hormone ◽  
Seed Germination ◽  
Key Words ◽  
Incubation Period ◽  
Seed Set ◽  
Summer Season ◽  
Conditioning Period ◽  
Root Parasite ◽  
One Year

To find out the ability of Orobanche seeds to germinate immediately after seed set, seeds were germinated periodically at an interval of three months for one year in GR24. Some Orobanche seeds were capable of germination immediately after seed set but most required about nine months as after ripening or incubation period to be able to germinate. The phenomenon of after ripening in Orobanche seeds could be taken as an ecological measure to dormant over following unfavorable wet summer season. The growth hormone studies on Orobanche seed germination have shown that GA3 at a concentration of 100 ppm substantially enhanced seed germination when applied during pre-conditioning period. NAA showed some stimulatory effect at 0.5 - 1.0 ppm when applied during post-conditioning period but the hormone if applied during pre-conditioning period inhibited the germination. Kinetin failed to stimulate the germination at all the concentrations tested. Key words: Germination, root-parasite, hormone. Ecoprint Vol.11(1) 2004.

Barth syndrome with severe dilated cardiomyopathy and growth hormone resistance: a case report

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Joel A. Vanderniet ◽  
Paul Z. Benitez-Aguirre ◽  
Carolyn R. Broderick ◽  
Richard I. Kelley ◽  
Shanti Balasubramaniam
Keyword(s):  
Growth Hormone ◽  
Dilated Cardiomyopathy ◽  
Corn Starch ◽  
Primary Hypothyroidism ◽  
Barth Syndrome ◽  
Height Velocity ◽  
Growth Delay ◽  
Hormone Resistance ◽  
Feeding Difficulties ◽  
Growth Hormone Resistance

Abstract Objectives To describe the metabolic and endocrine features of a patient with Barth syndrome who showed evidence of growth hormone resistance. Case presentation A male proband deteriorated rapidly with lactic acidosis after a circumcision at age three weeks and was found to have severe dilated cardiomyopathy. A cardiomyopathy gene panel led to the diagnosis of TAZ-deficiency Barth syndrome. He subsequently experienced hypotonia and gross motor delay, feeding difficulties for the first four years, constitutional growth delay and one episode of ketotic hypoglycaemia. Cardiomyopathy resolved on oral anti-failure therapy by age three years. He had a hormonal pattern of growth hormone resistance, and growth hormone treatment was considered, however height velocity improved spontaneously after age 3½ years. He also had biochemical primary hypothyroidism. Conclusions With careful metabolic management with l-arginine supplementation, overnight corn starch, and a prescribed exercise program, our patient’s strength, endurance, level of physical activity and body composition improved significantly by age six years.

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