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Biomedical subjects

A Shimatsu

Publications and source records attributed to A Shimatsu.

At least 55 records · Page 3Linked to original sources
PubMed1995

Acromegalic gigantism with low serum level of growth hormone and elevated serum insulin-like growth factor-I.

In a case of acromegalic gigantism with hyperprolactinemia is reported, the basal serum growth hormone (GH) levels ranged from 1.2 to 1.9 ng/ml. Serum GH response to either insulin-induced hypoglycemia or GH-releasing hormone was blunted. Frequent blood sampling showed non-pulsatile GH secretion. Serum prolactin and insulin-like growth factor-I (IGF-I) levels were elevated. After unsuccessful surgery, bromocriptine treatment normalized serum prolactin without affecting serum GH and IGF-I levels. Combined administration of octreotide with bromocriptine reduced serum GH and IGF-I levels. In this case, non-pulsatile GH secretion and enhanced tissue sensitivity to GH may induce hypersecretion of IGF-I and cause clinical acromegalic gigantism.

Acromegaly↗
PubMed1994

Identification of somatostatin receptor subtypes and an implication for the efficacy of somatostatin analogue SMS 201-995 in treatment of human endocrine tumors.

The presence of somatostatin receptors has been demonstrated in various endocrine tumors as well as in normal tissues. We recently have cloned five human somatostatin receptor subtypes (SSTR1-SSTR5). These mRNAs are expressed in a tissue-specific manner. In this study, we have determined the somatostatin receptor subtypes expressed in various endocrine tumors using a reverse transcriptase polymerase chain reaction method. In two cases of glucagonoma and its metastatic lymph nodes in one case, all the SSTR subtype mRNAs except SSTR5 mRNA were expressed. In four cases of insulinoma, SSTR1 and SSTR4 mRNAs were detected, but SSTR2 mRNA was not detected in one case and SSTR3 mRNA was not detected in two cases, indicating a heterogeneous expression of SSTR subtypes in insulinomas. Interestingly, SSTR3 mRNA, which is highly expressed in rat pancreatic islets, is not expressed in normal human pancreatic islets, while SSTR1, SSTR2, and SSTR4 mRNAs are expressed. In three cases of pheochromocytoma, SSTR1 and SSTR2 mRNAs were detected, showing an expression pattern identical to that of normal adrenal gland. In a carcinoid, SSTR1 and SSTR4 mRNAs were detected. We have also found that human SSTR2 shows a high affinity for SMS 201-995, which has been used clinically for the treatment of endocrine tumors. Since SMS 201-995 was effective in the treatment of a patient with glucagonoma in which SSTR2 mRNA was present, but had no effect in a patient with carcinoid in which SSTR2 mRNA was not detected, this study suggests that the efficacy of SMS 201-995 may depend, at least in part, on the expression of SSTR2 in tumors.

Adrenal Gland Neoplasms↗
PubMed1994

Insulin sensitivity and glycemic control before and after parathyroidectomy in a diabetic patient with familial multiple endocrine neoplasia type 1.

We treated a diabetic patient with familial multiple endocrine neoplasia type 1 (MEN 1) who had undergone total pancreatoduodenectomy. The patient received insulin and showed signs of symptomatic primary hyperparathyroidism (PHPT). The insulin requirement to control blood glucose before and after parathyroidectomy was compared by using an artificial pancreas. The insulin infusion rate during the day and at night was reduced to about one-third and half, respectively, after parathyroidectomy with autotransplantation of parathyroid tissues into the forearm. The daily insulin dose was reduced from 36 units to 14 units 2 weeks after surgery, and glycemic control showed further improvement 2 months after surgery with the same dose of insulin for up to 6 months. These observations suggest that insulin sensitivity increases after surgical correction of PHPT.

Adult↗
PubMed1994

Changes of gonadotrophin surge inhibiting/attenuating factor activity in pig follicular fluid in relation to follicle size.

The activity of GnSI/AF was measured in pig follicular fluid (pFF) from 58 individual follicles of various sizes, by bioassay using rat pituitary cells, to investigate the relationship between gonadotrophin surge inhibiting/attenuating factor (GnSI/AF) activity and follicular development. In addition, the correlation between GnSI/AF and inhibin activities and the content of sex steroids (oestradiol, progesterone and testosterone) of follicles was examined. The activity of GnSI/AF in pFF varied significantly (0.155-1.69 U microliter-1) with size of the follicle. The activities (mean +/- SEM) were intermediate and constant in follicles with diameters from 3 to 5 mm (0.583 +/- 0.080 U microliter-1, n = 24), were higher and reached the highest value in follicles with diameters between 6 and 8 mm (0.863 +/- 0.068 U microliter-1, n = 21), and were lower, reaching the lowest value in follicles with diameters of 9 and 10 mm (0.401 +/- 0.089 U microliter-1, n = 13). In contrast, inhibin activity was almost constant during the development of follicles, although individual values varied from 0.9 to 2.5 U microliters-1. For follicles with diameters of 4-8 mm, inhibin activity was 1.754 +/- 0.042 U microliters-1 (n = 39); activity was higher in the smallest follicles with diameters of 3 mm (2.063 +/- 0.015 U microliters-1, n = 6) and was lower in follicles with diameter of 9 mm, reaching the lowest value in follicles with diameter of 10 mm (1.176 +/- 0.068 U microliters-1, n = 7); inhibin activity was not significantly correlated with GnSI/AF activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Lymphocytic infundibuloneurohypophysitis as a cause of central diabetes insipidus.

BACKGROUND: Central diabetes insipidus may be familial, secondary to hypothalamic or pituitary disorders, or idiopathic. Idiopathic central diabetes insipidus is characterized by selective hypofunction of the hypothalamic-neurohypophysial system, but its cause is unknown. METHODS: We studied 17 patients with idiopathic diabetes insipidus, in whom the duration of the disorder ranged from 2 months to 20 years. Only four patients had been treated with vasopressin before the study began. All the patients underwent endocrinologic studies and magnetic resonance imaging (MRI) with a 1.5-T superconducting unit, and two patients had biopsies of the neurohypophysis or the pituitary stalk. RESULTS: Nine of the 17 patients had thickening of the pituitary stalk, enlargement of the neurohypophysis, or both and lacked the hyperintense signal of the normal neurohypophysis. In the remaining eight patients, the pituitary stalk and the neurohypophysis were normal, although the hyperintense signal was absent. The abnormalities of thickening and enlargement were seen on MRI only in the patients who had had diabetes insipidus for less than two years, and the abnormalities disappeared during follow-up, suggesting a self-limited process. In addition to vasopressin deficiency, two patients had mild hyperprolactinemia and nine had impaired secretory responses of growth hormone to insulin-induced hypoglycemia. The two biopsies revealed chronic inflammation, with infiltration of lymphocytes (mainly T lymphocytes) and plasma cells. CONCLUSIONS: Diabetes insipidus can be caused by lymphocytic infundibuloneurohypophysitis, which can be detected by MRI. The natural course of the disorder is self-limited.

Adult↗
PubMed1993

Galanin-induced growth hormone secretion in conscious rats: evidence for a possible involvement of somatostatin.

Intracerebroventricular administration of galanin (GAL) potently evoked growth hormone (GH) secretion in conscious male rats. Pretreatments with neostigmine and cysteamine blunted the GAL-induced GH secretion. Pretreatment of animals with a specific anti-somatostatin serum significantly inhibited the GAL-induced GH secretion. On the contrary, GH-releasing hormone-induced GH secretion was significantly enhanced with cysteamine and anti-somatostatin serum. These results suggest that somatostatin is involved in GAL-induced GH secretion in rats.

Animals↗
PubMed1993

Interaction between nicotinic cholinergic receptors and alpha-2 adrenergic systems in regulating growth hormone secretion in conscious rats.

The possible role and mechanism of central nicotinic cholinergic receptors in regulating growth hormone (GH) secretion were investigated in conscious, unrestrained male rats. The administration of galanin (GAL), a neuropeptide, GH-releasing hormone (GHRH) and UK 14304, an alpha-2 adrenergic agonist, caused increases in plasma GH levels. Pretreatment of the animals with hexamethonium significantly reduced GAL- and GHRH-induced GH secretion, but UK 14304-induced GH release was not affected. Neosurugatoxin, a nicotinic cholinergic neurotoxin, partially inhibited GAL-induced GH release. Pretreatment with neostigmine elevated basal plasma GH levels and partially inhibited GAL-induced GH secretion. However, GHRH- and UK 14304-induced GH release was additive to the effect of neostigmine. Yohimbine inhibited GH release induced by UK 14304, GAL and GHRH. Neostigmine-induced GH secretion was partially inhibited by yohimbine and phenoxybenzamine. These findings suggest that central nicotinic receptors have a stimulatory role in regulating GH secretion and that the nicotinic cholinergic system coupled with the alpha-2 adrenergic mechanism is involved in GH secretion induced by galanin in conscious rats.

Adrenergic alpha-Agonists↗
PubMed1993

[Alterations in receptor status and signal transduction mechanisms in pituitary tumors].

Recently evidence has been accumulating that important abnormalities in the receptor status and postreceptor signal transduction frequently occurred in human pituitary tumors. Several in vivo and in vitro studies suggest that during tumoral expansion, pituitary cells acquire functionally active receptors and respond to a variety of hypothalamic hormones. Alterations in proteins responsible for signal transduction have been reported. Somatic mutations of the alpha chain of Gs, the stimulatory regulatory protein of adenylate cyclase (AC), causing constitutive activation of AC have been identified in a subset of human GH-secreting adenomas. Alterations in receptor and signal transduction mechanisms in pituitary tumors triggered by hypothalamic hormones may result in amplification of stimulatory inputs and impairment of inhibitory inputs.

Adenylyl Cyclases↗
PubMed1992

Iodothyronine 5-deiodinase in rat posterior pituitary.

We first describe the presence of iodothyronine 5-deiodinase (5D) in the neural lobe of rat pituitary. 6-n-Propyl-2-thiouracil (PTU), a specific inhibitor of type-I deiodinase, had no effect, showing that 5D in neurohypophysis is of type-III isozyme, which is specific for 5-deiodination and has been found only in the brain, placenta and skin. The presence of 5D (type-III) together with our previous report of 5'-deiodinase (type-I in euthyroidism and type-II in hypothyroidism) shows that the isozymes of deiodinases in the neurohypophysis are quite similar to those in the brain. These data suggest a previously unrecognized role of thyroid hormone in posterior pituitary physiology.

Animals↗
PubMed1992

[A case of panhypopituitarism with normal height manifesting the transection of the pituitary stalk and the formation of the ectopic and eutopic posterior lobes].

A 33-year-old man with hypopituitarism is documented. He was born at breech presentation without asphyxia. He was the shortest in his class throughout his school days. He kept slowly growing and reached 172.8 cm at the age of 33. He was devoid of secondary sexual characteristics. Endocrinological studies showed panhypopituitarism with elevated levels of plasma TSH (15.0 microU/ml). TRH administration resulted in a marked increase in plasma TSH. Posterior pituitary function was normal. MR imaging showed transection of the pituitary stalk and the presence of ectopic and eutopic posterior lobes. The replacement of corticosteroid was initiated, and exaggerated response of TSH to TRH disappeared. Delayed bone maturation due to hypogonadism and hypothyroidism was one of the reasons why he had normal height without GH therapy. The significance of his peculiar MRI findings remains to be determined.

Adult↗
PubMed1992

[Long-term treatment of acromegaly and gigantism with octreotide (SMS 201-995)].

Twenty-one patients with active acromegaly and two patients with pituitary gigantism were treated with the long-acting somatostatin analogue octreotide (100-600 micrograms/day, sc, two or three times daily or 300-1500 micrograms daily by intermittent sc infusion) for 9-63 months. There was rapid clinical improvement. The fasting plasma GH levels were significantly suppressed (less than 50% of the values before treatment) in 17 patients and were normalized (less than 5 ng/ml) in 6 patients (27.3%). Plasma IGF-I levels were lowered by 50% and were normalized in 7 out of 18 cases. The effect of octreotide on pituitary tumor size was evaluated in 13 patients. In 4 cases, the shrinkage of the pituitary tumor was detected by computed tomographic scans and/or magnetic resonance imaging studies. The drug was generally well tolerated. However, there were probably newly formed gallstones in two patients during the therapy. Our study suggests that octreotide is an effective and relatively safe new approach for treating active acromegaly and gigantism.

Acromegaly↗
PubMed1992

Metastatic renal cell carcinoma to the pituitary gland presenting with hypopituitarism.

A 57-year-old man with pituitary metastasis from renal cell carcinoma is reported. He underwent right nephrectomy and total pancreatectomy for renal cell carcinoma and its pancreatic metastasis, respectively. Imaging studies showed an intrasellar mass lesion. The examination revealed panhypopituitarism, diabetes insipidus and bitemporal hemianospia. Metastatic renal cell carcinoma was diagnosed by the biopsy of the pituitary tumor. Metastatic renal cell carcinoma to the pituitary gland, which is extremely rare, appears to have unique features of presenting with hypopituitarism and visual disturbance more frequently than other metastatic pituitary tumors.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1992

Generalized resistance to thyroid hormone (GRTH) in a family: case studies.

A familial case of generalized resistance to thyroid hormone (GRTH) is described. A 17-year-old man (case 1), who had been treated with methimazole under the diagnosis of Graves' disease and his 11-year old sister (case 2) visited our clinic for the evaluation of their thyroid function. They lacked the signs and symptoms of thyrotoxicosis in spite of extremely high serum thyroid hormone levels. Their plasma TSH levels were not suppressed, but in fact markedly increased after TRH loading. Their peripheral indices of thyroid hormone were within normal limits and were not influenced by exogenous T3 administration. Even 150 micrograms T3 administration for 7 days did not fully suppress the TRH-stimulated TSH level in case 2. The two patients thus were diagnosed to have GRTH. Sera from their father and another sister showed identical abnormalities.

Adolescent↗
PubMed1992

[Effects of insulin-induced hypoglycemia on catecholamine secretion and blood pressure in neurological disorders affecting autonomic nervous system].

The effects of insulin-induced hypoglycemia on catecholamine secretion were investigated in patients with various neurological disorders affecting the autonomic nervous system. In control subjects, insulin-induced hypoglycemia resulted in marked increases in plasma epinephrine and norepinephrine levels. Heart rates were increased within 15 minutes after the insulin injection which were associated with slight elevation and depression of systolic and diastolic blood pressure, respectively. In patients with upper level spinal cord lesions (C1-T6) of various etiology, Shy-Drager syndrome and familial amyloidosis, insulin-induced hypoglycemia failed to increase plasma epinephrine and norepinephrine levels and resulted in falls in systolic and/or diastolic blood pressure 15 minutes after the injection. Heart rates were increased at 30-45 minutes after the injection. In patients with lower spinal cord lesions (T10-L1), neurosyphilis or brain stem tumor with orthostatic hypotension, the catecholamine responses were normal and blood pressure did not fall during insulin-induced hypoglycemia. In patients with Parkinson's disease and spinocerebellar degeneration with autonomic symptoms catecholamine responses were not impaired. These findings suggest that any lesion involving the sympathetic efferent systems of baroreflex such as the spinal descending pathway, sympathetic preganglionic neuron and peripheral nervous system causes both impairment of catecholamine secretion and a fall in blood pressure during hypoglycemia, and that lesions in sympatho-afferent system may not affect the secretion of catecholamine and neural control of blood pressure.

Adult↗