Nihon Naibunpi Gakkai zasshi最新文献

The history of the studies on stress and hormones is briefly reviewed. The two main stress transmission systems are the endocrine (CRH-ACTH-Cortisol) and the neural (Sympatho-adreno-medullary) systems. The junction of the two systems resides in the hypothalamus. It has been clarified that CRH has central suppressive effects on eating, sleeping and sexual behavior. The relationships between emotions such as fear, anger and neurotransmitters (noradrenaline or serotonin) are discussed. Recent studies have revealed that various kinds of cytokines secreted from leukocytes stimulate the secretions of CRH and ACTH. Thus the cooperative mechanisms and actions of the endocrine, neural and immune systems against stress to keep homeostasis are elucidated.

From 1969 to 1990, 15 children with acute suppurative thyroiditis (AST) were diagnosed in our hospital. Their clinical, laboratory and radiologic findings were reviewed. The characteristic features were as follows: 1) Males to female ratio was 1.5:1. 2) The ages at diagnosis ranged from 3 to 14 years, with a mean age of 6 years. 3) A painful, tender mass in the anterior neck was detected in all cases and fever was detected in 10 cases (67%). 4) The left lobe of the thyroid was affected in 11 cases (73%), whereas the right lobe was affected in the remaining 4 cases. No cases was bilateral. 5) Five cases (33%) were found to be recurrent. 6) Eight pathogenic organisms were identified on culture from 7 cases; among them 3 were due to anaerobic pathogen. 7) Leukocytosis was increased and acute-phase reactant tests were positive in most cases. 8) Thyroid function was found to be normal in all 9 cases examined. 9) Radiologic studies, which included radionuclide thyroid scan, ultrasonography, computed tomography and barium esophagogram, were very helpful for the diagnosis of AST. 10) A barium esophagogram was performed in 9 cases and a fistula originating from the pyriform sinus was found in 4 cases (44%). 11) Three cases (20%) had the complete removal of the fistula as a permanent cure. This report summarizes the clinical features of 15 children with acute suppurative thyroiditis diagnosed in our hospital during the past twenty years.

The primary objective of this study was to ascertain the usefulness of granulocyte count measurement after 4 hours of granulocyte colony-stimulating factor (G-CSF) injections for the detection of recovery from granulocytopenia. Four Graves' patients with antithyroid drug-induced granulocytopenia (granulocyte count between 500 and 1000/mm3) and three Graves' patients with antithyroid drug-induced agranulocytosis (granulocyte count < 500/mm3) each received a daily dose of 75 mu g of G-CSF administered subcutaneously. In all granulocytopenic patients, after 4 hours of G-CSF injection the granulocyte counts increased to 5623, 4050, 8923 and 4647/mm3, and the granulocyte count after 24 hours of G-CSF injection was 3008, 4634, 4854, 4200/mm3. In one of the three agranulocytic patients, the granulocyte count increased from 238/mm3 to 5982/mm3 after 4 hours of G-CSF injection, and the granulocyte count after 24 hours of G-CSF injection was 4800/mm3. Although the granulocyte counts before G-CSF injection of the remaining two agranulocytic patients were 138 and 126/mm3, the granulocyte counts after 4 hours of G-CSF injection were 837 and 59/mm3 and those after 24 hours of G-CSF injection were 817 and 0/mm3. These results indicated that granulocyte count measurement after 4 hours of G-CSF injection was useful for detecting the recovery from granulocytopenia and agranulocytosis.

The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension (EH) was explored. After the measurement of blood pressure in 15 EH patients and 8 control subjects, EH patients were divided into two groups by the elevation of plasma NE (delta NE) 5 min after standing: 7 normoadrenergic EH (delta NE < 140 pg/ml) and 8 hyperadrenergic EH (delta NE > or = 140 pg/ml). On the morning after a 12-h overnight fast, regular insulin (0.1 U/kg) was injected intravenously, and glucose disappearance rate (GDR) was measured and used as an index of insulin sensitivity. On the following day, the test was reinvestigated following the administration of mabuterol, a beta 2 agonist. Plasma growth hormone (GH), cortisol, norepinephrine (NE) and epinephrine (Epi) were measured before and after the mabuterol administration. Although there were no significant differences of basal GDR among these three groups, mabuterol induced a considerable decrease in GDR in EH patients but not in control subjects. There was no significant difference in the decrease of GDR between normo- and hyperadrenergic EH. The decrease in GDR tended to correlate with the mean blood pressure at rest in EH but not in normal subjects. Plasma glucose and serum insulin in EH patients were increased more than in normal subjects. Plasma GH, cortisol and Epi were not elevated by mabuterol, but plasma NE increased in each group, significantly in hyperadrenergic EH. There was no correlationship between the increase in plasma NE and the decrease in GDR after mabuterol.(ABSTRACT TRUNCATED AT 250 WORDS)

A 71-year-old man with a history of sarcoidosis was admitted to our hospital because of polyuria and polydipsia. On admission, the serum calcium concentration was elevated to 12.7mg/dl, and the creatinine clearance was 28.3ml/min. The initial serum 1,25-dihydroxyvitamin D concentration was 55.0pg/ml, while angiotensin-converting enzyme activity and serum PTH-rP concentration were within the normal range. Radiological studies revealed enlargement of bilateral hilar lymph nodes and a nodular lesion in the right lower lung field. Transbronchial lung biopsy showed noncaseous granuloma consistent with pulmonary sarcoidosis. After oral administration of 20mg prednisolone daily, the serum calcium and 1,25-dihydroxyvitamin D concentration returned to normal, and creatinine clearance was raised to 55ml/min. In conclusion, low dose glucocorticoid administration successfully reduced serum 1,25-dihydroxyvitamin D level with a prompt decrease in serum calcium level in a patient with sarcoidosis.

Vascular endothelial cells produce various biologically active factors regulating blood pressure, coagulation, and possibly cell growth of the vascular wall. Of the factors, nitric oxide (NO) has been the object of attention because of its quite simple molecular structure and variety of biological functions. In the present review, we focused on the physiologic and pathologic aspects of NO in hypertension. In experimental animals, both acute and chronic inhibition of NO synthase (NOS) with arginine derivatives produce a significant rise in blood pressure, indicating that tonic production of NO regulates basal vascular tonus. The chronic hypertension caused by NOS inhibitor is associated with cardiac hypertrophy and renal insufficiency. Sodium retention, though transient, and the plasma and tissue renin/angiotensin system in addition to the reduced production of NO have been implicated in the development of hypertension. Hypertension and the associated target organ failure can be reversed by co-administration of L-arginine or blockades of the renin/angiotensin system. Studies in which L-arginine as the substrate of NO or NOS inhibitor was administered demonstrated an important role of NO in the regulation of tonic vascular tonus also in normal subjects. In hypertensive subjects, however, endothelium-dependent vasorelaxation and production of NO are impaired, possibly due to a deficiency of L-arginine and/or a disorder of its utilization. Recent advances in the methods of detecting NO enabled us to demonstrate its diminished production from endothelial cells of hypertensive rats in vitro, although no definite biochemical evidence has been obtained in hypertensive subjects. The endothelial dysfunction, however, is not a primary cause of hypertension but a secondary result since it is commonly observed in various types of hypertension and can be reversed by correcting the blood pressure. Other common diseases including atherosclerosis and diabetes mellitus are also associated with similar abnormalities of the endothelium. NO has anti-atherogenic actions: inhibition of platelet functions and proliferation of vascular smooth muscle cells. Therefore, potentiation of endogenous NO and/or supplement of exogenous NO donors could be novel therapeutic approaches for the treatment of hypertension and atherosclerosis, while potential adverse effects of NO including cytotoxicity, immunosuppressibility, and hypotensive shock should be taken into account.

We report a patient with Addison's disease whose clinical features became worse during interferon therapy for chronically active hepatitis C. A 47-year-old male was admitted because somnolence developed during a 4 week treatment with interferon-alpha-2a (IFN: 900 x 104U/day). Serum Na level was 113mEq/l and plasma osmolarity was lowered to 238mOsm/kg on admission. Plasma ACTH level was high, while serum cortisol, urinary 17-OHCS and 17-KS excretion were far below the normal levels. On admission, serum prolactin, insulin levels and urinary CPR excretion increased. Normalization of serum Na level by NaCl administration attenuated hyperinsulinemia associated with the reduction of increased CPR excretion. It was supposed that IFN administration might increase cortisol consumption and worsen hypoadrenocortinism in a patient with Addison's disease. In addition, the present case raised the possibility that hyposmolarity may induce a hyperinsulinemic state in humans.

Little is known about the dopamine system in the ovary. The present study has been undertaken to investigate the effect of dopamine (DA) on the ovarian steroidogenic enzymes of pregnant mare serum gonadotropin (PMSG)-treated immature rats. Ovarian cells from PMSG-treated rats were cultured for 1-5 hours with or without DA, D1 agonists or bulbocapnine (Bul)(D1 antagonist). Progesterone (P) and estradiol (E2) in the media were assayed by specific RIAs. The enzyme activities were assayed by adding radioactive substrates in the media before incubation. DA and D1 agonists increased P in the media which was caused by the increment of 3 beta -hydroxysteroid dehydrogenase (3 beta -HSD) activity because cholesterol side chain cleavage enzyme (CSCC) activity showed no significant change. The stimulating effects of DA and DA agonists on P and 3 beta -HSD activity were inhibited by Bul. DA showed no effect on 17 alpha-hydroxylase activity. DA decreased 17.20 lyase activity, but this decrement was probably a non specific effect. DA alone did not affect the E2 level in the media and aromatase activity. The present results suggest that DA mainly stimulated 3 beta -HSD activity of the PMSG-treated rat ovary which regulated P synthesis.

Although many studies have been carried out on the dopaminergic system, little is known about the dopaminergic system in the ovary. The present study was undertaken to investigate the role of the dopamine (DA) system in ovarian function especially in steroidogenesis using rat ovaries. Ovarian cells from PMS-treated rats were incubated for 1 hour with or without DA or other drugs. DA, norepinephrine (NE) and isoproterenol (Iso) increased the levels of progesterone (P4) and cAMP in the media. D1 agonists (SKF38393, SKF82526-J, CY208-243) increased P4 secretion, whereas bromocriptine (D2 agonists) did not show any effect on the P4 level in the media. The effect of NE and Iso on P4 and cAMP levels was inhibited by propranolol (Pro; beta-blocker), while the increase of P4 and cAMP levels caused by DA or D1 agonists was suppressed by bulbocapnine (Bul; D1 antagonists). Propranolol (beta-blocker) or domperidone (D2 antagonists) did not affect the levels of P4 and cAMP. The presence of dopamine D1 receptor in the PMS-treated rat ovary was revealed by a kinetic study. The maximal number of binding sites (Bmax) of ovarian D1 receptor was 1.33fmol/mg tissue and the Kd value was 0.357nM. These results suggest that the DA system may physiologically play a role in the steroidogenesis in the ovary through D1 receptor.

We report a 54-year old man diagnosed as idiopathic hyperaldosteronism (IHA) at least 12 years after the onset. At the age of 42, he showed hypertension (162/100mmHg), hypokalemia, metabolic alkalosis, low plasma renin activity (PRA) and normal plasma aldosterone concentration (PAC) in a supine posture. Both PRA and PAC were elevated after a 2-hour ambulation following furosemide (60mg) injection. Since the accumulation of radioactivity following 131I-aldosterol injection with combined administration of dexamethasone was equally detected in both adrenal areas, he was diagnosed as low-renin essential hypertension (LREH). Blood pressure (BP) decreased to the normal range after treatment with nifedipine (40mg/day). At the age of 47, however, BP was hypertensive (164/106mmHg) serum potassium (K) level was normal. Although PAC was normal in a supine posture, it increased after a 2-hour ambulation following furosemide (60mg) injection. PRA after the stimulation was still suppressed despite the increase in PAC. At the age of 54, BP was 172/94mmHg. Serum K level was 3.4mEq/L. PRA was suppressed below 0.1 ng/ml/hr, while PAC was above the normal range (170pg/ml) in a supine posture. Serum cortisol and urinary excretion of 17-OHCS and 17-KS were within normal limits. PRA was still suppressed below 0.1 ng/ml/hr after a 2-hour ambulation following furosemide (60mg) injection, but PAC was markedly increased (330pg/ml). There was a diurnal rhythm of aldosterone, which was parallel to that of ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)