Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double paraneoplasic syndrome with hypersecretion of ADH and ACTH revealed the presence of a small cell bronchial cancer in a man aged 62 years. Water and electrolyte anomalies due to the hypersecretions were of such a degree that an occlusive syndrome occurred. Very high levels of ADH and ACTH were found in the tumoral tissue. The measurement of these levels is rarely conducted at the present time but was able to define the mechanism of abnormal secretion of these two hormones in this case.
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PMID:[Double paraneoplastic syndrome and anaplastic carcinoma of the lung. ADH and ACTH levels in the tumoral tissue (author's transl)]. 4 61

A 61 year old woman presented with profound hyponatremia and markedly low serum osmolality. Urine osmolality was greater than the serum osmolality, an abnormality that was corrected by water restriction, suggesting inappropriate ADH secretion. Although there were no physical signs of Cushing's syndrome, her serum potassium level was low and markedly elevated levels of plasma and urine corticosteroids were not altered by the administration of large amounts of dexamethasone, suggesting the ectopic ACTH-MSH syndrome. Plasma levels of immunoreactive ACTH and beta-MSH were elevated. At autopsy, a metastastic oat cell carcinoma of the lung, not detected antemortem by chest roentgenograms and bronchoscopy, was found. Immunoreactive ADH, ACTH and beta-MSH were detected in the primary tumor and in metastases to the liver. beta-MSH was also detected in the spleen, in which metastases were observed. This is the first documented case of the simultaneous production of ADH, ACTH and beta-MSH by neoplastic tissue associated with clinical manifestations of the syndrome of inappropriate ADH secretion and the ectopic ACTH-MSH syndrome.
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PMID:Ectopic production of antidiuretic hormone (adh), adrenocorticotrophic hormone (ACTH) and beta-melanocyte stimulating hormone (beta-MSH) by an oat cell carcinoma of the lung. 18 5

A case of pseudohypoparathyroidism has been investigated. Indirect evidence allows to eliminate a defect of renal 1 alpha-hydroxylase as the determining factor of this condition. Similarly, the increased size of the mean surface area of the cross-section of periosteocytic lacunae, as determined on decalcified sections of bone obtained by transiliac biopsy, shows the osteocytes to be sensitive to the endogenous PTH, discarding cAMP response to PTH in bone as a prerequisite for PTH action on bone. The authors conclude from these data and from previous experiments that the defect of parathyroid function in this condition probably relates to the existence of an abnormal PTH molecule and/or metabolism and/or interaction with the receptors sites. The endocrine function was studied as well. Prediabetes was demonstrated, as well as primary latent hypothyroidism (TRH test). Prolactin release could not be stimulated by TRH, levodopa, metoclopramide, chlorpromazine and insulin hypoglycemia. The latter produced a normal release of ACTH (as ascertained by plasma cortisol levels) and GH, and possibly a sluggish response of glucagon and gastrin. There was a deficiency of urinary concentration upon restriction of fluid intake. This was only partially corrected by ADH administration.
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PMID:[Physio-pathology of pseudohypoparathyroidism (author's transl)]. 22 97

The regulation of aldosterone was studied in a child with diabetes insipidus and adipsia, associated with holoprosencephaly. Plasma ADH was low and unresponsive to dehydration. Plasma renin concentration ranged from 52 to 1350 ng ml-1 h-1 at various degrees of hydration, and plasma aldosterone ranged from 4.7 to 104 ng/100 ml. Despite these wide ranges, the levels of the two hormones were not correlated. The aldosterone-renin ratio (log.) was inversely related to the plasma sodium concentration, while the plasma renin concentration (log.) was directly related to plasma sodium. Reduced values of both extracellular fluid volume (radiosulphate and sodium spaces) and total exchangeable sodium were measured when plasma sodium was elevated. Sodium depletion at the time when the patient was in a dehydrated state appeared to be caused, at least partly, by defective renal sodium conservation. Thus, in the dehydrated state, the patient showed the following unusual combination of abnormalities: hypernatraemia, sodium depletion, hyperreninaemia, and low to normal plasma aldosterone. The abnormal aldosterone-renin ratio was probably not caused by an intrinsic adrenal abnormality, since high levels of aldosterone were measured as long as a certain degree of hydration had been achieved with or without exogenous ADH, and since plasma cortisol was normal and responsive to exogenous ACTH. The results suggest that the responsiveness of the adrenal cortex to angiotensin may vary with extracellular sodium concentration. The direction of this effect, that is, suppression of aldosterone with increased sodium concentration, is not different from what is observed under experimental conditions, when extra-cellular sodium concentration is raised by infusions of hyperosmolar saline.
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PMID:Dissociation of renin and aldosterone during dehydration: studies in a case of diabetes insipidus and adipsia. 95 Mar 64

The radioimmunological dosages of renin and of aldosterone are used nowadays in clinical practice for research purposes only. The measurement of activity of plasma renin may be considered a significant indication of the concentration of the enzime in plasma and, indirectly, of its secretion. Several factors take a part in the regulation of renin secretion (mean arterial pressure, introduction of sodium and potassium, the sympathetic nervous system, ADH and concentration of angiotensin II in plasma). In pathological conditions such factors may cause alteration of the renin-angiotensin II system, thus determining hyperreninisms and hyporeninisms, whether associated with arterial hypertension or not. Several factors take a part on aldosterone secretion too (ACTH, sodiaemia, potassiaemia, renin-angiotensin II system). In pathological conditions the alteration of the regulation system may lead to hyperaldosteronism or to hypoaldosteronism of primary or secondary type. A survey of recent research on the physiopathology of the renin-aldosterone system is also given.
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PMID:[Renin and aldosterone]. 123 75

This study was undertaken to investigate the endocrine stress response during cataract surgery in local anaesthesia (LA) with or without additional sedation with midazolam (Dormicum). 20 patients for cataract surgery in LA were randomly allocated to the midazolam-group (before injection of LA, sedation with single doses of 1 mg midazolam until the patient was sleeping, but awakeable), and to the control-group without sedation. Premedication and LA were standardized. The investigation was performed at 7 measuring points starting at the arrival in the preparation room up to 30 min after surgery. Adrenaline in plasma was significantly lower in the midazolam-group. Intraoperatively, adrenaline increased in the control-group and decreased in the midazolam-group. In time course, noradrenaline in plasma decreased in the midazolam-group, in contrast to the control-group. With respect to ADH, ACTH and cortisol, no significant differences were found in group levels or time course, and concentrations remained within normal range. In contrast to the control-group, mean arterial pressure decreased in the midazolam-group during the course of time. There were no differences in heart rate or arterial oxygen saturation between the two groups. Local anaesthesia and premedication were sufficient to prevent psychic and surgical stressors. The slight sympathoadrenergic response in the control-group was significantly reduced by small doses of midazolam. Thus, a careful supplementation of local anaesthesia with midazolam appears advantageous for patients with cardiovascular disorders.
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PMID:[Endocrine stress response in cataract operations with local anesthesia]. 131 23

Some pituitary hormones secrete hormones while others do not. Nonsecreting tumors can interfere with normal pituitary hormone secretion and produce tumor symptoms and signs like headaches and visual field defects. The most frequent hormone-secreting tumors are prolactinomas. Growth hormone or ACTH or gonadotropin or gonadotropin-alpha and beta chain-producing tumors are less frequent, TSH producing tumors are extremely rare. The most important elements of the diagnostic work-up are clinical signs and symptoms, assessment of pituitary function (measurement of TSH, free T4, LH, FSH, oestradiol/free testosteron, growth hormone, IGF-1, prolactin, ACTH, Cortisol, serum and urine osmolality), CT and/or MRI and, in patients with large tumors, a visual field exam. The treatment of choice of pituitary tumors is often surgery. Alternative therapies are radiation treatment (in nonoperable patients or when hormone levels are persistently elevated after pituitary surgery) and drug treatment (dopamine agonists in hyperprolactinemia, somatostatin analogues in acromegaly). Pituitary hormone deficiencies are treated depending on the specific deficiency with thyroxine, cortisone, oestrogen/gestagen/testosterone gonadotropines or ADH analogues.
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PMID:[Hypophyseal dysfunction and tumors]. 158 68

Stress can be defined as a "reaction by living beings to any relevant impairment". The effect of anaesthesia on endocrine function is closely related to the actual stress concept based on the works by Cannon and Selye. Cannon described the role of catecholamines in stress and characterised the fight-flight reaction. Selye emphasised the role of the adrenocortical reaction defining the "general adaptation syndrome", which evolves in three stages ("alarm reaction", "stage of resistance", "stage of exhaustion"). Later, Henry postulated the dual stress concept. The sympathetic-adrenomedullary system is activated during the fight-flight reaction, thus representing an active role of the organism. The pituitary-adrenocortical system is activated during loss of control, submission and depression, especially in a social context. Main valid parameters of this endocrine stress response are adrenaline, noradrenaline, ADH, ACTH and cortisol. In the perioperative period, both pathways are "stressed". The most important factors are patient, operation, and anaesthesia. Anaesthesia can influence the stress response by afferent blockade (local anaesthesia), central modulation (general anaesthesia) or peripheral interactions with the endocrine system (etomidate). Up to now, a total peripheral blockade of the nociceptive system is impossible, due to surgical technique (destruction of nerve fibres) and release of mediator substances. With regard to reduction of endocrine stress response, inhalation anaesthesia with volatile anaesthetics and nitrous oxide may be less effective than neuroleptic, spinal or epidural anaesthesia. Immediately after extubation, rapid increases of endocrine parameters are observed. In addition to central modulation of pain and stress, both halothane and enflurane inhibit catecholamine release from the adrenal medulla. Neuroleptic anaesthesia and total intravenous anaesthesia are very potent and sufficient to control the increases in endocrine parameters even during major surgery, due to their central effects. Spinal and epidural anaesthesia alone as well as in combination with general anaesthesia can reduce the endocrine stress response more than necessary. This is due to the sympathetic blockade, combined with an afferent blockade of central cord fibers which modulate the pituitary-adrenocortical system. Only few data are available concerning the stress response during infiltration anaesthesia or nerve block, but additional sedation seems to be beneficial. Peripheral interactions with the endocrine system like blockade of the adrenal cortex by etomidate is dangerous and has caused a high mortality in intensive-care patients if the substance was admitted for a longer period. Assessment of endocrine stress response in anaesthesia and surgery is controversial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The endocrine stress reaction in anesthesia and surgery--origin and significance]. 175 50

A wide variety of tumour markers has been described in bronchial carcinoma. Clinical studies have been most frequently conducted with the substances CEA, NSE, CK-BB and for the peptid hormones ACTH, calcitonin and ADH. The serum levels for CEA, NSE and CK-BB correlate to a certain extent with the stage of the tumour disease, the prognosis and the survival time. On the other hand, the peptid hormones have no clinical significance on account of their low sensitivity and specificity. Outside of clinical studies the determination of tumour markers in bronchial carcinoma is clinically irrelevant.
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PMID:[Tumor markers, significance for clinical diagnosis]. 187 89

E2078, a new analgesic is a dynorphin derivative. E2078 shows strong affinity to kappa receptors and is not rapidly cleaved by peptidases. This analgesic is also considered to be free of tolerance and dependence. In the present study, to determine the effect of E2078 on pituitary-adrenocortical function the author administered E2078 (0.001, 0.05, 0.1, 1.0, 10.0 mg.kg-1) by intramuscular injection to 38 adult mongrel dogs under enflurane anesthesia (1.0%) and then investigated the changes in the plasma concentrations of ACTH, cortisol, beta-endorphin, PRA, aldosterone and ADH. In the animal groups which received E2078 at dosages of 0.001, 0.05, 0.1, and 1.0 mg.kg-1, no significant differences in the plasma concentrations of each hormone were detected compared with the control group which received physiological saline by intramuscular injection. However, in the dog group which received E2078 at 10.0 mg.kg-1, the plasma concentrations of PRA and aldosterone were significantly elevated.
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PMID:[Effects of E2078, a new dynorphin derivative, on pituitary-adrenocortical functions in dogs]. 197 31


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