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)

Many hormones initiate their biologic actions by augmenting the intracellular concentrations of 3',5'-adenosine monophosphate (cyclic AMP). The nucleotide has been found in body fluids; its determination in plasma and urine can be performed by a rapid, simple and specific method: the cyclic AMP assay kit of the Radiochemical Centre (Amersham, England). The assay is based on the competition between unlabelled cAMP and a fixed quantity of the tritium labelled compound for binding to a bovine muscle protein which has a high specificity and affinity for cAMP. Different factors must be considered in evaluating the 24 h urinary content of the nucleotide: the renal or extrarenal origin of cAMP and the functional status of the kidneys. In basal conditions the urinary cAMP excretion is significantly correlated with creatinine excretion (n = 67; r = 0.47; p less than 0.001) thus confirming that the most part of cAMP excreted is derived from the plasma by glomerular filtration. Parathyroid hormone (PTH) stimulates adenylate cyclase predominantly in the renal cortex, whereas vasopressin (ADH) stimulated the enzyme in the medulla; thus PTH and ADH could increase the amount of cAMP in the urine from the renal source. In a case of diabetes insipidus and infusion of ADH caused a prompt rise in cAMP urinary excretion. In 5 normals an infusion of bovine synthetic parathyroid hormone caused an increased excretion of cAMP that preceded the phosphaturic response. An infusion of salmon synthetic calcitonin caused a rise in phosphate excretion and no increase in cAMP urinary content. As it concerns the two calciotopic hormones, PTH and CT, it is reasonable to assume that renal receptors are distinct. The 24 h urinary excretion of cAMP in 55 control subjects (3613 +/- 1460 D.S. n moles) was contrasted with the lower excretion in 25 elderly subjects (70-93 years: 1804 +/- 699 n moles), with the high cAMP excretion in a patient with hyperparathyroidism (that fell to normal values following removal of the parathyroid adenoma) and with the low cAMP excretion in patients with primary or surgical hypoparathyroidism. The mean 24 h cAMP excretion in patients with renal insufficiency was significantly decreased when compared to control subjects. These findings and recent reports confirm that the 24 h urinary output of cAMP may be considered an useful index of pharathyroid function in man.
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PMID:[The diagnostic value of the determination of cyclic 3',5'-adenosine monophosphate (cAMP) in urine]. 19 Jun 33

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

The effects of angiotensin-converting-enzyme (ACE) inhibitors on circulatory regulating mechanisms in congestive heart failure (CHF) were studied by comparison of plasma levels of catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), substance P (SP-LI), calcitonin gene-related peptide (CGRP-LI), vasopressin (ADH-LI), atrial natriuretic peptide (ANP-LI) and renin activity (PRA) in patients with severe CHF (NYHA III-IV) with (n = 15) or without (n = 17) ACE inhibitors in addition to digoxin and diuretic therapy. Data were also compared with those for healthy subjects (n = 31) and patients with moderate CHF (NYHA I-II). Catecholamines and NPY-LI were increased to the same extent in both groups with severe CHF. CGRP-LI showed no changes relative to controls in any of the patient groups, and was not affected by ACE inhibitors. The SP-LI level was significantly increased in all patient groups. Patients with severe CHF on ACE inhibition had a SP-LI level of 4.05 +/- 0.79 pmol l-1, compared to a concentration of 2.28 +/- 0.30 pmol l-1 (P less than 0.05) in the patient group with a comparable degree of CHF but without ACE inhibition. In the latter group, an inverse relationship appeared between the SP-LI and the serum sodium levels (r = -0.68, P less than 0.05). The patients with severe CHF who received ACE inhibitors had significantly lower ADH-LI levels than the patients with a comparable degree of CHF who were not treated with ACE inhibitors, while the ANP-LI levels was increased to a similar extent in both groups.
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PMID:Increased plasma level of substance P in patients with severe congestive heart failure treated with ACE inhibitors. 171 29

In 51 patients with gastric adenocarcinoma the fasting blood concentrations of hCG, beta hCG, alpha subunits, ADH, calcitonin, enteroglucagon, gastrin, GH, melatonin, somatostatin, estradiol, CEA and pepsinogen I in the peripheral vein were estimated by radioimmunoassay at the time of diagnosis and, in those who underwent surgery, 7 days after the operation, to determine the incidence of the modifications of the above mentioned substances' blood levels and the existence of possible markers. In presence of increases of the examined parameters greater than 50%, considering M +/- 2 SD of 10 control subjects as normal range, the tumours were examined immunohistochemically. In patients with gastric adenocarcinoma, in comparison with normal subjects, we found significant higher blood levels of hCG alpha subunits, gastrin and CEA and lower of melatonin, pepsinogen I and GH. The immunohistological results demonstrated CEA in both examined cases, alpha subunits in 2 of 6 (respectively in dysplasic areas and in surrounding non neoplastic mucosa) and enteroglucagon in 1 of 3 (dysplasic areas). Our results indicate that none of the parameters we examined, because of their non-specificity or of the low incidence of their modifications, can be considered a marker of gastric adenocarcinoma.
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PMID:[Changes in hormonal and biochemical parameters in gastric adenocarcinoma]. 180 10

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

Small cell lung cancers are neuroendocrine tumours and therefore produce a lot of peptide hormones (calcitonin, ACTH, ADH), as well as the neuropeptide chromogranin A, which are all useful tumour markers. Furthermore, the tumour-associated antigens CEA and TPA, as well as the enzymes neuron specific enolase (NSE) and creatine kinase BB are used as markers in small cell lung cancer. At present, NSE appears to be the best marker for small cell lung cancer; elevated serum NSE levels are found in 65 to 85% of the patients. The serum level of the tumour markers is related to the stage of the tumour. When tumour regression occurs following therapy, elevated pretreatment levels decrease to the normal range. If the marker level increases again, tumour progression is indicated and this can be an early and sensitive sign denoting recurrence. Metastases in the central nervous system can be detected early by marker determination in the cerebrospinal fluid. At present, CEA appears to be the most valuable tumour marker for non-small cell lung cancer, but TPA may also be a useful marker.
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PMID:[Tumor markers in bronchus cancer]. 254 31

The effects of the absence of various hormones (antidiuretic hormone, thyroid hormone, parathyroid hormone, and calcitonin) on proximal and distal structures were studied in diabetes insipidus (DI) Brattleboro rats. The cross-sectional area of the first segment of proximal convoluted tubules (S1) was significantly reduced in thyroparathyroidectomized (TPTX) DI rats compared with Long-Evans rats (the strain of origin of DI rats) and untreated DI rats. Administration of triiodothyronine (T3, 10 micrograms/day for 7 days) to TPTX-DI rats restored the proximal tubule structure. In the distal convoluted tubule (DCT) the cross-sectional area of the epithelium and the number of nuclei per cross-sectional area were significantly greater in untreated ADH-deficient DI rats than in the control Long-Evans rats. Daily administration of 1-desamino-8-D-arginine vasopressin (dDAVP, 500 ng/day for 3 wk) significantly reduced the size and the number of DCT cells in DI rats. Cortical micropuncture data indicated that the Na+ concentration in the fluid delivered to the DCT and the absolute amount of Na+ reabsorbed along the DCT were higher in DI than in dDAVP-treated DI rats. It is concluded that functional changes in the PCT, subsequent to chronic TPTX, are accompanied by marked alteration of the cell anatomy of this nephron segment, and that the processes that modify the Na load delivered to the DCT and the Na transport in the DCT are accompanied by structural modifications of this segment.
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PMID:A structural study of the rat proximal and distal nephron: effect of peptide and thyroid hormones. 271 59

Bronchial carcinomas are frequently associated with ectopic secretion of hormones which may be responsible for paraneoplastic syndromes. In non small cells carcinomas, serum calcitonin levels may be raised. Hypercalcaemia can be found in squamous carcinomas and secretion of hCG (responsible for gynaecomastia) in large cells carcinomas. In small carcinomas, many hormones (ACTH, MSH, ADH, calcitonin) can be produced; however, their serial measurements as well as that of the carcino-embryonic antigen add nothing to the information available with standard staging investigations. More recent studies have identified three protein products: the BB-isoenzyme of creatine kinase, bombesin and neurone-specific enolase. The latter seems a promising marker to follow up the course of the disease.
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PMID:Role of biological markers and probes in lung carcinomas. 287 78

The most examined tumor markers in lung cancer patients are CEA, hormonal peptides, and some neurogenic enzymes in small cell carcinoma. Calcitonin, ACTH, ADH, CEA, neurophysin, oxytocin, beta-endorphin, neuron-specific enolase, and CK BB are elevated in serum specimens in 25-75% of cases of small cell carcinoma. The level of these markers is related to the stage of the disease in groups of patients; elevated pretreatment levels decrease with tumor regression. Marker levels are not valid in defining the tumor load and the presence of disease in the individual patient. It has not yet been documented that the markers can be used for clinical decisions on antineoplastic therapy. A recent development is the finding that measurement of CSF and plasma concentrations of ADH, calcitonin, CK BB, bombesin, and neuron-specific enolase may contribute in the diagnosis of CNS metastases including meningeal carcinomatosis.
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PMID:Tumor markers in patients with lung cancer. 300 40

The kidneys have primary responsibility for regulating the body's water and solute balance. Of the 180 L per day that are filtered at the glomerulus, about 98 to 99 per cent is reabsorbed throughout the course of the renal tubule. The kidney can produce a concentrated urine or a dilute urine, depending on the needs of the body. Several hormones, notably aldosterone, ADH, PTH, and calcitonin, as well as vitamin D, are important in the regulation of water and solutes. This article has not discussed other important renal functions as noted in the introduction.
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PMID:Renal and endocrine regulation of water and electrolyte balance. 331 85


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