Urinary Excretion Of 5-hydroxyindoleacetic Acid Research Articles

Die ausscheidung von 5-hydroxyindolessigsäure in normalen und pathologischen Zuständen

Excretion of 5-Hydroxyindoleacetic Acid in Normal and Pathological Conditions In order to investigate the metabolism of 5-hydroxytryptamine, the daily urinary excretion of 5-hydroxyindoleacetic acid was studied in 48 normal subjects and in 181 patients with various diseases: arterial hypertension, renal insufficiency, liver diseases, various types of tumours, carcinoids, haemorrhagic syndromes, haemochromatosis, recent myocardial infarction, bronchial asthma. Only in one case of functioning carcinoid was there found a significant increase in the urinary content of 5-hydroxyindoleacetic acid; in renal insufficiency and in haemochromatosis the values of the daily urinary excretion were constantly below normal. In the other diseases studied the excretion values were quite similar to those found in normal subjects.

Atypical phenylketonuric heterozygote: Deficiency in phenylalanine hydroxylase and transaminase activity

A child with an elevated serum level of phenylalanine, a typical phenylketonuria phenylalanine tolerance test, an absence of increased urinary concentrations of phenylketones, ortho- and parahydroxyphenyl acids, and phenolic acids, as well as no abnormality in urinary excretion of 5-hydroxyindoleacetic acid or in indole-3-acetic acid is reported. It appears that this child has marked limitation in phenylalanine transaminase activity and, as a consequence, the characteristic associated biochemical abnormalities related to limited activity of this enzyme were not expressed and could not be evoked. A child with an elevated serum level of phenylalanine, a typical phenylketonuria phenylalanine tolerance test, an absence of increased urinary concentrations of phenylketones, ortho- and parahydroxyphenyl acids, and phenolic acids, as well as no abnormality in urinary excretion of 5-hydroxyindoleacetic acid or in indole-3-acetic acid is reported. It appears that this child has marked limitation in phenylalanine transaminase activity and, as a consequence, the characteristic associated biochemical abnormalities related to limited activity of this enzyme were not expressed and could not be evoked.

Urinary excretion of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in relation with the survival-time of x-irradiated rats.

SummaryDeterminations of urinary 5-hydroxytryptamine (5-HT) and 5-hydroxy indoleacetic acid (5-HIAA) in x-irradiated rats (665 r) were performed.No significant association between the excretion of 5-HT and survival-time was found. However, the amounts of excreted 5-HIAA after irradiation, as well as the sum of 5-HT and 5-HIAA, gave a significant positive correlation with the survival-time.It seems that an intensive radiation-induced liberation of 5-HT, with its prompt degradation and excretion, might have a favourable influence on the fate of sub-lethally irradiated animals.

Psychopathology and 5-hydroxyindoleacetic acid excretion

Schizophrenics and nonschizophrenics do not differ in urinary excretion of 5-hydroxyindoleacetic acid on either a concentration or 24 h basis, nor do they differ in variability of excretion. Although a pattern was observed of decreasing psychopathology with increasing 5-hydroxyindoleacetic acid excretion, this pattern may be related to alterations in physical state accompanying psychopathology rather than to psychopathology per se.

The cardiac disease associated with the carcinoid syndrome (carcinoid heart disease)

The clinical and pathologic features of seventeen patients with the carcinoid syndrome are reviewed. Nine had carcinoid heart disease. The only clinical feature which distinguished those patients with carcinoid heart disease from those without was the presence of a precordial systolic murmur suggestive of tricuspid regurgitation or pulmonic stenosis. Urinary excretion of 5-hydroxyindoleacetic acid was similar in the two groups. The chest roentgenogram and the electrocardiogram was of no help in determining presence or absence of carcinoid heart disease. Cardiac catheterization in patients with carcinoid heart disease has shown that tricuspid regurgitation and pulmonic stenosis are the most frequent valvular alterations. Cardiac output appears to be increased in some patients who do not have carcinoid cardiac involvement. The cardiac lesions associated with the carcinoid syndrome were pathognomonic and bore little resemblance to lesions found in other cardiac diseases. Cardiac involvement in the carcinoid syndrome consisted of focal or diffuse collections of a peculiar type of fibrous tissue, which was free of elastic fibers and which was deposited on the endocardium of the valvular cusps, on the endocardium of the cardiac chambers and on the intima of the great veins, coronary sinus and occasionally great arteries. The valvular cusps per se remained normal as did the mural endocardium, and each was clearly separated from the fibrosing process by the elastic membrane which covered its surface. Left-sided cardiac lesions were commoner in the carcinoid syndrome than previously thought and were found in the absence of a right to left shunt or a pulmonary carcinoid tumor. The pathogenesis of the carcinoid cardiac lesions (carcinoid fibrous plaques) remains unknown. The morphologic appearance of the endocardial lesion suggests that it might be the result of the deposition of a material, possibly collagen, from the blood, but the identity of the substance which either directly or indirectly produced the endocardial fibrosis is unknown. The inability to produce these cardiac lesions in animals with serotonin and the present observation that the urinary excretion of 5-hydroxyindoleacetic acid was similar in the patient with carcinoid heart disease irrespective of the presence or absence of cardiac involvement suggest that mechanisms other than that involving serotonin should be considered.

Urinary 5-Hydroxyindoleacetic Acid Excretion in Scleroderma

Urinary 5-Hydroxyindoleacetic Acid Excretion in Scleroderma

Urinary 5-hydroxyindoleacetic Acid Excretion in Scleroderma

Urinary 5-hydroxyindoleacetic Acid Excretion in Scleroderma

The effect of some nucleotoxic agents on urinary excretion of 5-hydroxyindolacetic acid in rats

The effect of some nucleotoxic agents on urinary excretion of 5-hydroxyindolacetic acid in rats

URINARY EXCRETION OF 5-HYDROXYINDOLEACETIC ACID (5-HIAA) IN OVULATORY AND ANOVULATORY CYCLES.

Acta Obstetricia et Gynecologica ScandinavicaVolume 42, Issue S6 p. 147-149 Urinary Excretion of 5-Hydroxyindoleacetic Acid (5-HIAA) in Ovulatory and Anovulatory Cycles Anna-Riitta Fuchs, Anna-Riitta Fuchs Copenhagen, DenmarkSearch for more papers by this author Anna-Riitta Fuchs, Anna-Riitta Fuchs Copenhagen, DenmarkSearch for more papers by this author First published: January 1963 https://doi.org/10.3109/00016346309158276AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Volume42, IssueS6January 1963Pages 147-149 RelatedInformation

RELATIONSHIP BETWEEN THE DOSE OF WHOLE-BODY X-IRRADIATION AND THE URINARY EXCRETION OF 5-HYDROXYINDOLEACETIC ACID IN RATS.

SummaryThe dependency on x-irradiation dose of urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA) in rats was studied. A significant positive correlation between the applied doses: 50, 100, 150, 200, 400, 600 and 800 r, and 5-HIAA excretion-rate, was found. By means of this biochemical test it is possible to discriminate between animals irradiated with ‘low’ (50, 100, 150 r), ‘medium’ (200, 400 r) and ‘high’ (600, 800 r) doses. The maximal increase of 5-HIAA output after irradiation appears during the first 24 hours; excretion returns to normal values on the third day after irradiation. The females show a more pronounced response to radiation than the males. The dose of 200 r seems to be the lowest that significantly increases the output of 5-HIAA. The rats pre-treated with sub-lethal doses (50–200 r) respond to the subsequent dose of 800 r with somewhat delayed reaction.Some other urinary substances showing a certain irradiation dose-dependency are compared with 5-HIAA; the latter appears to be a good indicator for the evaluation of absorbed radiation dose.

EFFECT OF CHEMOPROTECTION BY CYSTAMINE ON URINARY EXCRETION OF 5-HYDROXYINDOLEACETIC ACID IN X-IRRADIATED RATS.

Studies were made on the excretion of 5-HIAA in the urine of lethally irradiated rats protected with a chemoprotector that is not a 5-hydroxyindole. It was concluded that cystamine produces inhibition of the post-irradiation increase in urinary excretion of 5-HIAA in rats but that inhibition is incomplete. Three possible explanations are given: cystamine prevents the discharge of 5-HT from body depots; it deviates the metabolic pathway of 5-HT; or inhibits the renal tubular secretion of 5-HIAA. (P.C.H.)

A biochemical approach to the mechanism of action of Jatamansone

We reported earlier that a single intraperitoneal injection of 100 mg/kg body weight Jatamansone produced demonstrate tranquilization in mice and monkeys. Since modifications of serotonin and/or catecholamine brain levels are intimately related with the above biological activity, estimations of these amines during peak pharmacological response were deemed pertinent and conducted. Preliminary observations revealed an average reduction of 52 per cent in serotonin and 10 per cent in catecholamine brain levels, 5–8 hr after Jatamansone administration thus implicating the former but absolving the latter for the observed pharmacological effects. The present investigation was, therefore, designed to study in detail serotonin levels, its biosynthesis and metabolism in rabbit's brain at various time intervals after the administration of Jatamansone. The estimation of 24 hr urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA), the end product of serotonin metabolism, was also included in this study.

A unique syndrome associated with secretion of 5-hydroxytryptophan by metastatic gastric carcinoids

Clinical and biochemical studies in a patient with metastatic gastric carcinoid are presented. The findings of this patient and in three similar patients described previously seem to justify consideration of a unique syndrome, consisting of distinctive flushes, persistently elevated urinary histamine and secretion of 5-hydroxytryptophan (5HTP) by carcinoid tumors of gastric origin. Elaboration of 5HTP, rather than serotonin, by the tumor is reflected in normal platelet serotonin values, and urinary excretion of 5HTP, serotonin and 5-hydroxyindoleacetic acid in proportions almost identical with those found following infusion of 5HTP in control subjects. The excretion of 5-hydroxyindoles and histamine in our patient with gastric carcinoid is compared with that in thirteen patients with carcinoid tumors from non-gastric or unknown primary sites. That the rate of tryptophan hydroxylation can be increased by raising substrate concentration is shown by the elevations in urinary 5HTP following oral administration of l-tryptophan in this patient. Evidence is presented that the increased excretion of histamine is not related to elevated tissue concentrations of 5HTP or serotonin. Thus treatment with the aromatic l-amino acid decarboxylase inhibitor, α-methyl-dopa, reduced 5HTP decarboxylation but failed to alter the urinary excretion of histamine. The clinical response to α-methyl-dopa therapy in the patient with gastric carcinoid was better than has been obtained in patients with the usual type of carcinoid syndrome. A possible explanation for this is offered and the importance of recognizing this variant syndrome is emphasized.

Urinary Excretion of 5-Hydroxyindoleacetic Acid in Normal Korean Adults and in Patients with Peptic Ulcer

Urinary Excretion of 5-Hydroxyindoleacetic Acid in Normal Korean Adults and in Patients with Peptic Ulcer

Tryptophan metabolism in phenylketonurics.

ALTHOUGH the genetic defect in the hereditary disorder phenylketonuria has been related to the lack of one of the enzymes involved in the hydroxylation of phenylalanine, the cause of the mental retardation remains unknown. Bickel et al. 1 and other workers noted dramatic improvement in intelligence and developmental quotients of certain phenylketonuric children who were fed diets low in phenylalanine content. Concomitantly, the blood phenylalanine levels of these children fell to within the range found in normal children. Hence, the mental retardation has been attributed to some metabolic disorder associated with elevated blood and tissue levels of phenylalanine. Armstrong et al. 2 found that phenylketonurics excrete more of certain tryptophan metabolites, such as indoleacetic acid, than do normal children, and Pare et al. 3 later showed that the blood levels of 5-hydroxytryptamine (serotonin) were lower, and the urinary excretion of 5-hydroxyindoleacetic acid was less, in phenylketonurics than in other mentally

Effect of L-tryptophan on diuresis and 5-hydroxyindoleacetic acid excretion in the rat.

Oral administration of L-tryptophan to rats produced two main biochemical and pharmacological effects: a marked increase in urinary 5-hydroxyindoleacetic acid excretion, and a significant reduction in the urine flow after a water load. Urinary 5-hydroxyindoleacetic acid excretion reached its maximum 2 to 6 hr after the administration of tryptophan, and it increased with the dose of the amino acid. Antidiuresis was seen after the administration of L-tryptophan, 200 mg/kg, or more. The effect appeared promptly and it was roughly proportional to the dose of the amino acid administered. Both antidiuretic effect and increase in urinary 5-hydroxyindoleacetic acid excretion were more intense after oral than after parenteral administration of L-tryptophan. D-Tryptophan, in oral doses up to 1,000 mg/kg, produced neither an increase in urinary 5-hydroxyindoleacetic acid nor a reduction of diuresis. Available evidence suggests that reduction of urine flow is a consequence of biosynthesis and release of 5-hydroxytryptamine by the gastrointestinal mucosa. Tryptamine produced by direct decarboxylation of L-tryptophan does not seem to play any important role.

Amino Acid Decarboxylases of Urticaria Pigmentosa Mast Cells

The association of histamine (1) and of his-tidine decarboxylase (2) with mast cells is now well established. However, there is no evidence for the presence of 5-hydroxytryptamine (5HT) in mast cells of any other animals than the rat, (3) and the mouse (4). Attempts by Parratt and West (5), to find an association of 5HT with mast cells in a number of species, including man, were only successful in the case of the rat and the mouse. Brogren et al (6) found no raised urinary excretion of 5-hydroxyindoleacetic acid (5HIAA) in urticaria pigmentosa. However, a recent report by Birt and Nickerson (7) of a five fold increase in urinary 5HIAA excretion following an induced attack of flushing of the skin in a child with generalized urticaria pigmentosa has suggested that human mast cells may in fact make and store 5HT.

Urinary Excretion of 5-Hydroxyindoleacetic Acid in Rosacea

Urinary Excretion of 5-Hydroxyindoleacetic Acid in Rosacea

Apparent absence of amines in cerebrospinal fluid of phenylketonurics.

THE mechanism by which mental defect is produced in phenylketonuria is unknown. No correlation has been found in patients having this disorder between the degree of mental defect and blood-levels of phenylalanine or phenylpyruvate, or urinary excretion of phenylalanine, phenyllactate, phenylpyruvate or o-hydroxyphenylacetate1. The possible implication of biologically active amines has been examined in several papers. Mitoma et al. 2 administered o-tyrosine and m-tyrosine to experimental animals and observed conversion to the corresponding amines in brain, with attendant central nervous system stimulation and convulsions. Association of the mental defect in phenylketonuria with an excessive production of o-tyramine was suggested. It also seems possible that overproduction of phenylethylamine may be responsible for the disturbance in cerebral metabolism. Jepson et al. 3 have recently shown that administration of a monoamine oxidase inhibitor to phenylketonuric individuals results in an increase much greater than normal in the urinary excretion of phenylethylamine, but not of o-tyramine. The mental defect in phenylketonuria may also be due to an underproduction of amines vital to normal brain function. Pare et al. 4 have reported low serum serotonin-levels and decreased urinary excretion of 5-hydroxyindoleacetic acid in phenylketonuria. They suggest that one or more aromatic acid metabolites of phenylalanine inhibit 5-hydroxytryptophan de-carboxylase, the enzyme responsible for the production of serotonin.

EFFECT OF ANTIBIOTICS ON THE 5‐HYDROXYTRYPTAMINE CONTENT OF THE SMALL INTESTINE AND OTHER ORGANS IN RATS AND MICE

Rats and mice were given antibiotics orally and by subcutaneous injection and the effects on tissue levels of 5-hydroxytryptamine and intestinal bacteria were studied. In mice it was found that antibiotics which caused a large reduction in the bacterial flora of the intestine when given orally also caused a significant increase in intestinal 5-hydroxytryptamine. In rats, neomycin caused a reduction in the urinary excretion of 5-hydroxyindoleacetic acid. In both rats and mice, many antibiotics caused a significant reduction in the weight of the spleen.