Catecholamines urinary

Metanephrines represent metabolites of the catecholamines urinary levels are greater than total catecholamines but less than those of VMA. In tumors, variations in the metabolic pathways can cause an increase in the metanephrines alone. 

Drugs can cause false results in clinical chemistry tests, e.g. plasma cortisol, urinary catecholamine, urinary glucose. 

Measurement of catecholamine metabolites can provide insight into the rate of release or turnover of catecholamines in the brain. In clinical studies, metabolites of catecholamines are generally assayed in the CSF because the large quantities derived from the peripheral sympa-thomedullary system obscure the small contribution from the brain to urinary concentrations. However, acid metabolites are actively excreted from the CSF more reliable estimates of turnover in the brain are obtained when this transport process is blocked by pretreatment with the drug probenecid. 

Disulfoton exposure altered catecholamine levels in animals, and this hormonal imbalance may be associated with elevated acetylcholine levels (Brzezinski 1969, 1972, 1973 Brzezinski and Ludwicki 1973 Brzezinski and Rusiecki 1970 Wysocka-Paruszewska 1970, 1971). In these studies, acute dosing with disulfoton caused increases in urinary and plasma noradrenaline and adrenaline levels, accompanied by decreases of adrenaline in the adrenal glands, in rats. In addition, the major urinary metabolite of catecholamine metabolism, 4-hydroxy-3-methoxymandelic acid (HMMA), was recovered in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1970,... 

Elevated catecholamine concentrations in the urine were also observed in rats dosed with 0.625 mg/kg/day of disulfoton every other day for 76 days (Brzezinski and Rusiecki 1970). Urinary catecholamine levels plateaued between 16 and 36 days, followed by a gradual decline for the next 40 days. However, these levels were still elevated at day 76. 

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

Increased levels of urinary catecholamines may also be associated with accumulation of acetylcholine that resulted from acetylcholinesterase inhibition by disulfoton. No human data were located to support this, but limited animal data provide some evidence. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in rats, respectively, within 72 hours (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). 

Pankow D, Ponsold W. 1978. Urinary catecholamine excretion and blood sugar response during acute poisonings with dinitrobenzenes. Toxicology 11 377-383. 

There are stability problems in urines stored for analysis. Fifty percent of delta-aminolevulinic acid was lost in specimens stored without preservative and exposed to light for 24 hours (V3). The loss increased to 80% in 48 hours, 85% in 72 hours, and 95% in 2 weeks. However, the same specimens acidified with tartaric acid and stored in the dark lost 2% of the aminolevulinic acid in 72 hours and 6% in 2 weeks (V3). The destruction of catecholamines collected in nonacidified urine specimens is well documented (Cll). Urinary acid phosphatase was destroyed on freezing (S15). The effect was related to increasing salt concentration during freezing and was prevented by the addition of albumin (S15). 

Oral contraceptives have their most significant effect on endocrine parameters. Blood cortisol, thyroxine, protein-bound iodine, T3 uptake, and urinary free cortisol are elevated. Urinary 17,21-dihydroxy steroids, 17-ketosteroids, and estrogens are decreased. There is no effect on urinary catecholamines or VMA (Table 10) (LIO). The effect of thyroid functions tests is due to the administered hormone stimulating an increase in the production of thyroid-binding globulin which in turn binds 1-thyroxine. The lowering of free thyroxine stimulates the anterior pituitary to produce thyrotropin, which in turn stimulates the thyroid to produce more thyroxine. Since the additional thyroxine is bound to the extra protein, there is an equilibrium and the patient remains clinically euthyroid, but the protein-bound iodine and the thyroxine are elevated. 

G5. Gifford, R. W., and Tweed, D. C., Spurious elevations of urinary catecholamines during therapy with alphamethyldopa. J. Amer. Med. Ase. 182, 493-495 (1962). 

Drug/Lab test interactions A labetalol metabolite may falsely increase urinary catecholamine levels when measured by a nonspecific trihydroxyindole reaction. Drug/Food interactions Food may increase bioavailability of the drug. 

Drug/Lab test interactions Methyidopa may interfere with tests for Urinary uric acid by phosphotungstate method serum creatinine by alkaline picrate method AST by colorimetric methods. Because methyidopa causes fluorescence in urine samples at the same wavelengths as catecholamines, falsely high levels of urinary catecholamines may occur and will interfere with the diagnosis of pheochromocytoma. 

Drug/Lab test interactions The antianabolic action of tetracyclines may cause an increase in blood urea nitrogen. During doxycycline or minocycline therapy, false elevations of urinary catecholamine levels may occur... 

Davidson J, Lipper S, KUts CD, Mahorney S, Hammett E (1985) Platelet MAO activity in posttraumatic stress disorder. Am J Psychiatry 142 1341-1343 Davis M (2002) The role of NMDA receptors and MAP kinase in the amygdala in extinction of fear clinical implications for exposure therapy. Eur J Neurosci 16 395-398 DeBellis MD, Letter L, Trickett PK, Putnam FW (1994) Urinary catecholamine excretion in sexually abused girls. J Am Acad Child Adoles Psychiatry 33 320-327 Debiec J, LeDoux JE, Nader K (2002) Cellular and systems reconsolidation in the hippocampus. Neuron 36 527-538... 

The initial report of sustained, lower urinary cortisol levels in PTSD highlighted the disassociation between cortisol and catecholamine levels in PTSD. Norepinephrine and epinephrine levels assayed from the same urine specimens revealed elevations in both of these catecholamines, while cortisol levels in PTSD fell within the normal range of 20-90 pg/day, indicating that the alteration was not in the hypoadrenal or endocrinopathologic range (Mason et al. 1986). This finding established the expectation that alterations in basal levels of cortisol might be subtle, and not easily differentiated from normal values (Mason et al. 1986). 

Glover D, Poland R (2002) Urinary cortisol and catecholamines in mothers of child cancer survivors with and without PTSD. Psychoneiu oendocrinology 27 805-819 Goeinjian AK, Pynoos RS, Steinberg Am, Endres D, Abraham K, Geffner ME, Fairbanks LA (2003) Hypothalamic-pituitary-adrenal activity amongArmenian adolescents with PTSD symptoms. J Trauma Stress 16 319-323... 

Halbreich U, Olympia J, Carson S, Glogowski J, Yeh CM, Axelrod S, Desu MM (1989) Hypothalamo-pituitary-adrenalactivityin endogenously depressedposttraumaticstress disorder patients. Psychoneuroendocrinology 14 365-370 Hawk LW, Dougall AL, Ursano RJ, Baum A (2000) Urinary catecholamines and cortisol in recent-onset posttraumatic stress disorder after motor vehicle accidents. Psychosom Med 62 423-434... 

The presence of a-methyldopa and its metabolites in the urine reduces the diagnostic value of urinary catecholamine measurements as an indicator of pheochro-mocytoma, since these substances interfere with the fluorescence assay for catecholamines. 

Urinary catecholamines preferred over phentolamine for screening for pheochro-... 

DeBellis, M.D., Lefter, L., Trickett, P.K., and Putnam F.W. (1994b) Urinary catecholamine excretion in sexually abused girls. / Am Acad Child Adolesc Psychiatry 33 320—327. 

Donnelly, M., Zametkln, A.J., Rapoport, J.L., Ismond, D.R., Wein-gartner, H., Lane, E., Oliver, J., Linnoila, M., and Potter, W.Z. (1986) Treatment of childhood hyperactivity with deslpramlne plasma drug concentration, cardiovascular effects, plasma and urinary catecholamine levels, and clinical response. Clin Pharmacol Ther 39 72-81. 

Jones ED, Maas JW, Dekirmenjian H, et al Urinary catecholamine metabolites during behavioral changes in a patient with manic-depressive cycles. Science 179 300-302, 1973... 

Pheochromocytoma is a tumor of the adrenal medulla or sympathetic ganglion cells. The tumor secretes catecholamines, especially norepinephrine and epinephrine. The patient in the case study at the beginning of the chapter had a left adrenal pheochromocytoma that was identified by imaging. In addition, she had elevated plasma and urinary norepinephrine, epinephrine, and their metabolites, normetanephrine and metanephrine. 

Methenamine mandelate, 1 g four times daily, or methen-amine hippurate, 1 g twice daily by mouth (children, 50 mg/kg/d or 30 mg/kg/d, respectively), is used only as a urinary antiseptic to suppress, not treat, urinary tract infection. Acidifying agents (eg, ascorbic acid, 4-12 g/d) may be given to lower urinary pH below 5.5. Sulfonamides should not be given at the same time because they may form an insoluble compound with the formaldehyde released by methenamine. Persons taking methenamine mandelate may exhibit falsely elevated tests for catecholamine metabolites. 

Dichloromethane (> 6.3 mmol/kg bw) administered to rats by gavage induced increased urinary excretion of catecholamines in the urine in rats cytomorphological changes and a decrease in chromafim reaction were observed in the adrenal medulla at a dose level of 15.6 mmol/kg bw (1330 mg/kg) (Marzotko Pankow, 1987). 

The catecholamines are a group of hormones secreted by the adrenal medulla. The major urinary metabolite of norepinephrine and epinephrine is vanillylmandelic acid (VMA). Urinary levels of VMA are considerably higher than those of total catecholamine. From the standpoint of laboratory methodology, VMA estimation is preferable to total catecholamine estimation, although it is not a simple procedure. VMA has been shown to be elevated in some patients who had phenochromocytoma and normal urinary catecholamines, even though patients with neuroblastoma have a normal VMA level and elevated catecholamine levels. 

Since dopamine is present in sympathetic nervous tissue as a precursor of norepinephrine, and it has a separate metabolic pathway that yields homovanillic acid (HVA), tumors such as neuroblastomas may cause elevations of the urinary dopamine and its metabolite HVA. In some cases these elevations have been observed with normal VMA, total catecholamine, and metanephrine. Urinary HVA is usually normal in patients with phenochromocytoma. Increased HVA is found in special fluids of patients with Parkinson s disease treated with L-dopa. 

Clonidine reduces plasma renin activity and urinary aldosterone and catecholamine concentrations (291). 

In one patient who took 900 mg of phenelzine, there was a marked excess of urinary and plasma catecholamines, analogous to pheochromocytoma, and the patient was successfully managed with alpha-adrenoceptor antagonists (44). In another patient, who probably... 

An IPC procedure assessed recoveries of urinary catecholamines during an innovative sample clean-up [95] and was optimized to avoid interferences by anti-TB drugs [96]. Adrenergic amines were determined in a variety of bitter orange-containing dietary supplements marketed as appetite suppressants a sodium dodecyl sulfate IPR and fluorescent detection were used [97]. Similarly, two classes of compounds. 

Manickum, T. Interferences by anti-TB drugs in a validated HPLC assay for urinary catecholamines and their successful removal. J. Chromatogr. B. 2008, 873, 124—128. 

Dexamphetamine sulphate acts by stimulating the release of norepinephrine and dopamine from storage sites and may also slow down the metabolism of catecholamines by inhibiting MAO. Usually about 30% is excreted unchanged in the urine this urinary excretion reaches 60% when the urine is acidic (pH 5.5-6). It is metabolized by cytochrome P450. 

There is debate over the association between caffeine intake and cardiovascular disease. Increases in mean blood pressure, blood glucose and free fatty acid concentrations, and urinary catecholamine excretion have been... 

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