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At least 19 recordsLinked to original sources
PubMed1997

Synthesis of tritium-labelled N tau-methylhistamine for the improvement of extraction efficiency of N tau-methylhistamine from biological fluids.

In order to trace the loss of N tau-methylhistamine, a principal metabolite of histamine, during extraction and purification from human plasma and urine samples, N tau-[3H]methylhistamine was prepared in two steps from N alpha t-butoxycarbonylhistamine (II). In the first step, compound II was deprotonated with NaH in an aprotic solvent and treated with [3H]methyl iodide. The products, N alpha t-butoxycarbonyl-N tau-[3H]methylhistamine (III) and N alpha t-butoxycarbonyl-N pi-[3H]methylhistamine (IV), were then hydrolysed with iodotrimethylsilane under mild and short reaction conditions. Facile purification with Sep-Pak silica cartridges gave the combined two isomers of N tau-[3H]methylhistamine and N pi-[3H]methylhistamine in 10.7% radiochemical yield with a radiochemical purity of > 94% and a ratio of approximately 2:1. Improvements in the extraction of methylhistamine using chromatography on Sep-Pak silica cartridges led to an overall recovery of 82.5 +/- 0.3% (n = 3) based upon total [3H]methylhistamine from normal human plasma.

Chemistry Techniques, Analytical↗
PubMed1985

Synthesis of N pi-methylhistamine and N alpha-methylhistamine by purified rabbit lung indolethylamine N-methyltransferase.

N tau-Methylhistamine is a major inactive metabolite of histamine and is formed by histamine N-methyltransferase (EC 2.1.1.8). However, a controversy exists concerning the presence of other N-methylated histamines, such as N pi- and N alpha-methylhistamine in mammalian tissues. Indolethylamine N-methyltransferase is present in mammalian tissues with the rabbit lung containing the highest concentration, but the physiologic function of this enzyme remains unclear. Using rabbit lung as a tissue source, we purified indolethylamine N-methyltransferase 260-fold and separated it completely from histamine N-methyltransferase. Histamine was a substrate for purified indolethylamine N-methyltransferase and unlike histamine N-methyltransferase which exclusively formed N tau-methylhistamine, indolethylamine N-methyltransferase catalyzed the in vitro formation of both N pi-methylhistamine and N alpha-methylhistamine. In contrast to histamine N-methyltransferase, indolethylamine N-methyltransferase activity was not inhibited by either high histamine concentrations or by quinacrine. Thus, mammalian tissues contain an enzyme capable of forming N pi-methylhistamine and N alpha-methylhistamine. This supports the concept of the existence of these compounds and suggests they may serve a physiologic function in mammals.

Animals↗
PubMed1986

Molecular determinants for the agonist activity of 2-methylhistamine and 4-methylhistamine at H2-receptors.

A model for drug action at the histamine H2-receptor has been evaluated computationally for the agonists 2- and 4-methylhistamine. Based on molecular properties calculated for molecular structures optimized with ab initio quantum mechanical methods, the activities of these compounds and their potencies relative to histamine are found to be explained by the previously proposed model. Recognized in the N3-H tautomeric form of their monocations, both compounds exhibit a change in ring tautomeric preference when the cationic side chain is neutralized. This change makes possible their participation in a proposed proton relay event that was postulated to initiate the receptor response of H2-agonists. The relative concentrations of the mono- and dication forms of the molecules in equimolar concentrations of histamine and the two derivatives are calculated from the values of the molecular electrostatic potentials at the ring protonation sites. Because the monocation is the species recognized at the H2-receptor, the reduced potency of 2-methylhistamine relative to histamine and to the 4-methyl derivative is explained by the finding that 2-methylhistamine will have the lowest concentration of the recognized species. The rank order of potencies obtained from the ratio of monocationic species of the molecules is in agreement with experimental results.

Methylhistamines↗
PubMed1996

Hemodynamic profile of activation of histamine H3 receptors by R-alpha-methylhistamine in the guinea pig.

1. The effect of R-alpha-methylhistamine, a histamine H1 receptor agonist, was studied on cardiovascular hemodynamics in bilateral vagotomized, anesthetized guinea pigs. 2. R-alpha-methylhistamine (100 micrograms/kg, IV) a dose that selectively activates histamine H3 receptors, produced hypotension and bradycardia. Total peripheral resistance (TPR) and rate pressure product (RPP) were also decreased at this dose. 3. Pretreatment with the ganglionic blocker hexamethonium (20 mg/kg, IV) blocked the blood pressure (BP), heart rate (HR), TPR, and RPP effects of R-alpha-methylhistamine (100 micrograms/kg, IV). Hexamethonium did not block the hypotensive and TPR lowering actions of the muscarinic agonist methacholine (1 and 3 micrograms/kg, IV). 4. Pretreatment with the alpha 1-adrenoceptor antagonist prazosin (0.5 mg/kg IV), blocked R-alpha-methylhistamine's (100 micrograms/kg, IV) effects on BP, TPR, and RPP. Prazosin did not antagonize the bradycardia effect of R-alpha-methylhistamine. 5. Pretreatment with the beta-adrenoceptor antagonist atenolol (1 mg/kg, IV) did not alter the BP, TPR, or RPP actions of R-alpha-methylhistamine. The HR effects of R-alpha-methylhistamine were blocked by atenolol. 6. The hemodynamic effects of R-alpha-methylhistamine were compared to the hemodynamic profile of the calcium channel blocker, verapamil (0.5 mg/kg, IV). Verapamil had little effect on TRP and had a greater cardiac depressant effect as evidenced by a significant reduction in HR and cardiac output (CO). 7. In summary, these results show that activation of prejunctional H3 receptors with R-alpha-methylhistamine decreases basal, BP, HR, TPR, and RPP in anesthetized guinea pigs. The fall in BP is mediated by a decrease in TPR. Furthermore, the inhibitory effects of R-alpha-methylhistamine on sympathetic control of the vasculature appears to impart a greater physiologic effect on the H3-histamine mediated hypotension than its inhibitory effects on sympathetic agents to the heart.

Animals↗
PubMed1993

Production by R-alpha-methylhistamine of a histamine H3 receptor-mediated decrease in basal vascular resistance in guinea-pigs.

1. The effect of the selective histamine H3 receptor agonist, R-alpha-methylhistamine given intravenously (10-100 micrograms kg-1) was examined on baseline total peripheral resistance (TPR), and cardiovascular haemodynamics in bilaterally vagotomized, anaesthetized guinea-pigs. 2. R-alpha-methylhistamine produced a dose-dependent hypotension and fall in TPR at 30 and 100 micrograms kg-1. A decrease in heart rate (HR) was observed at a dose of 100 micrograms kg-1. R-alpha-methylhistamine (10-100 micrograms kg-1) also produced a dose-dependent fall in rate pressure product (RPP). There was no effect on cardiac output (CO) or stroke volume (SV) at these doses. 3. Histamine H1 and H2 blockade in animals pretreated with a combination of chlorpheniramine (0.3 mg kg-1) and cimetidine (3.0 mg kg-1) did not alter the haemodynamic actions of R-alpha-methyl-histamine (100 micrograms kg-1, i.v.). Pretreatment with the selective H3 antagonist, thioperamide (1 mg kg-1), completely blocked the action of R-alpha-methylhistamine on haemodynamic parameters. 4. To study the mechanism of action of R-alpha-methylhistamine, the vasodilator hydralazine (1 mg kg-1, i.v.) was used. Hydralazine lowered BP, TRP and RPP in guinea-pigs pretreated with ipratropium (50 micrograms kg-1, i.v.). Hydralazine had no effect on HR, SV or CO. 5. R-alpha-methylhistamine (100 micrograms kg-1) did not affect the vasopressor action and increases in TPR produced by adrenaline (1 and 3 micrograms kg-1). On the other hand, the vasodilator hydralazine (1 mg kg-1, i.v.) inhibited the effects of adrenaline (3 micrograms kg-1) on TPR and RPP. The effect of both doses of adrenaline on BP were attenuated by hydralazine. Therefore, the inhibitory effects of R-alpha-methylhistamine are not mediated through a direct action on vascular smooth muscle.6. In adrenalectomized guinea-pigs, R-alpha-methylhistamine (100 microg kg-1) produced a drop in BP and HR.There was no difference between the effects of R-alpha-methylhistamine on blood pressure and heart rate in adrenalectomized and non-adrenalectomized guinea-pigs.7. These results show that activation of peripheral H3 receptors lowers basal BP, HR and TPR, most likely by a peripheral prejunctional mechanism. The fall in BP and TPR is probably due to a decrease in noradrenaline release from sympathetic effector nerves innervating the resistance blood vessels.

Adrenalectomy↗
PubMed1989

Analysis of histamine and N tau-methylhistamine in plasma by gas chromatography-negative ion-chemical ionization mass spectrometry.

Current methods of quantitation of histamine and its major metabolite N tau-methylhistamine are inaccurate and insensitive to the very low concentrations that exist in plasma samples. Therefore, an accurate and sensitive method for quantification in plasma has been developed using the stable isotope dilution assay with negative ion-chemical ionization mass spectrometry. For histamine, after the addition of [2H4]histamine to 2 ml of plasma, the plasma sample is deproteinized, extracted into butanol, back extracted into HCl, derivatized to the pentafluorobenzyl derivative (CH2C6F5)3-histamine, purified on silica gel columns, and then quantified with negative ion-chemical ionization mass spectrometry by selected ion monitoring of the ratio of ions m/z 430/434. For N tau-methylhistamine, after the addition of N tau-[2H3]methylhistamine to 2 ml of plasma, the plasma sample is deproteinized, extracted into butanol, back extracted into HCl, derivatized to the heptafluorobutyryl derivative (C3F7CO2)2-N tau-methylhistamine, purified on silica gel columns, and then quantified with negative ion-chemical ionization mass spectrometry by selected ion monitoring of the ratio of ions m/z 497/500. The precision of the histamine assay is 3.1% and the accuracy is 95.5 +/- 2.5% while the precision of the N tau-methylhistamine assay is 1.9% and the accuracy is 106.8 +/- 1.9%. The lower limits of sensitivity are 1 pg for histamine and 6 pg for N tau-methylhistamine injected on column. Using the assay in three normal human volunteers, plasma concentrations of histamine were 130, 92, and 85 pg/ml, and of N tau-methylhistamine were 229, 228, and 216 pg/ml. This assay provides a very sensitive and accurate method of quantitation of histamine and N tau-methylhistamine in plasma samples.

Animals↗
PubMed1980

Effects of the histamine H2-receptor agonists dimaprit and 4-methylhistamine on the central noradrenaline and serotonin system.

Effects of dimaprit and 4-methylhistamine, two histamine H2-receptor agonists, on noradrenaline and serotonin systems in the rat brain were investigated. Administration of dimaprit into the lateral brain ventricle produced 30% decrease in hypothalamal noradrenaline. 2 h after administration of dimaprit the level of 3-methoxy-4-hydroxyphenylglycol was increased by 50%. 4-Methylhistamine and histamine produced qualitatively the same effects as dimaprit. Dimaprit and 4-methylhistamine increased locomotor activity in tranylcypromine-treated rats. The hyperkinetic action of both drugs was prevented by phenoxybenzamine. Dimaprit had negligible effect on the serotonin system while 4-methylhistamine and histamine decreased serotonin and simultaneously increased 5-hydroxyindolcacetic acid. 4-Methylhistamine and histamine, but not dimaprit, evoked head-twitches in tranylcypromine-treated rats. It is concluded that dimaprit and 4-methylhistamine act similarly on the noradrenaline system, probably releasing noradrenaline, but having different effects on the serotonin system. 4-Methylhistamine (and histamine) probably releases serotonin from rat hypothalamus while dimaprit does not. The results are discussed in relation to a possible interaction of histamine with both noradrenaline and serotonin systems in the rat brain.

Animals↗
PubMed1986

Simultaneous determination of histamine and N tau-methylhistamine with high-performance liquid chromatography using electrochemical detection.

We have developed a liquid chromatographic method which uses electrochemical detection for the simultaneous quantitation of histamine and N tau-methylhistamine in rat brain. The amines are derivatized with the water-soluble Bolton-Hunter reagent (sulfo B-H). Perchloric acid extracts of rat brains are chromatographed on a strong cation-exchange resin. The eluate is evaporated and allowed to react with sulfo B-H at pH 9.8 at room temperature. The derivatization is complete after 30 s vortexing. The derivatives are purified using a cellulose-phosphate fibrous cation exchanger. They are quantified with an electrochemical detector at a potential of 0.56 V after preoxidizing the sample at 0.47 V. The derivatives of histamine, N tau-methylhistamine, and N alpha-methylhistamine are completely separated without interfering peaks. Since no N alpha-methylhistamine was detected in rat brain it was used as an internal standard. The detection limits are 0.1 pmol of histamine and 0.2 pmol of N tau-methylhistamine. The precision of this method is high, with within-run and between-run coefficients of variation of 2-7% and linearity of 0.999. Both histamine and N tau-methylhistamine peak heights increased significantly and selectively after treatment with pargyline. Because of the high sensitivity, accuracy, and precision, the histamine and N tau-methylhistamine contents of single nuclei of the rat hypothalamus can be routinely quantified.

Animals↗
PubMed1993

N alpha-methylhistamine inhibits intestinal transit in mice by central histamine H1 receptor activation.

The effects of (R)alpha-methylhistamine and N alpha-methylhistamine on intestinal transit were examined in mice. The passage of a charcoal meal in the gastrointestinal tract was dose dependently inhibited by N alpha-methylhistamine (1-20 mg/kg i.p.), but not by a selective H3 receptor agonist (R)alpha-methyl-histamine (1-50 mg/kg i.p.). The inhibitory effect of N alpha-methylhistamine (20 mg/kg) was attenuated by pretreatment with H1 receptor antagonists (mepyramine 5 mg/kg i.p. or 5 micrograms i.c.v. and triprolidine 5 mg/kg i.p.), but not by cimetidine (10 mg/kg i.p.), zolantidine (5 mg/kg i.p.), a brain-penetrating H2 receptor antagonist, or thioperamide (5 mg/kg i.p.), a selective H3 receptor antagonist. The effect of N alpha-methylhistamine was also attenuated by combined treatment with phentolamine and propranolol (5 and 15 mg/kg s.c., respectively) and by pretreatment with 6-hydroxydopamine (20 mg/kg i.p., 2 days before). N alpha-Methylhistamine markedly decreased histamine turnover in the mouse brain. These findings suggest that intestinal transit is inhibited by N alpha-methylhistamine via stimulation of central H1 but not H3 receptors and that stimulation of the sympathetic system is involved in this effect.

Animals↗
PubMed1995

Plasma N-methylhistamine concentration as an indicator of histamine release by intravenous d-tubocurarine in humans: preliminary study in five patients by radioimmunoassay kits.

Histamine disappears rapidly from plasma because of its short half-life. Because a metabolite of histamine, N-methylhistamine, is stable and has a longer half-life, determination of its plasma concentration can be useful in retrospective determination of histamine release. In this study, we measured plasma histamine and N-methylhistamine concentrations after d-tubocurarine (dTc) administration to evaluate the use of plasma N-methylhistamine measurement for confirming histamine release. After the induction of anesthesia, five patients received dTc, 0.8 mg/kg intravenously. A radioimmunoassay kit was used to determine plasma histamine and N-methylhistamine before and 1, 3, 5, and 10 min after administration of dTc. Histamine released by the injection of dTc reached a maximum level at 1 min, but decreased rapidly, whereas N-methylhistamine increased at 1 min and remained increased for at least 10 min. Good correlations were found between histamine concentration at 1 min and N-methylhistamine concentrations at 1, 3, 5, and 10 min, especially r = 0.999 (n = 5) at 10 min. N-Methylhistamine measurement with this kit can ascertain histamine release retrospectively in a semiquantitative manner.

Anesthesia↗
PubMed1980

Simultaneous determination of histamine and N tau-methylhistamine in human plasma and urine by gas chromatography--mass spectrometry.

A new and sensitive method is described for the determination of histamine and N tau-methylhistamine in human plasma and urine by gas chromatography--mass spectrometry. 15N2-Labeled histamine and N tau-[methyl-d3]methylhistamine were used as internal standards. Histamine and N tau-methylhistamine were converted to the derivatives N alpha-heptafluorobutyryl-N tau-ethoxycarbonylhistamine and N alpha-heptafluorobutyryl-N tau-methylhistamine, respectively. After these derivatives had been purified on a small column packed with CPG-10, the molecular ions were monitored during selected ion monitoring. Linear standard curves were obtained in the range of 0.5-10 ng/ml for both compounds. The reliability of the histamine analysis was demonstrated by using two different ion pairs, while a comparison with results from two different derivatizations on the same urine sample also established the specificity of the N tau-methylhistamine analysis. An increase of 1 ng of histamine in the plasma could be precisely determined by the present method. The histamine content of plasma from five normal subjects was determined as 0.83 +/- 0.37 (S.D.) ng/ml and the N tau-methylhistamine content in most subjects was below the limits of this measurement. High excretion of histamine was noted in the urine collected in the early morning from a patient with nephritis.

Gas Chromatography-Mass Spectrometry↗
PubMed1997

Determination of plasma Ntau-methylhistamine in vivo by isotope dilution using benchtop gas chromatography-mass spectrometry.

A practical sensitive and specific method for determination of the stable metabolite of histamine, Ntau-methylhistamine, in human plasma using benchtop gas chromatography-stable isotope dilution mass spectrometry has been developed. Ntau-Methylhistamine, a principal metabolite of histamine in humans, was extracted and purified from human plasma using a two-step procedure with Sep-Pak silica cartridges. Quantitation of Ntau-methylhistamine was made possible by the synthesis of Ntau-[2H3]methylhistamine used as an internal standard. Derivatization with pentafluoropropionyl anhydride of extracts of human plasma yielded the bis-pentafluoropropionyl derivative of Ntau-methylhistamine for measurement using selected ion monitoring of the m/z 417/420 ion pair after electron impact on a benchtop gas chromatography-mass spectrometry (GC-MS). By improvements in the plasma extraction technique, inclusion of a synthetic internal standard and the development of a sensitive and stable derivative of the histamine metabolite, Ntau-methylhistamine was found to be significantly elevated in the plasma of patients with the dermal fibroproliferative disorder, hypertrophic scarring as compared to age-matched normal volunteers (98.5+/-29.5 pg/ml, n=9, versus 43.3+/-16.5 pg/ml, n=8, p<0.05). As such, this method affords a sensitive, specific and practical approach to measurement of histamine metabolites in plasma and other biological fluids.

Burns↗
PubMed1997

Histological effect of (R)-alpha-methylhistamine on ethanol damage in rat gastric mucosa: influence on mucus production.

(R)-alpha-Methylhistamine, a selective agonist of histamine H3 receptors, prevents macroscopically visible gastric lesions by absolute ethanol in the rat. A further insight into its activity was the aim of our study. Rats were given saline or (R)-alpha-methylhistamine (100 mg/kg) intragastrically. After 30 min, absolute ethanol was given and gastric mucosa was sampled 60 min later. Histologic damage and intracellular and adherent mucus were quantified. Luminal surface and mucous cells were examined by scanning and transmission electron microscopy. (R)-alpha-Methylhistamine reduced the extent of lesions by ethanol from 96 to 18%. Surface mucous cells and mucous neck cells were increased in volume and number, packaging of intracellular mucus was modified, and the secretory processes were promoted by (R)-alpha-methylhistamine itself, although these modifications were mostly evident in stomachs subsequently exposed to ethanol. Adherent mucus layer thickness was increased by (R)-alpha-methylhistamine only after ethanol exposure. It is concluded that (R)-alpha-methylhistamine predisposes mucous cells to react to ethanol.

Animals↗
PubMed1989

Effects of the histamine H3-agonist (R)-alpha-methylhistamine and the antagonist thioperamide on histamine metabolism in the mouse and rat brain.

To study the feedback control by histamine (HA) H3-receptors on the synthesis and release of HA at nerve endings in the brain, the effects of a potent and selective H3-agonist, (R)-alpha-methylhistamine, and an H3-antagonist, thioperamide, on the pargyline-induced accumulation of tele-methylhistamine (t-MH) in the brain of mice and rats were examined in vivo. (R)-alpha-Methylhistamine dihydrochloride (6.3 mg free base/kg, i.p.) and thioperamide (2 mg/kg, i.p.), respectively, significantly decreased and increased the steady-state t-MH level in the mouse brain, whereas these compounds produced no significant changes in the HA level. When administered to mice immediately after pargyline (65 mg/kg, i.p.), (R)-alpha-methylhistamine (3.2 mg/kg, i.p.) inhibited the pargyline-induced increase in the t-MH level almost completely during the first 2 h after treatment. Thioperamide (2 mg/kg, i.p.) enhanced the pargyline-induced t-MH accumulation by approximately 70% 1 and 2 h after treatment. Lower doses of (R)-alpha-methylhistamine (1.3 mg/kg) and thioperamide (1 mg/kg) induced significant changes in the pargyline-induced t-MH accumulation in the mouse brain. In the rat, (R)-alpha-methylhistamine (3.2 mg/kg, i.p.) and thioperamide (2 mg/kg, i.p.) also affected the pargyline-induced t-MH accumulation in eight brain regions and the effects were especially marked in the cerebral cortex and amygdala. These results indicate that these compounds have potent effects on HA turnover in vivo in the brain.

Amygdala↗
PubMed1989

Sensitive radioimmunoassays for histamine and tele-methylhistamine in the brain.

Serum albumin conjugates of histamine or tele-methylhistamine, a major catabolite, were prepared using 1,4-benzoquinone as the coupling agent and used to raise polyclonal antibodies in rabbits. The same reagent was used to prepare the [125I]iodinated tracer and treat tissue extracts submitted to the radioimmunoassays. The IC50 values of prederivatized histamine and tele-methylhistamine in the radioimmunoassays were 0.3 nM and 0.5 nM, respectively, whereas nonderivatized histamine or tele-methylhistamine, histidine, a variety of histamine derivatives, amines, etc., had at least 1,000-fold higher IC50 values. Application of the radioimmunoassays to nonpurified extracts of rat brain allowed the quantification of the two amine immunoreactivities in samples corresponding to less than 1 mg of hypothalamus. The tissue immunoreactivity corresponded to authentic histamine or tele-methylhistamine, as shown by (a) the parallel 125I-tracer displacement curves, (b) the similar elution patterns from HPLC columns, (c) the regional levels of histamine and tele-methylhistamine in brain, similar to those obtained with other methods, and (d) the clearcut effects of treatments with inhibitors of L-histidine decarboxylase or monoamine oxidase. The two radioimmunoassays appear as simple and sensitive tools to evaluate steady-state levels and turnover rates of histamine and tele-methylhistamine.

Animals↗
PubMed1994

The disposition of (R)-alpha-methylhistamine, a histamine H3-receptor agonist, in rats.

Using a modified HPLC method with a fluorescence spectrophotometer and a weak cation exchanger, it was possible to separate (R)-alpha-methylhistamine (alpha-methylhistamine) from histamine in plasma and various tissues. The assay was used to study the disposition and pharmacokinetic analysis of alpha-methylhistamine after a bolus intravenous administration to rats. After rapid intravenous administration (12.6 mg kg-1), the plasma concentration declined biexponentially with a half-life of 1.3 min in the elimination phase. The area under the plasma concentration-time curve and total body clearance were 130 micrograms min mL-1 and 97 mL min-1 kg-1, respectively. After administration, alpha-methylhistamine was immediately transferred to various tissues. The concentration was high in the kidney, lung, and liver (kidney > lung > liver), but low in the brain. The tissue-to-plasma concentration ratios in peripheral tissues were greater than 1, suggesting that the transfer of alpha-methylhistamine to peripheral tissues was due to a specialized transport mechanism or possibly to tissue binding. However, the finding that the tissue/plasma ratio in the brain was lower than unity suggests that the transport system in this tissue depends on a concentration gradient, and that alpha-methylhistamine crosses the blood-brain barrier in rats with difficulty.

Animals↗
PubMed1991

Measurement of urinary N tau-methylhistamine excretion: correlation of a newly developed radioimmunoassay (RIA) with gas chromatography mass spectrometry (GCMS).

A newly developed radioimmunoassay (RIA, Y) for the determination of urinary N tau-methylhistamine concentrations was correlated with gas chromatography mass spectrometry (GCMS, X). In 34 urine samples, with histamine and N tau-methylhistamine levels within our reference values, the correlation was: Y = 1.47X -0.245 mumol/l (r = 0.92; p-slope less than or equal to 0.0001). In 14 pathological urine samples, derived from patients with mastocytosis and having upper reference values, the correlation was: Y = 1.75X - 1.02 mumol/l (r = 0.93; p-slope less than or equal to 0.001). In spite of the greater specificity of the monoclonal antibody for N tau-methylhistamine compared with that of histamine, relatively high urinary histamine concentrations gave a false positive influence on the RIA results, which was 100% when the histamine/N tau-methylhistamine ratio was about 19. Clear cases of mastocytosis can be diagnosed, using the RIA-kit, but for a more precise N tau-methylhistamine value GCMS analyses will remain necessary.

False Positive Reactions↗