Disease relevance of N-methyl-histamine

• Determination of N-methylhistamine in urine as an indicator of histamine release in immediate allergic reactions [1].
• Is urine methylhistamine a useful marker for interstitial cystitis [2]?
• Urinary excretion of N-methylhistamine as a marker of disease activity in inflammatory bowel disease [3].
• Value of urinary N-methylhistamine measurements in childhood mastocytosis [4].
• The excretion of MH but not MIMA increased in four patients (ages 37, 45, 61 and 65 years) and decreased in two patients (ages 26 and 48 years), including the only patient with paediatric-onset cutaneous mastocytosis [5].

High impact information on N-methyl-histamine

• The urinary excretion of histamine and its metabolite, N-methylhistamine, was measured in three persons who had scombroid-fish poisoning (scombrotoxism) after the ingestion of marlin [6].
• Histamine and methylhistamine were not elevated in MS [7].
• Here, cerebrospinal fluid from MS patients and controls with other neurologic diseases was assayed for histamine, its major metabolite methylhistamine, and the specific mast cell marker tryptase [7].
• The overall anatomical pattern of the histamine-evoked binding response closely reflects the known distribution of H3 binding sites and was faithfully mimicked by N(alpha)-methylhistamine, (R)-alpha-methylhistamine, and immepip, three H3-selective agonists [8].
• Brain methylhistamine levels were similar to or greater than histamine levels, indicating that histamine methylation is a major metabolic pathway in neonatal brain, as it is in adults [9].

Chemical compound and disease context of N-methyl-histamine

• An increase in urinary methylhistamine and LTE4 was seen during the acute allergic reaction in both groups of pigs [10].
• Comparison of serum tryptase and urine N-methylhistamine in patients with suspected mastocytosis [11].
• In addition, pretreatment with ICV injection of histamine H3-receptor antagonist, thioperamide, and histamine H3-receptor agonist, (R) alpha methylhistamine, enhanced and inhibited diazepam-induced hyperphagia (1 mg/kg, SC) in nondeprived rats, respectively [12].
• The median level of N-methylhistamine in the urine of patients with mastocytosis limited to the skin was 245 micro mol/mol creatinine [13].

Biological context of N-methyl-histamine

• Methylhistamine: evidence for selective deamination by MAO B in the rat brain in vivo [14].
• There was a significant positive relationship between mast cell number and the 24 h urine excretion of N-methylhistamine reflecting mast cell activity (p = 0.0001), and this latter measurement correlated negatively with bone mineral density (BMD) at the lumbar spine (p < 0.001) [15].
• In contrast, the urinary N-methylhistamine concentration did not change until the second trimester and was significantly decreased during the third trimester [16].
• 1. To investigate the role of mast cells and eosinophils in the pathogenesis of nocturnal asthma, the plasma methylhistamine concentration, serum eosinophil cationic protein level and peak expiratory flow rate were measured 2-hourly for 24 h in 10 patients with nocturnal asthma and in 10 healthy control subjects [17].
• 3. Both groups had equivalent decreases in blood pressure in response to methylhistamine [18].

Anatomical context of N-methyl-histamine

• This study demonstrates that exposure to diesel exhaust induces inflammatory response in healthy human airways, represented by an early increase in interleukin-6 and methylhistamine concentration and the percentage of neutrophils [19].
• CONCLUSION: In patients with PPH, increased levels of PGD-M, without increased synthesis of N-methylhistamine, suggest that macrophages are activated [20].
• An H3-agonist, R alpha methylhistamine strongly relaxed isolated and perfused rabbit middle cerebral artery precontracted with K+ [21].
• Six hours after exposure to DE, a significant increase was found in the percentage of sputum neutrophils (37.7 versus 26.2% p=0.002) together with increases in the concentrations of interleukin-6 (12.0 versus 6.3 pg x mL(-1), p=0.006) and methylhistamine (0.11 versus 0.12 microg x L(-1), p=0.024) [19].
• Endpoints were reductions in serum tryptase, urinary N-methylhistamine excretion, skin lesions, the number of mast cells in bone marrow sections, hepatomegaly and/or splenomegaly, and symptoms [22].

Associations of N-methyl-histamine with other chemical compounds

• RESULTS: Urine marker levels were similar for the 2 groups, including antiproliferative factor, epidermal growth factor, heparin binding epidermal growth factor-like growth factor, cyclic guanosine monophosphate, interleukins 6 and 8, and methylhistamine [23].
• Urinary EDN and N-methylhistamine concentrations were measured by radioimmunoassay and standardized with urinary creatinine concentration [16].
• We detected a significant variation in urinary methylhistamine excretion only in group C2 after 2 h, 6 h and 24 h (P < 0.0001) [24].
• TREATMENT: Confluent human endothelial cell layer were incubated with histamine (1 mM), H1, H2 or H3 receptor agonists: fluorophenylhistamine (10 microM), amthamine (10 microm), methylhistamine (10 microM), respectively [25].
• A high reaction velocity of human intestinal DAO is observed with putrescine, methylhistamine and histamine [26].

Gene context of N-methyl-histamine

• In the present study, we investigated the degranulation of eosinophils and mast cells within the normal course of pregnancy and after delivery by measuring the urinary concentrations of eosinophil-derived neurotoxin (EDN) and N-methylhistamine [16].
• The intradermal effects of the H3 receptor agonist R alpha methylhistamine in human skin [27].
• Methylhistamine as well as N-acetylated polyamine derivatives are selective substrates for monoamine oxidase type B (MAO-B) [28].
• The animals were pretreated with the histamine synthesis inhibitor alpha-fluoromethylhistidine, the H1 receptor antagonist mepyramine, the H2 receptor antagonist cimetidine or the H3 receptor agonist R (alpha) methylhistamine, which by binding to H3 autoreceptors inhibits histamine release and synthesis [29].
• In conclusion, the study presents an easy and reliable method for the detection of fecal ECP, EPX, and methylhistamine and may provide a tool to gain insight into the pathogenesis of inflammatory bowel diseases and have potential as diagnostic test [30].

Analytical, diagnostic and therapeutic context of N-methyl-histamine

• Methylhistamine and methylimidazolacetic acid (gas chromatography and mass spectrometry) were measured in urine 5 hours before and 5 hours after ingestion [31].
• The second radioimmunoassay using succinyl-glycine as an acylating reagent and monoclonal antibodies, which have been raised to acylated histamine, is the most sensitive assay without any cross-reactivity with methylhistamine [32].
• HNMT activity was unchanged in controls, but increased from 0.37 +/- 0.04 to 0.84 +/- 0.18 and 0.96 +/- 0.22 pmol methylhistamine/mg protein hour after 4 and 10 min reperfusion (p < 0.008 and p < 0.01) [33].
• Methylhistamine, which was separated from the enzymatic reaction system on reversed-phase high-performance liquid chromatography using an ion-paired chromatographic technique, was detected spectrophotometrically at 226 nm [34].
• Urinary excretion of histamine, methylhistamine (1-MeHi) and methylimidazoleacetic acid (MeImAA) in mastocytosis: comparison of new HPLC methods with other present methods [35].

References