Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine, 0.16, 0.33 and 0.66 microgram/kg/min, was infused intravenously to 13 normal non-headache-prone volunteers, 10 patients with chronic muscle contraction headache and 25 patients with common migraine. In the normal group no patients developed pulsating headache. In the migraine group 13 patients developed severe, 9 patients moderate and 2 patients mild pulsating headache, and only 1 patient failed to develop headache at all. The muscle contraction headache patients responded intermediately. At each infusion rate the headache was of constant quality and severity as long as the infusion continued, but disappeared shortly after its termination. Injection of an H1 blocking agent, mepyramine, almost immediately abolished the headache. The H2 blocker cimetidine was much less effective, but still significantly better than placebo. The i.v. histamine infusion test is a useful model for the study of experimental vascular headache.
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PMID:Headache provocation by continuous intravenous infusion of histamine. Clinical results and receptor mechanisms. 740 88

Sneezing, flush, headache, diarrhea, skin itch, and shortness of breath are symptoms occurring in patients intolerant to wine after drinking one glass of red wine. The role of histamine in wine intolerance was evaluated by a red wine provocation test in 28 patients with a history of wine intolerance and in 10 controls with good tolerance of wine. Patients were challenged with 125 ml red wine (equivalent to 50 micrograms histamine); blood samples were drawn before and after 15 and 30 minutes. Plasma histamine was assessed by a radioimmunoassay. Lung function tests were performed before and after the wine test. Twenty-two of twenty-eight patients had symptoms showing significantly higher plasma histamine levels 30 minutes after wine challenge (p < .01) compared with asymptomatic controls. Basal histamine levels of patients were higher (p < .05) than in controls. A slight asthmatic attack as well as a 30% decrease of FEF 25 was seen in 2/22 patients. Terfenadine premedication significantly eliminated symptoms in 10/12 patients (p < .05) in a subsequent wine test. Histamine assessment was done in 52 wines (red, white, and champagne) and in 17 beers by radioimmunoassay. Histamine levels ranged from 3-120 micrograms/l in white wines; 15-670 micrograms/l in champagnes; 60-3800 micrograms/l in red wines; and 21-305 micrograms/l in beers. Histamine is causing wine intolerance. Patients intolerant to wine seem to have diminished histamine degradation probably based on a deficiency of diamine oxidase.
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PMID:The red wine provocation test: intolerance to histamine as a model for food intolerance. 800 53

Food intolerance is not IgE-mediated but caused by histamine. A diminished histamine degradation based on a deficiency of diaminoxidase is suspected to be the reason. The therapeutic efficacy of a histamine-free diet was evaluated in 100 patients with food intolerance and allergic diseases, who were required to avoid fish, cheese, hardcured sausage, pickled cabbage, wine and beer for 4 weeks. Considerable improvement was observed in 57 patients, 15 of whom had total remission. The most striking treatment results were obtained in food or wine intolerance (80% P < 0.05; treatment of choice), bronchial asthma (80%), headache (64%) and urticaria (58%). After ingestion of food rich in histamine clearcut recurrence of atopic eczema was seen in 50% of the patients affected. Histamine plays a major part in food and wine intolerance. Histamine in food causes worsening of symptoms in atopics and patients suffering from headache. The results obtained indicate a deficiency of diaminoxidase in patients with intolerance to food or wine. Histamine levels in alcoholic beverages should be displayed on the labels.
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PMID:[The histamine-free diet]. 837 4

1. Increased histamine concentrations are found in the plasma and urine following allergen challenge in allergic subjects. This study compared a controlled challenge with clinically relevant doses of inhaled and injected histamine, as indicative of an allergic response, in an attempt to validate the use of urinary histamine or 1-methylhistamine measurements as an objective, non-invasive diagnostic test. 2. Inhalation of histamine produced peripheral vasodilation, increased heart rate, a fall in partial expiratory flow rate (pEFR) and blood pressure, 'tight chest' and cough. Subcutaneous injection produced vasodilation and headache but no change in heart rate or blood pressure. 3. Plasma histamine concentrations were similar in the two studies. Inhalation of increasing doses of histamine through a nebuliser (output 0.13 ml min-1) resulted in an increase from a mean of 0.30 to 1.65 ng ml-1, with return towards baseline within 20 min. Injection of 1 mg histamine s.c. produced an increase from 0.32 to 1.4 ng ml-1 within 5 min, remaining above 1 ng ml-1 for 30 min. 4. There was a significant increase of 15.2 ng mg-1 creatinine in urinary histamine concentration following the injection of histamine (P = 0.04) and an increase of 11.4 ng mg-1 creatinine when histamine was given by inhalation (P = 0.18). Histamine excretion rate increased by 108 ng min-1 (P = 0.04) after inhalation and by 37.2 ng min-1 (P = 0.09) after injection. Urinary 1-methylhistamine concentrations were significantly raised following both histamine inhalation (+ 238 ng mg-1 creatinine; P = 0.013) and injection (+ 180 ng mg-1 creatinine; P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma concentrations and urinary excretion of histamine after inhalation and subcutaneous injection of histamine. 844 35

Histamine poisoning is a foodborne chemical intoxication resulting from the ingestion of food products containing high levels of histamine. Historically, histamine poisoning has been attributed to the consumption of fish species belonging to the Scomberesocidae and Scombridae families and other sea fish, but histamine poisoning outbreaks may occur after the consumption of cheese, or other types of fermented foods. Also tyramine has been proved as a cause of adverse reactions, involving headache, hypertensive crisis and interactions with antidepressive drugs, which were observed after consumption of ripening cheeses. The formation of high levels of histamine and tyramine in foods is directly correlated to the level of microorganisms, possessing the enzymes: histidine and tyrozyne decarboxylases, and also with the concentration of histidine and tyrosine free substrate. Proteolysis, which takes place during ripening of cheeses may play role in the release of free histidine and tyrosine. This study reports on the levels of histamine and tyramine in ripening cheeses taken from Polish food market. 43 samples of soft and hard cheeses were investigated. Histamine was measured according to the AOAC fluorometric method. Tyramine was measured after column separation and purification, according to the spectrofluorometric technique with 1-nitroso-2-ortophtalate aldehyde, according to Carou with couple of modifications by authors. Histamine levels ranged from 0 to 157 mg/kg and tyramine levels ranged from 3.8 to 575 mg/kg. The very high levels of histamine and tyramine in many samples of cheeses support the opinion, that sometimes the storage temperature has not been sufficient to stop bacterial multiplication and in consequence enzymatic activity of decarboxylases of native amino acids--precursors of biogenic amines in ripening cheeses.
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PMID:[Level of histamine and tyramine in ripening cheeses]. 855 64

Peripheral blasts recovered from patients with acute myelogenous leukaemia (AML) were efficiently lysed by interleukin-2 (IL-2)-activated heterologous natural killer (NK) cells in vitro. The IL-2-induced killing of AML blasts was inhibited by monocytes, recovered from peripheral blood by centrifugal elutriation. Histamine, of concentrations within the micromolar range, abrogated the monocyte-induced inhibition of NK-cells; thereby, histamine and IL-2 synergistically induced NK-cell-mediated killing of AML blasts. The effect of histamine was apparently mediated by H2-type histamine receptors (H2R), since the H2R antagonist ranitidine completely blocked the response. Based on these in vitro findings, seven patients with AML in first (n=2), second (n=3) or third (n=2) complete remission (CR) were given home therapy with interleukin-2 (IL-2; O.9 x 10(6) IU x 2 s.c.) and histamine (0.4 - 0.7 mg x 2 s.c.) in cycles of 21 d, separated by 6-week intervals. The patients also received treatment with low dose cytarabine and thioguanine between cycles of histamine/IL-2. Toxicity was moderate and include local reactions to IL-2 at the site of injection and short-lasting flush, hypotension, and headache to histamine. The addition of histamine to treatment with IL-2 significantly enhanced the accumulation of CD25+ T cells in peripheral blood as compared to treatment with IL-2 alone (P< 0.003). Five patients remain in complete remission at 9, 18, 21, 24 and 26 months; the two patients in CR3 relapsed after 8 and 33 months, respectively. In the five patients with earlier relapse, the duration of remission after treatment with histamine/IL-2 has in each case exceeded that of previous remissions. We conclude that (i) histamine and IL-2 synergize to kill human AML blasts in vitro, and (ii) histamine/IL-2 is a safe and feasible approach to immunotherapy of AML which merits further investigation.
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PMID:Remission maintenance therapy with histamine and interleukin-2 in acute myelogenous leukaemia. 861 26

Headache can be induced by histamine in wine in patients suffering from histamine intolerance, a disease characterized by impaired histamine degradation based on reduced diamine oxidase activity or a lack of the enzyme. Diamine oxidase is localized in the jejunal mucosa and is the most important enzyme metabolising histamine. It is competitively inhibited by alcohol and numerous drugs. In preliminary investigations, assessment of diamine oxidase levels gave decreased activity (0.03 nKat/l) in patients with histamine intolerance compared to healthy controls (0.07 nKat/l). In pregnancy, diamine oxidase levels are known to be about 500-fold elevated, giving mean levels of 25.0 nKat/l. Other biogenic amines such as phenylethylamine or serotonin may be causative for wine/food-induced headache. In experimental models, headache has been induced by histamine infusion as well as red wine provocation. Histamine-induced headache is a vascular headache likely to be caused by nitric oxide which probably represents a key molecule in vascular headaches. A histamine-free diet is the treatment of choice for patients with histamine intolerance and chronic headache. To start treatment, an antihistamine (H1 blocker) for 14 days as well as a histamine-free diet for at least 4 weeks are recommended. Clinical improvement to the diet as well as in vitro tests for plasma histamine and diamine oxidase in the serum as well as vitamin B6 levels have to confirm the diagnosis. As supportive treatment, a vitamin B6 (pyridoxal phosphate) substitution appears useful in histamine-intolerant patients as pyridoxal phosphate seems to be crucial for diamine oxidase activity. Histamine intolerance, based on reduced diamine oxidase activity or a lack in the enzyme is causative for wine/food-induced chronic headache. According to the localization of diamine oxidase in the jejunal mucosa, histamine intolerance is primarily a disease of intestinal origin. A histamine-free diet is the treatment of choice in histamine-intolerant patients suffering from chronic headache. In addition, it is also important to avoid diamine-oxidase-blocking drugs and alcohol which act as inhibitors of diamine oxidase. As avoidance of histamine-rich food is simple, inexpensive and harmless treatment, histamine-containing food such as cheese and alcoholic beverages should be labeled.
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PMID:Wine and headache. 864 81

Numerous undesirable reactions to alcoholic beverages, foods, drugs and other substances are characterized by allergy-like signs and symptoms and yet show unambiguously negative allergy test results. Such persons should be assessed for evidence of histamine intolerance caused by histamine overload and/or diamine oxidase deficiency. Diamine oxidase is the main histamine degrading enzyme with a predominantly gut activity. This would explain why nutritional allergies are often primarily suspected. The clinical evidence for histamine intolerance is based on chronic headache, diarrhoea, vomiting, flush, urticaria, asthma-like symptoms, rhinitis and others. Histamine restricted food, supported if necessary by H1 antihistamine blockade are simple but highly efficacious measures as shown by us in large patient groups. Intolerance to red wine probably is the most outstanding clinical characteristic and a directed question must be included into any allergy history in order to avoid missing a very major diagnostic spectrum with good therapeutic maneuverability.
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PMID:[Pseudo-allergies are due to histamine intolerance]. 901 5

Histamine in food may be responsible for some cases of food intolerance. We previously demonstrated disturbances in the metabolism of ingested histamine in patients with chronic urticaria (CU) and proposed that this could be related to increased intestinal permeability to histamine. The present study was undertaken to look for ultrastructural changes in the intestinal tract that might explain this abnormality. We examined duodenal biopsies from seven patients with CU before and after intraduodenal administration of histamine (120 mg). Five subjects had clinical symptoms (diarrhea, urticaria, headache, accelerated heart rate, and drop in blood pressure) within 1 h of duodenal histamine challenge (DHC). Ultrastructural changes, including edema of the interstitial tissue, enlargement of the basal intercellular spaces, slight congestion of the endothelial cells, and pericapillary edema, were observed in six subjects 45 min after DHC. In all the biopsies, the epithelium was normal, and the tight junctions were not modified by DHC. This morphologic study demonstrates that histamine can induce edema in the basal intercellular spaces of the duodenal mucosa and in the submucosa without evident change in the integrity of intercellular junctions. The most plausible route for histamine to have taken would appear to be an intracellular one.
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PMID:Ultrastructural changes in the duodenal mucosa induced by ingested histamine in patients with chronic urticaria. 902 Apr 24

The aim of the present study was to examine if the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) can stimulate histamine release from mast cells in the dura mater and thereby play a role in cranial vasoregulation and local neurogenic inflammation. Dura mater mast cells were compared with peritoneal mast cells in the rat. Histamine was released from dura mater mast cells by compound 48/80, SP and CGRP but from peritoneal mast cells only by compound 48/80 and SP. NPY and VIP released quite small amounts of histamine from dural mast cells. The release of SP and CGRP from rat dura mater mast cells was blocked by the receptor antagonists FK888 and CGRP8-37 respectively, suggesting receptor mediated release mechanisms. None of the stimuli released histamine from human or porcine dural mast cells, possibly because the sampling procedure injures and incapacitates the cells.
Cephalalgia 1997 May
PMID:Release of histamine from dural mast cells by substance P and calcitonin gene-related peptide. 917 Mar 35


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