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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary excretion of histamine, as well as histaminuria following intravenous L-histidine loading, were studied in patients with so-called vascular headache. It was found that urinary excretion of histamine was increased on one or more occasions in 7 of 22 patients with cluster headache. The excretion was significantly higher on attack days than on attack free days. With migraine, increased excretion was found in 5 of 31 patients on days of an attack, whereas the corresponding figure for headache free days was 7 of 24 patients. Three patients showed increased histamine excretion during, as well as between, attacks. The excretion on attack days was not significantly different from that on attack free days. In cluster headache patients, L-histdine administration on attack days did not indicate that an increased histamine formation took place under such circumstances. The underlying mechanism behind the increased histamine output with cluster headache may be increased formation or liberation or altered catabolism. Histamine is more likely to be a consequence than the cause of an attack of cluster headache.
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PMID:Urinary histamine excretion in migraine and cluster headache. Further observations. 7 5

Out of 19 patients with extrinsic bronchial asthma challenged with 123 mug histamine acid phosphate by intravenous infusion only 13 responded with a fall in FEV1 of over 10% (mean 16%). Seventeen of these patients were given histamine 2 mg/ml by aerosol, and all responded with a mean decrease in FEV1 of 37.8%. When challenged with allergen extract by aerosol the mean decrease in FEV1 was 37.5%. After 40 mg sodium cromoglycate 15 of the 17 patients showed significant protection against allergen challenge with a mean decrease in FEV1 of only 23.6%. Inhalation of 40 mg sodium cromoglycate, however, failed to protect against histamine given by either the intravenous or aerosol route. Histamine given intravenously to asthmatic patients produces less of a bronchial response than when given by aerosol, even though the intravenous route produces many more systemic symptoms, such as flushing and throbbing headache. The protection of sodium cromoglycate against an allergen inhalation challenge is not due to histamine antagonsim.
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PMID:Bronchial reactivity to histamine before and after sodium cromoglycate in bronchial asthma. 81 11

Histamine release and leukotrienes (LTB4 and LTC4) production from circulating basophil have been studied in 13 patients with episodic cluster headache (CH) during the remission phase of symptoms, and in 9 normal subjects. Cell suspensions of basophils were stimulated with scalar dilutions of anti-IgE, f-met-peptide and Ca2+ ionophore A23187. Histamine was measured by an automated fluorimetric method; LTB4 and LTC4 with RIA in individual cases, and with Reverse-Phase HPLC in the two pools obtained from the supernatants of CH patients and controls. Mean values of histamine release in patients with CH were significantly lower when compared to those obtained in control subjects after stimulation with anti-IgE at the three dilutions used. LTC4 mean levels measured in CH patients were significantly lower than those of supernatants from controls after stimulation with 0.05 gamma/ml of A23187. A reduction of LTC4 and LTB4 levels in CH patients was also observed in R-P HPLC, which showed different elution patterns in the two groups. The histamine release in individual cases was related to leukotriene production: LTC4 levels were significantly (p less than .05) higher in "high histamine releasers" than in "low histamine releasers". Our results indicate that CH patients have complex abnormalities of histamine release and of leukotriene production during the painless phase of the disease.
Headache 1989 Jan
PMID:Basophil histamine release and leukotriene (LTB4-LTC4) production in cluster headache. 246 13

Histamine is well recognized as a product of both mast cells and basophils. Its release from these sources in IgE-mediated reactions unquestionably contributes to the allergic response. It is often stated that ingestion of foods rich in histamine can result in absorption of sufficient histamine to provoke signs and symptoms reminiscent of an allergic reaction. A review of literature relevant to this issue suggests that certain foods do indeed contain histamine as measured by current methodology. Further, histamine ingestion in excess of 36 to 250 mg may or may not result in a clinical response which includes abdominal complaints, feelings of warmth, flushing and headache. Taken together, this evidence supports the hypothesis that ingestion of large amounts of histamine-containing foods or foods which contain the histamine precursor, histidine, under some circumstances can result in adverse reactions.
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PMID:Histamine in foods: its possible role in non-allergic adverse reactions to ingestants. 330 58

Between 1976 and 1986, 258 incidents of suspected scombrotoxic fish poisoning were reported in Britain. Histamine analysis was carried out on 240 fish samples from these incidents, and 101 were found to contain greater than 5 mg histamine/100 g fish. The symptoms most consistently reported were rash, diarrhoea, flushing and headache. In recent years there has been a decrease in the number of confirmed scombrotoxic outbreaks and a trend towards more sporadic incidents. Of fish samples with greater than 20 mg histamine/100 g, 94% were from incidents in which scombrotoxic symptoms were characteristic, but where fish had 5-20 mg/100 g only 38% of incidents were clinically distinctive. Guidelines are presented based on the interpretation of quantitative histamine analysis of fish samples from scombrotoxic poisoning incidents.
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PMID:Scombrotoxic fish poisoning in Britain: features of over 250 suspected incidents from 1976 to 1986. 342 80

The Oriental flushing reaction is an adverse response to alcohol that appears to be genetically determined. In this study, the Oriental flushing reaction that was produced with ingestion of small amounts of alcohol was antagonized by antihistamine administration. A group of 17 subjects was tested. Each subject received placebo, diphenhydramine 50 mg (H-1 receptor antagonist), and cimetidine 300 mg (H-2 receptor antagonist) singularly and in combination. Alcohol was then administered orally. Most subjects given placebo experienced the typical flushing reaction that included a cutaneous flush, increase in skin temperature, decrease in blood pressure, increase in pulse rate and subjective symptoms such as dizziness, sleepiness, anxiety, headache, generalized weakness, and nausea. The flush, temperature and systolic hypotension were significantly blocked by the combined antihistamine administration. Cimetidine given alone blocked the flush, temperature increase, and systolic hypotension significantly more than diphenhydramine but less than the combined antihistamines. Diphenhydramine was similar to placebo in its effect on the flushing reaction. The role of histamine in the expression of tolerance to alcohol is not known. Antihistamine antagonism of the adverse flushing reaction suggests that histamine receptors may participate in the intolerance to ethanol in Orientals. Histamine may be an important protective factor in the low prevalence of alcoholism in Orientals.
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PMID:Histamine receptor antagonism of intolerance to alcohol in the Oriental population. 368 Dec 77

Histamine skin tests were performed in the painful area and on the opposite side in ten cluster headache patients. The studies were carried out with and without local anaesthesia. No differences between histamine skin response in the painful region compared with the contralateral side were revealed. This study concerns the part of the triple response which is the result of a direct action of histamine on the skin vasculature (mediated by both H1 and H2) histaminergic receptors, i.e. wheal and redness, and the flare, which is the result of neurohumoral mechanisms.
Cephalalgia 1985 Jun
PMID:Cluster headache: histamine skin tests in the painful area. 401 21

Spontaneous histamine release (SHR) from leucocytes (basophils) of 27 migraine patients was investigated during various phases of attack. Mean SHR during the first 3 h of attack (33.7%) was increased compared with the mean SHR from leucocytes of healthy persons (15.9%), but differed insignificantly from the mean SHR in symptom-free periods. Histamine release (HR) from leucocytes of healthy persons suspended in migraine sera from different time-periods of attack was also increased compared with HR in control sera, i.e. high HR could be induced by passive transfer of serum. But the mean HRs in sera from different time-periods of attack were insignificantly different from the mean HR in sera from symptom-free periods. The increased SHR may contribute to vascular hyperreactivity in migraine.
Cephalalgia 1984 Jun
PMID:Histamine release from leucocytes during migraine attack. 673 82

Regional cerebral blood flow (rCBF) was measured using the intra-arterial 133Xe technique in 35 or 256 areas of a hemisphere. In seven patients rCBF was measured in the resting state and following intracarotid (i.c.) infusion of histamine 10-50 microgram/min. In four patients histamine was infused intravenously in a dose of 25-40 microgram/min. Histamine caused no significant change in mean arterial blood pressure or arterial PCO2. There was no significant change in mean hemispheric blood flow during i.v. or i.c. histamine infusion. No change in the regional distribution of hemispheric blood flow was observed. Experimental histamine headache is most likely of extracranial origin.
Cephalalgia 1982 Mar
PMID:Effect of histamine on regional cerebral blood flow in man. 711 37

An 11-yr-old girl presented with a history of urticaria induced by warm or cool showers, exercise, and emotional stimuli. During evaluation she repeatedly developed generalized punctate urticaria, pruritus, palpitations, and headaches after warm baths or exercise, and she had a positive methacholine skin test. She developed similar lesions and pruritus after local application of sterile water, tap water, ethanol, normal saline, or 3% saline. The diagnosis of combined aquagenic and cholinergic urticaria was made and presented a unique opportunity to study and compare mediator release and clinical symptoms in both conditions. The patient was submerged in bath water at either 37 degree or 41 degree C to induce either aquagenic or cholinergic urticaria, respectively. Histamine was released into the systemic circulation in both conditions in a similar time course; however, systemic symptoms occurred only after the 41 degree C bath. After failure to induce tolerance to the 41 degree C bath water, hydroxyzine therapy was instituted. One week later she was rechallenged; few symptoms appeared, and a rise in serum histamine was not detected as had been shown in previous challenges. The data suggest that in our patient, hydroxyzine may have contributed to the inhibition of both histamine release and the appearance of symptoms during hot bath challenging.
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PMID:Evaluation of a patient with both aquagenic and cholinergic urticaria. 731 13


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