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)

The hyperimmunoglobulinaemia D and periodic fever (hyper-IgD) syndrome is typified by recurrent unpredictable febrile attacks with abdominal pain, joint involvement (arthralgias/arthritis), headache, skin lesions and a polyclonal elevation of serum IgD (> 100 U mL-1). Interferon-gamma (IFN-gamma) is a major proinflammatory cytokine which could play a role in the pathogenesis of the attacks. There is a need for parameters (if possible non-invasive) to monitor disease activity. A potential candidate is neopterin which is released by monocytes/macrophages when stimulated with IFN-gamma, excreted unchanged in urine, and appears to be an early and sensitive marker for activation of the immune system. We measured rectal body temperature, serum IFN-gamma, and urine neopterin in 10 hyper-IgD patients both during and between attacks. The body temperature rose to a mean of 38.9 degrees C on the first day of the attack and normalized within 5 days. Serum IFN-gamma during the first day of the attack was 2.98 IU mL-1 and was significantly lower during remissions. The urine neopterin excretion was 268 +/- 170 mumol mol-1 creatinine between attacks and was significantly increased to 638 +/- 275 mumol mol-1 creatinine on the first day of symptoms. Maximal urine neopterin values were reached on the fourth day of the attack (1051 +/- 387 mumol mol-1 creatinine) and excretion gradually declined and attained values below 400 mumol mol-1 creatinine after 9 days. There was a good correlation between serum IFN-gamma and urine neopterin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interferon-gamma and urine neopterin in attacks of the hyperimmunoglobulinaemia D and periodic fever syndrome. 749 43

Interferon-gamma (IFN-gamma) is produced by activated T cells and probably by NK cells. Its production can be induced by mitogens, antigens and other molecules. IFN-gamma interacts with cells by binding to specific membrane receptors. IFN-gamma--1b is an Escherichia coli--derived recombinant DNA product, which has biological activity identical to natural human IFN-gamma. This IFN type is a more potent immunomodulator than IFN-alpha and IFN-beta. Long term treatment with a therapeutic dosage of IFN-gamma--1b produces a significant reduction in the incidence of serious infections in patients with chronic granulomatous disease. This cytokine can be also useful in the treatment of patients with visceral leishmaniasis, Epstein-Barr virus infections, lepromatous leprosy and other infectious diseases. Phase I and II studies have demonstrated it to be capable of producing antitumor effects, especially in metastatic renal cell carcinoma and some hematologic malignancies. Clinical trials have suggested efficacy of IFN-gamma in the treatment of severe atopic dermatitis and rheumatoid arthritis. The most common adverse reactions are fever, headaches and erythema at the injection site.
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PMID:[Biological properties and clinical applications of interferon gamma (IFN-gamma)]. 820 10

Interleukin 1 alpha (IL-1 alpha) is a cytokine with pleiotropic effects, including cytotoxic-cytostatic activity against some tumor cell lines. We have conducted a phase I study of recombinant human IL-1 alpha (rhIL-1 alpha) in 17 patients with refractory malignancies to examine its toxicity and biologic activity. rhIL-1 alpha was given as a 2-h IV infusion daily for 5 days at five dose levels (0.08, 0.2, 0.8, 2.0, and 5.0 micrograms/m2). Seventeen patients with malignancies were treated, with no objective tumor responses noted. Common toxicities included: fever (100%), rigors and/or chills (96%), myalgia (54%), and headache (48%). Three patients developed grade III hypotension. The maximum tolerated dose was 2.0 micrograms/m2. rhIL-1 alpha induced a significant increase in absolute neutrophil count over baseline (p < 0.05), a delayed but significant increase in platelet count over baseline (p < 0.05), and there was a marked increase in the number of progenitors [colony-forming units (CFU)-G, CFU-M, CFU-GM, CFU-GEMM and burst-forming units (BFU-E)] observed in the peripheral blood. Nine of 12 evaluable patients showed an increase in bone marrow cellularity or myeloid:erthyroid ratio. Immunophenotyping did not demonstrate an increase in peripheral blood or bone marrow CD34+ cells. Interferon-gamma-mediated monocyte cytotoxicity (MCCTX) was significantly enhanced from baseline (p < 0.001), although an increase in direct MCCTX did not reach statistical significance. In summary, rhIL-1 alpha administration is well tolerated at a dose of 2.0 micrograms/m2 with fever, rigors, myalgia, and headache being the most frequent toxicities. Although there were no objective tumor responses, we have demonstrated significant biologic activity with increased neutrophil and platelet counts, increased peripheral blood progenitor cells, and enhanced interferon-gamma-mediated MCCTX.
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PMID:Biologic activity of interleukin 1 (IL-1) alpha in patients with refractory malignancies. 978 99

In the present study, 23 patients with migraine without aura were monitored during a migraine attack. Plasma levels of interleukin (IL)-4, IL-5, IL-10, and interferon-gamma were measured by enzyme-linked immunosorbent assay techniques. Interestingly, we observed low to undetectable IL-5 and IL-4 levels, whereas high IL-10 levels were seen in 52.2% of the patients. Interferon-gamma plasma levels were undetectable in all patients. After treatment with sumatriptan, 10 patients showed a subsequent decrease in IL-10 and an increase in both IL-4 and IL-5 plasma levels. Although these findings are derived from a limited number of patients, the apparent return to the IL-4 and IL-5 cytokine profile observed during the interictal period leads us to speculate that a preferential enhancement of TH2-type cytokine production may contribute to the pathogenesis of migraine.
Headache 2001 Sep
PMID:Immunological aspects in migraine: increase of IL-10 plasma levels during attack. 1157 99

Interferon-gamma release assay (IGRA) using specific tuberculous antigens is a rapid, specific and sensitive method for the detection of tuberculous infection, and usually done in peripheral blood sample. We examined IGRA in cerebrospinal fluid (CSF) in a patient strongly suspected of having tuberculous meningitis. A 53-year old woman had a month history of headache and fever with meningeal sign. Routine systemic bacterial, tuberculous and viral analyses all resulted in negative study except for increase of adenosine deaminase in CSF. Neither of antibacterial or antiviral treatments were effective, but she was successfully treated with antituberculous agents. In IGRA, the interferon-gamma concentration in her CSF was high in the background level and increased further after the antigen stimulation, suggesting theoretically that tuberculous antigen-specific T cells were presented in her CSF. IGRA of CSF in combination with peripheral blood-IGRA could be a useful and rapid method for diagnosing active tuberculosis in the central nervous system.
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PMID:[Interferon-gamma release assay in cerebrospinal fluid of a patient with tuberculous meningitis: a case report]. 1971 72

We report a 59-year-old immunocompetent man presenting with slowly progressive gait unsteadiness, dysarthria, and clumsiness in writing over 6 months. There were bilateral pyramidal signs, pseudobulbar palsy, and attention deficits. Cerebrospinal fluid examination showed mild mononuclear pleocytosis, and magnetic resonance imaging revealed pachymeningeal pattern of contrast enhancement beneath the calvarium and the posterior cranial fossa. Interferon-gamma release assay in whole blood after stimulation by specific tuberculosis antigens was positive and repeat polymerase chain reaction assay detected Mycobacterium tuberculosis genome in the cerebrospinal fluid. After combination therapy with anti-tuberculous agents and corticosteroids, the patient's pachymeningitis regressed. Tuberculous cranial pachymeningitis may present with chronic diffuse brain dysfunction without headache, fever, or cranial nerve dysfunction.
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PMID:[Tuberculous cranial pachymeningitis presenting with long-standing diffuse brain dysfunction]. 2159 96