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)

Human immunodeficiency virus (HIV), is able to replicate in many human cells such as helper lymphocytes, monocytes/macrophages and glial cells. Monocytes/macrophages must be considered an important reservoir of HIV in vivo and a producer of cytokines such as Interleukin-1 (IL1) and tumor necrosis factor (TNF). These substances lead to an autocrine feedback loop that produces an increased virus replication and a secondary induction of other cytokines such as Interleukin 6 (IL6) and granulocyte-macrophage colony stimulating factor (GM-CSF). These cytokines all together may be responsible for many clinical aspects of the disease such as headache, fever, anorexia, subtle cognitive changes, motor disfunctions and cachexia. The future strategies in the treatment of AIDS must be a combination of drugs acting on different points of viral replication and with synergistic potential. Omega 3 polyunsaturated fatty acids (omega-3) can be considered a candidate for their pleiotropic effects on immunological and metabolic systems. In particular, their use is considered for their ability to decrease IL1 and TNF production by monocytes/macrophages, as demonstrated by many authors. The decreased induction of these cytokines and consequently of IL6 and acute phase proteins may have beneficial effects on many clinical manifestations of AIDS such as cachexia.
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PMID:Omega-3 fatty acids as coadjuvant treatment in AIDS. 828 91

We report on a patient with clusterlike headache and multiple brain metastases of lung cancer. Initially, cluster headache was suggested clinically by characteristic symptoms without any focal central nervous system signs. However, magnetic resonance imaging demonstrated multiple brain metastases. It is possible that tumor necrosis factor may have played a role in initiating the clusterlike headache.
Headache 1996 Apr
PMID:Clusterlike headache as a first sign of brain metastases of lung cancer. 867 34

The role of infliximab in managing Crohn's disease (CD) is described. CD is characterized by chronic transmural inflammation at various sites of the gastrointestinal tract, particularly the ileum and colon. The major symptoms are diarrhea, abdominal pain, enterocutaneous and perianal fistulas, and weight loss. Management goals include alleviating symptoms, inducing remission, promoting healing of the intestinal mucosa and fistulas, and modifying the disease process. Drugs traditionally used to manage CD are aminosalicylates, antimicrobials, immunomodulatory agents, and corticosteroids. Infliximab is a chimeric (human-mouse) monoclonal antibody targeted at human tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine important in the pathogenesis of CD. Infliximab antagonizes the biological activity of TNF-alpha by binding to it on macrophage and T-cell surfaces. Clinical trials have shown infliximab to be effective in producing and maintaining a clinical response in patients with refractory, moderate to severe CD. Treatment helps promote healing of intestinal mucosa and closure of fistulas. Infliximab may act more rapidly than most traditional agents and produces less severe adverse effects. The most frequent adverse effects are headache, nausea, and upper-respiratory-tract infections. The recommended dosage is 5 mg/kg i.v. infused over a two-hour period. Infliximab may be given at eight-week intervals for maintenance or management of flare-ups. Infliximab appears useful in the treatment of CD and may improve patients' quality of life.
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PMID:Treatment of Crohn's disease with infliximab. 1122 67

E5564 is a second-generation synthetic analogue of the lipid A component of endotoxin (lipopolysaccharide [LPS]). The ability of E5564 to block the toxic activity of LPS was assessed in a double-blind, placebo-controlled study. A bolus infusion of endotoxin (4 ng/kg) was administered to healthy subjects to induce a mild transient syndrome similar to clinical sepsis. Single E5564 doses of 50-250 microg ameliorated or blocked all of the effects of LPS in a dose-dependent manner. All E5564 dose groups had statistically significant reductions in elevated temperature, heart rate, C-reactive protein levels, white blood cell count, and cytokine levels (tumor necrosis factor-alpha and interleukin-6), compared with placebo (P<.01). In doses of > or = 100 microg, E5564 acted as an LPS antagonist and completely eliminated these signs. E5564 also blocked or ameliorated LPS-induced fever, chills, headache, myalgia, and tachycardia (P<.01). These results demonstrate that E5564 blocks the effects of LPS in a human model of clinical sepsis and indicate its potential in the treatment and/or prevention of clinical sepsis.
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PMID:Blocking of responses to endotoxin by E5564 in healthy volunteers with experimental endotoxemia. 1259 80

We investigated whether anti-inflammatory effects of treatment with granulocyte colony-stimulating factor (G-CSF, filgrastim) are mediated via prostaglandin E(2) (PGE(2)) induction. In a double-blind crossover study, 10 healthy volunteers received 300 microg of filgrastim or saline 1 week apart. This was repeated after oral administration of 50 mg of flurbiprofen 1 h before injection. The increase in neutrophilic granulocytes initiated by G-CSF was augmented significantly by flurbiprofen. Lipopolysaccharide-induced PGE(2) and thromboxane (TxB(2)) release were increased 8 h after G-CSF treatment. This increase was abrogated by flurbiprofen. However, flurbiprofen did not affect G-CSF-mediated decrease in tumor necrosis factor-alpha or interferon-gamma release. Of the volunteers treated with G-CSF, eight reported side effects (headache and bone pain) against none in the saline group. When flurbiprofen was given before injection, one volunteer each reported side effects in the G-CSF and in the saline group. These data show that G-CSF primes for increased PGE(2) and TxB(2) release. Cyclooxygenase inhibition counteracts neither the hematopoietic nor the anti-inflammatory activity of G-CSF but reduces side effects.
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PMID:Granulocyte colony-stimulating factor (filgrastim) treatment primes for increased ex vivo inducible prostanoid release. 1461 Feb 36

Acupuncture has been widely used as a treatment for various conditions like headache and stroke, especially in Asian countries such as Korea and China. But few scientific investigations have been carried out. The aim of the present study is to investigate the effect of acupuncture on the production of inflammatory cytokines in patients with chronic headache (CH). Patients with CH were treated with acupuncture during the acute stage. Clinical signs of CH disappeared markedly after three months of treatment with acupuncture. Peripheral blood mononuclear cells obtained from a normal group and those from the patients with CH, before and after treatment with acupuncture, were cultured for 24 hours in the presence or absence of lipopolysaccharide (LPS). The amount of interleukin (IL)-1beta, IL-6 and tumor necrosis factor-alpha (TNF-alpha) in LPS culture supernatant was significantly increased in the patients with CH compared to the healthy control group (p < 0.05). But those cytokines came down toward the levels of the healthy group (p < 0.05) after treatment with acupuncture, although the levels still remained elevated. Plasma cytokine levels were analyzed to evaluate any change due to acupuncture treatment. There was little difference in the levels of IL-1 or IL-6 due to the treatment with acupuncture in the patients with CH, but significantly reduced plasma levels of TNF-alpha were observed. These data suggest that acupuncture treatment has an inhibitory effect on pro-inflammatory cytokine production in patients with CH.
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PMID:The effect of acupuncture on proinflammatory cytokine production in patients with chronic headache: a preliminary report. 1499 46

The role of B cells and antibodies in the pathogenesis of multiple sclerosis (MS) is controversial. We investigated the expression of B-cell-activating factor of the tumor necrosis factor family (BAFF), a protein indispensable for B-cell survival, and of its three receptors in MS patients and controls. BAFF mRNA levels in monocytes, and BAFF-receptor mRNA in B and T cells, were higher in patients than in healthy controls; yet, BAFF protein levels in cerebrospinal fluid and plasma were similar in patients and headache controls. In addition, each MS disease course was associated with a unique expression pattern for all four molecules.
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PMID:Expression of B-cell-activating factor of the TNF family (BAFF) and its receptors in multiple sclerosis. 1522 51

This report describes a case of aseptic meningitis induced by the tumor necrosis factor-alpha inhibitor infliximab. The patient, a 51-year-old female, was being treated for Crohn's disease. After an infliximab infusion, she had headache, fever, arthralgia, myalgia, and meningismus. Cerebrospinal fluid analysis was remarkable for a neutrophilic pleocytosis and elevated protein. Other potential causes of meningitis were excluded. Her symptoms completely resolved within 24 hours of presentation. Because infliximab commonly causes headache and is very immunogenic, we infer that infliximab-induced meningitis is immune-mediated and underrecognized. Potential risk factors and means for minimizing its occurrence are offered.
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PMID:Infliximab-induced headache and infliximab-induced meningitis: two ends of the same spectrum? 1595 16

Expression of the neuropeptide calcitonin gene-related peptide (CGRP) in trigeminal ganglion is implicated in neurovascular headaches and temporomandibular joint disorders. Elevation of cytokines contributes to the pathology of these diseases. However, a connection between cytokines and CGRP gene expression in trigeminal ganglion nerves has not been established. We have focused on the effects of the cytokine tumor necrosis factor-alpha (TNF-alpha). TNFR1 receptors were found on the majority of CGRP-containing rat trigeminal ganglion neurons. Treatment of cultures with TNF-alpha stimulated CGRP secretion. In addition, the intracellular signaling intermediate from the TNFR1 receptor, ceramide, caused a similar increase in CGRP release. TNF-alpha caused a coordinate increase in CGRP promoter activity. TNF-alpha treatment activated the transcription factor NF-kappaB, as well as the Jun N-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase pathways. The importance of TNF-alpha induction of MAP kinase pathways was demonstrated by inhibiting MAP kinases with pharmacological reagents and gene transfer with an adenoviral vector encoding MAP kinase phosphatase-1 (MKP-1). We propose that selective and regulated inhibition of MAP kinases in trigeminal neurons may be therapeutically beneficial for inflammatory disorders involving elevated CGRP levels.
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PMID:Tumor necrosis factor-alpha stimulation of calcitonin gene-related peptide expression and secretion from rat trigeminal ganglion neurons. 1627 6

Targeting tumor necrosis factor-a has proven of considerable value in treatment for rheumatoid arthritis, with substantial benefits achieved in a proportion of treated patients. However, a significant number of patients do not achieve sufficient improvement and as a result there remains considerable unmet clinical need. A number of cytokines have recently been described with proinflammatory activity in rheumatoid arthritis synovitis, including interleukin (IL)-6, IL-12, IL-15, and IL-18. We review recent data that support the notion that some or all of these moieties offer therapeutic potential. The possibility that some may be useful in partial responders to tumor necrosis factor blocking agents or in synergy with the latter is discussed.
Curr Pain Headache Rep 2005 Dec
PMID:Targeting cytokines beyond tumor necrosis factor-alpha and interleukin-1 in rheumatoid arthritis. 1628 41


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