Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic mastocytosis (SM), as opposed to cutaneous-only mastocytosis, implies the presence of neoplastic mast cell infiltration in extracutaneous tissue. Mast cell disease in adults is often systemic and often involves the bone marrow. Typical clinical and laboratory features of SM include urticaria pigmentosa, mast cell mediator symptoms (eg, headache, flushing, lightheadedness, urticaria and pruritus, nausea, diarrhea, abdominal pain, and vasodilatory shock), bone pain (eg, osteoporosis, lytic bone lesions, and fractures), hepatosplenomegaly, cytopenia, eosinophilia, elevated serum tryptase and histamine, and bone marrow fibrosis and angiogenesis. SM may be indolent (no evidence of organ dysfunction), aggressive (presence of organ dysfunction), associated with another often chronic myeloid hematologic disease (SM-AHD), or present as mast cell leukemia or sarcoma. Mast cell-mediator symptoms are treated with histamine antagonists and cromolyn sodium. Indolent SM does not require cytoreductive therapy. Aggressive SM and SM-AHD are managed based on their molecular profile. Recent information suggests that FIP1-like-1-platelet-derived growth factor receptor-alpha(+) SM responds well to imatinib mesylate, whereas interferon-alpha should be considered as a first-line treatment in all of the other cases, including patients with Asp816Val(+) SM. Cladribine has been shown to be effective in patients who develop resistance to interferon treatment.
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PMID:Systemic mastocytosis: current concepts and treatment advances. 1508 68

Infliximab is a tumour necrosis factor (TNF)-alpha antagonist that has revolutionised the treatment of Crohn's disease and rheumatoid arthritis. However, infliximab therapy can be complicated by a variety of adverse reactions. Acute infusion reactions occur during or shortly after infusion and typically consist of fever, chills, nausea, dyspnoea and headaches. Delayed reactions, characterised by myalgias, arthralgias, fever, rash, pruritus, facial, hand or lip oedema, dysphagia, urticaria, sore throat and headache may occur 3-12 days after infusion. Although the mechanisms of these reactions are not yet clearly defined, emerging evidence indicates that these reactions may be associated with the immune response against infliximab and the development of antibodies to infliximab.A number of studies have identified protective factors that may minimise adverse reactions, presumably related to the immune response against infliximab. Factors that may be protective by helping to establish immune tolerance for the foreign infliximab protein include concomitant administration of immunomodulators or corticosteroids, starting infliximab therapy with a 0, 2, 6-week induction regimen, maintenance dose administration with infusions every 8 weeks or less, and avoiding long periods between infusions. Infliximab therapy also may have other immunological consequences. There is evidence that infliximab may impede the appropriate immune response to a number of pathogens, prohibiting its use in patients with active infections. In addition, patients should be screened and appropriately treated for tuberculosis before initiating infliximab therapy. The development of autoantibodies, such as antinuclear antibody or anti-ds-DNA, has also been described with infliximab therapy, although the development of clinical lupus-like syndrome is rare. While there is a theoretical risk of increased rate of malignancies due to antagonism of TNFalpha, to date there is no clear evidence of such an effect. In addition, cardiac and neurological adverse events associated with infliximab therapy have been described. The mechanism for these adverse events is unclear. In summary, infliximab therapy can be an effective treatment for Crohn's disease; however, a number of immunological consequences and adverse events may complicate the infusion of this agent. Appropriate prophylaxis and therapy of these adverse reactions will allow infliximab to be used safely in the vast majority of patients.
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PMID:Managing immunogenic responses to infliximab: treatment implications for patients with Crohn's disease. 1530 61

Allergen immunotherapy (also called allergy vaccine therapy) involves the administration of gradually increasing quantities of specific allergens to patients with IgE-mediated conditions until a dose is reached that is effective in reducing disease severity from natural exposure. The major objectives of allergen immunotherapy are to reduce responses to allergic triggers that precipitate symptoms in the short term and to decrease inflammatory response and prevent development of persistent disease in the long term. Allergen immunotherapy is safe and has been shown to be effective in the treatment of stinging-insect hypersensitivity, allergic rhinitis or conjunctivitis, and allergic asthma. Allergen immunotherapy is not effective in the treatment of atopic dermatitis, urticaria, or headaches and is potentially dangerous if used for food or antibiotic allergies. Safe administration of allergen immunotherapy requires the immediate availability of a health care professional capable of recognizing and treating anaphylaxis. An observation period of 20 to 30 minutes after injection is mandatory. Patients should not be taking beta-adrenergic blocking agents when receiving immunotherapy because these drugs may mask early signs and symptoms of anaphylaxis and make the treatment of anaphylaxis more difficult. Unlike antiallergic medication, allergen immunotherapy has the potential of altering the allergic disease course after three to five years of therapy.
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PMID:Allergen immunotherapy. 1533 81

Hereditary periodic fever syndromes are a group of systemic disorders characterized by recurrent attacks of systemic inflammation (autoinflammation) without infectious or autoimmune cause. The hyper-IgD syndrome (HIDS) is a rare autosomal recessive inflammatory disorder characterized by recurrent fever, increased serum IgD (normal value < 100 U/ml) and generalized inflammation (lymphadenopathy, arthralgias/arthritis, abdominal complaints, skin rash, and headache). The attacks persist during the entire life although frequency and severity tend to diminish with age. HIDS is caused by specific mutations in the gene encoding mevalonate kinase, resulting in depressed enzymatic activity. At present the therapy for the syndrome is only supportive. Other than HIDS, other hereditary systemic inflammatory disorders have been described: the Familial Mediterranean Fever, the tumour necrosis factor receptor associated periodic syndrome (TRAPS), a disease related to the mutations of one of the TNF receptors, the Familial Cold Urticaria and the Muckle-Wells syndrome. The differential diagnosis with other causes of periodic fever is crucial for assessing appropriate management and treatment.
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PMID:[Hyper-IgD syndrome and other hereditary periodic fever syndromes]. 1547 May 20

Vardenafil is a potent selective and reversible inhibitor of the cGMP phosphodiesterase type 5 that has been shown to improve erectile function in men. Vardenafil is usually well tolerated; the most common adverse events are headache, flushing, rhinitis, sinusitis and dyspepsia. We report a case of a 48-year-old man with an acute episode of widespread urticaria following vardenafil consumption and in absence of other identifiable causative factors. The patient had no previous episodes of urticaria. This appears to be the first report of urticaria associated with vardenafil.
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PMID:Vardenafil-induced generalized urticaria. 1548 93

Aquagenic urticaria (AU) is a rare form of physical urticaria in which contact with water evokes hives. Extracutaneous manifestations of AU have been described but have not been controlled successfully to date. Selective serotonin reuptake inhibitors (SSRIs) have not been used previously in the treatment of AU. The aim of this study was to describe a case of AU with extracutaneous manifestations, to describe a novel treatment approach, and to review the literature on AU. Our patient presented with urticarial lesions and migraine-like headaches after contact with any type of water. A variety of prophylactic medications including antihistamines, anticholinergics, and SSRIs, were used and, ultimately, were successful in controlling the patient's symptoms. AU is a rare condition that can have extracutaneous manifestations. Multiple classes of medications, including SSRIs, may be necessary in the treatment and prophylaxis of such patients. Additional research is needed into the pathogenesis of AU.
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PMID:Aquagenic urticaria with extracutaneous manifestations. 1611 38

Acute urticaria is commonly observed in the prodromic stage of hepatitis A and B infection as well as in hepatitis C infection, although only rare cases have been published regarding the latter. Urticaria is considered one of the pre-icteric symptoms of viral hepatitis and is related to immune-complex deposits; subsequently, it may be associated with arthritis and headache (Caroli's triad). The absence of specific presentation of acute urticaria in patients with viral hepatitis is not surprising because many other viral infections can induce similar cutaneous symptoms. On the other hand, no convincing evidence exists in which hepatitis virus infection caused chronic urticaria. Data are lacking for hepatitis B, but several series and one controlled study showed the absence of a link between hepatitis C and chronic urticaria. Systematic hepatitis virus investigations in patients with chronic urticaria probably are not cost-effective. Hepatitis B or C can occasionally induce urticarial vasculitis, but this is probably related more to vasculitis than to true urticaria.
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PMID:Urticaria and hepatitis. 1646 92

Efalizumab is a recombinant humanised IgG1 kappa isotype monoclonal antibody against the CD11a molecule. Efalizumab is approved for the treatment of moderate-to-severe psoriasis and is currently administered as a weekly subcutaneous injection. Throughout October 2005, 19,000 patients were treated with efalizumab. According to the package insert that is based on 2762 subjects, the most common adverse reactions associated with efalizumab are a first dose reaction complex that includes headache, chills, fever, nausea and myalgia within two days following the first two injections. These reactions are dose-level-related in incidence and severity and were largely mild-to-moderate in severity when a conditioning dose of 0.7 mg/kg was used as the first dose. Adverse events occurring at a rate between 1 and 2% greater in the efalizumab group compared with placebo were arthralgia, asthenia, peripheral oedema and psoriasis. Efalizumab is associated with a rebound flare reaction in approximately 5% of patients when therapy is ceased. Antiefalizumab antibodies develop in approximately 5% of the subjects who were treated with efalizumab, but the clinical significance of these antibodies is unclear. Efalizumab has rare but serious haematological side effects. Immune-mediated thrombocytopenia platelet counts at or below 52,000 cells/microl have been observed in 0.3% of cases and monitoring of platelet counts monthly for the first 3 months of use and each 3 months thereafter. Reports of four cases of haemolytic anaemia diagnosed four to six months after patients started on the monoclonal antibody exist. Infrequent new onset or recurrent severe arthritis events, including psoriatic arthritis events, have been reported in clinical trials and postmarketing surveillance. Symptoms associated with a hypersensitivity reaction (e.g., dyspnoea, asthma, urticaria, angioedema, maculopapular rash) were rarely noted in the first 12 weeks of the controlled clinical studies. The overall incidence of malignancies of any kind was 1.8 per 100 patient-years for efalizumab-treated patients compared with 1.6 per 100 patient-years for placebo-treated patients. One case each of the following serious adverse reactions was observed: transverse myelitis, bronchiolitis obliterans, aseptic meningitis, idiopathic hepatitis, sialedenitis and sensorineural hearing loss. In the complete safety data from both controlled and uncontrolled studies, the overall incidence of hospitalis ation for infections was 1.6 per 100 patient-years for efalizumab-treated patients compared with 1.2 per 100 patient-years for placebo-treated patients. The rate of infection was 26% in the control group and 29% in treated cases. The most common findings on laboratory assessments in patients using efalizumab were reversible increases in lymphocyte count and total white blood cell. Efalizumab is a safe, effective, but expensive treatment for psoriasis.
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PMID:Efalizumab: a review of events reported during clinical trials and side effects. 1650 42

In addition to its U.S. Food and Drug Administration (FDA) approved conditions, immune globulin intravenous (IGIV) is now being used to treat a vast array of autoimmune disorders. Some of the reasons for this overall increase in the use of IGIV include its effectiveness and safety. Despite many years of safe use, side effects and adverse reactions still occur. Common and mild side effects associated with IGIV include: headache, malaise, nausea, low-grade fever, urticaria, arthralgias, and myalgia. These symptoms typically resolve within a few days after their onset. Although rare, the serious and potentially fatal side effects include: anaphylactic reactions, aseptic meningitis, acute renal failure, stroke, myocardial infarction, and other thrombotic complications. Many of these side effects have occurred in patients who have significant, underlying risk factors for the development of the event. Thus, it is vitally important that a thorough and comprehensive medical evaluation be performed on every patient who is being evaluated for potential IGIV therapy. This evaluation can, to some extent, significantly minimize the risk of these side effects. Careful, constant, and close monitoring by trained personnel during the infusion can also result in early detection of such events. Physicians should thoroughly discuss the risks and benefits of IGIV with patients who are being considered for this therapy.
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PMID:Adverse events associated with intravenous immunoglobulin therapy. 1650 16

The reported incidence of hypersensitivity reactions (HSRs) associated with oxaliplatin in patients with colorectal cancer (CRC) is approximately 12%, with 1 - 2% of patients developing grade 3 or 4 in severity. However, the recent rising incidence of HSR to oxaliplatin observed is the result of increasing clinical use. HSR to oxaliplatin may manifest as facial flushing, rash/hives, tachycardia, dyspnoea, erythema, pruritus, fever, tongue swelling, headache, chills, weakness, vomiting, burning sensations, dizziness and oedema. Anaphylactic shock is rare but serious, and must be considered in the event of hypotension. No definitive approaches to prevent and treat HSR associated with oxaliplatin are available; however, few successful strategies have been reported. Such strategies include: slowing the infusion rate, use of steroids and antagonists of type 1 and 2 histamine receptors, and desensitisation. Successful implementation of oxaliplatin desensitisation protocols based on other platinum-containing compounds have been reported, which could enable a small number of patients who experience severe HSR to further receive an effective therapy for CRC. However, reintroductions have only been reported as single case studies or small cohorts. Large-scale validation on desensitisation strategies are still missing. Recently, subcutaneous adrenaline has also been utilised as an alternative approach to manage HSR to oxaliplatin. Knowledge of this rare but real toxicity of oxaliplatin is paramount because the use of this drug continues to increase not only for the treatment of patients with stage II-IV CRC, but also other solid malignancies. In this article, the author discusses the incidence, clinical presentation, pathogenesis, risk factors and current strategies of management of HSR associated with oxaliplatin.
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PMID:Hypersensitivity reactions associated with oxaliplatin. 1690 58


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