Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of the myeloid growth factor G-CSF after allogeneic hematopoietic stem cell transplantation is usually well tolerated, and associated with rapid hematopoietic engraftment. We report a high incidence (50%) of side-effects associated with post-transplant G-CSF in patients with chronic phase chronic myeloid leukemia undergoing allogeneic HLA-identical sibling peripheral blood stem cell transplantation. One or more of the following signs and symptoms were observed shortly after the subcutaneous injection of G-CSF: dyspnea, chest pain, nausea, hypoxemia, diaphoresis, anaphylaxis, syncope and flushing. These reactions led to discontinuation of G-CSF in the majority of patients. Predictive factors could not be identified, and the underlying mechanism leading to these reactions is unknown.
 ...
PMID:Adverse side-effects associated with G-CSF in patients with chronic myeloid leukemia undergoing allogeneic peripheral blood stem cell transplantation. 1084 33

A 15 year old female with uterus bicornis bicollis was admitted for operation. She had a history of atopic dermatitis and allergy to buckwheat, raw egg and latex. Two months previously she had developed whole body flushing during dental treatment, and latex glove used by the dentist had been suspected as the cause. Prior to the operation she underwent internal examination and intrauterine echogram in which a latex glove was carelessly used by another gynecologist who had not confirmed her past history. After 30 minutes, dyspnea and urticaria without itching, appeared suddenly. Blood pressure decreased to 80/50 mmHg and heart rate increased to 120 beats.min-1. She was then transferred to our ICU. Methylprednisolone was administered intravenously for dyspnea and circulatory collapse. After 3 hours, the patient made an uneventful recovery. The increased plasma latex protein-specific IgE levels confirmed anaphylaxis to latex. The increasing incidence of potentially life-threatening allergic reactions to latex has caused mounting concern over recent years. We may suspect latex allergy when an anaphylaxic reaction or shock of unknown origin occurs. In hospitals, latex free products must be prepared for use with latex allergic patients and for protection of medical staff with this allergy.
 ...
PMID:[A case of anaphylaxic shock due to latex glove used on internal examination and on the probe of intrauterine echogram]. 1102 62

Anaphylaxis is an acute fatal or potentially fatal hypersensitivity reaction. Anaphylaxis represent a clinical diagnosis based on history and physical examination and includes symptoms of airway obstruction, generalized skin reactions, particularly flushing, itching, urticaria, angioedema cardiovascular symptoms including hypotension and gastrointestinal symptoms. These symptoms result from the action of mast cell mediators, especially histamine and lipid mediators such as leukotrienes and platelet activating factor on shock tissue. The shock tissue includes blood vessels, mucous glands, smooth muscle, and nerve endings. Anaphylaxis follows the typical immediate hypersensitivity time course, with a reaction beginning within minutes of antigen exposure. A late-phase reaction hours after the initial reaction may occur. Mast cell mediator release can be triggered by both IgE and non--IgE-mediated factors. Therefore, anaphylaxis may be termed anaphylaxis (IgE mediated) or anaphylactoid (non--IgE mediated). The most common IgE-mediated triggers are drugs, typically penicillin or other beta-lactam antibiotics, foods, most commonly nuts, peanuts, fish and shellfish, or hymenoptera stings. Non-IgE-mediated causes include factors causing marked complement activation such as plasma proteins or compounds which act directly on the mast cell membrane, such as vancomycin, quinolone antibiotics, or radiographic contrast media. The pathophysiology of some trigger factors, such as aspirin, remains unclear. Therapy of anaphylaxis revolves around patient education, avoidance, desensitization or pharmacologic pretreatment when agents causing anaphylaxis need to be readministered, and early recognition and prompt therapy of reactions should they occur.
 ...
PMID:Anaphylaxis and Anaphylactoid Reactions: Diagnosis and Management. 1186 83

Alcoholic drinks are involved in a variety of hypersensitivity reactions. These include flushing syndrome, anaphylactoid reactions (urticaria/angioedema and even shock), as well as the triggering of asthma, food allergy or exercise-induced anaphylaxis in susceptible subjects. In addition, there is increasing evidence that alcohol intake may play a role as a promoter of the development of immunoglobulin-E (IgE)-mediated hypersensitivity to different allergens. It seems clear that alcohol intake (alcohol abuse and even moderate alcohol consumption) is associated with increased total serum IgE levels. Similarly, alcohol intake may be associated with allergic (IgE-mediated) sensitization to environmental allergens. The clinical significance of these facts is probably moderate. The mechanisms by which alcohol can influence IgE responses are not entirely known, but further developments in this area could increase the understanding of both allergic diseases and alcohol-induced alterations in the immune system.
 ...
PMID:Alcohol, IgE and allergy. 1551 13

Carboplatin has established an important role in many different cancers. As its use increased, the documented cases of hypersensitivity also picked up. Although the mechanism of these reactions remains unknown, the immediate type of hypersensitivity reaction mediated by IgE may be involved. It takes a while for the reaction to develop, but cases are reported even after 1st cycle. The incidence of hypersensitivity is highest at about 8th cycle of therapy with decline after that. These reactions themselves ranged from facial flushing or itching to seizures, dyspnea, and anaphylaxis. Many physicians currently do not use skin testing prior to 8th cycle of carboplatin therapy and retreat their patients with carboplatin after the first hypersensitivity reaction. Therefore, it is suggested that skin test should be conducted prior to the 8th cycle, preferably before the 6th cycle, as hypersensitivity tends to increase on the 6th cycle-treatment. Methods published so far involve: desensitization, skin testing, switching therapy to another platinum analogue, and premedication. Despite all the process, the most effective drug toxicity prevention method remains skin testing prior to 8th cycle. It can accurately predict patients who will develop hypersensitivity reactions. Other methods so far have not shown consistent results.
 ...
PMID:Carboplatin hypersensitivity. 1617 60

Mastocytosis refers to a rare collection of disorders, both cutaneous and systemic, that are characterized by increased numbers of mast cells. Depending on the extent of the disease, these disorders may present with symptoms resulting from mast cell degranulation including flushing, diarrhea, vomiting, cramping, syncope, or anaphylaxis. In pediatric patients, cutaneous involvement is most prevalent in the form of urticaria pigmentosa, which is typically asymptomatic or minimally so with resolution by adolescence. In this case report and review of literature, we review a case of a 3-year-old child with uritcaria pigmentosa displaying recurrent syncope and anaphylaxis as the first presentation of systemic mastocytosis. We found data to be limited on this topic, and concluded that pediatric patients with prior diagnoses of cutaneous mastocytosis could benefit from either more aggressive screening for systemic disease or prophylactic treatment with antihistamines and rescue subcutaneous epinephrine.
 ...
PMID:Recurrent syncope and anaphylaxis as presentation of systemic mastocytosis in a pediatric patient: case report and literature review. 1663 42

A 21-year-old man, who had suddenly developed dyspnea with sneeze, cough and nasal congestion following supper, was admitted to our hospital because of hypoxemia and hypercapnia. Physical examination revealed wheezing in all lung fields and skin flushing. He took home-made Okonomi-yaki made from flour, which had been opened few months ago, and then had been remained uncooked at room temperature. Skin prick tests showed positive for problem flour and mite, but negative for just opened control flour. Collectively, we gave his diagnosis of anaphylaxis caused by mite-contaminated Okonomi-yaki.
 ...
PMID:[A case of anaphlaxis caused by mite-contaminated Okonomi-yaki]. 1688 95

A 60-year-old man suffered from inoperable recurrent undifferentiated thyroid cancer and was scheduled to undergo chemotherapy. He had no known allergy to medications. In the first regimen, he was given IV granisetron and betamethasone before IV 120 mg paclitaxel was administered. Five minutes after the paclitaxel infusion, he developed anaphylactic shock of hypotension, dyspnea, and flushing. He was treated by steroid and recovered. In the second regimen one week later, he was scheduled to be treated by other antineoplastic medication instead of paclitaxel for fear of anaphylaxis. Prechemotherapy the same as the first regimen, granisetron and betamethasone, were given,but he developed the same anaphylaxis before the antineoplastic medication was given. He was thus thought to develop anaphylaxis due to the granisetron itself. Anaphylaxis caused by granisetron has not yet been reported, and this experience prompted us to report this case.
 ...
PMID:[A case of anaphylactic shock caused by granisetron]. 1787 60

All chemotherapy agents can cause hypersensitivity reactions, which have limited the used of critical drugs in very sick patients for fear of inducing a more severe reaction and possibly death. The choice of an alternative chemotherapy regimen is often limited by tumor sensitivity and, because of the increasing number of cancer survivors, exposure to multiple courses of the same or similar chemotherapy agents. Increased exposures lead to sensitization and to hypersensitivity reactions in an increasing patient population. The need to offer first line therapy after cancer recurrence has spurred the clinical development of rapid desensitizations, which allow patients to be treated with medications to which they have presented hypersensitivity reactions. Desensitization protocols are available to treat hypersensitivity reactions to most chemotherapy agents including taxenes, platinums, doxorubicin, monoclonal antibodies and others, by gradual re-introduction of small amounts of drug antigens up to full therapeutic doses. Candidate patients include those who present mild to severe type I hypersensitivity, mast cell/IgE dependent, reactions during the chemotherapy infusion or shortly after. Symptoms include pruritus, flushing, urticaria, angioedema, respiratory and gastrointestinal distress, changes in blood pressure including hypotension, and shock with anaphylaxis. Associated musculoskeletal symptoms and pain can be present in patients reacting to taxenes as in anaphylactoid reactions, in which mast cell/IgE mechanisms cannot be demonstrated. There is now strong evidence that anaphylactoid reactions are amendable to treatment with the same rapid desensitization protocols as for type I hypersensitivity reactions. Initial rapid desensitizations should only be performed in settings with one on one nurse-patient care and where resuscitation personnel and resources are readily available. Temporary tolerization is achieved in a few hours. After the first desensitization, standard protocols are available for safe, repeated desensitizations in outpatient settings with similar conditions, which not only provides flexibility, but allows patients to remain in clinical studies. Breakthrough symptoms are less severe than the initial hypersensitivity reaction in all series reviewed, and deaths have not been reported. The aim of this review is to familiarize the medical community with the type of hypersensitivity reactions amendable to rapid desensitization and to review protocols for chemotherapy desensitization that can be used for most chemotherapy agents. Few studies have measured the cancer response to the chemotherapy agents delivered through rapid desensitizations. One patient population in which 26 patients were desensitized to carboplatin and 16 to paclitaxel had similar rates of remission as for non-desensitized patients. Education of nurses, pharmacists, oncology and allergy specialists will lead to the universal use of rapid desensitization protocols for all cancer patients with hypersensitivity reactions to chemotherapy agents. Basic research is needed to uncover the cellular and molecular mechanisms underlying the temporary tolerization induced by rapid desensitization, so that pharmacological interventions can improve its safety and efficacy.
 ...
PMID:Rapid desensitization of hypersensitivity reactions to chemotherapy agents. 1869 Sep 34

Mastocytosis denotes a wide range of disorders characterized by having abnormal growth and accumulation of mast cells. Mast cells contain histamine and other inflammatory mediators, which have diverse actions within the body, and play crucial roles in acquired and innate immunity. The diverse actions of these inflammatory mediators can lead to puzzling symptoms in individuals with mastocytosis. These symptoms can include flushing, pruritus, nausea, vomiting, abdominal pain, diarrhea, vascular instability, and headache. These clinical features generally divide into cutaneous and systemic manifestations, giving rise to the two divisions of mastocytosis: cutaneous mastocytosis (CM) and systemic mastocytosis. CM has a highly favorable clinical prognosis. Systemic mastocytosis has a range of severity, with the milder forms often remaining chronic conditions, while the severe forms have rapid complex courses with poor prognoses. Generally, treatment is aimed at avoiding mast cell degranulation, inhibiting the actions of the constitutive mediators released by mast cells and, in severe cases, cytoreductive and polychemotherapeutic agents. Behavioral intervention includes avoidance of triggers, such as heat, cold, pressure, exercise, sunlight, and strong emotions. Treatment for released histamine and other inflammatory mediators includes H1 antihistamines, H2 antihistamines, proton pump inhibitors, anti-leukotriene agents, and injectible epinephrine (for possible anaphylaxis). For severe cases, treatment includes cytoreductive agents (interferon alpha, glucocorticoids, and cladribine) and polychemotherapeutic agents (daunomycin, etoposide, and 6-mercaptopurine). For very specific and severe cases, tyrosine kinase inhibitors, imatinib and midostaurine, have shown promise.
 ...
PMID:Contemporary challenges in mastocytosis. 1963 28


<< Previous 1 2 3 4 5 Next >>