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)

The hypothesis that deficiencies of plasma protease inhibitors might play a role in the pathogenesis of chronic urticaria was evaluated. Plasma levels were measured in patients with urticaria and a matched control group for alpha1-antitrypsin, alpha2-macroglobulin, total trypsin-inhibiting capacity, kallikrein-inhibiting capacity, and the complement factors C1 esterase inhibitor, C3, and C4. A total of 92 patients with chronic urticaria or more than three months' duration was studied. Patients with acquired cold urticaria had significantly decreased levels of alpha1-antitrypsin and total antitrypsin activity. In patients with acquired angioneurotic edema, alpha1-antitrypsin levels and antichymotrypsin activities were lowered, with less significant decreases in anti-trypsin and antikallikrein activities. Levels of C1 esterase inhibitor , C3, and C4 were normal in all groups. There was no correlation between the increased sensitivity to intracutaneously administered kallikrein injection and deficiencies of of protease inhibitors.
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PMID:Protease inhibitors in plasma of patients with chronic urticaria. 6 Sep 15

A survey was made on workers handling powdered drugs in a pharmaceutical factory. In this factory, two kinds of anti-inflammatory enzyme (bromelain and trypsin), one anti-inflammatory agent (flufenamic acid), one antispasmodic (flopropion) and two kinds of antibiotics (ampicillin and cephalexin) are mainly produced. Twenty four workers were examined by interviews and checked by Cornell Medical Index, and 18 of them complained of respiratory symptoms. These 18 workers were physically examined by skin scratch tests, pulmonary function tests and serum immunological tests. Among 24 workers, 9 handled powdered drugs (A group), 5 handled the same in the past and had already been transferred to other sections for their symptoms (B group), 3 engaged in the process of capsul-filling (C group) and 7 handled several times occasionally during one year (D group). Their average months spent in handling powdered drugs were, in the case of anti-inflammatory enzyme, A group 53.2, B group 66.2, and in the case of antibiotics, 5 workers in A group 24.0, 2 workers in B group 7.0, 3 workers in C group 25.7. Twenty workers complained of symptoms which were mainly irritation of mucosa including the respiratory system and itching of the skin while they were working, and accelerated nasal discharge, urticaria and asthma after working. Group A and group B were higher than group D in the rate of respiratory complaints in C.M.I. (p less than 0.001). Fourteen workers pointed out anti-inflammatory enzyme as a cause of main symptoms, 7 workers flufenamic acid, 3 workers flopropion, 4 workers antibiotics. Three workers who had past history of asthma or articular rheumatism had been transferred to other sections. Of 18 workers who were physically examined, 11 workers showed positive reactions to skin scratch tests with handling drugs. On 8 workers of them, some kinds of drugs which were pointed out as drugs causing main symptoms reacted positively. Numbers of workers with increased immunoglobin values were, IgE 3, IgM 2, IgA 4, IgM 2. Two workers showed decreased FVC and FEV (1.0 sec.) values in pulmonary function tests. The causes of the occupational allergic reaction in this factory are guessed as follows: 1) control of powdered materials was incomplete in the process of production, 2) various kinds of sensitizing drugs were handled by the same workers.
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PMID:[Some experiments on the allergic reaction among workers in a pharmaceutical factory (author's transl)]. 16 Apr 71

During the year 1974, 111 patients with urticaria were studied in the Department of Dermatology, of the Saint Paul's Hospital (Autonomous University of Barcelona). Among those, 77 had chronic urticaria, of which 22 a had low blood iron values. After iron treatment the urticaria improved or was cured in some of these patients. The remaining cases in which the cause of their hives was unknown were followed for one year. Some systemic causatives for their urticaria may appear on longer follow-up. At the same time, blood levels of salicylates trypsin and alpha-chymotrypsin were checked in 14 patients, with the object of a possible relationship concerning the persistence of the urticaria.
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PMID:[Chronic urticaria and serum iron]. 124 Oct 79

Exercise is a physical cause of allergic reactions, including exercise-induced anaphylaxis (EIAna), exercise-induced urticaria (EIU), exercise-induced asthma (EIA), and exercise-induced rhinitis (EIR). Since its first description in 1979, EIAna has been reported with variable clinical manifestations, with exercise alone, and in combination with food ingestion. Elevated serum histamine levels and cutaneous mast cell degranulation have been noted. Exercise-induced urticaria appears as small, punctate lesions that differ from the classic coalescent type seen with EIAna. Variant forms of EIAna with cholinergic urticarial lesions manifesting systemic collapse and/or respiratory distress have been studied. Exercise-induced urticaria and cold-induced urticaria may cause elevated plasma histamine levels coincident with the onset of pruritus and hives. Theories accounting for EIA include respiratory heat loss, water loss, and mast cell activation. Although some studies have shown increased plasma histamine with EIA, others have not. Recently, bronchoalveolar lavage in atopic subjects with EIA has been evaluated preexercise and postexercise, with no significant differences in histamine or tryptase, suggesting a pathogenesis of EIA independent of the mast cell. Exercise-induced rhinitis, with varying degrees of rhinorrhea, congestion, and sneezing, has been increasingly recognized in athletes who run, cycle, and ski. Cold-air-induced rhinorrhea in laboratory challenges displays a mediator release pattern similar to that produced by allergen-induced nasal challenges. Therapeutically, H1 antihistamines are recommended for EIAna both as pretreatment and acute therapy. H1 antihistamines may be helpful in EIU, but are recommended for EIAna both as pretreatment and acute therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise-induced allergies: the role of histamine release. 137 Oct 41

Mast cells are the primary effector cell type in urticaria and angioedema. Recognition of different types of mast cells has increased the understanding of their cell biology and may help refine the therapy of human allergic diseases. Mast cells containing chymase and tryptase (MCTC) and tryptase alone (MCT) are two distinct types distinguished on the basis of the neutral protease composition of their granules. MCT cells are distributed primarily in the lung and gastrointestinal mucosa, whereas MCTC cells lie primarily in skin and gastrointestinal submucosa. The appearance of MCT cells in intestinal tissue is T-lymphocyte dependent, whereas MCTC cells is not. The granules in unstimulated mature MCT cells typically contain complete scrolls, whereas those of MCTC cells often contain grating or lattice substructures. Major categories for the mediators of mast cells include performed mediators present in the secretory granule, newly generated lipid-derived mediators, and cytokines.
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PMID:Mast cells and their role in urticaria. 186 92

The levels of tryptase in the suction-blister fluid from patients with chronic urticaria, urticaria pigmentosa, cholinergic urticaria, urticarial dermographism, prurigo of unknown origin, eczema, psoriasis, atopic dermatitis, and from healthy controls were studied. The blister fluid from controls contained up to 15 micrograms/l of tryptase, whereas that from patients with active urticaria contained greater than 50 micrograms/l. This study demonstrates that patients with urticaria have mast cells that readily release tryptase in both the lesional and non-lesional areas of skin.
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PMID:Increased tryptase levels in suction-blister fluid from patients with urticaria. 187 96

This study presents the clinical and laboratory findings of a novel syndrome associated with eosinophilia. Two young women presented with marked eosinophilia, and large, non-tender compressible articular nodules arising from the tenosynovium of extensor tendons, dermatitis, episodic swelling of the hands and/or feet and pain in adjacent muscles and joints. Tissue specimens were examined by routine haematoxylin and eosin staining, immunofluorescent staining for eosinophil granule major basic protein (MBP) and rhodamine-avidin or tryptase staining for mast cells. Plasma levels of MBP and eosinophil-derived neurotoxin (EDN) were quantitated by immunoassay. The first patient presented in 1967 at the age of 20 and had, in addition to nodules and eosinophilia, dermographism, recurrent episcleritis and axillary urticaria. Biopsy of a nodule showed tenosynovitis with necrotizing granulomas, non-specific vasculitis, eosinophils and eosinophil degranulation as shown by extracellular deposition of eosinophil granule MBP. Her symptoms responded to low-dose, alternate-day prednisone and have remained quiescent over the past 15 yr. The second patient presented in 1990 at the age of 28 with generalized pruritic dermatitis for 15 yr, eosinophilia for 2 yr, subcutaneous nodules and non-limiting pain in several joints. Biopsy of a nodule showed chronic mild tenosynovitis, numerous eosinophils and extracellular deposition of MBP. She remains untreated. Serum IgE values and plasma levels of MBP and EDN were elevated in both patients; mast cells were numerous in their synovial tissue. Based on their clinical courses, these patients reveal the existence of a distinctive, relatively benign eosinophilic disorder with good long-term prognosis.
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PMID:Nodules, eosinophilia, rheumatism, dermatitis and swelling (NERDS): a novel eosinophilic disorder. 822 Dec 54

We described a case of anaphylaxis diagnosed by the evaluation of plasma mast cell tryptase and a case of anaphylactoid reaction. In a patient undergoing pulmonary lobectomy, anaphylaxis, showing the elevation of plasma tryptase, was provoked by physiological glue for hemostasis during the operation. During the operation, cardiovascular collapse occurred suddenly, at which time the cause was not diagnosed. After completion of the operation and removal of drapes, diffuse urticaria with wide erythema on the torso and the upper extremity was noticed. Suspecting allergic adverse reaction, plasma tryptase was measured 2h and 5h after the start of the episode, showing 34.6 ng.ml-1 at 2h and 15.3 at 5h. Because these elevations of plasma tryptase indicated degranulation of mast cells, evaluation of the causative drugs was performed 7 weeks after the episode. Physiological glue was confirmed to be causative drug. In another patient for total hysterectomy and bilateral oophorectomy, adverse reaction occurred after completion of the operation and extubation. Increase in plasma histamine concentration to 4.94 ng.ml-1 that could induce systemic reaction was noticed; however, concentrations of plasma tryptase 25 min, 3h and 7h after the episode were not elevated. This finding indicated that the adverse reaction was not based on degranulation of mast cell, and was anaphylactoid reaction provoked by nonspecific histamine-release. In conclusion, measurement of plasma tryptase is a useful method for differential diagnosis of anaphylaxis and anaphylactoid reaction.
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PMID:[Usefulness of measurement of mast cell tryptase for differential diagnosis of anaphylaxis and anaphylactoid reaction]. 852 64

A girl, 5.7 years old, gained tolerance to egg white ingestion in spite of high immunoglobulin E (IgE) antibody titers to egg white but retained contact urticaria against egg white. She developed atopic dermatitis on her face at 2 months of age and showed high IgE antibody titers to egg white and cow's milk. Accidental ingestion of egg products initiated immediate symptoms such as wheezing, urticaria, erythema and edema of the eyelids and conjunctiva three times. These symptoms were confirmed by challenge tests using boiled egg white at 3.9 years of age. She also reacted positively to a 20 min patch test on her volar arm with raw egg white. However, there were no reactions to the oral challenge test by boiled egg and freeze-dried egg white at 5.1 and 5.7 years of age, respectively. This non-responsiveness was confirmed by a double-blind, placebo-controlled food challenge using freeze-dried egg white. Nevertheless, she showed positive reactions to a 20 min patch test with freeze-dried egg white. Her IgE antibody titers to the egg white components including ovomucoid, ovalbumin, ovotransferrin and lysozyme as well as egg white were high from 2.9 to 5.7 years old. Her IgE antibody titers for the ovomucoid fragments digested by pepsin, chymotrypsin and trypsin were not lower than those of positive control subjects. The binding activity of IgE antibody to ovomucoid, however, decreased from 2.9 to 5.6 years as shown by radioallergosorbent test (RAST) inhibition assays. The IgE antibody showed weaker binding activity to pepsin- and chymotrypsin-digested ovomucoid that were filtered through cut-off 10,000 filter at the age of 2.1 and 5.7 years. We speculated that the maturation of secretion of digestive enzymes was involved in the mechanisms of the acquisition of tolerance to egg white ingestion in spite of the persistence of contact urticaria.
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PMID:A case retaining contact urticaria against egg white after gaining tolerance to ingestion. 912 58

We present a 48-year-old patient who complained for 1 year about urticarial reactions which appeared always when he ingested alcoholic beverages. Skin prick tests with ethanol were negative but positive with 10% acetic acid in the patient. Normal controls tested negative with acetic acid. Skin prick tests to common immediate-type allergens were negative. The patient underwent a double-blind, placebo-controlled challenge test. A few minutes after challenge with ethanol but not with placebo, the patient developed erythema and wheals on the chest and the upper arms. The tryptase serum level rose from undetectable (0.1 U/ml) before challenge to 3.8 U/ml after skin lesions had appeared. This case demonstrates that increased tryptase serum levels can help in the diagnosis of ethanol-induced urticaria.
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PMID:Ethanol-induced urticaria: elevated tryptase levels after double-blind, placebo-controlled challenge. 973 72


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