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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

We report a case of cardiovascular collapse in a homozygous sickle cell patient undergoing elective orthopaedic surgery, following the intravenous administration of cefuroxime. This patient had no known previous drug allergies. She had been taking prophylactic penicillin V on a daily basis, for 10 years and had encountered no problems. She had received cefuroxime on at least four previous occasions, for the treatment of chest infections, with no reported problems. Her serum mast cell tryptase, 1 h after the onset of anaphylaxis, was greater than 200 microg x l(-1) (normal range 10-16). She was skin prick tested, 6 weeks after the event, to all the drugs administered during the course of the anaesthetic and reacted positively only to cefuroxime. Specific IgE levels for penicillin determinants and latex were negative (13 and 0 IU x ml(-1), respectively UniCAP Pharmacia & Upjohn).
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PMID:Anaphylactic shock due to cefuroxime in a patient taking penicillin prophylaxis. 1184 80

A 56-year-old patient was scheduled for coronary artery bypass surgery, because of a severe coronary artery disease. Soon after induction of anaesthesia, he rapidly developed a cardiovascular collapse with bronchospasm and rash. Specific immunoglobulin E and tryptase measurements supported the diagnosis of grade III anaphylactic shock due to rocuronium bromide. A few days later, a general anaesthesia was administered without muscle relaxant and was uneventful.
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PMID:[Anaphylaxis after rocuronium: advantage of blood tests for early diagnosis]. 1196 86

Mast cells accumulate in angiogenesis-dependent situations of lung adenocarcinoma. Human mast cells are divided into two major subsets: MCT (mast cells with immunoreactivity for tryptase but not chymase) and MCTC (reactive for tryptase and chymase). Chymase is an important mediator of tissue remodeling, but research into chymase-containing mast cell subpopulations has been hampered by the lack of reagents suitable for use with formalin-fixed tissue. We stained chymase using CC1 antibody in 66 cases of small sized lung adenocarcinoma as well as CD34 and tryptase. There were significant positive correlations of microvessel counts with MCT-type and MCTC-type mast cell counts in lung adenocarcinomas. When analyzed according to Noguchi's classification, MCT-type and MCTC-type mast cells were significantly increased in Noguchi type-C tumors [localized bronchioloalveolar carcinoma (LBAC) with active fibroblastic proliferation] compared with in Noguchi type-A (LBAC) plus type-B tumors (LBAC with alveolar collapse). Members in the high-count group of MCTC-type but not MCT-type mast cells showed a significantly worse outcome than those in the low-count group in LBACs. Counting chymase-positive (MCTC-type) mast cells in tumor stroma may be a good prognosis predictor for LBACs, especially Noguchi type-C tumors.
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PMID:Chymase-positive mast cells in small sized adenocarcinoma of the lung. 1282 14

Anaphylactic and anaphylactoid reactions during anaesthesia are rare, but potentially life-threatening allergic events. The worst manifestations are cardiovascular collapse, bronchospasm and laryngeal oedema. Anaphylactic and anaphylactoid reactions are clinically indistinguishable. The most incriminated agents are neuromuscular blocking drugs and latex. Treatment consists of instant interruption of contact with possible antigens, 100% oxygen, intubation, adrenaline and volume expansion. The incidence of cross-reactivity between neuromuscular blocking drugs is high. Further investigation of a suspected anaphylactic reaction is mandatory to find the responsible drug and to make future anaesthesia safe. Diagnosis is made with intraoperative tests (serum histamine and mast cell tryptase) and postoperative tests (skin tests and RASTs for specific IgE antibodies).
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PMID:Anaphylaxis during anaesthesia: diagnosis and treatment. 1551

Previous work has shown that endothelial cell (EC)-derived matrix metalloproteinases (MMPs) regulate regression of capillary tubes in vitro in a plasmin- and MMP-1 dependent manner. Here we report that a number of serine proteases can activate MMP-1 and cause capillary tube regression; namely plasma kallikrein, trypsin, neutrophil elastase, cathepsin G, tryptase and chymase. Plasma prekallikrein failed to induce regression without coactivators such as high molecular weight kininogen (HMWK) or coagulation Factor XII. The addition of trypsin, the neutrophil serine proteases (neutrophil elastase and cathepsin G) and the mast cell serine proteases (tryptase and chymase) each caused MMP-1 activation and collagen type I proteolysis, capillary tubular network collapse, regression and EC apoptosis. Capillary tube collapse is accompanied by collagen gel contraction, which is strongly related to the wound contraction that occurs during regression of granulation tissue in vivo. We also report that proMMP-10 protein expression is markedly induced in ECs undergoing capillary tube morphogenesis. Addition of each of the serine proteases described above led to activation of proMMP-10, which also correlated with MMP-1 activation and capillary tube regression. Treatment of ECs with MMP-1 or MMP-10 siRNA markedly delayed capillary tube regression, whereas gelatinase A (MMP-2), gelatinase B (MMP-9) and stromelysin-1 (MMP-3) siRNA-treated cells behaved in a similar manner to controls and regressed normally. Increased expression of MMP-1 or MMP-10 in ECs using recombinant adenoviral delivery markedly accelerated serine protease-induced capillary tube regression. ECs expressing increased levels of MMP-10 activated MMP-1 to a greater degree than control ECs. Thus, MMP-10-induced activation of MMP-1 correlated with tube regression and gel contraction. In summary, our work demonstrates that MMP-1 zymogen activation is mediated by multiple serine proteases and MMP-10, and that these events are central to EC-mediated collagen degradation and capillary tube regression in 3D collagen matrices.
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PMID:MMP-1 activation by serine proteases and MMP-10 induces human capillary tubular network collapse and regression in 3D collagen matrices. 1587 Jan 7

Granzyme K (Gzm K) and granzyme A (GzmA) are the only two tryptases among all the granzymes. Tryptase activity is necessary for cytotoxic T lymphocyte (CTL)/nature killer (NK) cells-mediated cytolysis. Granzyme K might be a potent granzyme to rescue the activity of granzyme A. Granzyme K expresses at high levels in CD56(high) NK cells, memory CD8+ T cells and CD56+ T cells. We recently demonstrated human granzyme K induces rapid cell death with rapid externalization of phosphatidylserine, nuclear morphological changes and single-stranded DNA nicks. Moreover, Granzyme K can induce rapid reactive oxygen species (ROS) generation and collapse of mitochondrial inner membrane potential. Blockade of reactive oxygen species accumulation suppresses granzyme K-induced cell death. However, it is unknown about how reactive oxygen species generate in Granzyme K-mediated apoptosis. Here we found the redox factor-1/apurinic apyrimidinic endonuclease Ape1 can antagonize reactive oxygen species generation. Overexpression of Ape1 inhibits, whereas silencing Ape1 expression potentiates reactive oxygen species accumulation under treatment with oxidative reagents or loading with granzyme K. Ape1 is a physiological substrate of granzyme K. Ape1 cleavage by granzyme K facilitates intracellular reactive oxygen species accumulation and enhances granzyme K-induced cell death.
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PMID:Granzyme K degrades the redox/DNA repair enzyme Ape1 to trigger oxidative stress of target cells leading to cytotoxicity. 1817 23

The true incidence of anaphylactic latex reactions and their associated morbidity and mortality remain poorly defined. It is noteworthy that a number of groups of individuals are at risk for anaphylactic reactions to latex during surgical and medical procedures; one of these groups is represented by the obstetric and gynaecologic population. A case of unrecognized first anaphylactic reaction to latex in a pregnant woman patient who underwent a caesarean section is presented. The diagnosis of latex allergy was missed and the following day the woman underwent a surgical re-exploration complicated by fatal cardiovascular arrest. At post-mortem examination, pulmonary mast cells in the bronchial walls and capillary septa were identified and a great number of degranulating mast cells with tryptase-positive material outside the cells was documented. A post-mortem latex-specific IgE test showed a high titre (14.00 U/I). Latex-induced fatal anaphylactic shock was recorded as the cause of death. This case highlights some of the practical difficulties in the initial diagnosis and subsequent investigation of fatal anaphylactic reaction during anaesthesia. Anaphylaxis is often misdiagnosed because many other pathologic conditions may present identical clinical manifestations, so anaphylactic shock must be differentiated from other causes of circulatory collapse. Although latex allergy usually has a delayed onset after the start of the surgery and most often a slow onset too, it should be always suspected if circulatory collapse and respiratory failure occur during surgery, even if the patient does not belong to a risk group; in the presence of identified risk factors for latex allergy a well-founded suspicion must be stronger, leading to an immediate discontinuation of the potential trigger.
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PMID:Anaphylactic latex reaction during anaesthesia: the silent culprit in a fatal case. 1846 22

Mastocytosis are characterized by an accumulation of abnormal mast cells in various tissues. Their incidence is estimated at 1/150,000 patients. Pure cutaneous mastocytosis which are mainly observed during childhood may resolve spontaneously during adolescence, whereas systemic mastocytosis involving one or more organs or tissues are more observed in adults. The initial event leading to mastocytosis is believed to be related to activating mutations in c-kit receptor, thus resulting in increased proliferation of mast cells precursors, migration in various tissues and degranulation leading to clinical signs. This nosologic entity does not belong to allergic diseases. Their perioperative management involves a multidisciplinary approach. The degranulation of mast cells with subsequent clinical symptoms can be triggered by psychological, chemical, traumatic, physical (rubbing, extreme temperatures...) agents. Avoiding these triggers should be realized whenever possible according to each patient. The premedication has not proven its efficiency. Tryptase measurement is part of the preoperative biological assessment. The clinical signs severity is related to the cardiovascular homeostasis disturbances (arterial hypotension, cardiovascular collapse, cardiac arrest). The cardiovascular symptoms do not correlate to the cutaneous versus systemic description of the disease. The drug of choice for the treatment of the severe cardiovascular signs is epinephrine associated to vascular loading. The aim of this literature review is to suggest the different modalities of perioperative care of patients with mastocytosis.
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PMID:[Mastocytosis and anaesthesia]. 1909 49


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