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PubMed2000

Idiopathic and allergic rhinitis show a similar inflammatory response

HYPOTHESIS: Idiopathic and allergic rhinitics have similar mucosal mast cell and IgE+ cell distribution. INTRODUCTION: The pathophysiology of idiopathic rhinitis (IR) is unknown but patients differ from those with allergic rhinitis (AR) in that they do not express IgE. Our study is novel because we investigated: (1) three study groups chosen prospectively using strict selection criteria over a 4-year period; and (2) mast cell and IgE+ cell counts were on full-thickness, full-length inferior turbinate mucosa. METHODS: Patient groups: allergic (n = 17); idiopathic: (n = 16); and normal controls (n = 9). Immunohistochemistry: mast cell and IgE+ cell detection using anti-mast cell tryptase and anti-IgE antibodies with an avidin-biotin (peroxidase) complex on paraffin processed tissue. Morphometry: sections were divided into three strata comprising an epithelial layer and two submucosal layers. Statistics: Mann-Whitney non-parametric analysis. alpha = 0.05, beta = 0.2. RESULTS: The power of the study was 89%. Mast cells (P = 0.03) and IgE+ cells (P < 0.05) were significantly increased in the epithelium of idiopahtic and allergic rhinitis mucosa compared to the normal control. More IgE+ cells were counted in the AR and IR groups compared to the controls in all three strata. CONCLUSION: Mast cells and IgE+ cells are involved in the pahtophysiology of IR. We propose that IR may be a variant form of AR involving a localized IgE-mediated inflammatory response.

Journal Article↗
PubMed2002

Dexamethasone inhibits maturation, cytokine production and Fc epsilon RI expression of human cord blood-derived mast cells.

BACKGROUND: Mast cells are responsible for eliciting the early phase and for contributing to the development of the late phase of allergic reactions, through the release of cytokines and other inflammatory mediators. OBJECTIVE: To assess whether the glucocorticoid dexamethasone has a direct effect on mast cell progenitor maturation and on mature cord blood-derived mast cell properties. METHODS: Mast cells were obtained by culturing human umbilical cord blood mononuclear cells with stem cell factor, IL-6 and prostaglandin E2. Mast cell numbers were assessed by Toluidine Blue staining and immunocytochemistry of tryptase positive cells. The expression of Fc epsilon RI, CD49d and c-kit was assessed by flow cytometry. Histamine release was determined by a radioenzymatic assay. Cys-LT, GM-CSF and TNF-alpha production and release were determined by ELISA. RESULTS: Dexamethasone (10(-6) M-10(-9) M) time- and dose-dependently inhibited the maturation of the mast cell progenitors. Dexamethasone did not affect the basal expression of Fc epsilon RI, CD49d and c-kit, but it inhibited the IgE-dependent enhanced expression of Fc epsilon RI. Dexamethasone (10(-6) M-10(-9) M) had no significant effect on Fc epsilon RI-dependent histamine release or the synthesis and release of Cys-LT from the mature mast cells. However, pre-incubation of the mast cell cultures with dexamethasone for 1 h, prior to cross-linking of Fc epsilon RI, dose-dependently inhibited the production and secretion of both GM-CSF and TNF-alpha. CONCLUSIONS: From these in vitro data we propose that glucocorticosteroids are effective drugs in the management of allergic inflammation due to their capacity to inhibit mast cell development, IgE-dependent Fc epsilon RI expression and mast cell production of GM-CSF and TNF-alpha.

Administration, Topical↗
PubMed2002

Haptoglobin interacts with the human mast cell line HMC-1 and inhibits its spontaneous proliferation.

Haptoglobin (Hp) is an acute phase reactant produced by hepatocytes. There is evidence for an immunomodulatory potential of Hp, though there is no clear evidence yet about the mechanisms of this action. We have previously shown that Hp interacts with the beta2-integrin CD11b/CD18. In addition, other investigators reported the binding of Hp to B lymphocytes through the CD22 receptor, and to neutrophils through two different receptors. In the present study, we investigated the interaction of haptoglobin with the human mast cell line HMC-1. We report that fluorescein isothiocyanate (FITC)-labelled haptoglobin binds to this cell line and that binding is increased by calcium in a dose- and time-dependent manner. Hp binding sites on HMC-1 were upregulated upon stimulation with phorbol myristate acetate (PMA)/A23187 and after treatment with anti-CD43 and anti-CD44 monoclonal antibodies (MoAbs). HMC-1 cells do not express either CD11b/CD18 or CD22 receptors, indicating that the haptoglobin-binding receptor on this cell line is different from the known receptors. Assessment of cell function showed that Hp inhibits the spontaneous growth of HMC-1 up till 40% at higher Hp concentrations, but it did not exhibit any effect on the expression of CD54 on the release of either tryptase or IL-1ra. In conclusion, haptoglobin binds specifically to human mast cells via a receptor different from CD11b/CD18 and CD22, and may play a role in the modulation of mast cell functions. Exploration of Hp effects in mast cell-dependent diseases such as allergic rhinitis and urticaria seems warranted.

Antigens, CD↗
PubMed2000

Search for evidence of a Th2 profile in HIV+ patients.

BACKGROUND: Hypersensitivity dermatoses are common in human immunodeficiency virus-positive (HIV+) patients, particularly as the disease progresses. Studies have shown that a switch to T-helper 2 (Th2) might represent a turning point in HIV. This study investigated whether increases in the number of skin mast cells, immunoglobulin E (IgE) serum levels, and eosinophilia, involved in the Th2 response in allergic disease, might also be present in HIV+ patients. If so, these alterations might explain one of the mechanisms of skin hypersensitivity in these patients. METHODS: Forty-five skin biopsies from the normal skin of the upper arm of HIV+ patients and 15 controls were included in the study. HIV+ individuals were classified into three equal categories according to their immunologic status: Category I (< 200/microL), Category II (200-499/microL), and Category III (> 500/microL). Anti-tryptase antibody was employed in tissue sections to show mast cells; IgE serum levels and eosinophils in peripheral blood count were investigated; delayed-type hypersensitivity (DTH) skin tests (candidin, trichophytin, and PPD 2U) were evaluated. RESULTS: Normal cutaneous mast cell and eosinophil counts were the same in all categories and in the control group, but increased IgE levels (P < 0. 01) and DTH skin test anergy (P < 0.006) were observed among acquired immunodeficiency syndrome (AIDS) patients. CONCLUSIONS: The density of skin mast cells in HIV infection was not modified in the course of the disease. Mast cells do not seem to be primarily responsible for triggering hypersensitivity dermatoses among AIDS patients, although data in support of the Th2 response, as seen in increased IgE serum levels and DTH anergy, are present.

Adult↗
PubMed2004

Mucosal T-cell phenotypes in persistent atopic and nonatopic rhinitis show an association with mast cells.

BACKGROUND: Allergic rhinitis is characterized by selective expansion of T cell subsets with a CD4+ phenotype. Recently, we identified a subpopulation of nonallergic rhinitis subjects with increased epithelial mast cell and eosinophil populations, suggestive of local mucosal allergy. Previously, T cell subsets have not been characterized in this subselection of nonallergic subjects and furthermore, their relationship to mast cell and basophil effector cells remain unidentified. OBJECTIVE: To determine if a subpopulation of nonallergic subjects with idiopathic rhinitis (IR) have localized allergy confined to their nasal mucosa by comparing the T cell subsets and major histocompatibility complex (MHC) II expressing cells to persistent allergic rhinitis (PAR). Furthermore, the relationship between T cell subsets and mast cells/basophils was investigated. METHODS: None of the symptomatic patients in this study were clinically allergen-challenged. Nasal turbinate mucosa was removed from patients with PAR, IR and normal controls. Morphometry was performed on immunostained sections for T cell subset populations including CD3+, CD4+, CD8+, CD25+, CD45RA+, CD45RO+, human leucocyte antigen (HLA)-DRalpha (MHC class II), mast cell tryptase and for basophils. RESULTS: Subjects with persistent allergic rhinitis differed to normal controls in showing significantly increased numbers of total (CD3+), activated (CD25+) and allergen-naïve (CD45RA+) T lymphocytes in their nasal mucosa (P < 0.025). The naïve CD45RA+ memory T cells correlated to mucosal mast cells in PAR (P = 0.03). IR patients differ to allergic subjects in showing significantly reduced numbers of epithelial HLA-DRalpha+ cells (P = 0.007), but increased numbers of CD8+ lymphocytes (P = 0.02). The CD8+ T cells correlated with mucosal mast cell numbers (P = 0.02). In both rhinitis groups, basophils were present in very low numbers obviating the need for statistical analysis. CONCLUSION: PAR is characterized by increased numbers of CD3+, CD25+ and CD45RA+ T lymphocytes compared with normal mucosa. Allergic and nonallergic rhinitis groups can be separated by significant differences in the number of epithelial antigen presenting cells (APCs) (HLA-DRalpha+) and sub-epithelial activated (CD25+) T cells. Moreover, IR patients do not significantly differ to their allergic counterparts with respect to total (CD3+) and naïve (CD45RA+) T cell numbers, or numbers of epithelial activated (CD25+) lymphocytes. IR subjects show significantly increased numbers of CD8+ lymphocytes compared with control mucosa and although our findings suggest that the initiating inflammatory events may differ, both rhinitis groups show a similarity in pathology involving mucosal mast cells with an association to infiltrating T cells.

Adolescent↗
PubMed2003

Expression, purification and characterization of the second Kunitz-type protease inhibitor domain of the human WFIKKN protein.

Recently we have described a novel secreted protein (the WFIKKN protein) that consists of multiple types of protease inhibitory modules, including two tandem Kunitz-type protease inhibitor-domains. On the basis of its homologies we have suggested that the WFIKKN protein is a multivalent protease inhibitor that may control the action of different proteases. In the present work we have expressed the second Kunitz-type protease inhibitor domain of the human protein WFIKKN in Escherichia coli, purified it by affinity chromatography on trypsin-Sepharose and its structure was characterized by CD spectroscopy. The recombinant protein was found to inhibit trypsin (Ki = 9.6 nm), but chymotrypsin, elastase, plasmin, pancreatic kallikrein, lung tryptase, plasma kallikrein, thrombin, urokinase or tissue plasminogen activator were not inhibited by the recombinant protein even at 1 microm concentration. In view of the marked trypsin-specificity of the inhibitor it is suggested that its physiological target may be trypsin.

Amino Acid Sequence↗
PubMed2001

Mini-plasmin found in the epithelial cells of bronchioles triggers infection by broad-spectrum influenza A viruses and Sendai virus.

Extracellular cleavage of virus envelope fusion glycoproteins by host cellular proteases is a prerequisite for the infectivity of mammalian and nonpathogenic avian influenza viruses, and Sendai virus. Here we report a protease present in the airway that, like tryptase Clara, can process influenza A virus haemagglutinin and Sendai virus envelope fusion glycoprotein. This protease was extracted from the membrane fraction of rat lungs, purified and then identified as a mini-plasmin. Mini-plasmin was distributed predominantly in the epithelial cells of the upward divisions of bronchioles and potentiated the replication of broad-spectrum influenza A viruses and Sendai virus, even that of the plasmin-insensitive influenza A virus strain. In comparison with plasmin, its increased hydrophobicity, leading to its higher local concentrations on membranes, and decreased molecular mass may enable mini-plasmin to gain ready access to the cleavage sites of various haemagglutinins and fusion glycoproteins after expression of these viral proteins on the cell surface. These findings suggest that mini-plasmin in the airway may play a pivotal role in the spread of viruses and their pathogenicity.

Amino Acid Sequence↗
PubMed2001

Mast cells in the rat liver are phenotypically heterogeneous and exhibit features of immaturity.

Gastrointestinal hypersensitivity to food allergens is a significant but relatively poorly understood allergic disease. Recent evidence from a rat model of IgE-mediated gastrointestinal hypersensitivity has suggested that hepatic mast cells (HMC) may play an important role in such reactions. The present study was undertaken to better define their phenotype. Livers from Australian albino Wistar (AaW), Brown Norway (BN) and PVG/c rats were examined using traditional histological techniques and reverse transcription-polymerase chain reaction (RT-PCR). Hepatic mast cells were overwhelmingly Alcian blue positive, sensitive to formalin fixation and predominantly rat mast cell protease (RMCP) 1+/2- (AaW 57%; BN 53%). Such a phenotype has previously been associated with an immature mast cell phenotype. A significant number of HMC also stained RMCP 1-/2+ (AaW 15%; BN 19%) or were RMCP 1+/2+ (AaW 24%; BN 26%). In contrast to previous reports, RT-PCR showed that the liver expressed mRNA of other mast cell proteases, including the chymase RMCP 5 as well as two tryptases, RMCP 6 and RMCP 7. These results suggest that HMC are a heterogeneous population of mast cells with some characteristics previously associated with immature cells.

Animals↗
PubMed2001

Regulation of the inflammatory response in asthma by mast cell products.

In airways, mast cells lie adjacent to nerves, blood vessels and lymphatics, which highlights their pivotal importance in regulating allergic inflammatory processes. In asthma, mast cells are predominantly activated by IgE receptor cross linking. In response to activation, preformed mediators that are stored bound to proteoglycans, for example, TNF-alpha, IL-4, IL-13, histamine, tryptase and chymase, are released. New synthesis of arachidonic acid metabolites (leukotriene C4 (LTC4), leukotriene B4 (LTB4) and prostaglandin D2 (PGD2)) and further cytokines is stimulated. Mediators from degranulating mast cells are critical to the pathology of the asthmatic lung. Mast cell proteases stimulate tissue remodelling, neuropeptide inactivation and enhanced mucus secretion. Histamine stimulates smooth muscle cell contraction, vasodilatation and increased venular permeability and further mucus secretion. Histamine induces IL-16 production by CD8+ cells and airway epithelial cells; IL-16 is an important early chemotactic factor for CD4+ lymphocytes. LTC4, LTB4 and PGD2 affect venular permeability and can regulate the activation of immune cells. The best characterized mast cell cytokine in asthmatic inflammation is TNF-alpha, which induces adhesion molecules on endothelial cells and subsequent transmigration of inflammatory leucocytes. IL-13 is critical to development of allergic asthma, although its mode of action is less clear.

Animals↗
PubMed2002

Anaphylactic shock due to cefuroxime in a patient taking penicillin prophylaxis.

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).

Adolescent↗
PubMed2003

Indolent systemic mast cell disease: immunophenotypic characterization of bone marrow mast cells by flow cytometry.

BACKGROUND: Mast cell disease has a low prevalence and is difficult to diagnose in the absence of the characteristic skin lesions that usually accompany the condition. Extracutaneous involvement is not easy to assess. There are reports in the recent literature on the use of tryptase as a reliable immunohistochemical marker as well as on the study of the immunophenotype of bone marrow mast cells. The latter is of great help for the diagnosis of systemic involvement as, after the skin, the bone marrow is the organ most commonly affected by the disease. OBJECTIVE: We describe two cases of indolent systemic mast cell disease (SMCD) where flow cytometry was used to identify immunophenotypical characteristics of bone marrow mast cells. Recent advances in the application of this technique prove it can be a good diagnostic tool for assessing systemic involvement of the disease. PATIENTS AND METHODS: Two adult subjects with indolent SMCD had multiple clinical symptoms. Cutaneous lesions were the clue to the diagnosis but, subsequently, in the presence of disturbing symptoms, involvement of other organ systems was confirmed. In both cases, the authors used flow cytometry techniques, as described by Escribano et al. (1998) to define the immunophenotype of bone marrow mast cells. RESULTS: Both patients were diagnosed with indolent SMCD with cutaneous and bone marrow involvement. Also, they presented visible clues to the presumptive bone, cardiovascular and nervous system involvement. Gastrointestinal manifestations were documented in one case. CONCLUSIONS: The use of flow cytometry on bone marrow samples from patients with mastocytosis reveals immunophenotypic differences that can serve to allow classification of these subjects in the category of indolent SMCD even though involvement of another organ system may not be thoroughly confirmed.

Aged↗
PubMed2003

Identification of a potential effector function for IgE autoantibodies in the organ-specific autoimmune disease bullous pemphigoid.

Bullous pemphigoid (BP) is an autoimmune skin disease characterized by autoantibodies against the hemidesmosomal protein BP180. In addition to IgG autoantibodies, IgE class autoantibodies have been reported in BP patients. Because animal models utilizing only IgG antibodies do not totally replicate human BP, we examined the specificity and potential relevance of IgE autoantibodies in this disease. Thirty BP patients participated in these studies. Serum IgE was measured and the IgE specificity was determined by immunoblotting. Double labeling Immunofluorescence was performed using combinations of specific antibodies to human mast cell tryptase, IgE and BP180. BP180-stimulated histamine release was measured from basophils of untreated BP patients (n=9), BP patients undergoing immunosuppressive therapy (n=9) and controls (n=16). Elevated IgE levels were found In 70% of untreated BP patients. IgE autoantibodies directed against BP180 were detected in 86% of untreated patients and in all but one of these patients the IgE reacted with the NC16A domain of BP180. IgE-coated mast cells were detected in perilesional skin of the BP patients. Moreover, BP180 peptides were detected on these mast cells. BP180-stimulated histamine release was significantly higher in basophils obtained from untreated BP patients compared with control basophils (p=0.006) or from treated BP patients (p=0.01). These findings support the hypothesis that IgE autoantibodies are involved in the pathogenesis of BP. IgE and IgG BP autoantibodies share the same antigenic specificity. Antigen-specific degranulation of basophils and/or mast cells from BP patients suggests a mechanism by which IgE may contribute to lesion development.

Autoantibodies↗
PubMed2003

Mast cell infiltration and chemokine expression in progressive renal disease.

BACKGROUND: Mast cells are growth factor-rich, bone marrow-derived cells that infiltrate injured tissue where they have been implicated in the pathogenesis of progressive fibrosis. METHODS: Mast cell infiltration and the expression of related chemoattractants was examined following 5/6 nephrectomy, a model of progressive, nonimmune-mediated renal injury. In addition, expression of the profibrotic cytokine, transforming growth factor-beta (TGF-beta) within mast cells and the effects of renoprotective therapy with angiotensin-converting enzyme (ACE) inhibition were also determined. RESULTS: Renal injury was accompanied by mast cell infiltration, in close proximity to areas of tubulointerstitial fibrosis. Mast cells displayed toluidine blue metachromasia and were immunopositive for TGF-beta1 as well as chymase and tryptase. The expression of several mast cell chemokines, including stem cell factor, interleukin-8 (IL-8), and also TGF-beta1, were increased in 5/6 nephrectomized kidneys. ACE inhibition with ramipril led to a reduction in renal injury in association with attenuation of mast cell infiltration and chemokine expression. CONCLUSION: Mast cell infiltration and related chemokine expression are prominent and early features following renal mass reduction and may contribute pathogenetically to progressive renal injury.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Proteinases and proteinase-activated receptor 2: a possible role to promote visceral hyperalgesia in rats.

BACKGROUND & AIMS: PAR-2s are highly expressed throughout the gastrointestinal tract. These receptors are cleaved by trypsin and mast cell tryptase and can be activated by peptides corresponding to the tethered ligand of the receptor (SLIGRL-NH2 for rat). The aim of this study was to determine whether colonic administration of PAR-2 agonists affects visceral sensitivity to rectal distention in conscious rats. METHODS: Abdominal contractions (a criteria of visceral pain) were recorded in rats equipped with intramuscular electrodes. Rectal distention was performed at various times after intracolonic infusion of SLIGRL-NH2 and trypsin. Inflammation parameters and permeability were followed in the colon after the intracolonic injections. Fos expression at a spinal level (L4-L6) was also studied 2 hours after intracolonic injection of SLIGRL-NH2. RESULTS: Rectal distention significantly increased abdominal contractions starting at the RD volume of 0.8 mL. Intracolonic injection of SLIGRL-NH2 (200 microg/rat) and trypsin (200 U/rat), but not vehicle, LRGILS-NH2 (control peptide), boiled trypsin, or SLIGRL-NH2 injected IP, significantly increased (P < 0.05) abdominal contractions for high volumes of distention, 10- and 24-hour postinfusion. SLIGRL-NH2-induced hyperalgesia was inhibited by a NK1 receptor antagonist (SR 140333) but not by indomethacin. Intracolonic injection of SLIGRL-NH2 elevated spinal Fos expression and caused increased intestinal permeability but did not cause detectable inflammation. CONCLUSIONS: Intracolonic infusion of subinflammatory doses of PAR-2 agonists activated spinal afferent neurons and produced a delayed rectal hyperalgesia that involves changes in intestinal permeability and the activation of NK1 receptors. These results identify a possible role for proteinases and PAR-2 in the genesis of visceral hyperalgesia.

Animals↗
PubMed2002

Serine proteases excite myenteric neurons through protease-activated receptors in guinea pig small intestine.

BACKGROUND & AIMS: Serine proteases are postulated to influence gastrointestinal function by stimulating protease-activated receptors (PARs). This study identified the effects on myenteric neurons of activating PARs and investigated underlying mechanisms of action. METHODS: Intracellular electrophysiologic methods were used to study the effects of proteases on electrical and synaptic behavior of morphologically identified neurons in the guinea pig enteric nervous system. Fluorescent immunohistochemistry was used to study the chemical coding of neurons that responded to PARs stimulation. RESULTS: Application of thrombin, trypsin, or mast cell tryptase evoked slowly activating excitatory responses reminiscent of slow synaptic excitation in enteric neurons. Synthetic activating peptides for PAR-1, -2, and -4 receptors mimicked the actions of the proteases. The depolarizing responses evoked by PARs were insensitive to cyclooxygenase inhibitors and were suppressed by agents that inhibit phospholipase C (PLC) or block intraneuronal receptors for inositol triphosphate. A majority of PAR-sensitive uniaxonal neurons expressed immunoreactivity for nitric oxide synthase. Most of the PAR-sensitive AH Dogiel morphologic type II neurons were immunoreactive for calbindin. CONCLUSIONS: Excitatory responses to the serine proteases are mediated by PAR-1, -2, and -4 receptors. The mechanism of signal transduction involves stimulation of PLC and intraneuronal calcium mobilization and is independent of prostanoid formation.

Animals↗
PubMed2000

Reduction of pulmonary mast cells in areas of acute inflammation in calves with Mannheimia (Pasteurella) haemolytica pneumonia.

Mast cells in the left cranial pulmonary lobe of colostrum-deprived neonatal calves were quantified 2 and 6 h after intrabronchial inoculation with Mannheimia (Pasteurella) haemolytica A1. The mast cells were detected (1) immunohistochemically with a mouse anti-human mast cell tryptase monoclonal antibody, and (2) by metachromatic staining with low pH toluidine blue. A greater number of mast cells was demonstrated by the second method than by the first. At 6 h after inoculation, but not at 2 h, the number of mast cells was significantly reduced at the site of the main lesions. Treatment of calves with a sialyl Lewis mimetic (TBC1269) did not appreciably affect the results at 6 h.

Acute Disease↗
PubMed2000

Intrahepatic mast cell population correlates with clinical outcome in biliary atresia.

PURPOSE: To determine if mast cells influence the clinical outcome in biliary atresia (BA), the authors examined the intrahepatic mast cell population in BA. METHODS: Mast cells were identified histochemically using Toludin Blue and immunohistochemically using antimast cell tryptase antibody in formalin-fixed paraffin-embedded sections from 21 cases of BA. Patients were divided into 3 groups; group I (n = 8) with good liver function, group II (n = 8) with moderate liver dysfunction, and group III (n = 5) with severe liver dysfunction. Liver biopsies from patients with choledochal cysts (CDC, n = 5), and normal liver (NL, n = 4) served as controls. The results were compared among the groups. RESULTS: Both histochemical and immunohistochemical methods showed similar data. Mast cells were seen mostly in the portal tracts. Mast cell numbers per medium power field (20 x magnification) were higher in BA than in the controls (15. 03 +/- 2.25 v 3.85 +/-.65, [mean +/- SEM], P <.05, BA v CDC; 15.03 +/- 2.25 v 1.73 +/-.06, [mean +/- SEM], P <.05, BA v NL, immunohistochemical data). Clinical correlation showed an association between higher mast cell number and liver dysfunction (32.62 +/-.80 v 8.52 +/-.87 [mean +/- SEM], group III v group I; P <. 05, immunohistochemical data). CONCLUSION: Increased mast cell population in BA adversely affects liver function and raises the possibility that type I allergic reaction may play role in the pathology of BA.

Biliary Atresia↗
PubMed2001

Angio-oedema following rectal diclofenac after caesarean section.

We report a case of an acute allergic reaction to rectal diclofenac following elective caesarean section in a patient taking ibuprofen. The reaction presented as severe angio-oedema affecting the face and tongue. Serial blood samples failed to show the rise in tryptase levels characteristic of an anaphylactic or anaphylactoid reaction. Diclofenac is widely used for postoperative pain relief in women undergoing caesarean section. To our knowledge this is the first time that an adverse reaction to diclofenac given via this route has been reported in an obstetric patient.

Journal Article↗

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